sports medicine Volume 41 Issue 2 February 2011

Sports Med 2011; 41 (2): 91-101 0112-1642/11/0002-0091/$49.95/0

CURRENT OPINION

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The Menstrual Cycle and Anterior Cruciate Ligament Injury Risk Implications of Menstrual Cycle Variability Jason D. Vescovi School of Kinesiology and Health Science, York University, Toronto, Ontario, Canada

Abstract

The menstrual cycle and associated hormonal fluctuations are considered risk factors for non-contact anterior cruciate ligament (ACL) injuries in female athletes. Researchers have used a ‘normal’ 28-day cycle and relied upon menstrual history questionnaires or a biological sample (i.e. blood, saliva) taken on a single day to identify the phase of the menstrual cycle where an ACL tear has occurred. However, evidence from available studies lack adequate consideration of menstrual cycle variability that exists in the general population and neglect to acknowledge the greater prevalence of subtle menstrual disturbances in physically active and athletic women. Inter- and intrawoman menstrual cycle variability is large for total cycle, follicular phase and luteal phase length ranging from 22 to 36, 9 to 23 and 8 to 17 days, respectively (95% CI). More importantly, subtle menstrual disturbances such as anovulation and luteal phase defects are common in athletic women with a high prevalence of cycle-to-cycle variations. To complicate matters further, menstrual history questionnaires inaccurately quantify cycle length compared with prospective monitoring of cycle length, highlighting the need to implement more sophisticated methods for identifying menstrual cycle/phase characteristics. Regardless of variability and/or the presence of subtle menstrual disturbances, women may still have regularly occurring menses, making it extremely difficult to accurately identify the phase of the menstrual cycle where an ACL tear has occurred based on a menstrual history questionnaire or a single biological sample. Therefore, the assumption that normal ovarian endocrine function is synonymous with regularly occurring menses in physically active and athletic women is unjustified. Thus, definitive conclusions are not warranted regarding the association between the menstrual cycle and non-contact ACL injury risk based on currently available data. Future work in this area must incorporate methods to prospectively evaluate and accurately characterize menstrual cycle characteristics if we are to link the hormonal fluctuations of the menstrual cycle to non-contact ACL injury risk.

1. Introduction The menstrual cycle and sex steroid hormones have been implicated as risk factors for the greater

occurrence of non-contact anterior cruciate ligament (ACL) injuries observed in female athletes compared with male athletes[1-7] (for reviews see Hewett et al.[8] and Renstrom et al.[9]). An apparent

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non-random distribution of this particular injury across the menstrual cycle suggests that fluctuations in sex steroid hormones during the menstrual cycle are associated with non-contact ACL tears in female athletes. Some clinical investigators have reported more non-contact ACL injuries around the time of ovulation (i.e. late follicular phase) when there is a sharp rise in the concentration of estradiol, compared with the early follicular and luteal phases of the menstrual cycle;[1-4] however, not all reports support this view and indicate ACL injury risk may be greater around menses when both estrogen and progesterone concentrations are low.[5-7] Additionally, numerous studies have attempted to determine if biomechanical,[10,11] musculoskeletal[12,13] and neuromuscular[10,13] properties vary across the menstrual cycle, but outcomes have been equivocal.[12-23] The challenge with many studies is the methods used to determine phases of the menstrual cycle. Consequently, results from these studies make it difficult to discern the role of the menstrual cycle and sex steroid hormones on ACL injury risk as well as risk factors associated with ACL tears. At the molecular level, sex steroid hormones are considered a possible risk factor because they are involved with the regulation of collagen metabolism. It was reported that the size[24] and structural properties[25,26] of the ACL differ between men and women, suggesting that sex differences in the cellular remodelling process may play an important role in how the ACL resists loading conditions. Furthermore, estrogen receptors have been identified on fibroblasts in human ACLs[27] indicating that estrogen could have a direct regulatory effect on fibroblast function, collagen remodelling and, ultimately, alter the structural, material and mechanical properties of the ACL in vivo. Indeed, Liu et al.[28] demonstrated a doseresponse relationship between 17-b estradiol concentration and a reduction of fibroblast proliferation and collagen synthesis in vitro indicating a direct effect of estrogen on collagen remodelling. Shultz et al.[12,14,15] have demonstrated that knee joint laxity varies across the menstrual cycle and is associated with the absolute concentrations of sex steroid hormones, with their model being more predictive when a time delay was considered. Collectively, these findings indicate that it is ª 2011 Adis Data Information BV. All rights reserved.

plausible there could be (i) an immediate or slightly delayed effect on knee joint laxity[12] and potential ACL injury risk, resulting from the regulation of specific proteins involved with collagen and matrix metabolism subsequent to large absolute changes in sex steroid concentrations across the menstrual cycle;[15] or (ii) a chronic effect on the size, shape and quality of the ligament as a result of the accumulated exposure to sex steroid hormones on ligament remodelling. As a result of the conflicting evidence available for an association between a specific phase or particular hormonal fluctuations during the menstrual cycle and non-contact ACL injury risk, as well as with particular risk factors, a consensus has yet to be reached on these topics.[29] One reason for the disparity in findings is that the methods for determining which phase of the menstrual cycle a female athlete is in at the time of injury have relied on questionnaires used to identify cycle day and/or a biological sample taken from a single day. These methods limit the ability to accurately identify the follicular and luteal phases in physically active and athletic women.[30] Additionally, methodological strategies to account for normal intra-individual menstrual cycle variability and/or menstrual dysfunction have been lacking and preclude any definitive conclusions from being made based on currently available research. While there are implications for the accurate assessment of menstrual status and menstrual cycle phases for investigators seeking to determine physiological, biomechanical, structural or functional difference across the various phases of the menstrual cycle, due to space limitations this article will focus on ACL injury risk. The aim of this article is to provide an overview of menstrual cycle variability in young women and, more importantly, to clearly illustrate that normal ovarian function is not synonymous with regularly occurring menses, especially when working with physically active and athletic women.[31,32] 2. Menstrual Cycle Variability The ‘normal’ length of the menstrual cycle or particular phases of the menstrual cycle have been repeatedly used to standardize study outcomes;[4-6] Sports Med 2011; 41 (2)

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however, there is a substantial body of evidence that illustrates menstrual cycle variability (both intra- and inter-person) is actually the norm.[33-41] Many investigators have reported that the average length of the menstrual cycle is approximately 28 days;[33,34,39,42,43] however, the 95% confidence intervals (CIs) for menstrual cycle length is substantially large. For example, Fehring et al.[34] reported that in 165 women between 21 to 44 years of age, the 95% CI for cycle length was 22–36 days. More recently, Cole et al.[33] demonstrated that in 167 women aged 18–36 years, the 95% CI for cycle length was 23–32 days. In addition to inter-woman cycle variability, intrawoman cycle variability is also an important consideration when attempting to identify phases for a particular cycle. Cycle-to-cycle variability is >7 days, but <14 days in 42–46% of women aged 18–44 years.[34,39] What’s more, Creinin et al.[39] reported that from a sample of 130 women who prospectively recorded menstrual cycle length, one in five had cycle-to-cycle variability of 14 days or more. Because of the large inter-woman variability, and considering nearly half of the women aged 18–44 years demonstrate cycle variability of more than 1 week, it would seem prudent for researchers to avoid the assumptions that (i) all women have 28-day cycles; and (ii) any one woman will have consistent cycle lengths. A possible limitation of the studies examining cycle and phase length is the applicability of outcomes from women older than the ACL injury at-risk age group (i.e. 15–25 years). However, notable changes in cycle length primarily occur in the 1–3 years prior to menopause,[44] and this window of transition is unlikely to happen before the age of 44 years[45] (highest age of participant from Fehring et al.[34]). Therefore, these data should accurately represent menstrual cycle variability within the targeted atrisk age range. In addition to total cycle length variability, follicular and luteal length variability has also been reported in the literature.[33,34,46,47] Fehring et al.[34] had 165 premenopausal women use a commercially available electronic fertility monitor to characterize 1060 menstrual cycles, and demonstrated the average follicular and luteal phase lengths were 16.5 – 3.4 days and 12.4 – 2.0 days; ª 2011 Adis Data Information BV. All rights reserved.

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however, the 95% CI for each phase was 9–23 days and 8–17 days, respectively. Cole et al.[33] used daily urine samples collected over three to eight menstrual cycles to determine cycle phase characteristics, which was based on the timing of the luteinizing hormone (LH) peak and reported mean follicular and luteal phase lengths of 14.7 – 2.4 days and 13.2 – 2.0 days, and 95% CI for each menstrual cycle phase of 10–20 days and 9–17 days, respectively. Accordingly, when classifying cycle phase for an injured athlete, a greater understanding of cycle phase dynamics is needed. Yet, this aspect of menstrual cycle variability largely goes overlooked and any deviation from the ‘normal’ 28-day cycle has been presumed to be reflective of a change in follicular phase length with no impact on luteal length[4,48] or simply ignored.[2,3] In contrast to this view, figure 1 displays the results from a woman who prospectively collected daily urine samples for eight consecutive menstrual cycles.[33] Total cycle length varied from 25 to 29 days, and follicular and luteal length ranged from 10 to 17 days and 11 to 17 days, respectively. More notable, is that four of the eight cycles have a total length of 27 days, yet the follicular length and luteal length ranged from 10 to 15 days and 12 to 17 days, respectively, indicating that even when multiple cycles from the same individual are identical in total cycle length, both follicular and luteal phase length can vary considerably. Taken together with reports on total cycle length variability these data highlight that cycle phase variability should be a major consideration for investigators interested in determining the relationship between the menstrual cycle and non-contact ACL injuries. To compound the issue of variability and increase the potential of cycle phase misclassification is the use of retrospective menstrual cycle questionnaires to quantify cycle history as well as to determine which phase of the cycle an injury occurred based on the timing of previous menses. Self-reported menstrual history is not sufficiently accurate for verifying current cycle length,[39,42,43] with prospective cycles being longer compared with historical estimates.[42,43] When reporting retrospective cycles, women tend to cluster around 28 days or 30 days and although 39% of women Sports Med 2011; 41 (2)

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Consecutive menstrual cycles

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Days since start of last menstrual period Fig. 1. Cycle length and luteinizing hormone peak (arrow) of eight consecutive menstrual cycles from a single participant determined from the analysis of daily urine samples (reprinted from Fertility and Sterility, 91(2), Cole LA et al. The normal variabilities of the menstrual cycle, 525, 2009, with permission from Elsevier).

reported having 28-day cycles, only 12% actually did.[43] Additionally, Small and colleagues[43] demonstrated that 68% of retrospective cycles from 398 women were different compared with prospectively monitored cycle length by up to 3 days, and Steiner et al.[42] indicated that approximately half of the cycles from 195 women had a difference between actual (prospective) length and selfreported historical estimates of up to 7 days. When women were categorized into groups based on selfreported total cycle length (i.e. <26 days, 26–35 days or >35 days), one in five were misclassified.[43] To demonstrate how the use of menstrual questionnaires in combination with cycle length and phase length variability can result in misclassification of cycle phase or misrepresent the expected hormonal milieu at the particular time of an injury, three menstrual cycles from a hypothetical eumenorrheic ovulatory woman are displayed in figure 2. These cycles differ in total cycle length, but are characterized with the same hormonal profile and temporal characteristics around ovulation. Figure 2a is a classic hormonal profile of a ‘normal’ 28-day ovulatory menstrual cycle – the estrogen peak occurs on day 12 (solid arrow), an LH peak occurs approximately 24 hours later on day 13 (dashed arrow)[49] and ovulation occurs within 36 hours after the LH peak on day 14–15 (shaded area).[49,50] Therefore, if on the day ª 2011 Adis Data Information BV. All rights reserved.

of an ACL tear a female athlete indicated that her previous menses began 14 days ago, it would be concluded that she was injured around the time of ovulation (i.e. late follicular phase) just following the peak concentration of estradiol. Figures 2b and c show the same sex steroid profile; however, there is a change in total cycle length, which will consequently alter the phase of the cycle that a woman is in at the time of injury if her menses began 14 days earlier. If an individual has a short 22-day cycle (figure 2b) then she would be in the early luteal phase (with high concentrations of both sex steroid hormones); however, a longer 35-day cycle (figure 2c) would place a female athlete in the late follicular phase (with low concentrations of both sex steroid hormones). This simple illustration demonstrates the complexity associated with determining if a particular phase of the menstrual cycle or hormonal milieu is related to non-contact ACL injuries in female athletes simply by utilizing a menstrual cycle questionnaire. In truth, only if an ovulatory woman experienced a non-contact ACL tear within the first 5–6 days of menses could we be relatively sure the injury occurred in the early follicular phase. This example was based on hypothetical cycles with identical estrogen and progesterone profiles. However, even eumenorrheic, ovulatory women with regularly occurring menses are likely to have Sports Med 2011; 41 (2)

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Day Fig. 2. Three menstrual cycles from a hypothetical eumenorrheic ovulatory woman with matching sex steroid hormone profiles around ovulation, but consisting of varying total cycle lengths. (a) 28-Day cycle; (b) 22-day cycle; (c) 35-day cycle. Solid arrow indicates estradiol peak; dashed arrow indicates luteinizing hormone peak; shaded area indicates ovulation.

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Sports Med 2011; 41 (2)

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hormone profiles that differ from cycle to cycle. This will further increase the difficulty for investigators to assess sex steroid hormones at the time of an injury and presume that those concentrations accurately reflect previous or subsequent cycles. Michaud et al.[51] and Missmer et al.[52] reported similar group mean concentrations for single samples of estradiol (follicular and luteal) and progesterone (luteal) taken from two cycles in a group of women from the Nurses’ Health Study II cohort. However, the intraclass correlation coefficients (ICC) for estrogen (follicular r = 0.38–0.53 and luteal r = 0.19–0.45) and progesterone (luteal r = 0.29–0.54) were low to moderate suggesting that within-person variability of these hormone concentrations vary widely from one cycle to the next. Similar to these studies, Shultz et al.[53] reported moderate ICC values for nadir and peak concentrations of estradiol (r = 0.56–0.58) and progesterone (r = 0.44–0.67) in a group of ovulatory and anovulatory premenopausal women. Interestingly, when the anovulatory cycles were removed from the analysis, the ICC values were reduced slightly indicating that considerable cycleto-cycle variations in sex steroid hormone concentrations exist even in ovulatory women. Only when mean concentrations were compared from samples taken over several days in the follicular and luteal phases did ICC values improve for estradiol (r = 0.81–0.83) and progesterone (r = 0.54–0.90). This strategy of sampling may help improve reliability, although 11 participants were determined to have one or two anovulatory cycles and another three were excluded prior to analysis as a result of negative ovulation detection tests. Taken together, these findings highlight the difficulty with quantifying the hormonal milieu of premenopausal women and, as will be discussed in section 3, physically active women are likely to have cycleto-cycle inconsistencies in hormonal and cycle phase characteristics that must be considered. 3. Menstrual Dysfunction in Physically Active Women Thus far, menstrual cycle variability has been described for the general population and while these characteristics are present in physically acª 2011 Adis Data Information BV. All rights reserved.

tive women, there is an additional challenge to consider when attempting to identify menstrual cycle phases within this particular population, namely, the greater prevalence of menstrual dysfunction.[54-58] In particular, subtle menstrual disturbances such as anovulation and luteal phase defects (LPD) are associated with exercise[59-63] and are prevalent in 12–29% and 48%[61,62,64,65] of cycles, respectively, in physically active women. More importantly, anovulatory and LPD cycles have altered sex steroid hormone profiles (see figures 3a and b) and/or cycle phase length (i.e. LPD luteal phase £10 days) compared with ovulatory cycles with normal follicular development and luteal function.[59,61,64] Unlike overt menstrual dysfunction (i.e. amenorrhea and oligomenorrhea), which is easily identifiable due to the absence of menses or longer than normal cycle lengths (35–90 days), anovulation and LPD are undetectable via menstrual history questionnaires because menstrual bleeding occurs at regular intervals. Therefore, the assumption that a eumenorrheic athlete has normal ovarian endocrine function and typical cycle characteristics is unjustified. Evidence that acute and chronic exercise is associated with or can initiate menstrual disturbances has been available for several decades[63,66] with 42% of physically active women having cycleto-cycle variations to include ovulatory, anovulatory and LPD cycles.[61] In a case report of a female runner, Shangold et al.[66] demonstrated that adding mileage during the second half of the menstrual cycle resulted in lower peak progesterone and estradiol concentrations by ‡50% during the luteal phase. These investigators also reported that weekly mileage was inversely related with luteal phase length (r = –0.81) and that when mileage was £8 km per week, luteal phase length was 13–14 days, but when mileage was ‡56 km per week, short luteal phases (<9 days) were evident, suggestive of the presence of LPD. Winters et al.[32] demonstrated that 40% of trained female runners had anovulatory or LPD cycles, and that urinary estrogen and progesterone concentrations were 24–42% and 22% lower during the follicular phase and luteal phase, respectively, compared with physically active controls. Pirke et al.[64] and Broocks et al.[65] also provided evidence of compromised Sports Med 2011; 41 (2)

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Fig. 3. Hypothetical examples of subtle menstrual disturbances. (a) Luteal phase defects (LPD) cycle that is short (<9 days) and inadequate; (b) 28-day anovulatory cycle. Solid arrow indicates estradiol peak; dashed arrow indicates luteinizing hormone peak; shaded area indicates ovulation.

ovarian function in female athletes with regularly occurring menses as evidenced by suppressed estrogen and progesterone concentrations compared with control participants. More recently, De Souza et al.[61] reported suppressed concentrations of urinary estrogen by 33–39% (mean follicular and luteal phase concentrations) and urinary progesterone by 80% (mean luteal phase concentration) in exercising women with anovulatory cycles. In addition, follicular and luteal phase ª 2011 Adis Data Information BV. All rights reserved.

lengths were approximately 18 and 8 days, respectively, and ovulation was observed as late as day 20 in exercising women with LPD.[61] Collectively, these findings demonstrate that physically active women and female athletes who appear to be eumenorrheic may not have normal sex steroid hormone profiles simply because they have regularly occurring menses.[31] Consequently, it would seem to be extremely difficult to conclude with any certainty which phase of the menstrual cycle Sports Med 2011; 41 (2)

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an athlete is in during the time of an ACL injury from a questionnaire. The sizeable variations in total cycle and individual phase lengths, as well as the unpredictable variation in sex steroid hormone patterns from cycle to cycle in physically active women, likely confounds any corroboration for cycle phase identification with the use of estrogen and/or progesterone concentration from a single day. Wojtys et al.[1] attempted to confirm cycle phase by the assessment of urinary sex steroid concentrations taken within 24 hours after an ACL injury and again within 24 hours of the first day of the following menses. However, a close examination of table 5 (page 185) from these authors,[1] indicates that total estrogen concentration was similar among the follicular, ovulatory and luteal phases, although there is typically a 4- to 7-fold increase from the early follicular phase to peak levels just prior to ovulation in urinary estrogen metabolites.[61,67] The mean progesterone concentration in the study by Wojtys et al.[1] increased by approximately 3- to 4-fold from the follicular to the luteal phase, which is substantially less than the 6- to 7-fold increase in urinary progesterone metabolite concentrations between the same phases observed in ovulatory women,[61,67] although similar to the observed follicular-luteal phase difference in exercising women with LPD.[61] This suggests that subtle menstrual disturbances were present in the sample of women from the Wojtys et al.[1] study or that cycle phase was not appropriately identified. In another investigation examining the relationship between ACL injuries and menstrual cycle phase, Slauterbeck et al.[5] used a single salivary sample taken within 72 hours after an ACL injury to measure estradiol and progesterone concentrations and concluded that a greater number of ACL injuries occurred during days 1–2 of the menstrual cycle (i.e. early follicular phase). However, there is a high amount of interand intra-person variability, as well as small differences noted in salivary estradiol between the follicular and luteal phases.[68,69] There is also a low correlation for single salivary progesterone samples from cycle to cycle,[68] leaving questions as to whether the concentration of sex steroid ª 2011 Adis Data Information BV. All rights reserved.

hormones from a one saliva sample can provide sufficient evidence to adequately determine if ovulation has occurred and subsequently identify cycle phases. Additionally, De Cree et al.[70] demonstrated that salivary progesterone and estrogens increased by 14.8% and 13.9–21.1%, respectively, following a 21 km run in a group of athletic women with menstrual dysfunction, indicating the influence of exercise on salivary hormone concentrations. The results reported by Wojtys et al.[1] and Slauterbeck et al.[5] highlight how difficult it is for investigators to confirm a particular menstrual cycle phase in physically active women based on a single biological sample and suggest that (i) subtle menstrual disturbances were likely to be present in the studies with female athletes; and (ii) the methodology used to identify menstrual cycle phases in athletic women needs improvement. 4. Conclusion In future studies, researchers are strongly encouraged to determine menstrual status (i.e. ovulatory, anovulatory, LPD) prior to and following an ACL rupture, correctly identify menstrual cycle phases (i.e. menses, follicular phase and luteal phase) and to properly quantify hormonal profiles if they are to maximize the likelihood of truly determining if an association exists between ACL injury risk and menstrual cycles in female athletes. This can be accomplished by prospectively collecting frequent biological samples (e.g. blood, urine, saliva), and routinely implementing the use of ovulation detection kits to provide evidence whether ovulation has occurred and to identify the transition into the luteal phase. The author acknowledges that this would be a massive undertaking and would require a multicentre investigation implemented over several years, given that the occurrence of non-contact ACL injuries is unknown and infrequent. The next best strategy would be to take multiple samples over several days at the time an injury occurs and continue monitoring into the subsequent menstrual cycle, tracking when menses happens and using an ovulation detection kit. Investigators should avoid relying solely on questionnaires and the use of cycle days, even when combined with single biological Sports Med 2011; 41 (2)

Menstrual Cycle and ACL Injury Risk

samples, to identify menstrual status or menstrual cycle phase in physically active women, since this methodology does not provide proof of menstrual status, nor does it accurately identify menstrual cycle phases. Admittedly, implementing proper methodologies may prove challenging, but until more appropriate strategies are employed within this area of research, caution is warranted about opinions based on the data currently available.

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Acknowledgements 14.

The author extends his thanks to Dr James R. Slauterbeck for his careful review and suggestions on this article. No funding was provided for the preparation of this article. The author declares no conflicts of interest that are directly relevant to the content of this article.

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and correlation with biomechanical properties. J Orthop Res 2008 Jul; 26 (7): 945-50 Liu SH, al-Shaikh R, Panossian V, et al. Primary immunolocalization of estrogen and progesterone target cells in the human anterior cruciate ligament. J Orthop Res 1996 Jul; 14 (4): 526-33 Liu SH, Al-Shaikh RA, Panossian V, et al. Estrogen affects the cellular metabolism of the anterior cruciate ligament: a potential explanation for female athletic injury. Am J Sports Med 1997 Sep-Oct; 25 (5): 704-9 Griffin LY, Albohm MJ, Arendt EA, et al. Understanding and preventing noncontact anterior cruciate ligament injuries: a review of the Hunt Valley II meeting, January 2005. Am J Sports Med 2006; 34 (9): 1512-32 Vescovi JD. The menstrual cycle and ACL injury risk [letter]. Am J Sports Med 2008; 36 (11): E4-5 Bonen A. Effect of exercise training on reproductive hormones. Int J Sports Med 1984; 5: 195-7 Winters KM, Adams WC, Meredith CN, et al. Bone density and cyclic ovarian function in trained runners and active controls. Med Sci Sports Exerc 1996 Jul; 28 (7): 776-85 Cole LA, Ladner DG, Byrn FW. The normal variabilities of the menstrual cycle. Fertil Steril 2009 Feb; 91 (2): 522-7 Fehring RJ, Schneider M, Raviele K. Variability in the phases of the menstrual cycle. J Obstet Gynecol Neonatal Nurs 2006 May-Jun; 35 (3): 376-84 Vollman RF. The degree of variability of the length of the menstrual cycle in correlation with age of woman. Gynaecologia 1956 Nov; 142 (5): 310-4 Treloar AE, Boynton RE, Behn BG, et al. Variation of the human menstrual cycle through reproductive life. Int J Fertil 1967 Jan-Mar; 12 (1 Pt 2): 77-126 Beach SA. Length and variability of the menstrual cycle [letter]. JAMA 1968 Jun 17; 204 (12): 1148 Chiazze Jr L, Brayer FT, Macisco Jr JJ, et al. The length and variability of the human menstrual cycle. JAMA 1968 Feb 5; 203 (6): 377-80 Creinin MD, Keverline S, Meyn LA. How regular is regular? An analysis of menstrual cycle regularity. Contraception 2004 Oct; 70 (4): 289-92 Harlow SD, Ephross SA. Epidemiology of menstruation and its relevance to women’s health. Epidemiol Rev 1995; 17 (2): 265-86 Lenton EA, Lawrence GF, Coleman RA, et al. Individual variation in gonadotrophin and steroid concentrations and in the lengths of the follicular and luteal phases in women with regular menstrual cycles. Clin Reprod Fertil 1983 Jun; 2 (2): 143-50 Steiner MJ, Hertz-Picciotto I, Taylor D, et al. Retrospective vs. prospective coital frequency and menstrual cycle length in a contraceptive effectiveness trial. Ann Epidemiol 2001 Aug; 11 (6): 428-33 Small CM, Manatunga AK, Marcus M. Validity of selfreported menstrual cycle length. Ann Epidemiol 2007 Mar; 17 (3): 163-70 Ferrell RJ, Simon JA, Pincus SM, et al. The length of perimenopausal menstrual cycles increases later and to a greater degree than previously reported. Fertil Steril 2006 Sep; 86 (3): 619-24

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45. O’Connor KA, Holman DJ, Wood JW. Menstrual cycle variability and the perimenopause. Am J Hum Biol 2001 Jul-Aug; 13 (4): 465-78 46. Lenton EA, Landgren BM, Sexton L. Normal variation in the length of the luteal phase of the menstrual cycle: identification of the short luteal phase. Br J Obstet Gynaecol 1984 Jul; 91 (7): 685-9 47. Lenton EA, Landgren BM, Sexton L, et al. Normal variation in the length of the follicular phase of the menstrual cycle: effect of chronological age. Br J Obstet Gynaecol 1984 Jul; 91 (7): 681-4 48. Ruedl G, Ploner P, Linortner I, et al. Are oral contraceptive use and menstrual cycle phase related to anterior cruciate ligament injury risk in female recreational skiers? Knee Surg Sports Traumatol Arthrosc 2009 Sep; 17 (9): 1065-9 49. Pauerstein CJ, Eddy CA, Croxatto HD, et al. Temporal relationships of estrogen, progesterone, and luteinizing hormone levels to ovulation in women and infrahuman primates. Am J Obstet Gynecol 1978 Apr 15; 130 (8): 876-86 50. Temporal relationships between ovulation and defined changes in the concentration of plasma estradiol-17 beta, luteinizing hormone, follicle-stimulating hormone and progesterone. I: probit analysis. World Health Organization, Task Force on Methods for the Determination of the Fertile Period, Special Programme of Research, Development and Research Training in Human Reproduction. Am J Obstet Gynecol 1980 Oct 15; 138 (4): 383-90 51. Michaud DS, Manson JE, Spiegelman D, et al. Reproducibility of plasma and urinary sex hormone levels in premenopausal women over a one-year period. Cancer Epidemiol Biomarkers Prev 1999 Dec; 8 (12): 1059-64 52. Missmer SA, Spiegelman D, Bertone-Johnson ER, et al. Reproducibility of plasma steroid hormones, prolactin, and insulin-like growth factor levels among premenopausal women over a 2- to 3-year period. Cancer Epidemiol Biomarkers Prev 2006 May; 15 (5): 972-8 53. Shultz SJ, Levine BJ, Wideman L, et al. Some sex hormone profiles are consistent over time in normal menstruating females: implications for sports injury epidemiology. Br J Sports Med. Epub 2009 Oct 23 54. De Souza MJ, Williams NI. Physiological aspects and clinical sequelae of energy deficiency and hypoestrogenism in exercising women. Hum Reprod Update 2004 Sep-Oct; 10 (5): 433-48 55. Torstveit MK, Sundgot-Borgen J. The female athlete triad: are elite athletes at increased risk? Med Sci Sports Exerc 2005; 37 (2): 184-93 56. Beals KA, Manore MM. Disorders of the female athlete triad among collegiate athletes. Int J Sport Nutr Exerc Metab 2002 Sep; 12 (3): 281-93 57. Beals KA, Hill AK. The prevalence of disordered eating, menstrual dysfunction, and low bone mineral density among US collegiate athletes. Int J Sport Nutr Exerc Metab 2006; 16 (1): 1-23 58. Nichols JF, Rauh MJ, Lawson MJ, et al. Prevalence of the female athlete triad syndrome among high school athletes. Arch Pediatr Adolesc Med 2006 Feb; 160 (2): 137-42 59. Beitins IZ, McArthur JW, Turnbull BA, et al. Exercise induces two types of human luteal dysfunction: confirmation by urinary free progesterone. J Clin Endocrinol Metab 1991 Jun; 72 (6): 1350-8

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60. Williams NI, Bullen BA, McArthur JW, et al. Effects of short-term strenuous endurance exercise upon corpus luteum function. Med Sci Sports Exerc 1999 Jul; 31 (7): 949-58 61. De Souza MJ, Miller BE, Loucks AB, et al. High frequency of luteal phase deficiency and anovulation in recreational women runners: blunted elevation in follicle-stimulating hormone observed during luteal-follicular transition. J Clin Endocrinol Metab 1998 Dec; 83 (12): 4220-32 62. McConnell HJ, O’Connor KA, Brindle E, et al. Validity of methods for analyzing urinary steroid data to detect ovulation in athletes. Med Sci Sports Exerc 2002 Nov; 34 (11): 1836-44 63. Bullen BA, Skrinar GS, Beitins IZ, et al. Induction of menstrual disorders by strenuous exercise in untrained women. N Engl J Med 1985 May 23; 312 (21): 1349-53 64. Pirke KM, Schweiger U, Broocks A, et al. Luteinizing hormone and follicle stimulating hormone secretion patterns in female athletes with and without menstrual disturbances. Clin Endocrinol (Oxf) 1990 Sep; 33 (3): 345-53 65. Broocks A, Pirke KM, Schweiger U, et al. Cyclic ovarian function in recreational athletes. J Appl Physiol 1990 May; 68 (5): 2083-6

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66. Shangold M, Freeman R, Thysen B, et al. The relationship between long-distance running, plasma progesterone, and luteal phase length. Fertil Steril 1979 Feb; 31 (2): 130-3 67. Cekan SZ, Beksac MS, Wang E, et al. The prediction and/or detection of ovulation by means of urinary steroid assays. Contraception 1986 Apr; 33 (4): 327-45 68. Gann PH, Giovanazzi S, Van Horn L, et al. Saliva as a medium for investigating intra- and interindividual differences in sex hormone levels in premenopausal women. Cancer Epidemiol Biomarkers Prev 2001 Jan; 10 (1): 59-64 69. Chatterton Jr RT, Mateo ET, Hou N, et al. Characteristics of salivary profiles of oestradiol and progesterone in premenopausal women. J Endocrinol 2005 Jul; 186 (1): 77-84 70. De Cree C, Lewin R, Ostyn M. The monitoring of the menstrual status of female athletes by salivary steroid determination and ultrasonography. Eur J Appl Physiol Occup Physiol 1990; 60 (6): 472-7

Correspondence: Dr Jason D. Vescovi, 4700 Keele Street, School of Kinesiology and Health Science, York University, Toronto, ON M3J 1P3, Canada. E-mail: [email protected]

Sports Med 2011; 41 (2)

REVIEW ARTICLE

Sports Med 2011; 41 (2): 103-123 0112-1642/11/0002-0103/$49.95/0

ª 2011 Adis Data Information BV. All rights reserved.

Two Emerging Concepts for Elite Athletes The Short-Term Effects of Testosterone and Cortisol on the Neuromuscular System and the Dose-Response Training Role of these Endogenous Hormones Blair T. Crewther,1,2,3 Christian Cook,3,4,5 Marco Cardinale,6,7 Robert P. Weatherby 2 and Tim Lowe8 1 The New Zealand Institute for Plant & Food Research Limited, Hamilton, New Zealand 2 Department of Exercise Science and Sport Management, Southern Cross University, Lismore, New South Wales, Australia 3 Hamlyn Centre, Institute of Global Health Innovation, Imperial College, London, UK 4 United Kingdom Sport Council, London, UK 5 Sport, Health and Exercise Science, Bath University, Bath, UK 6 British Olympic Medical Institute, London, UK 7 University College London, Division of Surgical and Interventional Science, London, UK 8 School of Applied Sciences, Bay of Plenty Polytechnic, Tauranga, New Zealand

Contents Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2. Literature Search Methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3. Hormonal Effects on the Neuromuscular System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.1 Long-Term Effects of Exogenous Hormones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.1.1 Muscle Development. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.1.2 Neural Development . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.2 Short-Term Effects of Exogenous Hormones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.2.1 Steroid Receptors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.2.2 Second Messengers and Lipid/Protein Pathways . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.2.3 Behaviour and Cognition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.2.4 Motor System. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.2.5 Muscle Properties . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.2.6 Energy Metabolism. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.3 Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4. Hormonal Contribution to Resistance Training . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.1 Acute Modifications in Endogenous Hormones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.1.1 Workout Design . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.1.2 Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.1.3 Training Status and Type . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.1.4 Genetic Variation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.2 Chronic Modifications in Endogenous Hormones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.2.1 Training Status . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.2.2 Training Type . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.3 Acute and Chronic Modifications in Steroid Receptors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.3.1 Androgen Receptors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

104 104 105 105 106 106 106 106 106 107 107 107 107 108 108 109 109 109 110 110 111 111 111 112 113 113

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5. 6.

4.3.2 Glucocorticoid Receptors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4 Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Limitations and Challenges with Hormonal Research. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Abstract

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The aim of this review is to highlight two emerging concepts for the elite athlete using the resistance-training model: (i) the short-term effects of testosterone (T) and cortisol (C) on the neuromuscular system; and (ii) the doseresponse training role of these endogenous hormones. Exogenous evidence confirms that T and C can regulate long-term changes in muscle growth and performance, especially with resistance training. This evidence also confirms that changes in T or C concentrations can moderate or support neuromuscular performance through various short-term mechanisms (e.g. second messengers, lipid/protein pathways, neuronal activity, behaviour, cognition, motor-system function, muscle properties and energy metabolism). The possibility of dual T and C effects on the neuromuscular system offers a new paradigm for understanding resistance-training performance and adaptations. Endogenous evidence supports the short-term T and C effects on human performance. Several factors (e.g. workout design, nutrition, genetics, training status and type) can acutely modify T and/or C concentrations and thereby potentially influence resistance-training performance and the adaptive outcomes. This novel short-term pathway appears to be more prominent in athletes (vs non-athletes), possibly due to the training of the neuromuscular and endocrine systems. However, the exact contribution of these endogenous hormones to the training process is still unclear. Research also confirms a dose-response training role for basal changes in endogenous T and C, again, especially for elite athletes. Although full proof within the physiological range is lacking, this athlete model reconciles a proposed permissive role for endogenous hormones in untrained individuals. It is also clear that the steroid receptors (cell bound) mediate target tissue effects by adapting to exercise and training, but the response patterns of the membrane-bound receptors remain highly speculative. This information provides a new perspective for examining, interpreting and utilizing T and C within the elite sporting environment. For example, individual hormonal data may be used to better prescribe resistance exercise and training programmes or to assess the trainability of elite athletes. Possible strategies for acutely modifying the hormonal milieu and, thereafter, the performance/training outcomes were also identified (see above). The limitations and challenges associated with the analysis and interpretation of hormonal research in sport (e.g. procedural issues, analytical methods, research design) were another discussion point. Finally, this review highlights the need for more experimental research on humans, in particular athletes, to specifically address the concept of dual steroid effects on the neuromuscular system.

1. Introduction Resistance training provides an effective stimulus for improving the morphological (e.g. musª 2011 Adis Data Information BV. All rights reserved.

cle size) and/or functional (e.g. strength, power) qualities of the neuromuscular system in athletic and non-athletic populations.[1-3] The steroid hormones are recognized as one important mediator Sports Med 2011; 41 (2)

Two Emerging Concepts for Elite Athletes

for these training adaptations. Specifically, the biological effects of testosterone (T) and cortisol (C) help to control long-term changes in muscle growth and subsequent performance, especially with resistance training.[4-6] However, in light of recent advancements in this area, a more complex model may be needed to explain the T and C contribution to resistance-training adaptations. Greater understanding of the steroid hormones, especially through animal research, has led to suggestions that they can also influence neuromuscular function (e.g. behaviour, neuronal activity, intracellular signalling, muscle force) through various rapid or short-term mechanisms (see reviews[7-10]). Therefore, T and C may well contribute to the adaptive responses to training by regulating longterm muscle performance and/or the short-term expression of neuromuscular performance. To date, little research has addressed the concept of dual steroid effects with the second tier being a possible moderator of human movement during normal everyday and sport-specific activities. Debate also exists regarding the permissive (i.e. need to be present) and dose-response (i.e. changes need to occur) training roles of these endogenous hormones. Recent studies on untrained males suggest that physiologically elevated hormones do not enhance muscle size and strength.[11-14] However, elite athletes can differ considerably from lesser trained or untrained individuals in terms of both endocrine and neuromuscular function and development,[15-20] thereby accounting for many of the differences and discrepancies found with regards to the training roles of T and C. The possibility of short-term steroid effects offers a further avenue to explain the observed or expected differences between athletes and non-athletes. This review will highlight two emerging concepts for elite athletes using the resistance-training model: (i) the short-term T and C effects on the neuromuscular system; and (ii) the dose-response training role of these endogenous hormones. Within the athlete model, we will also discriminate between highly trained and trained individuals to emphasize the different hormonal effects and roles. Section 2 outlines the literature search methods. Section 3 uses exogenous evidence to investigate the possibiª 2011 Adis Data Information BV. All rights reserved.

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lity of dual T and C effects on the neuromuscular system, focusing on potential mechanisms, their time course and target tissue. Section 4 uses endogenous evidence to examine how modifications in T and/ or C concentrations may contribute to resistancetraining performance and adaptations. This section also examines the exercise and training responses of the steroid receptors. Section 5 highlights some of the limitations and challenges associated with hormonal research. 2. Literature Search Methods The databases searched were PubMed and Scirus. Literature searches were undertaken using several key words including ‘testosterone’, ‘androgen’, ‘cortisol’, ‘glucocorticoid’, ‘non-genomic’, ‘rapid’, ‘androgen receptors’, ‘glucocorticoid receptors’, ‘neuronal’, ‘nervous system’, ‘behaviour’, ‘brain’, ‘neuromuscular’, ‘muscle’, ‘resistance training’, ‘resistance exercise’, ‘strength training’, ‘adaptation’, ‘power’, ‘strength’, ‘muscle’, ‘athlete’, ‘nutrition’, ‘supplementation’ and ‘males’. Following electronic searches, the reference lists of included studies were screened for additional relevant research. The inclusion criteria for research in section 3 were randomized, placebo-controlled trials (preferably blinded). The inclusion criteria for research in section 4 were less stringent, particularly for those studies involving elite athletes, because of inherent limitations with performing research on athletes and within the elite sporting environment (see section 5). Given the broad nature of this review, other relevant studies and reviews of literature have been included in all sections. 3. Hormonal Effects on the Neuromuscular System Human movement is controlled by the physiological interactions of the CNS (i.e. brain, spinal cord) and the peripheral nervous system (PNS) [i.e. motor unit-neuron and innervated muscle fibres, collectively termed the neuromuscular system].[21] Briefly, during voluntary movement, neural signals from the brain are transmitted down the spinal cord to activate the Sports Med 2011; 41 (2)

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motor neurons and stimulate muscle fibre contractions to produce (and coordinate) muscle force for the expression of human movement during normal everyday and athletic tasks.[21,22] Force development also depends upon other morphological, neurological, metabolic and biomechanical factors.[3,21,22] This section will examine the effects of exogenous T and C on some of these factors. 3.1 Long-Term Effects of Exogenous Hormones 3.1.1 Muscle Development

In animals, the most recognized effect of T[23-29] and C[30-33] lies in the remodelling of skeletal muscle protein, especially the type II muscle fibres.[24,25,28,31-33] The influence of T[34-40] and C[41-44] on protein metabolism and muscle size are also well documented in humans, but the fibrespecific effects are less clear,[36,37,44] probably because of differences in experimental design between animal and human studies (e.g. treatment dose and duration, muscles assessed). Nevertheless, T is considered a primary anabolic hormone, by increasing protein synthesis and decreasing protein degradation, and C the primary catabolic hormone, as it increases protein degradation and decreases protein synthesis.[6,45-47] The net result is an increase, decrease or maintenance in muscle fibre and whole muscle size. The force-generating capacity of muscle is related to its cross-sectional area,[48] so it is generally agreed that T and C contribute to the expression of human performance by regulating longer term (i.e. weeks to months) changes in skeletal muscle size. We do recognize that several other events and pathways (e.g. activation of satellite cells, local growth and mechanical factors, feeding) may contribute to net changes in muscle size, along with other morphological adaptations (e.g. tendon and connective tissue, muscle architecture),[3,45,46] but these will not be addressed in this review. Resistance training provides an effective stimulus for maximizing muscle form and function. For example, the exogenous manipulation of T in males enhanced muscle size and/or performance in a dose-dependent manner,[34-38,40,49] but comª 2011 Adis Data Information BV. All rights reserved.

bining T with resistance training produced greater adaptation than either alone.[50-52] Likewise, suppressing total T and free T attenuated the training gains in muscle size and strength.[53] Exercise and training can also counteract the catabolic effects of total C and free C.[30,31,33,43,44,54] However, the initial (<8 weeks) force changes with training are primarily ascribed to neural adaptation, after which muscle growth predominates.[55-59] Some of this evidence also supports a permissive hormonal role in regulating overall changes in muscle size and strength, which will be addressed in more detail in section 4. 3.1.2 Neural Development

Skeletal muscle growth is not the only outcome influenced by these steroids. The motor neuron exhibits T-sensitive plasticity in terms of soma size,[29,60] dendritic length[60,61] and synaptic input,[62] along with the size[63] and number[64] of motor neurons. Likewise, different C treatments have been shown to influence dendritic growth,[65,66] soma size[66] and the structural and functional characteristics of the neuromuscular junction.[67] Still, it remains to be seen if these neural modifications can occur independently of the contractile proteins and whether or not exercise and training can enhance, or attenuate, the steroid effects. 3.2 Short-Term Effects of Exogenous Hormones 3.2.1 Steroid Receptors

In general, the long-term effects of T and C are mediated by specific receptors (e.g. androgen receptors [AR] and glucocorticoid receptors [GR]) located in the cytosol of target cells, which regulate the transcription of deoxyribonucleic acid.[8,10,68] The identification of steroid receptors on the membrane of cells provides a new viewpoint for understanding the biological effects of steroid hormones.[10] These newly identified receptors include ion channels, neurotransmitters, protein kinases and G-proteins.[10] The exact role of these receptors has yet to be clearly defined, but they are thought to mediate cellular effects that are independent of the cytosol receptors and Sports Med 2011; 41 (2)

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gene transcription, with these effects also occurring on a much shorter timescale.[8,10,68] 3.2.2 Second Messengers and Lipid/Protein Pathways

Steroid binding to membrane receptors can facilitate the rapid (i.e. seconds) activation of many second messenger signals, such as the intracellular release of ions (e.g. Ca2+, adenosine triphosphate [ATP], K+) in different cells,[69-76] with downstream effects on various lipid (e.g. inositol trisphosphate, phosphatidylinositol 3-kinase)[72-74,77] and protein kinase (PK) pathways (e.g. mitogen-activated PK, PKC, PKA).[69,70,74,78,79] These modifications in the cellular environment can subsequently affect neuronal excitation or inhibition within minutes, as seen in different brain regions.[80-84] Ultimately, the hormonal induction of these signals, along with changes in the membrane kinetics of cells, could affect the functioning of neuromuscular tissue/systems to which the cells belong. The following sub-sections will address different aspects of neuromuscular function important to human movement and performance. 3.2.3 Behaviour and Cognition

Studies on animals have demonstrated rapid (i.e. minutes) T- or C-induced modifications in behaviour[85-88] that are likely to originate from alterations in brain neuronal activity. Likewise, in humans, long-term users of anabolic steroids often exhibit behavioural traits (e.g. mood disturbances, aggression) that reflect alterations in central neural activity.[89] Research on humans[90-96] and primates[97,98] also confirms a steroidal role in regulating or supporting different aspects of cognitive function (e.g. memory, decision making, learning). The T or C effects on behaviour and cognition do appear to be more delayed in humans, occurring several hours after initial treatment,[90-96] but this is probably due to methodological reasons (e.g. timing of assessment, treatment type) rather than any inherent delay in the transduction processes influencing the CNS. 3.2.4 Motor System

The motor system is another important steroid target. In one study,[99] the motor-evoked potential of muscle increased after the electrical stimª 2011 Adis Data Information BV. All rights reserved.

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ulation of the motor cortex when salivary free C concentrations were low, but an oral C dose prevented this response. The free C concentrations of subjects also correlated (negatively) to the motor cortex response. Similarly, an increase in total T concentrations, induced by a single injection of human chorionic gonadotropin, decreased the cortical motor threshold in humans[100] and this can also influence muscle activity. These results are partially supported by human studies where exogenous treatments were found to modify the secretory levels of these hormones and muscle performance.[34,35,39,40,44,49-51,53] Together, the hormonal data presented has possible implications for transmitting and processing neural information to and from skeletal muscle, as well as the putative effects on behaviour and cognition. The biological effects of these steroids on the CNS are complex. The brain uptake of T involves various distribution routes including cerebrospinal fluid, diffusion through brain tissue and transport through nerve projections.[101] Experimental data also suggests that T secretion is regulated by a direct neural connection between the brain and testes, via the catecholamines.[102-104] Thus, the dual effects of T may be mediated by two pathways, the ‘slow-release’ hypothalamicpituitary-gonadal axis and a ‘rapid-release’ hypothalamic-gonadal pathway. Even then, the target response may depend on the peripheral conversion of T or C to other metabolites (e.g. estradiol, dehydrotestosterone, tetrahydrocortisol)[105-108] or mediated through other neurotransmitters (e.g. serotonin).[109] To complicate matters, many of the androgens and glucocorticoids influencing behaviour and cognition are themselves synthesized within the CNS.[106,107] 3.2.5 Muscle Properties

Exogenous T and C may contribute to the muscular properties of the PNS by rapidly modulating Ca2+ influx in skeletal muscle cells.[71-74] These findings are important because intracellular Ca2+ not only triggers the muscle contraction, but is also involved in twitch relaxation, energy metabolism and helps to maintain the structural integrity of the muscle fibre.[110] The expression of Ca2+ channels in skeletal muscle are also Sports Med 2011; 41 (2)

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sensitive to T[111] and C[112] treatments. Another mechanism by which steroid hormones may help to regulate muscle contractility is through the acute and chronic modification of NA+-K+ pump activity and content, along with other peptides and growth factors.[113] Animal studies have demonstrated rapid T or C effects on the electrophysiological and contractile properties of muscle (e.g. reflex response, neuromuscular transmission, end plate potential).[114,115] The effects of longer term steroidal treatments on muscle performance have been widely investigated in animals[23,28,116] and humans.[34,35,39,40,44,49-51,53] In humans, the performance gains (or losses) observed were generally proportional to the temporal changes in muscle size, but few studies have examined specific or relative performance to address the prospect of a mass-independent mechanism[44,49] and those that have are with conflicting results. In animals, T manipulation did influence relative forces,[23,28,116] but there was a lack of uniformity across different tests and muscle groups. The lack of experimental research in this area highlights the need for more studies on humans with a specific focus on the dual steroid effects. 3.2.6 Energy Metabolism

The primary role of C as a glucocorticoid is to stimulate gluconeogenesis and glycogenolysis via glycogen, protein and lipid metabolism and through its permissive actions on other hormones (e.g. catecholamines and glucagon).[41,42,47,117,118] Exogenous C can also affect human sympathetic nerve activity within hours,[119,120] which has further consequences for metabolic and cardiovascular function. The metabolic role of T is less clear. T promoted rapid effects on substrate transport and metabolism in cultured myotubes[121] and regulated insulin sensitivity in rats.[122,123] However, no differences in substrate use and endurance performance were found in humans with either low, normal or high total T concentrations.[124] The long-term response to T manipulation is equally unclear with reports of increases, decreases or no changes in various metabolites and substrates involved in the energy-yielding processors.[25-27,125-128] ª 2011 Adis Data Information BV. All rights reserved.

Long-term T administration has been found to improve the fatigue resistance of specific muscles in rats.[24,116] Hence, the metabolic effects of T may only be realized when muscle fatigue occurs and is more localised. In fact, many of the fatigue mechanisms are sensitive to the rapid actions of this androgen, including neural drive to the motor neurons, neuromuscular propagation, excitation coupling, metabolic substrates and the intracellular milieu.[129] However, an exogenous protocol that modified T levels in humans did not affect fatigability.[49] Once again, differences in research design make comparisons difficult and there is a clear need for more experimental studies on humans. Research confirms that T and C can influence neuromuscular performance via one or many mechanisms that can be broadly classified as being either a short-term or long-term effect, thereby potentially contributing to human movement (figure 1). It is also clear that these effects are dose dependent, although a permissive role cannot be dismissed. Other issues remain unresolved, such as whether the opposing long-term steroid actions also apply in the short term, or any interactions thereof. Indeed, the rapid steroid actions may prepare target cells for chronic adaptations and induce early adaptive changes that are opposite to the delayed effects.[8,10] Since the use of exogenous hormones has moral, legal and health implications, another key issue is whether the observed responses can occur under physiological conditions (i.e. endogenous hormones). Whether we can utilize the novel short-term steroid pathway to achieve the best performance outcomes, and practical strategies for doing so, are unknown. 3.3 Summary

Exogenous evidence confirms that T and C can regulate long-term changes in muscle growth and performance, especially with resistance training. This evidence also confirms that changes in T or C concentrations can moderate or support the performance capacity of the neuromuscular system through various short-term mechanisms (e.g. second messengers, lipid/protein pathways, neuronal activity, behaviour, cognition, motor system function, muscle properties and energy metabolism). Sports Med 2011; 41 (2)

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Long-term effects

Tissue/system Protein metabolism Skeletal muscle growth Neural modifications

Short-term effects

Cellular Second messenger signalling Lipid and protein pathways Neuronal activation

Development of the PNS

Tissue/system Behaviour and cognition Motor system function Muscle electrophysiological and contractile properties Energy metabolism

Functioning of the CNS and PNS

Neuromuscular performance (e.g. power, strength, speed, work)

Human performance (e.g. jumping, sprinting, lifting, throwing) Fig. 1. Summary of the dual effects of testosterone and cortisol on the neuromuscular system and the implications for human performance. PNS = peripheral nervous system.

The possibility of dual T and C effects on the neuromuscular system offers a new paradigm for understanding their contribution to resistance-training performance and adaptations. 4. Hormonal Contribution to Resistance Training 4.1 Acute Modifications in Endogenous Hormones 4.1.1 Workout Design

Resistance exercise workouts are prescribed, in part, on the premise that acute elevations in endogenous hormones increase the likelihood of receptor interactions, thereby mediating the longterm adaptive responses.[4,6] For example, hypertrophy workouts produce acute increases in various anabolic (e.g. T, growth hormone, growth factors) and catabolic (e.g. C) hormones to promote protein metabolism and muscle growth during the recovery period.[130-134] Conversely, maximal strength and power workouts typically ª 2011 Adis Data Information BV. All rights reserved.

produce little or no hormonal change,[130-135] so the adaptive changes are generally limited to the neural pathways. This perspective may be too simplistic given the potential for dual steroid effects on the neuromuscular system and human performance outcomes (e.g. power, strength, speed, work), which are major determinants of power and strength adaptation.[136-138] It is possible that acute changes in physiological hormones may offer short-term benefits for training performance and long-term adaptations. Some studies on athletes have used intense exercise as a stimulus to acutely elevate T concentrations and improve power or strength during later exercises.[139,140] However, this approach did not enhance training adaptation in rugby players,[141] partly due to individual variation in the exercise responses. In untrained males,[142] a protocol that combined arm and leg exercises was also used to elevate the anabolic hormones during individual workouts, thereby resulting in greater training gains in arm strength (vs arm only training). Sports Med 2011; 41 (2)

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These findings are limited by differences in baseline strength between training groups[142] and the lack of control data.[140] Recent work on untrained males has found that physiologically elevated hormones do not necessarily enhance protein metabolism, muscle growth or strength.[11-14] Taken in perspective with other exogenous evidence,[34-38,40,49,53] it appears that anabolic hormones may have a permissive effect on improving muscle form and function in untrained males. That is, adaptive changes in muscle size and performance may result from resistance training protocols as long as basal T concentrations are within the physiological range (i.e. T value within this range is less important). However, elite athletes involved in power sports can often express much higher T values,[143-145] so a greater training stimulus may be needed to evoke acute alterations in the hormonal milieu (i.e. dose response) and thereby allow such individuals to achieve further increases in muscle size and performance. 4.1.2 Nutrition

Nutritional adjustments offer another strategy for modifying the hormonal and performance outcomes. One study noted improvements in the power and strength of recreational lifters using a multi-nutrient supplement for 7 days.[146] As a possible mechanism to explain these gains, the total T and free T responses to exercise (along with other anabolic markers) were elevated after supplementation. Further evidence comes from training studies. Carbohydrate and/or protein supplementation has been found effective in acutely elevating T and/or reducing C concentrations during workouts and this appeared to promote greater resistance training gains in body mass, muscle size and performance,[147-149] whilst also attenuating the strength losses that occurred during overreaching.[150] There are still some conflicting reports regarding the efficacy of carbohydrate and/or protein supplementation. These include acute modifications in the workout responses of T and/or C but without any alterations in training performance,[151-153] no hormonal alterations but improved performance[154,155] or no changes in ª 2011 Adis Data Information BV. All rights reserved.

either of these outcomes.[156-158] These inconsistencies could be explained by differences in the supplementation procedures, workout design and the training background of subjects. Nevertheless, the possibility exists for using different strategies (e.g. workout design, nutrition) to acutely modify the hormonal milieu and thereafter, the performance/training outcomes. 4.1.3 Training Status and Type

Resistance training can enhance the T responses and/or reduce the C responses to workouts in previously untrained males,[57,147,159-161] probably as an early-phase adaptation to assist muscle growth. Strength athletes can also produce greater workout changes in T than non-athletes,[16,17] with more experienced weightlifters producing greater T responses than less experienced lifters.[162] Since strength athletes are already highly adapted to the training stimulus, and given their limited ability (and sometimes desire) to induce further muscle growth, these response patterns could represent a longer term adaptation to support workout performance. This idea is supported by correlations between the T and performance responses to exercise in athletes,[17,139,163-166] but a lack of a correlation in non-athletes.[17] The type of training performed is an important consideration. Athletes who often train to induce muscle fatigue (e.g. bodybuilders, 400 m sprint runners) have shown little-to-no changes, or a reduction, in T after exercise bouts.[163,167-169] Likewise, the T and C responses of endurance athletes to resistance exercise were less pronounced than resistance-trained athletes.[16] Similar patterns have been noted during other exercise forms. In response to a 400 m sprint,[167] the total T and free T concentrations of elite runners were lowered despite an increase in luteinizing hormone, which stimulates T production. Conversely, non-elite runners had elevated T, but luteinizing hormone levels did not change. These findings have led to speculation of enhanced T uptake and utilization to attenuate muscle fatigue.[6,163] Literature confirms that acute modifications in these endogenous hormones may have different training roles for highly trained, trained and Sports Med 2011; 41 (2)

Two Emerging Concepts for Elite Athletes

untrained individuals. The different roles may be likened to the morphological and neural contributions to training adaptation, where one predominates during the early phase and another during later phases.[1-3] It is important to note that strength and power athletes also exhibit ideal neuromuscular profiles for promoting the steroid effects, such as greater type II fibre area and a higher percentage of type II fibres (vs untrained individuals).[19,170,171] Thus, the effects of physiological changes in T or C concentrations may be further linked to the recruitment and training of those neuromuscular structures that are more sensitive to these steroids.[24,25,28,31-33] 4.1.4 Genetic Variation

Genetic variation is a major limiting factor in human movement and may account for up to half of the variation in performance between athletes.[172] In male athletes, large individual variation has also been observed in the T and/or C responses to resistance exercise[141,173,174] and other exercise forms.[140,169,174-176] These individual patterns may reflect genetic differences in our ability to respond to, and cope with, different stressors,[169] and this could be important for moderating physiological adaptation to training stress.[169,173,174,176] Therefore, repeated exposure to the stressors of exercise, training and competition may result in steroid responses akin to our genetic makeup. It is important to note other genetic factors (e.g. body and muscle composition, anatomy, physiology, behaviour) as potential moderators of athlete performance and training.[172] A recent study of rugby players addressed the prospect of prescribing training based on individual hormonal response patterns.[177] Four different workouts were compared to determine which would produce the maximal and minimal changes in salivary free T concentrations for each player. Training with the maximal T workouts (irrespective of their design) promoted increases in strength and body mass, whereas training with the minimal T workouts had no effect upon or reduced strength in most players. The prescription of resistance exercise and training programmes based on individual hormonal data is a novel ª 2011 Adis Data Information BV. All rights reserved.

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area for research and should be pursued with adhoc studies with large athletic populations. 4.2 Chronic Modifications in Endogenous Hormones 4.2.1 Training Status

Resting or basal T and C concentrations are thought to represent the current state of muscle tissue and tissue homeostasis.[4,5] Modifications in basal T and/or C concentrations with resistance training are generally non-existent in untrained males.[14,15,57,142,147,149,161,178-180] There have been some reports of basal alterations in these hormones in studies on untrained males,[55,159,160,181] but these changes still tended to occur during the later training stages. In all of these studies, the relative improvements in performance were found to be much greater, and occurred much earlier, than any changes in body and/or muscle size. These data support the notion that the initial performance gains with training are largely due to neural adaptations, although endogenous T and C may still play a permissive role in this process. Resistance training can modify the basal T and/ or C concentrations of trained males.[15,150,182-194] This difference from untrained males may be attributed to adaptive changes in the neuromuscular and endocrine systems, combined with the greater training capacity (e.g. training intensity, total volume lifted) of trained men. Thus, whilst the training role of endogenous T and C may be permissive for untrained individuals, a dose-response role might exist for trained individuals. Indeed, these hormonal modifications have been used to explain the accompanying changes in speed, power or strength with training.[15,150,183-188,190-192,194] Nevertheless, some training studies on this population have noted performance changes without any modifications in basal T and/or C concentrations,[50,141,148,195-197] or vice versa.[52,158,198-201] Interpretation is limited by a lack of uniformity in study design, in particular the training status of subjects, as the term ‘trained’ can include a mixture of novice, intermediate or advanced lifters. For elite athletes, alterations in basal hormones may be needed to induce further improvements in individual performance. Support Sports Med 2011; 41 (2)

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comes from correlations between the individual changes in basal T and/or C concentrations and strength adaptation in elite strength athletes.[182,183,186,187,192,202] If these individual responses to training were related to genetic makeup, as discussed in section 4.1.4, then such data could be used to assess the trainability of some athletes. Research on power and strength athletes also indicates that basal changes in T and/or C concentrations may help to moderate, or maintain, performance during periods of detraining.[186,192,203] These findings corroborate a dose-dependent training role for endogenous T and C, especially for elite athletes, although full proof within the physiological range is still lacking. This model reconciles recent training studies that have proposed a permissive role for endogenous hormones in untrained individuals.[11,12,53]

higher total T concentrations than soccer players, whilst soccer players in turn had higher total T than cross-country skiers.[143] Similar findings have been reported.[144,145] Conversely, endurance athletes often exhibit lower T concentrations than more explosive athletes and controls (table I). Thus, explosive training practices might lead to increases in T secretion whereas endurance training may lower T, possibly to meet the performance demands of each respective group. Training volume is one variable to consider with lower T identified in high mileage runners (vs moderate mileage runners and controls);[205] hence, a training threshold may well exist. The timing of assessment across the season can also influence the measured T values.[20] Alternatively, the differences identified between each athletic group could represent a genetic predisposition for a selected sport. In general, basal C concentrations are no different between sporting and control groups (table I). There are still reports of greater basal

4.2.2 Training Type

The type of training undertaken might also influence basal T. For example, sprinters had

Table I. Summary of the basal testosterone (T) and cortisol (C) concentrations of different sporting groups and controls No. of subjects

Sessions

Samplesa

Results

Arce et al.

28 ER, BB and controls

1

1

Total T, free T: ER and BB < controls

De Souza et al.[205]

30 HER, MER and controls

1

1

Total T, free T: HER < MER and controls Total C, urinary free C: no group differences

Wittert et al.[206]

12 ETA and controls

1

22 (blood) 1 (urine)

Total C, urinary free C: no group differences

Lucı´a et al.[20]

40 ER, RC, TRI and controls

3

1

Total T: ER, RC and TRI < controlsb Free T, total C: no group differences

Grasso et al.[207]

25 SP and controls

1

1

Total T: SP < controls Total C: no group differences

Hackney et al.[208]

88 ETA and controls

1

1

Total T, free T: ETA < controls Total C: no group differences

Maı¨moun et al.[209]

48 ETA and controls

1

1

Total T: ETA < controls Total C: no group differences

Izquierdo et al.[210]

41 WL, RC and controls

1

1

Total T, free T: RC < WL and controls Total C, T : C: no group differences

Bambaeichi and Rahnama[145]

45 SR, ER and controls

1

1

Total T: ER < SR

Timon et al.[211]

30 ETA and controls

1

1

Urinary free T: ET < controls Urinary free C: no group differences

Bonifazi et al.[212]

26 SW, LTR and controls

1

1

Total C: no group differences

Study [204]

a

All hormones measured in blood unless otherwise stated.

b

First session only.

BB = bodybuilders; ER = endurance runners; ETA = endurance trained athletes; HER = high mileage endurance runners; LTR = low trained runners; MER = moderate mileage endurance runners; RC = road cyclists; SP = soccer players; SR = sprint runners; SW = swimmers; TRI = triathletes; WL = weightlifters.

ª 2011 Adis Data Information BV. All rights reserved.

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levels of adrenocorticotropic hormone (which stimulates C production) in endurance athletes than controls,[206,213] thereby suggesting a reduction in adrenal sensitivity with training. The acrophase and early morning increase in adrenocorticotropic hormone and total C also occurred earlier in endurance athletes than controls.[206] Together, these cross-sectional data on athletes and non-athletes highlight the potential of different training methods for regulating T secretion and the adrenal pathway that controls C secretion. One must remain cognizant of the limitations of cross-sectional research, such as the number of sessions monitored and the frequency and timing of sample collection, and the assumption that the observed results were due to training alone. It appears from literature that the short-term effects of T and C may predominate in elite athletes, as others have suggested.[7,139,144] This supposition is based on the assumption that these endogenous hormones can moderate the performance/training outcomes and that muscle growth is either limited or non-existent in this athletic group. We acknowledge that the long-term T and C effects might still play a supporting role by maintaining lean body mass in some elite populations. Regardless, the exact contribution of these steroids to the training process is still unclear, because most endocrine studies have not taken accurate measurements of muscle size (e.g. muscle fibre cross-sectional area) and neural activity (e.g. electromyography, V-wave, Hoffmann reflex) to identify the training mechanisms involved. There is also a paucity of experimental studies on elite athletes that have specifically addressed the concept of dual steroid effects. More work is needed to delineate the specific hormonal mechanisms contributing to resistance training performance and adaptation. 4.3 Acute and Chronic Modifications in Steroid Receptors 4.3.1 Androgen Receptors

Steroid receptors mediate the hormonal effect by either up-regulating (i.e. increase in receptor content and/or binding sensitivity) or downª 2011 Adis Data Information BV. All rights reserved.

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regulating (i.e. decrease in receptor content and/ or binding sensitivity) in response to exercise and training.[4] If explosive training methods increased basal T production to support athlete performance, as indicated previously, then one may also expect the AR to be up-regulated. As supporting evidence, greater AR content was found in the trapezius muscle of power-lifters (vs controls), especially those taking anabolic steroids,[214] who themselves may exhibit a greater number and proportion of type II fibres. Transient adaptations are also evident, with resistance exercise promoting acute increases in both AR mRNA and/or protein content and T concentrations.[215-219] There are other reports of no changes, or decreases, in these AR measures after resistance exercise[220,221] and probably arising from their dynamic recovery patterns post-exercise. It has been demonstrated that AR expression can vary between different muscles, muscle fibres and cells;[214,222-224] therefore, the responses evoked by different training methods may well show similar specificity. In rats,[225] resistance training down-regulated AR content in the soleus, which is predominantly a slow oxidative muscle, but up-regulated AR content in the extensor digitorum longus, which is primarily a fast glycolytic muscle. Conversely, endurance training increased AR content in the soleus, but did not change AR content in the extensor digitorum longus. Similar to basal T secretion, there does appear to be a loading threshold before acute exercise-induced changes in AR content may occur.[226,227] 4.3.2 Glucocorticoid Receptors

The GR are similarly responsive to exercise and training. In humans, a bout of resistance exercise acutely increased GR content in one study,[228] but not another,[221] although the workout tested and training background of subjects were different between these studies. Resistance training did provide an effective stimulus for increasing GR content in untrained males[229] and, in handball players, 10 weeks of training improved GR binding capacity.[230] Conversely, animal research have identified a reduction in GR content after endurance-type exercise,[231,232] Sports Med 2011; 41 (2)

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with endurance training also reducing GR content in an intensity- and load-volume-dependent manner.[231,233,234] Cross-sectional evidence in humans supports these results.[207,212,233] The specificity of the AR and GR responses to exercise and training is likely to support the biological effects at target tissue, by activating those signalling processes that contribute to the longterm steroid actions (i.e. gene transcription). However, because of compliance issues associated with muscle biopsies, most training studies in humans have used blood cells as indirect measures of muscle receptors; in particular, only the cell-bound type. Whether or not the membrane-bound receptors exhibit similar patterns of change with exercise and training, the time-course of these responses remains highly speculative. 4.4 Summary

Endogenous evidence supports the existence of short-term T and C effects on human performance within the resistance-training model. Several factors (e.g. workout design, nutrition, genetics, training status and type) can modify T and/or C concentrations and thereby potentially influence resistance-training performance and the adaptive outcomes. This novel pathway appears to be more prominent in athletes, possibly due to the training of the neuromuscular and endocrine systems. However, the exact contribution of these hormones to the training process is still unclear. A dose-response training role for endogenous T and C was confirmed, especially for elite athletes, but full proof is lacking. It is also clear that the steroid receptors (cell bound) mediate target tissue effects by adapting to exercise and training, but the response patterns of the membrane-bound receptors remain highly speculative. 5. Limitations and Challenges with Hormonal Research This review has focused on the effects of T and C concentrations on the neuromuscular system. However, steroid concentrations still only reflect the secretory and clearance mechanisms.[235] Other important endocrine features include transport ª 2011 Adis Data Information BV. All rights reserved.

proteins, hormone-protein dissociation, hormone degradation rates and the intracrine and paracrine pathways.[235] The physiological meaning of the free and total steroids adds to this complexity, as does the different secretory mechanisms (e.g. rapid vs slow, blood vs brain). As outlined in section 3.2.4, the neuromuscular responses may also depend upon the actions and interactions of other steroid metabolites, neurotransmitters, peptides, amines and growth factors. The importance of procedural issues (e.g. volume shifts, specimen collection, sleep) in endocrine research has been highlighted.[6,236,237] As an example, corrections should be made for plasma volume shifts when examining the T responses to exercise.[238,239] On the other hand, uncorrected hormonal values better represent what target tissue is actually exposed to, so the need to account for plasma volume depends on the research questions.[6] The collection of control data (or lack thereof) is another consideration because of the normal circadian variation in T and C secretion.[206,240-242] In fact, the exercise responses of T and/or C can also exhibit circadian variation.[243-245] The influence of other biological factors (e.g. age, sex, race, body composition) on these hormones and the implications for research analysis and interpretation have been discussed elsewhere.[236,237] The analytical techniques employed can also influence research interpretation. Some of the endogenous evidence is based on correlations, which only imply cause and effect. However, correlations can help to identify relationships for further experimental testing[246] and may be useful when comparing group, sub-group and individual trends on athletes.[141,144,202] The method used for hormone testing (e.g. immunoassays, bioassays, chromatography) and their sensitivity, accuracy and repeatability for assessing hormones also requires attention.[236,237] A major limiting factor in the application of research into the sporting environment is the retrospective use of hormonal data because most testing methods require several hours for sample preparation and analysis. A real-time analysis system is implicit in being able to maximize the use of the hormonal information gained, for instance, by indicating a Sports Med 2011; 41 (2)

Two Emerging Concepts for Elite Athletes

readiness to train or compete at a certain level, by determining the most appropriate warm-up strategy and/or by assisting with the design of workouts to promote optimal training gains. Issues relating to research design are another consideration. Most of the exogenous evidence in this review comes from blinded, placebocontrolled, randomized trials whereas the endogenous evidence from athletes rarely meets this criterion. The strict control of training protocols is also difficult to achieve within the sporting environment and, notwithstanding, the confounding effects of other variables (e.g. competition, training periodization, psychology). Further bias comes from the selection criteria, smaller sample sizes and the lack of control data when undertaking research on elite athletes. Nevertheless, this research does represent the actual responses to, and inherent limitations within, elite sport and thus better represents the real-world setting. From a training perspective, the interplay between the neuromuscular and endocrine systems presents a myriad of strategies for inducing performance gains with differential responses based on factors such as workout and training design, training status and type, age, sex, genetic predisposition and nutrition.[1,3,6,247] Resistance training can also induce other muscular (e.g. muscle fibre phenotype, fibre architecture), metabolic (e.g. substrate stores, enzyme activities) and/or neural changes (e.g. motor unit activation, firing rate, synchronization and reflex activity) to regulate the adaptive responses of the neuromuscular system.[3,21,22,247] Finally, many athletes often use resistance training to compliment other fitness- and sport-specific practices within a periodized programme,[2,172] so they may present multiple and sometimes conflicting systems of adaptation to produce the desired training effect. 6. Conclusion Exogenous evidence confirms the existence of short-term T and C effects on the neuromuscular system and, through this, the expression of human performance. Whilst not conclusive, endogenous evidence from athletes provides some support regarding the short-term effects of these steroids ª 2011 Adis Data Information BV. All rights reserved.

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on resistance training performance and the adaptive outcomes. Both forms of evidence also support a dose-dependent training role for T and C in moderating the performance capabilities and development of the neuromuscular system. For some elite athletes, changes (acute or basal) in endogenous T and C would seem to be one possible moderator of training performance and long-term adaptations. This athlete model reconciles a proposed permissive role for endogenous hormones in untrained individuals. Acknowledgements This review was written as part of the PhD thesis for Southern Cross University by the first author. Support for the preparation of this manuscript was provided by The New Zealand Institute for Plant & Food Research Limited, UK Sport and the Engineering and Physical Sciences Research Council of the UK. The authors have no conflicts of interest that are directly relevant to the content of this review.

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Two Emerging Concepts for Elite Athletes

heavy-resistance exercise in weight-trained men. Chronobiol Int 2004; 21 (1): 131-46 244. Deschenes MR, Kraemer WJ, Bush JA, et al. Biorhythmic influences on functional capacity of human muscle and physiological responses. Med Sci Sports Exerc 1998; 30 (9): 1399-407 245. Kanaley JA, Weltman JY, Pieper KS, et al. Cortisol and growth hormone responses to exercise at different times of day. J Clin Endocrinol Metab 2001; 86 (6): 2881-9 246. Bishop D. An applied research model for the sport sciences. Sports Med 2008; 38 (3): 253-63

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247. Kraemer WJ, Fleck SJ, Evans WJ. Strength and power training: physiological mechanisms of adaptation. Exerc Sport Sci Rev 1996; 24: 363-97

Correspondence: Dr Blair Crewther, Hamlyn Centre, Institute of Global Health Innovation, Bessemer Building, Imperial College, South Kensington Campus, London SW7 2AZ, UK. E-mail: [email protected]

Sports Med 2011; 41 (2)

Sports Med 2011; 41 (2): 125-146 0112-1642/11/0002-0125/$49.95/0

REVIEW ARTICLE

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Developing Maximal Neuromuscular Power Part 2 – Training Considerations for Improving Maximal Power Production Prue Cormie,1 Michael R. McGuigan2,3 and Robert U. Newton1 1 School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Joondalup, Western Australia, Australia 2 New Zealand Academy of Sport North Island, Auckland, New Zealand 3 Institute of Sport and Recreation Research New Zealand, Auckland University of Technology, Auckland, New Zealand

Contents Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1. Role of Strength in Maximal Power Production . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2. Movement Pattern Specificity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.1 Traditional Resistance Training Exercises. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.2 Ballistic Exercises . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.3 Plyometrics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.4 Weightlifting Exercises . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3. Load Specificity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.1 Heavy Loads . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.2 Light Loads . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.3 The ‘Optimal’ Load . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.4 Combination of Loads . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4. Velocity Specificity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.1 Actual Movement Velocity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.2 Intention to Move Explosively. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.3 Actual versus Intended Movement Velocity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5. Window of Adaptation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6. Integration of Power Training Modalities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7. Conclusions and Implications. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Abstract

125 127 129 129 129 133 134 134 135 136 136 137 138 138 139 140 140 140 141

This series of reviews focuses on the most important neuromuscular function in many sport performances: the ability to generate maximal muscular power. Part 1, published in an earlier issue of Sports Medicine, focused on the factors that affect maximal power production while part 2 explores the practical application of these findings by reviewing the scientific literature relevant to the development of training programmes that most effectively enhance maximal power production. The ability to generate maximal power during complex motor skills is of paramount importance to successful athletic

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performance across many sports. A crucial issue faced by scientists and coaches is the development of effective and efficient training programmes that improve maximal power production in dynamic, multi-joint movements. Such training is referred to as ‘power training’ for the purposes of this review. Although further research is required in order to gain a deeper understanding of the optimal training techniques for maximizing power in complex, sportsspecific movements and the precise mechanisms underlying adaptation, several key conclusions can be drawn from this review. First, a fundamental relationship exists between strength and power, which dictates that an individual cannot possess a high level of power without first being relatively strong. Thus, enhancing and maintaining maximal strength is essential when considering the long-term development of power. Second, consideration of movement pattern, load and velocity specificity is essential when designing power training programmes. Ballistic, plyometric and weightlifting exercises can be used effectively as primary exercises within a power training programme that enhances maximal power. The loads applied to these exercises will depend on the specific requirements of each particular sport and the type of movement being trained. The use of ballistic exercises with loads ranging from 0% to 50% of one-repetition maximum (1RM) and/or weightlifting exercises performed with loads ranging from 50% to 90% of 1RM appears to be the most potent loading stimulus for improving maximal power in complex movements. Furthermore, plyometric exercises should involve stretch rates as well as stretch loads that are similar to those encountered in each specific sport and involve little to no external resistance. These loading conditions allow for superior transfer to performance because they require similar movement velocities to those typically encountered in sport. Third, it is vital to consider the individual athlete’s window of adaptation (i.e. the magnitude of potential for improvement) for each neuromuscular factor contributing to maximal power production when developing an effective and efficient power training programme. A training programme that focuses on the least developed factor contributing to maximal power will prompt the greatest neuromuscular adaptations and therefore result in superior performance improvements for that individual. Finally, a key consideration for the longterm development of an athlete’s maximal power production capacity is the need for an integration of numerous power training techniques. This integration allows for variation within power meso-/micro-cycles while still maintaining specificity, which is theorized to lead to the greatest long-term improvement in maximal power.

Part 1[1] of this review discussed the biological basis for maximal power production. Part 1 highlighted that maximal muscular power is influenced by a wide variety of interrelated neuromuscular factors including muscle fibre composition, crosssectional area, fascicle length, pennation angle and tendon compliance as well as motor unit recruitment, firing frequency, synchronization and inter-muscular coordination. Maximal power is ª 2011 Adis Data Information BV. All rights reserved.

also affected by the type of muscle action involved and, in particular, the time available to develop force, storage and utilization of elastic energy, interactions of contractile and elastic elements, potentiation of contractile and elastic filaments as well as stretch reflexes. Furthermore, acute changes in the muscle environment impact the ability to generate maximal power. Thus, development of training programmes that enhance Sports Med 2011; 41 (2)

Training to Improve Maximal Power

maximal power must involve consideration of these factors and the manner in which they respond to training. The purpose of part 2 is to explore the practical applications of the findings of part 1 by reviewing the scientific literature relevant to the development of training programmes that most effectively improve maximal power production in dynamic athletic movements. The search for scientific literature relevant to this review was performed using the US National Library of Medicine (PubMed), MEDLINE and SportDiscus databases. The specific search terms utilized included ‘maximal power’, ‘muscular power’, ‘power training’, ‘ballistic training’, ‘plyometric training’ and ‘weightlifting training’. Relevant literature was also sourced from searches of related articles arising from the reference list of those obtained from the database searches. The studies reviewed examined factors that could potentially influence the ability to improve maximal power production through training. 1. Role of Strength in Maximal Power Production A fundamental relationship exists between strength and power, which dictates that an individual cannot possess a high level of power without first being relatively strong. This assertion is supported by the robust relationship that exists between maximal strength and maximal power production as well as countless empirical observations of the differences in strength and power capabilities between elite and sub-elite athletes.[2-9] Cross-sectional comparisons have revealed that individuals with higher strength levels have markedly superior power production capabilities than those with a low level of strength[7,10-17] (table I). Furthermore, research has demonstrated that heavy strength training programmes involving untrained to moderately trained subjects resulted not only in improved maximal strength but also increased maximal power output.[9,18-27] While strength is a basic quality that influences maximal power production, the degree of this influence diminishes somewhat when the athlete maintains a very high level of strength.[28] As maximal strength is increased, the window of ª 2011 Adis Data Information BV. All rights reserved.

127

adaptation for further strength enhancement is reduced. Consequently, increases in maximal power output following strength training are expected to be lower in stronger individuals and more velocity specific in that the changes would impact primarily on the high-force end of the forcevelocity relationship.[29-34] Theoretically, if a well trained, strong athlete was able to enhance maximal strength at the same rate as an untrained novice through either steroid use and/or creative strength training protocols, the degree to which strength training would influence maximal power production would be quite similar. In any case, the current strength level of an athlete will always dictate the upper limit of their potential to generate maximal muscular power because the ability to generate force rapidly is of little benefit if maximal force is low.[32] Therefore, the ability to generate superior maximal muscular power is considerably influenced by the individual’s level of strength. Stronger individuals possess favourable neuromuscular characteristics that form the basis for superior maximal power production. For example, following the first 3 years of a periodized strength training programme the neuromuscular profile would be significantly enhanced. Whole muscle cross-sectional area (CSA) would be considerably greater[35-56] as a result of increased myofibrillar CSA of type I and, to a greater degree, type II fibres.[35,37,41,42,44,45,57-60] It is highly likely that pennation angle[46,52] and possibly even fascicle length[48,49,55,61] would be greater. Additionally, neural drive[21,29,40,62-68] as well as inter- and possibly even intra-muscular coordination[66,68-73] would be far superior after the 3 years of training. These neuromuscular characteristics would result in a shift in the forcevelocity relationship so that the force generated by muscle would be greater for any given velocity of shortening.[9,20,25,26] As a result, maximal muscular power output would be far superior following the 3 years of strength training.[20,24-26,41,56,74,75] Therefore, enhancing maximal strength is a vital consideration when designing training programmes that maximize the long-term development of maximal muscular power. While previous research has demonstrated that improvements in strength are accompanied Sports Med 2011; 41 (2)

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Table I. Summary of cross-sectional studies comparing maximal power production between stronger and weaker subjects Study (year)

No. of subjects stronger weaker

Subject demographics stronger weaker

Strength test conducted

Strength level (mean – SD) stronger weaker

Power test conducted

Maximal power (mean – SD) stronger weaker

8

8

Well trained male volleyball and badminton players

Well trained M longdistance runners

Smith machine squat 1RM (kg/kg)

2.36* – 0.74

1.74 – 0.32

Maximum CMJ power (W/kg)

76.3* – 10.8

59.2 – 11.1

Baker and Newton[14] (2006)

6

6

M 1st division national rugby league players

M 2nd division state rugby league players

BP 1RM (kg/kg)

1.46* – 0.12

1.19 – 0.13

Maximum BP throw power (W/kg)

6.97* – 0.64

5.51 – 0.55

Baker and Newton[15] (2008)

20

20

M 1st division national rugby league players

M 2nd division state rugby league players

Squat 1RM (kg)

175.0* – 27.3

149.6 – 14.3

Maximum CMJ power (W)

1897* – 306

1701 – 187.0

Cormie et al.[17] (2010)

12

18

Stronger physically active men

Weaker physically active men

Squat 1RM (kg/kg)

1.97* – 0.08

1.32 – 0.14

Maximum CMJ power (W/kg)

59.8* – 3.8

50.2 – 5.2

Cormie et al.[11] (2009)

12

18

Division I M football and track athletes

Untrained men

Squat 1RM (kg/kg)

1.93* – 0.22

1.40 – 0.27

Maximum CMJ power (W/kg)

71.7* – 10.7

55.9 – 8.0

McBride et al.[12] (1999)

8

8

National level M power lifters

Moderately active men

Smith machine squat 1RM (kg/kg)

2.88* – 0.14

2.13 – 0.14

Maximum CMJ power (W/kg)

56.9* – 2.5

49.4 – 2.6

6

8

National level M Olympic lifters

Moderately active men

Smith machine squat 1RM (kg/kg)

2.86* – 0.15

2.13 – 0.14

Maximum CMJ power (W/kg)

63.0* – 2.7

49.4 – 2.6

6

8

National level M sprinters

Moderately active men

Smith machine squat 1RM (kg/kg)

2.66* – 0.16

2.13 – 0.14

Maximum CMJ power (W/kg)

63.8* – 2.9

49.4 – 2.6

14

13

National level F weightlifters

Untrained women

VJ height (m)

0.50* – 0.08

0.32 – 0.07

5

5

Strongest out of a pool of 22 resistance trained men

Weakest out of a pool of 22 resistance trained men

Squat 1RM (kg)

212.5* – 8.4

95.0 – 6.3

Maximum CMJ power (W)

5391* – 2566

3785 – 376

10

10

M track athletes with international experience

Physically active men

Leg press 1RM (kg)

364.5 – 115.1

304.0 – 47.3

Maximum CMJ height (m)

0.40* – 0.05

0.30 – 0.05

Stoessel et al.[13] (1991) Stone et al.[7] (2003) Sports Med 2011; 41 (2)

Ugrinowitsch et al.[16] (2007)

1RM = one-repetition maximum; BP = bench press; CMJ = countermovement jump with no arm swing; F = female; kg/kg = the ratio between 1RM in kg and body mass in kg; M = male; VJ = vertical jump a CMJ with an arm swing; * indicates significant (p £ 0.05) difference between stronger and weaker groups.

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Bourque[10] (2003)

Training to Improve Maximal Power

by increased power output,[9,18-24,27] much of this research involved training relatively novice subjects with low to moderate strength levels, in which improvements in muscular function are easily invoked and relatively non-specific. Further improvement in maximal muscular power and performance enhancement in well trained athletes, requires a multifaceted approach incorporating a variety of training strategies targeting specific areas of the force-velocity relationship.[28,31] 2. Movement Pattern Specificity The ability to generate maximal power in dynamic, multi-joint movements is dependent on the nature of the movement involved.[76,77] Therefore, the exercises selected for a power training programme may influence the magnitude of performance improvements and type of adaptations observed. A range of movements have been previously prescribed for improving maximal power output including traditional resistance training exercises, ballistic exercises, plyometrics and weightlifting exercises (table II). 2.1 Traditional Resistance Training Exercises

Inherent in traditional resistance training exercises such as the squat or bench press, is a substantial period where the load is decelerated towards the end of the range of motion.[77,84] For example, in the bench press the deceleration has been reported to last for 23% of the total duration of a one-repetition maximum (1RM) and is increased to 52% of the total duration when the load was reduced to approximately 80% of 1RM.[84] When the movement is performed rapidly with a lower load of 45% of 1RM in an attempt to increase sports specificity, the deceleration phase still extends for approximately 40–50% of the total movement duration.[77] Thus, even if traditional resistance training exercises are performed with light loads and the athlete is instructed to perform these movements rapidly, this deceleration results in movement velocities lower than those typically encountered in sporting movements such as jumping or throwing.[76,77] Furthermore, this deceleration phase is associated ª 2011 Adis Data Information BV. All rights reserved.

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with decreased muscle activation of the agonists and the possibility of increased muscle activity in the antagonist muscles in order to stop the load at the end of the range of motion.[77] As a result of this decreased mechanical specificity, the transfer of training effect following a programme involving traditional resistance training exercises is reduced. Despite this, traditional resistance training exercises have been successfully used to improve maximal power output in dynamic, sports-specific movements.[22-24,32,85-88] While performance of these exercises requires the generation of relatively high power outputs, improvements in maximal power following training have primarily been a result of the physiological adaptations responsible for increasing maximal strength including increased CSA and neural drive.[35,85,89] Consequently, significant increases in maximal power following training with traditional resistance training exercises occur in relatively untrained subjects with low to moderate strength levels and diminish as strength level increases.[29-32] It is possible, however, that if maximal strength did not become asymptotic as a result of anabolic steroid use, enhancing maximum strength through the use of traditional resistance training exercises would continue to improve maximal muscular power. Therefore, without consideration of anabolic steroid use, increases in maximal power output following training with these exercises are prominent in the early phases of training or in athletes who maintain a relatively low level of strength such as endurance athletes.[32,90] While the use of traditional resistance training exercises are vital in the development of strength and power, further training induced improvement in maximal power requires the involvement of other, more mechanically specific movements. 2.2 Ballistic Exercises

Ballistic exercises including the jump squat and bench press throw circumvent any deceleration phase by requiring athletes to accelerate throughout the entire range of motion to the point of projection (i.e. takeoff or release).[77] Ballistic exercises are overloaded by increasing the load required to be projected. Typically, these Sports Med 2011; 41 (2)

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ª 2011 Adis Data Information BV. All rights reserved.

Table II. Summary of studies examining changes in maximal power production following a power training intervention Study (year)a

No. of Subject demographics subjects

Experimental groups Power training programmeb

Cormie et al.[17] (2010)

24

Physically active men with a variety of training backgrounds; squat 1RM : BM ~1.35–1.97

Ballistic training in weaker subjects (n = 8); ballistic training in stronger subjects (n = 8); control (n = 8)

Cormie et al.[27] (2010)

24

Physically active men who could perform a back squat with proficient technique; squat 1RM : BM ~1.34

Ballistic training 3 sessions/wk: (n = 8); TRTE training Ballistic: jump squats 5–7 · 5–6 at 0–30% 1RM; (n = 8); control (n = 8) TRTE: squats, 3 · 3–5 at 75–90% 1RM

Cormie et al.[78] (2007)

26

Recreationally trained men; squat 1RM : BM ~1.47

Hawkins et al.[79] (2009)

29

Holcomb et al.[80] (1996)

51

Training Major findings duration (wk) Both weaker and stronger ballistic: › PP, MP and PD in 0%, 20% and 40% 1RM*, › PD in CMJ*; › RFD in isometric squat and CMJ*, › 40 m sprint performance*, 2 squat 1RM; no difference in › maximal P between the training groups; CON: 2 any outcome measures

10

Ballistic: › PP, MP and PD in 0%, 20% and 40% 1RM*, › PD in CMJ*; › RFD in isometric squat and CMJ*, › 40 m sprint performance*, 2 squat 1RM; TRTE: › PP, MP and PD in 0%, 20%, 40% and 60% 1RM*, › PD in CMJ*; › RFD in CMJ*, › 40 m sprint performance*, › squat 1RM*; no difference in › maximal P between the training groups; CON: 2 any outcome measures

Ballistic training (n = 10); ballistic + TRTE training (n = 8); control (n = 8)

2 sessions/wk: 12 Ballistic: jump squats, 7 · 6 at 0% 1RM; strengthballistic + TRTE: jump squats, 5 · 6 at 0% 1RM and squats, 3 · 3 90% 1RM

Ballistic: › PP and PD in 0, 19% 1RM*, 2 squat 1RM; strength-power EXP: › PP and PD in 0%, 17%, 35%, 52%, 70% 1RM*, › squat 1RM*; no difference in › maximal P between the training groups; CON: 2 any outcome measures

Non-athlete collegeaged M; squat 1RM : BM ~1.35

TRTE training (n = 10); plyometric training (n = 10); weightlifting training (n = 9)

3 sessions/wk: 8 TRTE: squat, deadlift, lunges, etc., 3 · 4–10RM; plyometric: drop jumps, CMJ, hops, bounding, etc. 3 · 3–10; weightlifting: hang clean, high pull, split jerks, etc. 3 · 2–8RM

TRTE: › PD in VJ*, › squat 1RM*; plyometric: › PD in VJ*, › squat 1RM*; weightlifting: › PP in CMJ*, › PD in VJ*, › squat 1RM*; no difference in › maximal P between the training groups

Men recruited from university physical education classes; 1RM, NR

Ballistic training (n = 10); TRTE training (n = 12); plyometric training (n = 10); ‘modified’ plyometric training (n = 10); control (n = 9)

8 3 session/wk: Ballistic: jump squat, 9 · 8 at 0% 1RM; TRTE: leg press, knee extension, knee flexion, etc., 3 · 4–8RM; plyometric: drop jumps, 3 · 8 at 0.4–0.6 m heights; ‘modified’ plyometric: drop jump variations, 3 · 8 at 0.4–0.6 m heights

All training groups: › PP in CMJ and static jump*, › PD in CMJ and static jump*; no difference in › maximal P between any of the training groups; CON: 2 any outcome measures

Continued next page

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10

3 sessions/wk: Ballistic: jump squats, session 1 and 3, 7 · 6 at 0% 1RM; session 2, 5 · 5 at 30% 1RM

No. of Subject demographics subjects

Experimental groups Power training programmeb

Training Major findings duration (wk)

Kaneko et al.[20] (1983)

20

M who had not been specifically trained before; 1RM, NR

0% Fmax TRTE training (n = 5); 30% Fmax TRTE training (n = 5); 60% Fmax TRTE training (n = 5); 100% Fmax TRTE training (n = 5)

3 sessions/wk: TRTE: elbow flexion, 0% Fmax group: 1 · 10 at 0% Fmax; 30% Fmax group: 1 · 10 at 30% Fmax; 60% Fmax group: 1 · 10 at 60% Fmax; 100% Fmax group: 1 · 10 holds at 100% Fmax

12

All TRTE groups: › maximal P in elbow flexion*, › maximal velocity in elbow flexion*; 0% and 30% Fmax groups: 2 Fmax in elbow flexion; 60% and 100% Fmax groups: › Fmax in elbow flexion*; no difference in › maximal P between groups

Kyro¨la¨inen et al.[81] (2005)

23

Recreationally active men; 1RM, NR

Ballistic + plyometric training (n = 13); control (n = 10)

2 sessions/wk: Ballistic + plyometric: jump squat, 5–10 repetitions at 30–60% 1RM; drop jumps from 0.2 m to 0.7 m heights; hops and hurdle jumps

15

Ballistic + plyometric: › knee joint P during a drop jump*, › PD in a drop jump*, › RFD in isometric knee extension*; CON: 2 any outcome measures

Lyttle et al.[82] (1996)

33

Men who participate in various regional level sports but had no resistance training experience; squat 1RM : BM ~1.33

Ballistic training (n = 11); TRTE + plyometric training (n = 11); control (n = 11)

2 sessions/wk: Ballistic: jump squat, and bench press throw, 2–6 · 8 at 30% 1RM; TRTE + plyometric: squat, 1–3 · 6–10RM; bench press, 1–3 · 6–10RM; drop jump, 1–2 · 6–10 at 0.2 m–0.6 m heights and drop medicine ball throws, 1–2 · 6–10 at 0.0–1.6 m drop heights

8

Both ballistic and TRTE + plyometric: › MP in 6 s cycle*, › PD in CMJ*, › squat 1RM*, › PD in medicine ball and shot put throws*, › impulse during SSC and concentric-only push up*; no difference in › maximal P between the training group; CON: 2 any outcome measures

McBride et al.[21] (2002)

26

Athletic men with varying levels of resistance training experience; Smith machine squat 1RM : BM ~1.84

30% 1RM ballistic training (n = 9) 80% 1RM ballistic training (n = 10) control (n = 7)

2 sessions/wk: Ballistic: jump squats, 30% 1RM group: 5 sets at 30% 1RM; 80% 1RM group: 4 sets at 80% 1RM; as many reps until a 15% fl in PP

8

30% 1RM ballistic: › PP in 30%, 50% and 80% 1RM jump squat*, › squat 1RM*, NS › 20 m sprint performance; 80% 1RM ballistic: › PP in 50% and 80% 1RM jump squat*, › squat 1RM*, fl 20 m sprint performance*; no difference in › maximal P between the training groups; CON: › PP in 80% 1RM jump squat*; 2 any other outcome measures

Moss et al.[9] (1997)

30

M physical education 90% 1RM TRTE students; elbow flexion training (n = 9); 1RM ~20 kg 35% 1RM TRTE training (n = 11); 15% 1RM TRTE training (n = 10)

3 sessions/wk: TRTE: elbow flexion, 90% 1RM group: 3–5 · 2 at 90% 1RM; 35% 1RM group: 3–5 · 7 at 35% 1RM; 15% 1RM group: 3–5 · 10 at 15% 1RM

9

All TRTE groups: › PP at 2.5 kg, 15%, 25%, 35% 1RM in elbow flexion*, › 1RM elbow flexion*; 90% and 35% 1RM group: also › PP at 50%, 60% and 90% 1RM in elbow flexion*; no difference in › maximal P between TRTE training groups; CON: 2 any outcome measures Continued next page

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Study (year)a

Training to Improve Maximal Power

ª 2011 Adis Data Information BV. All rights reserved.

Table II. Contd

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ª 2011 Adis Data Information BV. All rights reserved.

Table II. Contd Study (year)a

No. of Subject demographics subjects

Experimental groups Power training programmeb

Newton et al.[33] (1999)

16

NCAA division I, M volleyball players; squat 1RM : BM ~1.69

8 2–4 sessions/wk: Ballistic training (n = 8); TRTE training Ballistic: jump squats 2 · 6 at 30% 1RM, 2 · 6 at 60% 1RM, 2 · 6 at 80% 1RM; TRTE: squat (n = 8) 3 · 6RM and leg press 3 · 6RM

Ballistic: › PP and PD in 30%, 60% and 80% 1RM jump squat*, › PD in VJ*, › 3-step approach VJ*, 2 squat 1RM; TRTE: › PP and PD in 30% 1RM jump squat*, 2 any other outcome measures; no difference in › maximal P between the training groups

Toji and Kaneko[25] (2004)

21

M college students who had not exercised regularly for at least 1 y; 1RM, NR

30 + 60% Fmax TRTE training (n = 7); 30 + 100% Fmax TRTE training (n = 7); 30 + 60 + 100% Fmax TRTE training (n = 7)

8 3 sessions/wk: TRTE: elbow flexion, 30 + 60% Fmax group: 1 · 6 at 30% Fmax and 1 · 6 at 60% Fmax; 30 + 100% Fmax group: 1 · 6 at 30% Fmax and 1 · 6 5 s holds at 100% Fmax; 30 + 60 + 100% Fmax group: 1 · 4 at 30% Fmax, 1 · 4 at 60% Fmax and 1 · 4 5 s holds at 100% Fmax

All TRTE groups: › maximal P in elbow flexion*, › maximal velocity in elbow flexion*, › Fmax in elbow flexion*; › maximal P greater in 30% + 60% + 100% Fmax group vs 30% + 100% Fmax group ›

Toji et al.[26] 12 (1997)

M college students who had not exercised regularly for at least 1 y; 1RM, NR

30 + 0% Fmax TRTE training (n = 6); 30 + 100% Fmax TRTE training (n = 6)

11 3 sessions/wk: TRTE: elbow flexion, 30 + 0% Fmax group: 1 · 5 at 0% Fmax and 1 · 5 at 60% Fmax; 30 + 100% Fmax group: 1 · 5 at 30% Fmax and 1 · 5 3 s holds at 100% Fmax

Both TRTE groups: › maximal P in elbow flexion*, › maximal velocity in elbow flexion*; 30% + 0% group: 2 Fmax in elbow flexion; 30% + 100% group: › Fmax in elbow flexion*; › maximal P greater in 30% + 100% Fmax group vs 30% + 0% Fmax group-

Wilson et al.[24] (1993)

Previously trained men; Ballistic training 1RM : BM, NR (n = 16); TRTE training (n = 16); plyometric training (n = 16); control (n = 16)

2 sessions/wk: Ballistic jump squats 3–6 · 6–10 at ~30% Fmax; TRTE: squat 3–6 · 6–10RM; plyometric: drop jumps 3–6 · 6–10 at 0.2–0.8 m heights

10

Ballistic: › MP in 6 s cycle*, › PD in CMJ and SJ*, NS › 30 m sprint performance; TRTE: › PD in CMJ and SJ*, › Fmax *; plyometric: › PD in CMJ*. CON: 2 any outcome measures; no difference in › maximal P between the training groups

8

Ballistic: › PP in 30% 1RM jump squat*; › RFD in isometric mid-thigh pull*; 2 squat 1RM; CON: 2 any outcome measures

64

Winchester 14 et al.[83] (2008)

M with at least 3 mo training experience; squat 1RM : BM ~1.45

Ballistic training 3 session/wk: (n = 8); control (n = 6) Ballistic: jump squat 3 · 3–12 at 26–48% 1RM

Only studies that included a specific measurement of power output were included in this table.

b

Training programme is expressed as sets · repetitions.

BM = body mass; CMJ = countermovement jump with no arm swing; CON = control group; Fmax = maximal isometric force; M = male(s); MP = mean power; NCAA = National Collegiate Athletic Association; NR = not reported; NS = non-statistically significant change; P = power; PD = peak displacement; PP = peak power; RFD = rate of force development; RM = repetition maximum; SJ = concentric-only jump with no arm swing; SSC = stretch shorten cycle; TRTE = traditional resistance training exercise; VJ = vertical jump a CMJ with an arm swing; › indicates improvement following training; fl indicates decrease following training; 2 indicates no change following training; ~ indicates approximately; * indicates significant (p £ 0.05) change following training; - indicates significant (p £ 0.05) difference between training groups.

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Sports Med 2011; 41 (2)

a

Training Major findings duration (wk)

Training to Improve Maximal Power

exercises are performed across a variety of loading conditions from 0–80% of 1RM in a similar traditional resistance training exercise such as the squat or bench press based on the specific exercise utilized and the requirements of the sport. Stemming from the continued acceleration throughout the range of motion, concentric velocity, force, power and muscle activation are higher during a ballistic movement in comparison to a similar traditional resistance training exercise.[76,77] As a result, many researchers and coaches recommend the inclusion of ballistic exercises rather than traditional resistance training exercises in power training programmes.[24,28,31,33,76,77,91] These recommendations are based on the fact that ballistic exercises are generally more sport specific for a vast number of sports and therefore may prompt adaptations that allow for greater transfer to performance. Supporting such recommendations is research demonstrating significant improvements in maximal power output during sports-specific movements following training with ballistic exercises.[21,24,33,78,81-83,92] Furthermore, the ability to generate power is also improved across a variety of low- and high-load conditions following training.[21,33,78] For example, an 8-week training intervention involving well trained male volleyball players with a squat 1RM to body mass ratio of approximately 1.69 revealed that training with ballistic jump squats resulted in a significantly greater change in sport-specific vertical jump performance than training with traditional resistance training exercises including the squat and leg press.[33] Therefore, training with ballistic exercises allows for athletes with various training ages and strength levels to improve power production in a variety of sports-specific movements. The precise mechanisms driving adaptation to power training involving ballistic exercises are not clearly defined. It is possible that these movements elicit adaptations in neural drive, the rate of neural activation and inter-muscular coordination that are specific to movements typically encountered in sports. These adaptations are hypothesized to contribute to observations of enhanced rate of force development (RFD) and result in the ability to generate more force in shorter periods of time.[19,21,33,78,81] Hence, the ª 2011 Adis Data Information BV. All rights reserved.

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use of ballistic exercises in power training programmes is very effective at enhancing maximal power output in sports-specific movements as well as power production capabilities under a variety of loading conditions. 2.3 Plyometrics

Plyometrics are exercises characterized by rapid stretch-shorten cycle (SSC) muscle actions.[93] A great deal of exercises are classified as plyometric including a range of unilateral and bilateral medicine ball throws, push ups, bounding, hopping and jumping variations.[93] While plyometric exercises are ballistic in nature, they are delineated from specific ballistic exercises within this review due to the way these exercises are overloaded. Typically, plyometric exercises are performed with little to no external resistance, such as with body mass only or light medicine ball, and overload is applied by increasing the stretch rate by minimizing the duration of the SSC and/or stretch load by, for example, increasing the height of the drop during drop jumps.[94] Plyometric exercises can therefore be tailored to train either short SSC movements characterized by a 100–250 ms duration (i.e. ground contact in sprinting, long or high jump), or long SSC movements characterized by duration greater than 250 ms (i.e. countermovement jump [CMJ] or throw).[95] As a result of the ability to target both short and long SSCs as well as the ballistic nature of these movements, plyometric exercises are very specific to a variety of movements typically encountered in sport. Hence, it is not surprising that the use of plyometrics in power training programmes has been shown to significantly improve maximal power output during sports-specific movements.[24,80,82,88,96-102] These improvements are, however, typically restricted to low-load/highvelocity SSC movements.[24,102] The current literature involving the use of plyometric training does not provide much insight into the mechanisms driving improvements in maximal power. Similar to ballistic exercises, plyometrics are theorized to elicit specific adaptations in neural drive, the rate of neural activation and intermuscular control, which result in improved RFD Sports Med 2011; 41 (2)

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capacity.[98,103] Adaptations to the aforementioned mechanisms driving enhanced performance during SSC movements are also hypothesized to contribute to improved maximal power production following plyometric training.[98,103] Therefore, the high degree of specificity of plyometric training to a range of sporting movements make power training programmes incorporating plyometric exercises very effective at improving maximal power in sports-specific movements.[24,80,82,97-99] 2.4 Weightlifting Exercises

Weightlifting exercises such as the snatch or clean and jerk and their variations, some of which include the hang/power clean, hang/power snatch and high pull, are commonly incorporated into power training programmes of athletes who compete in all types of sports.[104-106] Similar to ballistic exercises, weightlifting exercises require athletes to accelerate throughout the entire propulsive phase or second pull, causing the projection of the barbell and often the body into the air.[107,108] However, they differ from ballistic exercises in that they require the athlete to actively decelerate their body mass in order to catch the barbell. The inherent high-force, high-velocity nature of weightlifting exercises creates the potential for these exercises to produce large power outputs across a variety of loading conditions. In fact, power output during weightlifting exercises has commonly been found to be greatest at loads equivalent to 70–85% of 1RM in snatch or clean.[76,109,110] Additionally, the movement patterns required in weightlifting exercises are generally believed to be very similar to athletic movements common to many sports such as jumping and sprinting.[111] Empirical observations are supported by evidence of similarities in the kinetic features of the propulsive phase in both weightlifting and jumping movements.[107,112] Significant relationships have also been observed between weightlifting exercises and power output during jumping (r = 0.58–0.93) as well as sprint performance (r = -0.57).[4,113] Despite the widespread use of weightlifting exercises to enhance power and the evidence highlighting its specificity to athletic movements common to many sports, little reª 2011 Adis Data Information BV. All rights reserved.

search exists examining the efficacy of power training with weightlifting exercises. In previously untrained men, Tricoli et al.[102] observed significant improvements in static jump and CMJ height as well as 10 m sprint performance following 8 weeks of power training with weightlifting exercises. In addition, the improvement in CMJ height was greater than the improvement following 8 weeks of plyometric training.[102] Power training with weightlifting exercises is theorized to significantly improve not only maximal power output but, more specifically, power output against heavy loads. Thus, the use of these movements in training is ideal for athletes who are required to generate high velocities against heavy loads including wrestlers, rugby union front rowers and American football linemen. The mechanisms responsible for improvements following power training using weightlifting exercises have not yet been investigated. The skill complexity involved with such movements together with the use of heavy loads are hypothesized to elicit unique neuromuscular adaptations that allow for improved RFD and superior transfer to performance. Therefore, the nature of weightlifting exercises coupled with the specificity of their movement patterns to numerous athletic movements, creates the potential for weightlifting exercises to be very effective power training exercises. 3. Load Specificity Not only is the ability to generate maximal power during sports-specific movements dependent on the type of movement involved but also the load applied to that movement. Power output varies dramatically as the load an athlete is required to accelerate during a movement changes.[9,20,76,114,115] For example, absolute peak power output during a jump squat, which is defined as a CMJ with a bar held across the shoulders, ranges from 6332 – 1085 W at 0% of 1RM to 3986 – 564 W at 85% of 1RM, a 37% variation.[76] Consequently, the loading parameters utilized in power training programmes influence the type and magnitude of performance improvements observed as well as the nature of Sports Med 2011; 41 (2)

Training to Improve Maximal Power

the physiological adaptations underlying the improvements. Kaneko et al.[20] illustrated that different training loads elicited specific changes in the force-velocity relationship and subsequently power output. Four groups completed 12 weeks of elbow flexor training at different loads – 0%, 30%, 60% and 100% of maximum isometric force (Fmax). While all groups displayed significant improvements in maximal power, the most pronounced alterations in the force-velocity relationship were seen at, and around, the load utilized during training. For example, the 0% Fmax group predominately improved power in low-force, highvelocity conditions while the 100% Fmax group predominately improved power under high-force, low-velocity conditions.[20] Stemming from this seminal research, a range of loading conditions have been endorsed to elicit improvements in maximal power output throughout the literature including heavy loads, light loads, the ‘optimal’ load as well as a combination of loads (table II). 3.1 Heavy Loads

Despite the ensuing low movement velocity, training with heavy loads equivalent to ‡80% of 1RM has been suggested to improve maximal power output based on two main theories. First, due to the mechanics of muscle contraction (i.e. force-velocity relationship) and the positive association that exists between strength and power, increases in maximal strength following training with heavy loads results in a concurrent improvement in maximal power production.[9,19,20,22,24,41,56,74] The second theory forming the basis for the prescription of heavy loads is related to the size principle for motor unit recruitment.[116-118] According to the size principle, high-threshold motor units that innervate type 2 muscle fibres, are only recruited during exercises that require near maximal force output.[119-121] Therefore, the type 2 muscle fibres, which are considered predominately responsible for powerful athletic performances, are theorized to be more fully recruited and thus trained when training involves heavy loads.[21,24,95,122] Heavy loads are typically utilized in conjunction with either traditional resistance training exercises in strength training ª 2011 Adis Data Information BV. All rights reserved.

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programmes or both ballistic and weightlifting exercises in power training programmes in an attempt to improve maximal power. Heavy loads are often prescribed in conjunction with traditional resistance training exercises in strength training programmes with the primary goal being to improve maximal strength. As a result of the subsequent increase in Fmax following training, and based on the inherent force-velocity relationship of muscle, the stronger athlete is able to generate greater maximal power output and improved power output throughout the loading spectrum.[9,19,20,22,24,41,56,74] These observations hold true for relatively weak individuals or those with a low training age and are driven by increases in myofibrillar CSA especially of type II muscle fibres, maximal neural drive and RFD capabilities.[27,56,62,74,89,123] Changes to maximal power following such training in strong, experienced athletes are of a much smaller, nonstatistically significant magnitude.[29-32] While it is possible that even small increases in elite athletes are meaningful, the use of traditional resistance training exercise with heavy loads plays an important role in initial improvements in maximal power but typically not beyond the time in which a reasonable level of strength is reached and maintained.[28] Heavy loads are also commonly used in power training programmes incorporating ballistic and/ or weightlifting exercises. While there is a paucity of research investigating the adaptations following such training, the adaptations are theorized to be different to heavy load training with traditional resistance training exercises.[21,76] Ballistic and/or weightlifting training with heavy loads would still allow for the recruitment of high threshold motor units.[124,125] However, improvements in power output following such training are hypothesized to also be due to improved RFD capabilities as well as improved rate of neural activation and inter-muscular coordination rather than being primarily driven by increased maximal strength, CSA and maximal neural activation typical of training at heavy loads with traditional resistance training exercises.[19,21] While these adaptations are theorized to positively influence maximal power output, they Sports Med 2011; 41 (2)

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would have their greatest impact at the loads utilized during training resulting in load/movement velocity specific adaptations.[9,20,21] Thus, heavy load ballistic and/or weightlifting training has the potential to beneficially influence power output in both novice/weak and experienced/strong athletes. Unfortunately, little research exists examining the efficacy of power training with heavily loaded ballistic and/or weightlifting exercises. Tricoli et al.[102] reported that weightlifting training using 4–6RM loads resulted in significant improvements in maximal jump height and 10 m sprint performance. However, this study involved relatively untrained individuals who also performed 6RM half squats as part of their programme and showed a significant improvement of approximately 43% in half squat 1RM following the training.[102] McBride et al.[21] observed improvements in peak power during 55% and 80% of 1RM jump squats but not during a 30% of 1RM jump squat following 8 weeks of ballistic jump-squat training with 80% of 1RM. These improvements were associated with improved muscle activity of the vastus lateralis during 55% and 80% of 1RM jump squats suggesting load/velocity specific adaptations.[21] While more research is required to elucidate the impact of heavy load ballistic and weightlifting training on power production and the mechanisms responsible for performance improvements, such training is theorized to be ideal for athletes required to generate high power outputs against heavy loads such as wrestlers, rugby union front rowers and American football linemen.

demonstrated that ballistic and/or plyometric training with light loads results in increases in maximal power output during sports-specific movements and improved athletic performance including various jumping, sprinting and agility tasks.[9,19-21,24,78,80-83,97-99,126] Furthermore, comparisons between light and heavy loads in ballistic training programmes that involve exercises with the same movement patterns have revealed that maximal power has a tendency to be improved to a greater degree following training with light loads.[20,21] Thus, it is well established that ballistic and/or plyometric power training with light loads is very effective at improving maximal power output in sports-specific movements. Research investigating the mechanisms responsible for these improvements is limited. The high movement velocity, RFD and power requirements of ballistic and/or plyometric power training involving light loads are theorized to elicit adaptations in the rate of neural activation and inter-muscular coordination that drive improvements.[19,21,33,78,81] Therefore, ballistic and/or plyometric training with light loads is recommended for athletes who are required to generate high power outputs during fast movements against low external loads such as in sprinting, jumping, throwing and striking tasks.[114] It is important to note, however, that these findings are only relevant when light loads are utilized with ballistic and plyometric exercise. The use of light loads with traditional resistance training exercises is not recommended because such training would not provide an adequate stimulus for adaptation in either the force or velocity requirements of such exercises.[31,77]

3.2 Light Loads

The use of light loading conditions equivalent to 0–60% of 1RM in conjunction with ballistic and/or plyometric exercises is commonly recommended and utilized in power training programmes.[9,19-21,24,80,82,83,97-99] Such training parameters permit individuals to train at velocities similar to those encountered in actual onfield movements. Furthermore, light loads are recommended due to the high RFD requirements and the high power outputs associated with such resistances.[19-21] A great deal of research has ª 2011 Adis Data Information BV. All rights reserved.

3.3 The ‘Optimal’ Load

Throughout the literature, the load that elicits maximal power production in a specific movement is commonly referred to as the ‘optimal’ load.[24,76,109,114,127] Training with the ‘optimal’ load provides an effective stimulus to elicit increases in maximal power output for a specific movement as improvements in power are most pronounced at the load used in training.[20,21] Power is maximized at approximately 30% Fmax in single muscle fibres and single-joint movements.[20,25,26,128-132] However, Sports Med 2011; 41 (2)

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the load that maximizes power in multi-joint, sports-specific movements varies depending on the type of movement involved. For example, the ‘optimal’ load typically ranges from 0% of squat 1RM in the jump squat[17,27,76,133-136] to 30–45% of bench press 1RM in the bench press throw[115,135] and up to 70–80% of snatch and/or clean 1RM in weightlifting exercises.[76,109,110] These ‘optimal’ loads vary significantly across different exercises because power output is influenced by the nature of the movement involved. Ballistic exercises allow for high forces to be generated in light load situations due to the continued acceleration throughout the movement. While the jump squat and bench press throw are both ballistic exercises, the ‘optimal’ load differs when expressed relative to a 1RM due to the differences in the load that must be projected. The jump squat requires both the mass of the body as well as any external load to be projected while only the external load is projected in the bench press throw. Although jump squats and weightlifting exercises are characterized by similar degrees of ankle, knee and hip joint kinematics, they differ markedly in the load that maximizes power output.[76] This is due primarily to the fact that only the external load is being projected in weightlifting movements and the ballistic versus semi-ballistic nature of the movements. While weightlifting exercises are performed at high velocities, the body mass must be actively decelerated in order to catch the barbell so these exercises require greater external load in order to generate the high forces necessary to optimize power output. Furthermore, the ‘optimal’ load of weightlifting exercises would be much lower if expressed as a percentage of an equivalent traditional resistance training exercise such as the deadlift, which would be similar to how the load is expressed for ballistic exercises. Additionally, the load that maximizes power in multi-joint, sports-specific movements may also vary depending on the strength level and/ or training history of the athlete. Previous research has observed the ‘optimal’ load to occur at higher loads in individuals with significantly greater maximal strength.[7,137] However, conflicting evidence exists indicating that the ‘optiª 2011 Adis Data Information BV. All rights reserved.

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mal’ load does not vary between individuals with significantly different strength levels (i.e. stronger vs weaker individuals).[17,136] Further study is required to clarify the role of maximal strength level and/or training history on the load-power relationship. Although the exact mechanisms underlying superior adaptations after training with a specific load remain unidentified, it is theorized that the ‘optimal’ load provides a unique stimulus due to specific adaptations in the rate of neural activation.[19-21] This theory is supported by several investigations demonstrating that training with the ‘optimal’ load resulted in superior improvements in maximal power production than other loading conditions.[9,20,21,24] While the scientific evidence illustrates that training at the ‘optimal’ load is very effective for improving maximal power output in a specific movement over short-term interventions lasting only 8–12 weeks, this does not necessarily mean that training at the ‘optimal’ load is the best or only way to increase maximal power over a long-term training programme. Furthermore, it is unknown if similar results would be observed when training well trained or elite athletes as much of this research has involved homogeneous groups of low to moderately trained subjects. Even so, power training programmes in which movements are performed at the ‘optimal’ load are a potent stimulus for improving maximal power output in a specific movement. 3.4 Combination of Loads

Power training using light loads improves muscular performance in the high-velocity area of the force-velocity relationship (i.e. power at high velocities against low loads), and the use of heavy loads enhances muscular performance in the high-force portion of the curve (i.e. power at low velocities against heavy loads).[9,19-21,62,130,138] The theory behind the use of a combination of loads in a power training programme is to target all areas of the force-velocity relationship in an attempt to augment adaptations in power output throughout the entire curve. Thus, it is argued that training with a combination of loads may Sports Med 2011; 41 (2)

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allow for all-round improvements in the forcevelocity relationship that results in superior increases in maximal power output and greater transfer to performance than either light or heavy load training alone.[25,26] Research has established that significant improvements in maximal power output and various athletic performance parameters occur following training with a combination of loads.[25,26,33,78,81,82,88,122,139] Furthermore, results from some of these investigations suggest that improvements in maximal power and athletic performance are more pronounced in combined light and heavy load training programmes compared with programmes involving training at a single load or other load combinations.[25,26,78,88,122] However, most of these studies did not control for the total work completed by various groups[25,26,88,122] and thus it is difficult to delineate whether the loading parameters or the differences in total work performed contributed to their observations. While equalizing the work of different training programmes has the potential to impact the optimum programme design, it is an important consideration when examining the efficacy of using a combination of loads. Cormie et al.[78] reported no differences in maximal power output or maximal jump height between a light load only programme and a combined light and heavy load programme when the total work done during training was equivalent. However, the combined training group also displayed improvements in power and jump height throughout a range of loaded jump squats and improved both Fmax and dynamic 1RM. No such improvements were observed in the light load only group.[78] These results suggest that the combination of light and heavy loads elicits greater all round improvements in the strength-power profile than power training with a light load only. However, each of the research investigations relevant to this topic were conducted on relatively in-experienced, weak subjects and typically involved a combination of ballistic exercises and traditional resistance exercises such as jumps and squats rather than a combination of ballistic exercises or weightlifting exercises with light and heavy loads (i.e. 0–80% of 1RM jump squats or 40–80% of ª 2011 Adis Data Information BV. All rights reserved.

1RM snatch/clean). Consequently, it is unknown if these findings apply to well trained athletes who already maintain a high level of strength. Additionally, it is not clear if a combination of loads within 10–30% of 1RM of the ‘optimal’ load may be more beneficial at enhancing maximal power in subjects who are well trained. Further research is also required to determine if adaptations are influenced by whether the combination of loads are used within a single set such as with complex training, a single session or in separate training sessions. 4. Velocity Specificity The theory of velocity specificity in resistance training suggests that adaptations following training are maximized at or near the velocity of movement used during training.[20,40,140-144] However, another theory exists in which training adaptations are theorized to be influenced to a greater degree by the intention to move explosively regardless of the actual movement velocity.[18] These conflicting theories have led to confusion surrounding the appropriate selection of loads and exercises to utilize during power training. Therefore, the development of an effective power training programme must include consideration of the actual and intended velocity of movement involved with training exercises. 4.1 Actual Movement Velocity

Research comparing isokinetic training at a variety of different velocities has found a velocityspecific response to training.[40,140-144] The results of these investigations typically show that highvelocity training produces greater improvements in force and power at higher movement velocities than those seen at low movement velocities. This research also demonstrates that training with low velocities results in increased force and power predominately at low movement velocities, with nonsignificant changes at higher velocities.[140-144] Some evidence also indicates smaller but significant improvements in force and power at velocities both above and below the specific training velocity.[140,143] Results of research comparing isoinertial loading in single-joint movements have also indicated Sports Med 2011; 41 (2)

Training to Improve Maximal Power

a velocity-specific response. Specifically, improvements in both force and power output were most pronounced at the velocities encountered in training.[9,20] Less research is available examining whether a velocity-specific response occurs following isoinertial training with dynamic, sportsspecific movements. McBride and co-workers[21] observed subjects who trained with low velocities using jump squats with 80% of 1RM to improve performance at low and moderate velocities and no changes in performance at high velocity. In contrast, training with the higher velocity movement of jump squats with 30% of 1RM resulted in significant improvements in power across high, moderate and low velocities. Furthermore, training with high movement velocities resulted in a trend towards improved 20 m sprint performance while training with low velocities significantly decreased sprint performance.[21] These results suggest that the training did elicit some velocityspecific adaptations that transferred to athletic performance. While the bulk of the current research indicates the presence of a velocity-specific response, the mechanisms responsible for this effect have not been determined. A comparison of the results from two studies conducted by Ha¨kkinen and associates[19,62] offer some insight into possible mechanisms. High-velocity training involving jump squats with 0–60% of 1RM resulted in a 24% improvement in isometric RFD and 38% increase in the rate of onset in muscle activation during an isometric knee extension.[19] In contrast, low-velocity training involving squats with 70–120% of 1RM did not affect either the isometric RFD or rate of muscle activation onset during the isometric knee extension.[62] These findings suggest that velocity-specific adaptations in the rate of neural activation contribute to a velocity-specific response in RFD capabilities. However, more recent research has reported that both the RFD and the rate of neural activation are enhanced in response to heavy strength training that is performed at relatively low velocities.[123] Specific adaptations to muscle architecture and contractile mechanics may also contribute to velocity-specific improvements in performance. For example, Blazevich and colleagues[49] reported ª 2011 Adis Data Information BV. All rights reserved.

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pennation angle to decrease following high-velocity training involving jumping and sprinting, and increase in response to low-velocity training involving heavy squatting. Due to the rotation of fibres required during contractions in pennate muscles, these architectural adaptations favour high and low velocity of muscle shortening, respectively.[49,145] Therefore, while it is possible that neuromuscular adaptations to training are specific to the actual velocity of movement, further research is necessary to determine the precise mechanisms driving velocity-specific adaptations. 4.2 Intention to Move Explosively

The theory that training with the intention to move explosively determines velocity-specific adaptations centres primarily on the findings of a study by Behm and Sale.[18] The study involved untrained, physical education students who trained using unilateral ankle dorsiflexions for two 8-week training blocks separated by a 3-week non-training period. One limb was trained with isometric contractions, while the other limb was trained using a high-velocity dynamic movement. Subjects attempted to make maximal ballistic dorsiflexion movements with both legs, being specifically instructed to ‘‘attempt to move as rapidly as possible regardless of the imposed resistance.’’[18] When data were pooled across both legs, the results indicated a velocity-specific response in peak torque typically expected following training with a high-velocity movement. Specifically, the greatest significant improvement in torque occurred at the training velocity and progressively smaller increases were observed as the velocity of movement decreased. No significant differences in peak torque across any of the velocities were observed between the isometric and dynamically trained legs. Based on these findings, the authors concluded that training with highvelocity movements is not necessary to elicit highvelocity-specific improvements in performance. They hypothesized that improvements are instead driven by the characteristic high rate of neural activation associated with intended ballistic contractions and the high RFD requirements of such contractions regardless if the resulting Sports Med 2011; 41 (2)

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movement is isometric or dynamic.[18] These findings have not been attempted to be replicated in a different exercise to ankle dorsiflexions, with a similar subject pool of relatively untrained students or with well trained athletes – a population commonly expected to show more sensitive adaptations to training.[72,73] Investigations comparing purposefully fast and slow movements with the same load offers no further support or rejection of this theory as these studies cannot delineate if adaptations were due to the intention to move explosively or the ensuing higher velocity movement of intentionally fast contractions.[87,146] 4.3 Actual versus Intended Movement Velocity

Two different paradigms have been suggested as the critical stimulus for velocity-specific adaptations, actual versus intended movement velocity. Training with the intention to move explosively is believed to influence adaptations to training and is vitally important during power training irrespective of the contraction type, load or movement velocity of the exercises used.[18,146] However, the bulk of the literature indicates that velocity-specific improvements in maximal power are more likely elicited by the actual movement velocity utilized during training.[9,19-21,40,49,62,140-144] Therefore, the intention to move explosively and the actual movement velocity are both vital stimuli required to elicit neuromuscular adaptations driving performance improvements following training. In order to maximize the transfer of training to performance, training should include loads that allow for similar movement velocities to those typically encountered in their sport. Additionally, athletes should attempt to perform these exercises as explosively as possible. 5. Window of Adaptation The ability to generate maximal power is influenced by a multitude of neuromuscular factors including muscle mechanics, muscle morphology, neural activation as well as the muscle environment, and the interested reader should refer to part 1[1] in this series of reviews for a detailed ª 2011 Adis Data Information BV. All rights reserved.

discussion of these factors. The multifaceted nature of maximal power production is reflected in the variety of different training stimuli that have been previously shown to effectively improve maximal power in some individuals but not in others. For example, heavy strength training improved maximal power output in relatively untrained subjects[22-24,32,85-88] but not in stronger or more experienced athletes.[32,33] The magnitude of potential adaptations in maximal power or the window of adaptation to training is heavily influenced by the specific neuromuscular characteristics of each individual athlete.[31] These neuromuscular factors can be classified by a number of main components contributing to maximal power production: slow-velocity strength, highvelocity strength, RFD, SSC ability as well as intra- and inter-muscular coordination and skill.[31] As an athlete develops a certain component and the associated neuromuscular factors to a high level, the potential for further improvements to contribute to increases in maximal power diminish. Therefore, the window of adaptation for that component decreases. For example, Wilson and associates[32] showed that 8 weeks of heavy strength training improved vertical jump and sprint performance in weak individuals, but not already strong individuals (squat 1RM : body mass = 1.16 – 0.20 and 1.80 – 0.26, respectively). As a result of a large window of adaptation for maximal power development in untrained individuals, they tend to respond to virtually any type of training,[9,20,78,82,88] whereas well trained athletes require much greater specificity and variation.[33] A training programme that focuses on the least developed component contributing to maximal power will prompt the greatest neuromuscular adaptations and thus result in superior performance improvements. Therefore, it is vital to consider an individual’s window of adaptation for each component contributing to maximal power production when developing effective and efficient power training programmes. 6. Integration of Power Training Modalities The concept of periodization has been endorsed and used frequently to maximize long-term Sports Med 2011; 41 (2)

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improvements in strength.[147-150] Through the use of cycles within an overall programme, periodization allows for variations in the intensity, volume and specificity of strength training.[147-150] This systematic approach to training is based on the General Adaptation Syndrome, which describes the ability of the body to react and adapt to stress.[151] When exposed to a new or more intense stress, their initial response usually involves a temporary drop in performance that is classified as the alarm stage.[151,152] The resistance phase represents the period in which the body is going through the process of adapting to the stimulus and is typically associated with improved performance.[148,151,152] However, if the stress is too great or continues for an extended period of time, the desired adaptations are no longer possible. Under these circumstances the exhaustion phase is reached and will result in a continued decrease in performance associated with overtraining.[151,152] The variations involved with a periodized strength training programme, which include alterations in the load, volume and exercises selected, allow for athletes to continuously adapt to training by moving from the alarm phase to the resistance phase whilst avoiding the exhaustion phase.[147-150] Therefore, the integration of various strength training techniques such as hypertrophy, basic strength and strength/ power is commonly used to elicit superior longterm improvements in maximal strength and sports performance.[147-150] Based on the same principle, there is a need for the integration of power training modalities (i.e. a periodized power training programme) if long-term improvements in maximal power are to be optimized.[31] Such an integrated approach would, for example, allow for the use of traditional resistance training with heavy loads to develop strength at slow velocities and RFD, ballistic training with light loads to enhance highvelocity strength and RFD, plyometric training to improve SSC performance and sport-specific technique training in order to advance intermuscular coordination and skill. While the use of some of these methods will improve maximal power and transfer to sports performance to a greater degree in the short term, exclusive exª 2011 Adis Data Information BV. All rights reserved.

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posure to a single power training modality renders inferior long-term developments due to the exhaustion phase being reached.[30,151,152] It is imperative that each of the modalities used involve a degree of movement, load and velocity specific to the requirements involved with the athlete’s sport. Furthermore, programme design must also specifically target the components of maximal power with the greatest window of adaptation for each athlete. A key limitation of most of the literature examining improvements in maximal power production following training is the fact that interventions typically represent an isolated mode of training monitored over a short period of time. However, with the aforementioned considerations in mind, the neuromuscular adaptations resulting from an integrated approach to power training are theorized to result in greater improvements in maximal power production than any of these modalities used in isolation.[31] 7. Conclusions and Implications The ability to generate maximal muscular power is considerably influenced by the individual’s level of strength therefore enhancing and maintaining maximal strength is essential when considering the long-term development of power. Strength training using traditional resistance training exercises with heavy loads is therefore a pivotal component of any athlete’s training programme. In order to maximize the transfer of training to performance, power training must involve the use of movement patterns, loads and velocities that are specific to the demands of the individual’s sport. Ballistic, plyometric and weightlifting exercises can be used effectively as primary exercises within a power training programme that enhances maximal power in dynamic, multi-joint movements common to many sports. The loads applied to these exercises will depend on the specific requirements of each particular sport and the type of movement being trained. The use of ballistic exercises with loads ranging from 0% to 50% of 1RM and/or weightlifting exercises performed with loads ranging from 50% to 90% of 1RM appears to be the most Sports Med 2011; 41 (2)

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potent loading stimulus for improving maximal power in complex movements. Furthermore, plyometric exercises should involve stretch rates as well as stretch loads that are similar to those encountered in each specific sport and should involve little to no external resistance. These loading conditions allow for superior transfer to performance because they require similar movement velocities to those typically encountered in sport. The window of adaptation in maximal muscular power, or the magnitude of potential for training-induced improvement following different training stimuli must be considered in light of the neuromuscular characteristics of the individual athlete. Such consideration will allow for the least developed neuromuscular factors to be targeted and, therefore, the greatest potential for improvements in maximal power output. The integration of numerous power training techniques is essential as it allows for variation within power meso-/ micro-cycles while still maintaining specificity, which is theorized to lead to the greatest longterm improvement in maximal power. Acknowledgements The authors have no potential conflicts of interest to disclose and no funding was received for this review.

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107. Garhammer J, Gregor R. Propulsion forces as a function of intensity for weightlifting and vertical jumping. J Appl Sport Sci Res 1992; 6 (3): 129-34 108. Schilling BK, Stone MH, O’Bryant HS, et al. Snatch technique of collegiate national level weightlifters. J Strength Cond Res 2002; 16 (4): 551-5 109. Kawamori N, Crum AJ, Blumert PA, et al. Influence of different relative intensities on power output during the hang power clean: identification of the optimal load. J Strength Cond Res 2005; 19 (3): 698-708 110. Haff GG, Stone MH, O’Bryant HS, et al. Force-time dependent characteristics of dynamic and isometric muscle actions. J Strength Cond Res 1997; 11 (4): 269-72 111. Hori N, Newton RU, Nosaka K, et al. Weightlifting exercises enhance athletic performance that requires highload speed strength. Strength Cond J 2005; 27 (4): 50-5 112. Canavan PK, Garrett GE, Armstrong LE. Kinematic and kinetic relationships between an Olympic-style lift and the vertical jump. J Strength Cond Res 1996; 10 (2): 127-30 113. Hori N, Newton RU, Andrews WA, et al. Does performance of hang power clean differentiate performance of jumping, sprinting, and changing of direction? J Strength Cond Res 2008; 22 (2): 412-8 114. Kawamori N, Haff GG. The optimal training load for the development of muscular power. J Strength Cond Res 2004; 18 (3): 675-84 115. Newton RU, Murphy AJ, Humphries BJ, et al. Influence of load and stretch shortening cycle on the kinematics, kinetics and muscle activation that occurs during explosive upper-body movements. Eur J Appl Physiol Occup Physiol 1997; 75 (4): 333-42 116. Schmidtbleicher D, Buehrle M. Neuronal adaptation and increase of cross-sectional area studying different strength training methods. In: de Groot G, Hollander AP, Huijing PA, et al., editors. Biomechanics X-B. Amsterdam: Free University Press, 1987: 615-20 117. Schmidtbleicher D, Haralambie G. Changes in contractile properties of muscle after strength training in man. Eur J Appl Physiol Occup Physiol 1981; 46 (3): 221-8 118. Sale DG. Influence of exercise and training on motor unit activation. Exerc Sport Sci Rev 1987; 15: 95-151 119. Hannerz J. Discharge properties of motor units in relation to recruitment order in voluntary contraction. Acta Physiol Scand 1974; 91 (3): 374-85 120. Henneman E, Clamann HP, Gillies JD, et al. Rank order of motoneurons within a pool, law of combination. J Neurophysiol 1974; 37: 1338-49 121. Henneman E, Somjen G, Carpenter DO. Functional significance of cell size in spinal motoneurons. J Neurophysiol 1965; 28: 560-80 122. Harris GR, Stone ME, O’Bryant HS, et al. Short-term performance effects of high power, high force, or combined weighttraining methods. J Strength Cond Res 2000; 14 (1): 14-20 123. Aagaard P, Simonsen EB, Andersen JL, et al. Increased rate of force development and neural drive of human skeletal muscle following resistance training. J Appl Physiol 2002; 93 (4): 1318-26 124. Desmedt JE, Godaux E. Ballistic contractions in man: characteristic recruitment pattern of single motor units of the tibialis anterior muscle. J Physiol 1977; 264: 673-93

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125. Desmedt JE, Godaux E. Ballistic contractions in fast or slow human muscles: discharge patterns of single motor units. J Physiol 1978; 285: 185-96 126. Newton RU, Rogers RA, Volek JS, et al. Four weeks of optimal load ballistic resistance training at the end of season attenuates declining jump performance of women volleyball players. J Strength Cond Res 2006; 20 (4): 955-61 127. Dugan EL, Doyle TL, Humphries B, et al. Determining the optimal load for jump squats: a review of methods and calculations. J Strength Cond Res 2004; 18 (3): 668-74 128. Bottinelli R, Pellegrino MA, Canepari M, et al. Specific contributions of various muscle fibre types to human muscle performance: an in vitro study. J Electromyogr Kinesiol 1999; 9 (2): 87-95 129. de Haan A, Jones DA, Sargent AJ. Changes in velocity of shortening, power output and relxation rate during fatigue of rat gastrocnemius muscle. Pflugers Arch 1989; 412 (4): 422-8 130. Duchateau J, Hainaut K. Isometric or dynamic training: differential effects on mechanical properties of human muscle. J Appl Physiol 1984; 56: 296-301 131. Faulkner JA, Claflin DR, McCully KK. Power output of fast and slow fibers from human skeletal muscles. In: Jones NL, McCartney N, McComas AJ, editors. Human muscle power. Champaign (IL): Human Kinetics Inc., 1986: 81-94 132. van Leeuwen JL. Optimum power output and structural design of sarcomeres. J Theor Biol 1991; 149: 229-56 133. Cormie P, McBride JM, McCaulley GO. Power-time, force-time, and velocity-time curve analysis during the jump squat: impact of load. J Appl Biomech 2008; 24 (2): 112-20 134. Sheppard JM, Cormack S, Taylor KL, et al. Assessing the force-velocity characteristics of the leg extensors in well-trained athletes: the incremental load power profile. J Strength Cond Res 2008; 22 (4): 1320-6 135. Bevan HR, Bunce PJ, Owen NJ, et al. Optimal loading for the development of peak power output in professional rugby players. J Strength Cond Res 2010; 24 (1): 43-7 136. Nuzzo JL, McBride JM, Dayne AM, et al. Testing of the maximal dynamic output hypothesis in trained and untrained subjects. J Strength Cond Res 2010; 24 (5): 1269-76 137. Driss T, Vandewalle H, Quievre J, et al. Effects of external loading on power output in a squat jump on a force platform: a comparison between strength and power athletes and sedentary individuals. J Sports Sci 2001 Feb; 19 (2): 99-105 138. Jones K, Bishop P, Hunter G, et al. The effects of varying resistance-training loads on intermediate- and high-

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Correspondence: Dr Prue Cormie, School of Exercise and Biomedical Health Sciences, Edith Cowan University, 270 Joondalup Drive, Joondalup, WA 6027, Australia. E-mail: [email protected]

Sports Med 2011; 41 (2)

Sports Med 2011; 41 (2): 147-166 0112-1642/11/0002-0147/$49.95/0

REVIEW ARTICLE

ª 2011 Adis Data Information BV. All rights reserved.

Physiological Profiles of Elite Judo Athletes Emerson Franchini,1 Fabrı´cio B. Del Vecchio,1,2 Karin A. Matsushigue1 and Guilherme G. Artioli1,3 1 Martial Arts and Combat Sports Research Group, School of Physical Education and Sport, University of Sa˜o Paulo, Sa˜o Paulo, Brazil 2 Superior School of Physical Education, Federal University of Pelotas, Pelotas, Brazil 3 Laboratory of Applied Nutrition and Metabolism, School of Physical Education and Sport, University of Sa˜o Paulo, Sa˜o Paulo, Brazil

Contents Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2. Somatotype and Body Composition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3. Maximal Strength . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.1 Isometric Strength . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.2 Dynamic Strength . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4. Muscle Power . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5. Muscular Endurance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6. Anaerobic Profile . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7. Aerobic Profile . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8. Conclusions and Future Directions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Abstract

147 148 149 149 150 152 155 156 156 158 164

To be successful in international competitions, judo athletes must achieve an excellent level of physical fitness and physical condition during training. This article reviews the physiological profiles of elite judo athletes from different sex, age and weight categories. Body fat is generally low for these athletes, except for the heavyweight competitors. In general, elite judo athletes presented higher upper body anaerobic power and capacity than nonelite athletes. Lower body dynamic strength seems to provide a distinction between elite and recreational judo players, but not high-level judo players competing for a spot on national teams. Even maximal isometric strength is not a discriminant variable among judo players. However, more studies focusing on isometric strength endurance are warranted. Although aerobic power and capacity are considered relevant to judo performance, the available data do not present differences among judo athletes from different competitive levels. Typical maximal oxygen uptake values are around 50–55 mL/kg/min for male and 40–45 mL/kg/min for female judo athletes. As for other variables, heavyweight competitors presented lower aerobic power values. The typical differences commonly observed between males

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and females in the general population are also seen in judo athletes when analysing anaerobic power and capacity, aerobic power, and maximal strength and power. However, further research is needed concerning the differences among the seven weight categories in which judo athletes compete.

1. Introduction Currently, there are seven weight categories for both male (<60 kg, 66 kg, 73 kg, 81 kg, 90 kg, 100 kg and >100 kg) and female judo competitors (<48 kg, 52 kg, 57 kg, 63 kg, 70 kg, 78 kg and >78 kg). Judo competitions are also divided according to athletes’ age, as follows: cadets (15–16 years of age), junior (17–19 years of age), senior (>20 years of age, although younger athletes might compete) and master (>30 years of age). The main competitions in judo are the Olympic Games and World Championship for each age category. Each weight division implies marked differences in technical and tactical aspects as well as in physiology, performance and body composition among competitors of the different weight classes. Thus, it directly influences some key aspects of athletes’ preparation, including the management of bodyweight and body composition. Judo is a dynamic, high-intensity intermittent sport that requires complex skills and tactical excellence for success.[1] As judo athletes have to perform a great number of actions during each match, the physical demand of a single match is high. Typically, judo medalists perform five to seven matches during international competitions, with each match having a 5-minute time limit. If a judo athlete obtains an ippon (full point), the match ends. On the other hand, since 2003, when the time allotted for the contest finished and the scores/penalties are equal for both athletes (i.e. the match draws), the result of the contest is decided by a ‘Golden Score’. If neither athlete obtains any score in the Golden Score period the match continues for another 3 minutes and is decided by the referees (Hantei decision). Thus, a judo match may last from a few seconds to 8 minutes, depending on the scores obtained by the contestants. However, a typical high-level judo match lasts 3 minutes, with 20- to 30-second ª 2011 Adis Data Information BV. All rights reserved.

periods of activity and 5–10 seconds of interruption.[2,3] Moreover, a significant portion of the matches last 3–4 minutes.[2] To be effective, judo techniques should be applied with accuracy, within a good ‘window of opportunity’, with strength, velocity and power. This short burst of energy is supplied mainly by anaerobic metabolism. In contrast, the maintenance of the intermittent work performed during a match, as well as the recovery process during the short intervals, are mainly supported by aerobic metabolism. Additionally, aerobic metabolism is especially important for an effective recovery between matches.[4] With these facts, it can be established that judo is a complex sport with demands comprising a number of specific characteristics to achieve a high level in competition. It is well known that understanding the characteristics of elite athletes can provide insightful information regarding what is needed for competitive success. Therefore, the objective of the present narrative review is to present and discuss the knowledge currently available on the main physical and physiological characteristics of judo competitors. When available, specific considerations will be directed to age, sex, weight and competitive level differences across groups of athletes. For this purpose, a literature search of PubMed, SportDiscus and ISI Web of Knowledge was performed with the specific keywords ‘judo’, ‘judo and performance’, ‘judo and physical fitness’, ‘judo and body composition’, ‘judo and aerobic fitness’, ‘judo and anaerobic fitness’, ‘judo and strength’ and ‘judo and physiology’. The retrieved studies were further selected based on their purpose, methodology, and number and characteristics of the judo athletes evaluated. Additionally, references cited in these articles were considered whenever limited information in a specific topic was evident. Sports Med 2011; 41 (2)

Physiological Profiles of Elite Judo Athletes

2. Somatotype and Body Composition In judo, as occurs in any other combat sport, where competitors are divided by weight classes, optimal body composition is a major concern.[5] Thus, judo athletes attempt to maximize the amount of lean tissue, minimize the amount of body fat, and minimize total bodyweight. Considering the broad range of weight classes (48 kg to >78 kg for female judo athletes and 60 to >100 kg for male judo athletes), it is impossible to establish a single body type or anthropometric profile for all judo athletes.[6] Nevertheless, there is some similarity throughout much of the range in terms of characteristic somatotypes and a predominance of mesomorphy (table I).[8,10] In terms of somatotype, the judo athlete is generally thought to have a profile that accentuates the mesomorphic properties (very high muscularity, low linearity and low fat). Among females, the endomorphic component has values near to the mesomorphic one. However, caution should be exercised when interpreting these results as they could have been influenced by the inclusion of heavyweight athletes. Table II presents the body composition of high-level judo athletes. World and Olympic level male judo athletes usually have <10% body fat.[6,14,32] However, caution is needed when using this value as a re-

149

ference, because most studies predicted body fat by skinfold thickness measurements and, therefore, the specific mean error of estimate of each equation should be taken into consideration. Ideally, a prospective judo athlete should employ sound nutrition and aerobic training principles to reach a steady-state fat percentage of 7–10%.[26] Since they compete at their weight categories, it is not surprising that they are very strong per kilogram of bodyweight. This means that they must have a very small percentage of body fat compared with an average male of the same height and age. Indeed, the range of fat percentage extends from approximately 4% to 9%, with the exception of the heavyweights (>78 kg for females and >100 kg for males). Only one study presented a significant difference in body fat among bestranked judo athletes and lower ranked athletes.[19] 3. Maximal Strength Maximal strength can be defined as the maximal torque that a muscle or a muscle group can generate at a specified or determined velocity.[33] It depends upon the ability of the nervous system to recruit motor units, the ability of the muscle to utilize the energy anaerobically (mainly adenosine triphosphate and phosphocreatine) for muscle contractions, the amount of motor units simultaneously

Table I. Somatotype of high-level judo athletes Athlete characteristics

Endomorphy (mean – SD)

Mesomorphy (mean – SD)

Ectomorphy (mean – SD)

Reference

Hungarian team (n = 18)

3.6 – 1.9

7.0 – 1.5

1.6 – 0.9

Farmosi[7]

Japanese (n = 13)

3.4 – 2.0

8.5 – 1.4

1.0 – 0.6

Kawamura et al.[8]

French (n = 10)

1.2 – 0.5

7.6 – 0.9

1.5 – 0.7

Kawamura et al.[8]

Brazilian team 1999 (n = 7)

2.7 – 1.3

7.9 – 1.6

1.1 – 0.6

Silva et al.[9]

WCP under 71 kg (n = 18)

2.3 – 0.4

5.6 – 0.5

1.9 – 0.4

Claessens et al.[10]

WCP 71–86 kg (n = 9)

3.0 – 0.5

6.0 – 0.7

1.7 – 0.7

Claessens et al.[10]

WCP >86 kg (n = 11)

4.1 – 0.9

6.2 – 0.6

1.3 – 0.4

Claessens et al.[10]

Brazilian university team 1996 (n = 6)

2.7 – 1.8

6.2 – 1.5

1.6 – 1.2

Franchini et al.[11]

Brazilian university team 1996 (n = 7)

4.1 – 1.3

5.0 – 1.1

1.7 – 1.2

Franchini et al.[11]

Brazilian team 1999 (n = 7)

4.3 – 1.3

5.1 – 0.9

1.1 – 1.0

Franchini et al.[12]

Brazilian elite (n = 28)

3.6 – 1.9

5.1 – 1.7

1.5 – 0.9

Mello and Fernandes Filho[13]

Male

Female

WCP = World Championship players.

ª 2011 Adis Data Information BV. All rights reserved.

Sports Med 2011; 41 (2)

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Table II. Percentage body fat in judo athletes Athlete characteristics

Body mass (kg) [mean – SD]

Body fat (%) [mean – SD]

Prediction equation reference

Reference

8.9 – 0.8

Enilina[14]

Farmosi[7]

14.0 – 7.3

[14]

Farmosi[7]

Male Hungarian team (n = 7) Hungarian team (n = 11) Canadian team 1987 (n = 22) US (elite; n = 8)

60–70a >70

b

75.4 – 12.3 91.5 – 2.7

9.3 – 2.1 10.8 – 1.9

Enilina

Lohman

[15]

Thomas et al.[16]

Jackson and Pollock

[17]

Callister et al.[18]

Jackson and Pollock

[17]

Callister et al.[19]

US (elite; n = 18)

83.1 – 3.8

8.3 – 1.0

Canadians (n = 17)

79.3 – 14.6

10.5 – 1.0

Drinkwater and Ross[20]

Little[21]

Brazilian university team (n = 6)

86.9 – 34.4

11.1 – 5.1

Drinkwater and Ross[20]

Franchini et al.[11]

Polish (n = 15)

82.9 – 16.4

13.7 – 3.4

Slaughter et al.[22]

Sterkowicz et al.[23]

Brazilian university team 2000 (n = 13)

89.0 – 16.0

13.7 – 5.2

Drinkwater and Ross

[20]

[25]

Franchini et al.[24] Koury et al.[26]

Brazilian Olympic team 2000 (n = 7)

NR

7.0 – 3.0

Croatians (elite; n = 6)

NR

12.0 – 1.2

NR

Sertic et al.[27]

Brazilian team A (n = 7)

90.6 – 23.8

11.4 – 8.4

Jackson and Pollock[17]

Franchini et al.[6]

Brazilian team B (n = 15)

86.5 – 16.3

10.1 – 5.7

Jackson and Pollock[17]

Franchini et al.[6]

59.1 – 7.9

20.9 – 2.0

Piechaczek[28]

Obuchowicz-Fidelus et al.[29]

Lohman et al.

Female Polish team (n = 22) Canadians (n = 8) US (elite; n = 7)

62.3 – 5.2 56.3 – 0.9

15.2 – 2.1 15.8 – 1.2

Drinkwater and Ross

[20]

Little[21]

Jackson et al.

[30]

Callister et al.[18]

[30]

Callister et al.[19]

US (elite; n = 9)

53.8 – 1.6

15.2 – 1.0

Jackson et al.

Brazilian university team (n = 7)

66.9 – 16.3

16.1 – 3.0

Drinkwater and Ross[20]

Franchini et al.[11]

Brazilian Olympic team 2000 (n = 9)

66.0 – 8.0

22.0 – 5.0

Jackson et al.[30]

Koury et al.[31]

Croatians (n = 8)

NR

16.6 – 4.3

NR

Sertic et al.[27]

a

Athletes body mass ranged from 60 kg to 70 kg.

b

Athletes body mass was >70 kg.

NR = not reported.

active and the size of cross-sectional area of muscle fibres present. Because of the relationship to crosssectional area and size, strength is often analysed relatively to bodyweight; the so-called relative strength is especially informative in bodyweight classified sports such as judo.[34] As muscle contractions might occur in different manners, they will be discussed separately in the next sections. 3.1 Isometric Strength

An isometric action results in no change in muscle length and although force is developed, as no movement occurs, no work is performed.[33] As judo athletes have to grip the opponent’s uniform (judogi), early studies have focused on isometric grip strength. Table III presents the grip strength of different groups of judo athletes. ª 2011 Adis Data Information BV. All rights reserved.

Isometric grip strength has not been investigated in detail for different weight categories, while only two studies[7,36] have addressed this topic. In one study,[36] greater left isometric grip strength was observed in the middle weight category compared with the light weight category. However, there is no mention concerning the number of left-handed athletes in each group, which prevents any conclusion on whether the difference is caused by the weight category or by the number of left-handed athletes in the first group. The other study did not identify any difference among weight categories.[7] A third study presented in table III did not perform any statistical comparison among the different weight groups, but it seems that the isometric strength increases according to the weight category.[35] When correlation analysis is conducted, one study[16] Sports Med 2011; 41 (2)

Physiological Profiles of Elite Judo Athletes

identified a positive relationship (r = 0.76) between body mass and isometric grip strength. Sex differences were reported in only one study.[11] The male group presented higher absolute right and left isometric grip strength compared with the female group. However, when

151

values were presented relative to body mass, no difference was observed. In Canadian judo players,[21] no statistical comparison between male and female athletes was reported, but it is possible to infer that both absolute and relative isometric grip strength were higher for the male group.

Table III. Isometric handgrip strength (IHGS) of judo athletes Study

Athlete characteristics; sex

Right IHGS (kgf) [mean – SD]a

Left IHGS (kgf) [mean – SD]a

Matsumoto et al.[35]

Japanese university athletes (~66 kg); M (n = 12): 1967

43.8

43.8

1968

49.3

49.3

Candidates to the 1967 World Championship

44.9

45.1

1967

50.8

47.7

1968

53.3

52.2

Candidates to the 1967 World Championship

56.8

52.0

1967

55.3

49.5

1968

59.6

55.6

Candidates to the 1967 World Championship

54.2

51.5

All (n = 24)

64.9 – 8.9

59.7 – 8.8

<71 kg (n = 13)

56.8 – 7.7

54.4 – 7.5

71–86 kg (n = 9)

59.7 – 6.1

59.3 – 7.6

All (n = 18)

59.9 – 11.2

55.7 – 10.7

<71 kg (n = 7)

54.3 – 5.4

50.9 – 5.4

>71 kg (n = 11)

63.9 – 12.8

59.0 – 12.4

Elite (n = 26)

51.0 – 10.0

49.0 – 10.0

Non-elite (n = 66)

42.0 – 11.0

40.0 – 10.0

54.3 – 8.3

53.2 – 7.4

M (n = 6)

49.5 – 12.8

47.2 – 12.4

F (n = 7)

32.3 – 7.6

32.2 – 7.8

56.4 – 6.6

55.7 – 6.6

Junior F (n = 9)

32.1 – 3.5

29.3 – 5.3

Senior F (n = 8)

31.8 – 5.8

30.6 – 5.4

Cadet M (n = 17)

39.8 – 12.7

39.4 – 10.0

Junior M (n = 9)

52.0 – 8.3

50.6 – 8.5

Senior M (n = 17)

57.7 – 9.0

54.0 – 10.4

World Championship university athletes (~73 kg; n = 18):

University athletes (~83 kg; n = 8):

Claessens et al.[36]

Farmosi[7]

Franchini et al.[37]

Franchini et al.[24]

High-level Belgian judo athletes:

Hungarian team; M:

Brazilian judo athletes; M:

Brazilian university team (2000); M: All (n = 13)

Franchini et al.[11]

Thomas et al.[16]

Brazilian university team (1996):

Canadian team (1987); M: All (n = 22)

Little[21]

a

Canadian athletes:

Data for Matsumoto et al.[35] presented as mean values.

F = female; kgf = kilogram force; M = male.

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Thus, it can be hypothesized that high-level male and female judo athletes differ less in isometric grip strength when compared with lower level male and female judo athletes, probably because high-intensity training can decrease the difference in relative strength. Differences in isometric grip strength were reported between cadet judo athletes and both junior and senior judo athletes.[21] However, when an index of isometric strength (including grip, back and arm) was expressed relative to body mass, only cadet and senior athletes differed.[21] It is also interesting to note that the isometric grip strength of high-level judo athletes has not exhibited an increase over the last 40 years, because the values measured in Japanese athletes during the 1960s[35] are quite similar to those reported later in more recent studies. Furthermore, an important aspect for consideration is the fact that no difference was observed between elite and non-elite judo players,[37] and most of the groups on table III would be classified only as ‘good’ compared with the US population.[38] Thus, it is likely that measurement of isometric strength endurance may be more relevant to judo athletes’ evaluation than the measurement of maximal strength, since the athletes have a near continuous grip during a judo match and the maximal strength is not maintained for a long period. However, no studies were found concerning isometric grip strength endurance in judo athletes. 3.2 Dynamic Strength

The one-repetition maximum (1RM) test has been used for both evaluating and prescribing strength training.[39] However, 1RM data from judo athletes are limited in the literature. Table IV presents the 1RM results found in judo athletes from different levels and for different exercises. In one study,[34] maximal absolute and relative squat strength differed between recreational and international level judo athletes, while no differences were found among groups for the bench press exercise. However, when athletes of similar competitive level were compared (main team vs ª 2011 Adis Data Information BV. All rights reserved.

reserves in a national squad) no differences were reported for bench press, row and squat 1RM values.[6] It is important to highlight that the bench press values presented in table IV are in the 60–80th percentile of the US population,[38] which suggests that these judo athletes do not present an excellent maximal strength profile. Studies on female judo athletes’ maximal strength are scarcer, but one study[32] has reported values lower than their male counterparts and comparable to those verified in non-athletes.[38] Some studies[40,41] presented values of strength on specific judo machines, which can provide a more realistic perspective and a more specific and performance-related evaluation. Tests conducted on isokinetic equipment, although not specific to judo movements, seem to be important to establish relations of torque or strength among muscles with antagonist actions as well as different speeds of movement. Table V presents the results of strength tests conducted on isokinetic equipment in judo athletes. When judo athletes from different age classes are compared,[43] both knee and shoulder flexion and extension strength (measured in two velocities, 60/s and 240/s) were higher in seniors compared with juniors. Only one study presented a statistical comparison between male and female judo athletes.[19] The results showed a similar trend to that observed in non-athletes, i.e. the male athletes presented a higher absolute strength. This difference decreased when the value was relative to the fat-free mass.[19] In a study conducted with the 1996 Japanese Olympic Team,[44] women’s elbow extension was lower than that measured in men using both 60/s (92% of men values) and 180/s (88% of men values). However, when values were expressed relative to the cross-sectional area, a different result was obtained, with higher dynamic strength in females. Both men and women were stronger in their knee extensor than in their knee flexor muscles. Women were also stronger in their elbow extensor than in their elbow flexor muscles (flexor values represented 77% from that measured in the extensor muscles). However, men attained almost the same value for both elbow muscle groups (extensor and flexor).[19] Other studies with male judo Sports Med 2011; 41 (2)

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153

Table IV. One-repetition maximum (1RM) data in different exercises performed by judo athletes Study

Sample characteristics; sex

Exercise

1RM (kg) [mean – SD]

Thomas et al.[16]

Canadian team (1989); M (n = 22)

Bench press

100 – 21

Fagerlund and Ha¨kkinen[34]

Finnish athletes; M: International (n = 7)

Bench press Squat

National (n = 7)

Bench press Squat

Recreational (n = 7)

Bench press Squat

Franchini et al.[6]

96 – 12 166 – 32 87 – 20 140 – 36

Brazilian team (2002); M: Main team (n = 7)

Reserves (n = 13)

Sbriccoli et al.[32]

96 – 20 185 – 25

Italian Olympic team (2004): M (n = 6)

F (n = 5)

Bench press

110 – 25

Row

116 – 21

Squat

104 – 27

Bench press

110 – 23

Row

115 – 24

Squat

104 – 18

Bench press

160 – 30

Lat machine

142 – 15

Leg press

397 – 8

Deadlift

127 – 11

Leg curl

77 – 4

Bench press

74 – 13

Lat machine

84 – 11

Leg press

305 – 19

Deadlift

94 – 6

Leg curl

40 – 4

F = female; M = male.

athletes reported similar values of extensor-flexor ratio for shoulder (71–77%)[43] and knee (74%).[42] Trunk flexion corresponded to 71–81% of the extension value.[45] Despite the fact that righthanded judo athletes (i.e. the right hand grabs the lapel on judogi) perform a left trunk rotation in many techniques, no difference was observed in the dynamic strength between sides, suggesting that rotation dominance seems to be determined more by coordination than by strength.[45] A comparison among weight categories using isokinetic equipment was not found in the literature. The available information on this aspect indicates that in absolute values heavier athletes are stronger than lighter athletes. The halfheavyweight category (<95 kg when the study was conducted) were considered the weakest among ª 2011 Adis Data Information BV. All rights reserved.

the seven weight classes;[19] however, there is no clear explanation for this finding. When judo athletes of different competitive levels are compared, the only evidence found was that higher ranked female US judo athletes tend to present a higher elbow flexor and extensor muscles isokinetic strength compared with lower ranked athletes.[19] Tumilty et al.[43] have compared isokinetic shoulder flexion and extension between judo athletes and other athletic groups. The authors have found that the Australian junior judo athletes were weaker, and the senior group were stronger. The results presented by Kort and Hendriks[45] for trunk flexion, extension and rotation demonstrated higher values for judo athletes compared with cyclists. Sports Med 2011; 41 (2)

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Table V. Torque (Nm or Nm/kg) or strength (N or N/cm2) during isokinetic maximal tests performed by judo players Study

Sample characteristics; sex

Exercise

Taylor and Brassard[42]

1979 Canadian team; M (n = 19)

Knee extension:

Result (mean – SD)

right

148.0 – 41.0 Nm

left

146.0 – 28.0 Nm

Knee flexion:

Tumilty et al.[43]

Australian junior; M (n = 9)

right

105.0 – 17.0 Nm

left

108.0 – 23.0 Nm

Shoulder: 60/s extension

1.1 – 0.2 Nm/kg

60/s flexion

0.8 – 0.1 Nm/kg

240/s extension

0.7 – 0.2 Nm/kg

240/s flexion

0.6 – 0.1 Nm/kg

Knee:

Senior; M (n = 8)

60/s extension

2.6 – 0.4 Nm/kg

60/s flexion

1.6 – 0.3 Nm/kg

240/s extension

1.4 – 0.2 Nm/kg

240/s flexion

1.1 – 0.2 Nm/kg

Shoulder: 60/s extension

1.4 – 0.2 Nm/kg

60/s flexion

1.1 – 0.1 Nm/kg

240/s extension

1.0 – 0.1 Nm/kg

240/s flexion

0.8 – 0.1 Nm/kg

Knee: 60/s extension

Ichinose et al.[44]

1.7 – 0.2 Nm/kg

240/s flexion

1.4 – 0.2 Nm/kg

Elbow extension:

M (n = 5)

60/s

215.9 – 11.8 N

180/s

188.8 – 16.9 N

60/s

198.2 – 14.9 N

180/s

165.7 – 4.6 N

M (n = 5) F (n = 6) Kort and Hendriks

2.0 – 0.4 Nm/kg

240/s extension Japanese Olympic team (1996):

F (n = 6)

[45]

3.1 – 0.4 Nm/kg

60/s flexion

Dutch national and international levels; M (n = 28)

60/s

14.5 – 1.0 N/cm2

180/s

12.7 – 1.1 N/cm2

60/s

16.7 – 0.9 N/cm2

180/s

14.3 – 1.2 N/cm2

Trunk flexion: 30/s

3.3 – 0.3 Nm/kg

60/s

3.3 – 0.2 Nm/kg

90/s

3.3 – 0.2 Nm/kg

120/s

3.3 – 0.3 Nm/kg

Trunk Extension: 30/s

4.7 – 0.8 Nm/kg

60/s

4.6 – 0.6 Nm/kg

90/s

4.6 – 0.5 Nm/kg

120/s

4.1 – 0.5 Nm/kg Continued next page

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155

Table V. Contd Study

Sample characteristics; sex

Result (mean – SD)

Exercise Trunk rotation:







30/s

2.8 – 0.4 N m/kg

60/s

2.8 – 0.5 N m/kg

90/s

2.8 – 0.5 N m/kg

120/s

2.8 – 0.5 N m/kg

F = female; M = male.

4. Muscle Power Muscle power has been characterized in judo athletes through the use of free weight exercises[34] or vertical jump tests.[16,36,43,46] A study conducted with Finnish judo athletes[34] demonstrated that international level athletes presented higher values in the strengthvelocity curve for the squat jump compared with a group of recreational practitioners: the time to achieve half of the maximal strength was shorter for the international level group. Given that the

muscle groups mainly activated during a judo throwing technique are those of the lower body, and considering that these techniques have to be performed at high speed and against a great resistance from the opponent, this difference can be a consequence of this adaptation. However, when the bench press exercise was used to determine the strength-velocity curve, no difference was found in international, national or recreational level groups. This may be due to the multiple actions (power, endurance and strength) performed by the upper body during a typical judo

Table VI. Vertical jump height in judo athletes of different age, weight categories and competitive levels Study Ishiko and Tomiki

Athlete characteristics; sex [46]

Claessens et al.[36]

Farmosi[7]

Tumilty et al.[43]

Sertic et al.[27]

a

Height (cm) [mean – SD]a

Judo practitioners from Kodokan; M: 20–29 y (n = 5)

51.6

30–39 y (n = 6)

45.7

40–49 y (n = 7)

46.3

50–59 y (n = 10)

37.1

60–69 y (n = 5)

29.8

70–79 y (n = 2)

20.0

Belgian athletes; M: Total (n = 24)

52.5 – 6.7

<71 kg (n = 13)

53.3 – 6.4

71–86 kg (n = 9)

50.2 – 7.4

Hungarian team; M: Total (n = 18)

53.3 – 5.6

<71 kg (n = 7)

50.6 – 5.5

>71 kg (n = 11)

55.2 – 5.0

Australian athletes; M: Junior (n = 9)

44.0 – 7.0

Senior (n = 8)

52.0 – 8.0

Croatian athletes: M (n = 6)

58.3 – 5.4

F (n = 8)

40.8 – 4.3

Data for Ishiko and Tomiki[46] presented as mean values.

F = female; M = male.

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match. Table VI presents the vertical jump test results in judo athletes. One of the first studies of power characteristics of judo athletes used the vertical jump test[46] to compare different age groups. It demonstrated a significant decrease after the athletes reached 50 years of age. Another study[43] compared junior and senior judo players and found a higher performance in the vertical jump test in seniors compared with juniors. Only one study presenting results from male and female athletes was found,[27] but no comparison between groups was made. A comparison among weight categories was conducted in 729 college judo athletes.[47] When all the weight categories were considered, a small variation was observed from the under 60 kg to the under 95 kg weight categories, being lower than values found in the over 95 kg category. As no correction by weight was presented, only the absolute power of these athletes can be fully compared. The relevancy of this measurement (vertical jump height) can be inferred from one study that presented a positive correlation between the percentage of winnings during the European World Cup competitions and the vertical jump performance in male judo athletes (r = 0.69). This can be an indicator that lower body power is important for judo performance, probably because a powerful action is needed during many throwing techniques.[48] 5. Muscular Endurance Muscular endurance is the ability of a muscle or group of muscles to sustain repeated contrac-

tions against a resistance for an extended period of time.[33] In judo, most of the studies on muscular endurance have evaluated this capacity using sit-ups and push-ups.[16,42,49] The results from these studies are presented in table VII. Based on the results depicted above, it is possible to conclude that judo athletes are, in general, above the 90th percentile for push-ups, and between the 80th and 90th percentile for sit-ups in classificatory tables.[38] This can be interpreted as a high need for muscular endurance in these muscle groups for a successful judo performance. 6. Anaerobic Profile High-intensity, intermittent sports rely mostly on anaerobic sources, as the decisive actions depend on powerful movements.[50] During a judo match, the anaerobic contribution seems to be very important, although other sources also contribute significantly to the total work performed.[1] The anaerobic evaluation is quite complex because no gold standard test is available.[51] However, as is seen in other sports, the Wingate test has been used to evaluate the anaerobic profile of judo athletes.[16,32] The typical Wingate test evaluates variables (peak power, mean power and fatigue index)[52] that have been reported for upper and lower body actions in judo athletes.[21,23,29,37] In athletes from sports in which upper body actions are important, such as wrestling and judo, the upper body Wingate test has been used more often than the lower body test.[52-54] Table VIII presents the main results of studies evaluating judo players’ anaerobic performance.

Table VII. Muscular endurance in different exercises performed by judo athletes Study

Athlete characteristics; sex

Exercise

Result (repetitions) [mean – SD]

Taylor and Brassard[42]

Canadian team (1979); M (n = 19)

Push-ups

72 – 16

Thomas et al.[16]

Canadian team (1989); M (n = 22)

Sertic et al.[27]

Croatian athletes: M (n = 6)

Sit-ups

48 – 10

Bench press at 70% 1RM

16 – 3

Sit-ups

F (n = 8) Krstulovic et al.[49]

Croatian junior athletes; M (n = 40)

58 – 6 55 – 4

Push-ups

56 – 8

Sit-ups

42 – 12

1RM = one-repetition maximum; F = female; M = male.

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Table VIII. Upper body Wingate test performance in judo players Study

Athlete characteristics; sex

AMP (W) [mean – SD]

Little[21]

Canadians (various competitive levels); M:

RMP (W/kg) [mean – SD]

APP (W) [mean – SD]

RPP (W/kg) [mean – SD] 7.1 – 1.6

Cadet (n = 17)

282 – 70

4.9 – 1.0

407 – 172

Junior (n = 9)

395 – 62

5.7 – 0.6

573 – 117

8.4 – 1.1

Senior (n = 17)

447 – 87

5.6 – 0.5

675 – 133

8.5 – 0.7

Canadians (various competitive levels); F:

Franchini et al.[12]

Franchini et al.[37]

Junior (n = 9)

219 – 48

3.8 – 0.6

322 – 88

5.5 – 1.1

Senior (n = 8)

253 – 41

4.0 – 0.6

366 – 59

5.9 – 0.9

Brazilian team (1999 Panamerican Games); F (n = 5) 70 days before

NR

4.3 – 0.2

NR

5.8 – 0.3

30 days before

NR

4.5 – 0.6

NR

5.8 – 0.8

Brazilians; M: Elite (n = 34)

468 – 63

5.7 – 0.8

623 – 80

7.6 – 1.0

Non-elite (n = 56)

394 – 53

5.4 – 0.8

493 – 92

7.0 – 1.3

Franchini et al.[24]

Brazilian university team; M (n = 13)

555 – 63

6.2 – 0.7

724 – 67

8.1 – 0.8

Mickiewitz et al.[55]

Polish juniors (n = 85)

671 – 89

8.8 – 0.8

NR

NR

Sharp and Koutedakis[56]

British team; M (n = 6)

736 – 221

8.5 – 0.5

916 – 301

10.6 – 0.8

Thomas et al.[16]

Canadian team; M (n = 22)

653 – 87

8.7 – 1.2

852 – 131

11.3 – 0.8

Obuchowicz-Fidelus et al.[29]

Polish team; F (n = 20)

253 – 36

4.3 – 0.5

331 – 50

5.7 – 0.6

AMP = absolute mean power; APP = absolute peak power; F = female; M = male; NR = not reported; RMP = relative mean power; RPP = relative peak power.

The values presented by the judo athletes from a range of different national teams were quite high and their performance during the upper body Wingate test was above the 90th percentile for lower body values measured in non-athletes.[57] This result has been interpreted as a consequence of the high upper body demand during judo-specific activities performed in the training sessions.[16] A comparison among age groups using the upper body Wingate test[21] has shown that cadet judo athletes have lower absolute peak and mean power when compared with both junior and senior athletes, and lower relative peak power compared with senior judo athletes. These differences are probably related to maturational aspects and have also been reported in wrestlers[58] and in non-athletes.[59-62] When athletes from different competitive levels are compared for performance in the upper body Wingate test, higher values of peak and mean power were measured in elite (national or international medalists) than in non-elite athletes (non-medalists).[37] Further evidence supporª 2011 Adis Data Information BV. All rights reserved.

ting the relevance of upper body anaerobic performance for judo was found in a correlational study,[48] which reported moderate and significant correlations between the percentage of wins during European World Cup competitions and upper body Wingate test peak power (r = 0.66) and mean power (r = 0.68) in female judo players. In high-level male judo athletes there was a moderate, yet significant, correlation (r = 0.76) between relative total work performed in two consecutive upper body Wingate tests (separated by 3-minute intervals) and the number of attacks performed during a match simulation.[48] Although the comparison of upper body anaerobic performance of judo athletes in different weight categories has not been carried out with a large number of athletes, it is possible to conclude that the athletes from heavyweight categories have higher absolute values of both peak and mean power than the lighter athletes. In contrast, when body mass values are considered (i.e. relative mean and peak power are the variables), Sports Med 2011; 41 (2)

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lighter athletes present higher power than the heavyweight athletes. This fact is probably due to the higher percentage body fat of heavier athletes compared with lighter athletes combined with the fact that a higher percentage fat has been associated with lower relative total work during two Wingate tests (r = -0.87) in high-level judo athletes.[24] When sexes are compared, females present values of approximately 70% of those observed in males, which is similar to what has been observed in the general population.[52] However, it is important to note that high-level female judo athletes showed values similar to that presented by males from lower competitive levels or from younger age groups, indicating that the strategy of mixed training sessions by sex is possible when anaerobic fitness is the variable considered. In fact, it is common in actual training environments for high-level female judo athletes to perform ‘randori’ (free sparring) with male athletes of lower age or less skill. Performance of judo athletes in lower body Wingate tests has also been investigated. Table IX presents the main published results. When different competitive level groups are compared for performance, the pattern largely differs from that observed in the upper body Wingate test (i.e. the lower body Wingate test is not an adequate performance predictor compared with the upper body test). This probably occurs due to the low demand imposed on the lower body in judo. However, it is possible to verify differences between weight categories and to confirm the inferences raised in the upper body test concerning the lower relative results presented by heavyweight categories compared with lighter categories in both males and females.[65] Additionally, it is possible to verify that women’s values are about 80% of the male values, which are slightly higher than the percentage observed in the upper body test and somewhat similar to that observed in non-athletic groups.[57] In healthy male non-athletes, the ability to perform anaerobic work with their arms was about 51% of the capacity to perform anaerobic work with the lower limbs, while data of Canadian Judo Team athletes[16] show a ratio of 81%. When analysing a group of judo players at the regionª 2011 Adis Data Information BV. All rights reserved.

al level[66] the ratio was closer to the healthy subjects than the elite wrestling or judo athletes. The highest upper/lower body ratio may be due to differences in distribution of muscle fibre type in the upper and lower body (a higher percentage of fast twitch fibres in the upper body) and/or due to a greater emphasis on training directed to the upper body rather than the lower body.[66,67] Other studies have assessed judo athletes in a variety of anaerobic tests. Some have used cycle ergometer tests,[43,68] jumps[69,70] or tests involving a running time trial.[42,49] Based on these studies it can be concluded that judo athletes of both sexes show great power and anaerobic capacity when exercise involves the upper body, and this aspect is a potential discriminating factor in performance. Moreover, power and anaerobic capacity values from the lower body are not prominently higher than that observed in other athletic groups[68] or even in active individuals.[38,52,57] Additionally, these variables do not appear to be predictors of performance and success in judo. 7. Aerobic Profile Although decisive actions in judo are mainly dependent on anaerobic metabolism, aerobic fitness seems to be important in high-intensity intermittent exercise,[71] which is the case with judo, as it permits better recovery during the short rest periods between efforts. The aerobic fitness of judo players has been assessed essentially via maximal oxygen uptake . . (VO2max) or peak oxygen uptake (VO2peak) for the aerobic power component and via the socalled anaerobic threshold for the aerobic capacity component. Both aerobic power and capacity have been considered relevant to judo performance because it has been hypothesized that a higher value for these variables should allow judo athletes to maintain a higher intensity during the match, delay the accumulation of metabolites associated with fatigue processes (e.g. H+ and Pi) and improve the recovery process between two consecutive matches.[63,72] In fact, there is some evidence that judo athletes who normally obtain their scores in the final Sports Med 2011; 41 (2)

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Table IX. Lower body Wingate test performance in judo athletes from different levels and nationalities Study

Sample characteristics; sex

Gariod et al.[63]

French athletes (inter-regional and national); M:

AMP (W) [mean – SD]

RMP (W/kg) [mean – SD]

APP (W) [mean – SD]

RPP (W/kg) [mean – SD]

Endurance (n = 10)

860 – 74

12.0 – 1.0

1051 – 65

14.6 – 0.9

Explosive (n = 6)

861 – 67

12.0 – 0.9

1166 – 79

16.2 – 1.1

Wojczuk et al.[64]

Polish junior class (different levels); M (n = 19)

666 – 91

8.7 – 1.0

Mickiewitz et al.[55]

Polish (different levels); M:

870 – 100

11.3 – 1.0

Junior (n = 109)

871 – 115

11.4 – 1.2

NR

Senior (n = 257)

917 – 149

11.5 – 1.2

NR

NR

F senior (n = 16)

571 – 66

9.6 – 0.9

NR

NR

Sterkowicz et al.[23]

Polish (high-level); M (n = 15)

713 – 120

8.6 – 0.7

942 – 194

11.4 – 0.9

Sbriccoli et al.[32]

Italian Olympic team (2004): 12.1 – 2.4

NR

M (n = 6)

558 – 86

5.4 – 1.1

1236 – 202

F (n = 5)

286 – 11

4.3 – 0.5

635 – 21

9.5 – 1.1

Thomas et al.[16]

Canadian M team (n = 22)

804 – 138

10.7 – 0.7

1032 – 161

13.7 – 1.1

Borkowski et al.[65]

Polish team 1994–7a; M: <60 to >95 kg

NR

8.8 – 0.8

NR

12.1 – 1.2

<60–95 kg

NR

9.0 – 0.8

NR

12.4 – 0.8

+95 kg

NR

7.1 – 0.9

NR

9.6 – 1.0

NR

9.1 – 0.6

NR

12.5 – 0.9

Polish team 1998–9b; M: <60 to <100 kg Polish team 1994–9c; M:

Borkowski et al.[65]

Principal

NR

9.0 – 0.5

NR

12.3 – 0.9

Reserves

NR

9.0 – 0.6

NR

12.1 – 0.9

<48 to >72 kg

NR

7.8 – 0.7

NR

10.5 – 1.0

<48 to <72 kg

NR

8.0 – 0.6

NR

10.7 – 0.8

>72 kg

NR

6.7 – 0.8

NR

8.9 – 1.1

NR

7.8 – 0.5

NR

10.6 – 0.6

Polish team 1994–7d; F:

Polish team 1998–9e; F: <48 to <78 kg Polish team 1994–9f; F:

a

Principal

NR

7.7 – 1.0

NR

10.3 – 1.3

Reserves

NR

7.7 – 0.8

NR

10.2 – 1.0

Fifty-eight subjects, no specifications about the number in each category.

b

Seventeen subjects, no specifications about the number in each category.

c

Seventy-five subjects, no specifications about the number of principal and reserve athletes.

d

Forty-nine athletes, no specifications about the number in each category.

e

Eighteen athletes, no specifications about the number in each category.

f

Sixty-seven athletes, no specifications about the number of principal and reserve athletes.

AMP = absolute mean power; APP = absolute peak power; F = female; M = male; NR = not reported; RMP = relative mean power; RPP = relative peak power.

. moments of a match present higher VO2max values and were able to resynthesize gastrocnemius creatine phosphate faster compared with others who score earlier in the match and had better perª 2011 Adis Data Information BV. All rights reserved.

formance in lower body Wingate tests.[63] Furthermore, a faster recovery after high-intensity intermittent exercise has also been associated with aerobic fitness.[73,74] Athletes with higher aerobic Sports Med 2011; 41 (2)

160

power are probably able to perform supramaximal activities at a relatively lower intensity compared with those with lower aerobic power. This would be even more important considering the matches that last several minutes and probably explains the importance of aerobic power for judo performance.[75] Table X presents the aerobic power of male and female judo players. Although the studies reported on table X have used different protocols and exercise modes, it seems that most of the male judo players have . VO2max values between 50 and 60 mL/kg/min, while most of the females have values between 40 and 50 mL/kg/min. This difference between sexes is quite similar to that reported in non-athletic groups.[89] Regarding the influence of aerobic power on judo performance, it is important to consider that the studies comparing elite versus non-elite male judo athletes,[37] principals versus reserves in national teams[6,65] or athletes involved in direct competition,[81] did not observe any significant difference between these groups. Thus, although aerobic power can be relevant to judo performance, its development is not enough to discriminate the competitive level of judo athletes. When considering female judo athletes, the only study found comparing members and reserves of the Brazilian Olympic judo team, also did not find any difference in aerobic power between the groups.[48] However, it is important to point out that most of these studies were cross sectional and analysed lower body modes of exercise (e.g. treadmill or . cycle ergometer) to determine VO2max. In fact, one study reported a decrease in lower body aerobic power in judo athletes prior to their main competition, but conversely presented an increase on upper body aerobic power at the same period.[48] Thus, if the high demand on the upper body during a typical judo match was taken into the analysis it is possible to suggest that the upper body aerobic power should be of greater focus and study than lower body aerobic power. When weight categories are compared, it is possible to note a decrease in relative aerobic power (mL/kg/min) parallel to an increase in the body mass.[16,32] It is common to find values <50 mL/kg/min in heavyweight male and ª 2011 Adis Data Information BV. All rights reserved.

Franchini et al.

<45 mL/kg/min in heavyweight female judo athletes. However, only one study statistically com. pared VO2max among weight categories. Male heavyweights presented lower values compared with athletes from all other weight classes, yet, . VO2max among female athletes was similar regardless of weight class.[65] Aerobic capacity in judo players has been evaluated through the so-called anaerobic threshold velocity (ATV). Table XI presents the ATV of judo athletes. As shown in table XI, judo athletes of different levels have similar ATV, which is not as high as in aerobically trained athletes. Additionally, ATV did not change in the final phase of competitive preparation in highly trained female judo players.[12] Thus, based on these observations, in the evaluation process of judo athletes, other aspects should be focused on. On the other hand, Franchini et al.[88] reported a negative, significant correlation between the ATV and blood lactate after a judo match simulation (r = -0.69 to -0.87, depending on the moment blood lactate was measured) and a positive, significant correlation between ATV and mean power in an upper body Wingate test performed 17 minutes after the judo match simulation either when the recovery after this simulation was passive (r = 0.61) or active (r = 0.84). This suggests that a higher aerobic capacity could be important in the recovery process between consecutive matches. In view of this, future studies should focus on the effect of aerobic capacity training, especially for the upper body on the recovery process between typical judo matches. Regarding upper body aerobic capacity, one study has used onset blood lactate accumulation (OBLA; 4 mmol/L of blood lactate concentration) to evaluate this variable in high-level Polish judo athletes.[65] The author found that male athletes presented their OBLA at a higher intensity (2.08 – 0.29 to 2.25 – 0.24 W/kg, depending on the weight category) than female judo athletes (1.10 – 0.24 to 1.79 – 0.32 W/kg, depending on the weight category). No difference was found in upper body cycle ergometry OBLA between principals and reserves in either male (principals = 2.17 – 0.26 W/kg; reserves = 2.11 – 0.26 W/kg) or female groups (principals = 1.64 – 0.28 W/kg; Sports Med 2011; 41 (2)

Physiological Profiles of Elite Judo Athletes

161

Table X. Aerobic power of judo athletes Ergometer

. VO2max (mL/kg/min) [mean – SD]

Reference

US judo players (elite; n = 8)

Treadmill

53.2 – 1.4

Callister et al.[18]

US judo players (elite; n = 18)

Treadmill

55.6 – 1.8

Callister et al.[19]

Japanese team (n = 13)

Treadmill

45.9 – 4.8

Ebine et al.[76]

Japanese (university level; n = 17)

Bicycle

40.0 – 5.5

Ikai et al.[77]

Japanese (university level; n = 6)

Treadmill

Sample characteristics Male

Sugiyama[78] 50.5 – 3.0

pre-training

52.5 – 3.4

after 1-y judo training Koreans (elite; n = 29)

Treadmill

Canadian

Treadmill

61.1 – 10.6

Little[21]

cadets (n = 17)

57.6 – 3.4

juniors (n = 9)

59.3 – 4.0

seniors (different levels; n = 17)

Oh et al.[79]

53.8 – 5.6

Junior French (different levels; n = 9)

NR

Polish

NR

juniors (n = 54)

Majean and Gaillat[80]

59.8 – 8.5

Mickiewitz et al.[55] 60.2 – 6.8

seniors (different levels; n = 157)

60.2 – 8.7

Canadian team (n = 19)

NR

57.5 – 9.5

Taylor and Brassard[42]

Canadian team (n = 22)

Treadmill

59.2 – 5.2

Thomas et al.[16]

Australians (elite; n = 17)

Bicycle

53.2 – 5.1

Tumilty et al.[43]

Spanish

Bicycle

winners (n = 14)

Suay et al.[81] 52.8 – 0.8

defeated (n = 14)

50.4 – 1.11

Spanish (n = 17)

Bicycle

French

Bicycle

45.6 – 1.5a

Gariod et al.[63]

endurance profile; regional level (n = 10)

63.2 – 7.9

power profile; regional level (n = 6)

54.6 – 3.0

Polish team 1994–7b

Borkowski et al.[65]

Bicycle

<60 to >95 kg

Salvador et al.[82]

56.6 – 5.6

<60 to 95 kg

57.6 – 4.6

>95 kg

45.2 – 3.9

Polish team 1998–9c <60 to <100 kg

55.6 – 3.2

Polish team 1994–9d principal

54.5 – 4.9

reserves

54.4 – 5.6

Polish (national level; n = 15)

Treadmill

Sterkowicz et al.[23]

50.1 – 6.5 a

Degoutte et al.[1]

French (regional level; n = 16)

Bicycle

55.0 – 0.5

French (regional level; n = 16)

Bicycle

55.0 – 2.9

Degoutte et al.[83]

French (national level; n = 10)

Bicycle

44.5 – 6.0

Cottin et al.[84]

Spanish (7 men and 1 woman; national and international level)

Treadmill

48.4 – 7.4

Bonitch et al.[85]

Bicycle

53.8 – 5.2

Vidalin et al.[86]

Bicycle (indirect)

50.9 – 7.0

French (regional level; n = 8)

Continued next page

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Sports Med 2011; 41 (2)

Franchini et al.

162

Table X. Contd Sample characteristics

Ergometer

French (different levels)

NR

junior (n = 8)

. VO2max (mL/kg/min) [mean – SD]

Reference Maejan and Gaillat[80]

53.0 – 5.4

juvenile (n = 13)

46.3 – 7.8

French (practitioners; n = 8)

Bicycle

52.0 – 5.3

Ahmaidi et al.[87]

French regional and inter-regional levels (n = 20)

Bicycle (indirect)

47.6 – 7.1

Frings-Dresen et al.[68]

Brazilians

Treadmill

Franchini et al.[88]

national and international levels (n = 5)

63.0 – 10.3

state level (n = 7)

62.9 – 9.3

city level (n = 5) Brazilians

64.9 – 5.5

elite (n = 15)

58.1 – 10.8

non-elite (n = 31) Brazilian team

63.3 – 10.6 Franchini et al.[6]

Cooper test

principal (n = 7)

48.3 – 8.1

reserves (n = 15) Italian Olympic team 2004 (n = 6)

Franchini et al.[37]

Treadmill

49.6 – 5.5 Treadmill

47.3 –10.9

Sbriccoli et al.[32]

Female Polish team 1994–7e

Borkowski et al.[65]

Bicycle

<48 to >72 kg

49.9 – 6.6

<48 to <72 kg

50.7 – 5.5

>72 kg

39.5 – 12.0

Polish team 1998–9f <48 to <78 kg

49.9 – 4.8

Polish team 1994–9g 48.6 – 8.6

principals

47.2 – 6.0

reserves French (regional level; n = 4)

Bicycle

44.0 – 14.7

Bicycle (indirect)

43.0 – 11.8

Polish seniors (different levels; n = 15)

NR

49.9 – 5.1

Canadians (different levels)

Treadmill

juniors (n = 9)

Vidalin et al.[86] Mickiewitz et al.[55] Little[21]

45.1 – 3.7

seniors (n = 8)

43.7 – 3.5

US (elite; n = 7)

Treadmill

51.9 – 0.8

Callister et al.[18]

US (elite; n = 9)

Treadmill

52.0 – 1.4

Callister et al.[19]

Cuban team (n = 8)

NR

47.4 – 10.3

Pujadas et al.[73]

Japanese team (n = 16)

Treadmill

42.1 – 4.4

Ebine et al.[76]

Italian Olympic team 2004 (n = 5)

Treadmill

52.9 –4.4

Sbriccoli et al.[32]

a

Standard error.

b

Fifty-eight athletes, no details concerning number of judo players per weight category.

c

Seventeen athletes, no details concerning number of judo players per weight category.

d

Seventy-five athletes, no details concerning the number of principal and reserve members.

e

Forty-nine athletes, no details concerning the number of judo athletes per weight category.

f

Eighteen athletes, no details concerning the number of judo athletes per weight category.

g

Sixty-seven athletes, no details concerning the number of principal and reserve judo athletes per weight category. . NR = not reported; VO2max = maximal oxygen uptake.

ª 2011 Adis Data Information BV. All rights reserved.

Sports Med 2011; 41 (2)

Physiological Profiles of Elite Judo Athletes

163

Table XI. Anaerobic threshold velocity (ATV) in judo players Study

Sample characteristics

ATV (km/h) [mean – SD]

Sterkowicz et al.[23]

Polish (national level; n = 15)

12.0 – 0.9

Franchini et al.[12]

Female Brazilian team (n = 5):

Franchini et al.[88]

70 days before the Panamerican Games (1999)

9.3 – 1.60

30 days before the Panamerican Games (1999)

9.7 – 1.3

Brazilians: National and international levels (n = 5)

Franchini et al.[37]

10.7 – 0.8

State level (n = 7)

9.3 – 1.7

City level (n = 5)

9.2 – 1.5

Brazilians: National and international level (n = 16)

10.8 – 1.5

State level (n = 40)

10.8 – 1.7

reserves = 1.69 – 0.29 W/kg), suggesting that this variable is not discriminant for judo performance, at least in this level. Similar findings were observed with running as the exercise model. In the same study, both male and female heavyweight judo athletes presented their OBLA at a lower intensity compared with judo players from other

weight categories,[65] confirming the findings from Thomas et al.[16] concerning the. lower aerobic fitness (in that case measured by VO2max) of heavyweight judo players. Ventilatory threshold (VT) has also been used to evaluate the aerobic capacity of judo players. The main results are presented in table XII.

Table XII. Ventilatory threshold (VT) intensity in judo athletes during treadmill exercise Study Ebine et al.

Sample characteristics [76]

. VT (%VO2max) [mean – SD]

Japanese team (VT1): M (n = 13)

57.5 – 3.3

F (n = 16)

57.0 – 4.3

Oh et al.[79]

Elite Korean (VT1; n = 29)

66.3 – 18.7

Bonitch et al.[85]

8 Spanish (7 men and 1 woman; national and international level):

Little[21]

VT1

63.7 – 6.6

VT2

79.3 – 7.2

Canadians (different levels; VT2) M: Cadets (n = 17)

78.6 – 4.8

Juniors (n = 9)

77.0 – 5.5

Seniors (n = 17)

78.7 – 6.6

F:

Callister et al.[19]

Sbriccoli et al.[32]

Juniors (n = 9)

80.7 – 7.8

Seniors (n = 8)

85.1 – 5.7

Americans (elite): M (n = 18)

84.4 – 1.0

F (n = 9)

87.9 – 1.2

Italian Olympic team (2004): M (n = 6)

80.7 – 20.0

F (n = 5)

87.1 – 11.0

. F = female; M = male; %VO2max = percentage of maximal oxygen uptake.

ª 2011 Adis Data Information BV. All rights reserved.

Sports Med 2011; 41 (2)

Franchini et al.

164

. . The percentage of VO2max (%VO2max) in which the VT identified was similar to those found in physically active individuals, but lower than in highly aerobically trained athletes.[89] This fact strengthens the belief and provides more evidence that aerobic metabolism is not highly developed in high-level judo athletes. Additionally, the only study comparing different age groups did not find any difference for VT.[21] When males and females are compared, . the results seem to indicate higher values (%VO2max) in males, although no detail about this aspect was given in these studies.[19,21,32,76] 8. Conclusions and Future Directions Successful judo athletes have very low levels of body fat – both male and female – with the exception of heavyweight athletes. Mesomorphy is the most predominant somatotype component in male athletes, while females have similar components of mesomorphy and endomorphy. Moreover, highlevel competitive judo athletes present with highly developed dynamic strength, muscular endurance, anaerobic power and capacity as well as aerobic power and capacity. These variables seem to be more prominent in the upper body than in the lower body, suggesting that physical preparation should focus on improvement in the upper body. Muscle power, in contrast, appears to be better developed in the lower body. Isometric grip strength is only slightly above the average of the non-athlete population. However, aerobic power and capacity are not highly developed in these athletes. Although the above-mentioned characteristics have been consistently demonstrated in high-level judo athletes and, therefore, this may be considered as an ideal profile when preparing an athlete for engaging in high-level judo, much less is known regarding the differences among weight classes and sexes. Indeed, the development of evaluation tools more specific to judo and more longitudinal studies, would greatly contribute to elucidating the determination of weight class- and sex-specific profiles. Moreover, studies using allometric scaling would be of great importance for a better characterization of the weight classes and for understanding the differences among them. ª 2011 Adis Data Information BV. All rights reserved.

Acknowledgements No sources of funding were used to assist in the preparation of this review. The authors have no conflicts of interest that are directly relevant to the content of this review.

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55. Mickiewitz G, Starczenska J, Borkowski L. Judo, ovvero sforzo breve di grande intensita`. Athlon 1991; 4: 42-6 56. Sharp NCC, Koutedakis Y. Anaerobic power and capacity measurements of the upper body in elite judo players, gymnasts and rowers. Australian J Sci Med Sport 1987; 19 (3): 9-13 57. Maud P, Shultz BB. Norms for the Wingate anaerobic test with comparison to another similar test. Res Q Exerc Sport 1989; 60 (2): 144-51 58. Terbizan DJ, Seljevold PJ. Physiological profile of age-group wrestlers. J Sports Med Phys Fitness 1996; 36 (3): 178-85 59. Falk B, Bar-Or O. Longitudinal changes in peak aerobic and anaerobic mechanical power of circumpubertal boys. Pediatric Exerc Sci 1993; 5: 318-31 60. Nindl BC, Mahar MT, Harman EA, et al. Lower and upper body anaerobic performance in male and female adolescent athletes. Med Sci Sports Exerc 1995; 27 (1): 235-41 61. Inbar O, Bar-Or O. Anaerobic characteristics in male children and adolescents. Med Sci Sports Exerc 1986; 18 (3): 264-9 62. Blimkie CJ, Roache P, Hay JT, et al. Anaerobic power of arms in teenage boys and girls: relationship to lean tissue. Eur J App Physiol Occup Physiol 1988; 57: 667-83 63. Gariod L, Favre-Juvin A, Novel V, et al. Evaluation du profit energetique des judokas par spectroscopie RMN du P31. Sci Sports 1995; 10 (4): 201-7 64. Wojczuk J, Wojcieszak I, Zdanowicz R. Anaerobic work capacity in athletes. Biol Sport 1984; 1 (2): 119-30 65. Borkowsky J, Faff J, Starczewska-Czapowska J. Evaluation of the aerobic and anaerobic fitness in judoists from the Polish national team. Biol Sport 2001; 18: 107-11 66. Franchini E, Teixeira S, Vecchio FB, et al. Poteˆncia aero´bia e anaero´bia para membros superiores e inferiores em judocas. III Congreso de la Asociacio´n Espan˜ola de Ciencias del Deporte, 2004 [compact disk]. Valencia: Gra´ficas Mari Montan˜ana, S.L., 2004 67. Horswill CA, Miller JE, Scott JR, et al. Anaerobic and aerobic power in arms and legs of elite senior wrestlers. Int J Sports Med 1992; 13 (8): 558-61 68. Frings-Dresen M, Eterradossi J, Favre-Juvin A. Puissances maximales ae´robie, anae´robie alactique et force musculaire isome´trique des skieurs alpins, skiurs de fond et judokas. Med Sport 1987; 61 (2): 98-102 69. Carratala´ V, Pablos C, Carque´s L, et al. Valoracio´n de la fuerza explosiva, ela´stico-explosiva de los judokas infantiles y cadetes del equipo nacional espan˜ol [online]. Available from URL: http://www.judoinfo.com/pdf/re search2.pdf [Accessed 2004 Nov 5] 70. Pujadas A, Collazo Garay BC, Rodriguez Leal EA. Aptitud anaerobia en deportistas de combate del sexo femenino. Rev Int Meda Cienc Actividad Fı´ s Dep 2005; 19: 283-94 71. Tomlin DL, Wenger HA. The relationships between aerobic fitness, power maintenance and oxygen consumption during intense intermittent exercise. J Sci Med Sport 2002; 5 (3): 194-203 72. Castarlenas JL, Sole´ J. El entrenamiento de la resistencia en los deportes de lucha com agarre: una propuesta integradora. Apunts: Educ Fı´ s Deportes 1997; 1 (47): 81-6 73. Franchini E, Takito MY, Nakamura FY, et al. Influeˆncia da aptida˜o aero´bia sobre o desempenho em uma tarefa anaero´bia la´ctica intermitente. Motriz 1999; 5 (1): 58-66

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74. Muramatsu S, Horiyasu T, Sato Si, et al. The relationship between aerobic capacity and peak power during intermittent anaerobic exercise of judo athletes. Bull Assoc Sci Study Judo 1994; 8: 151-60 75. Gorostiaga EM. Coste energe´tico del combate de judo. Apunts: Educ Fı´ s Deportes 1988; 25: 135-9 76. Ebine K, Yoneda I, Hase H, et al. Physiological characteristics of exercise and findings of laboratory tests in Japanese elite judo athletes. Med Sport 1991; 65 (2): 73-9 77. Ikai M, Haga S, Kaneko M. The characteristics of physical fitness of judoists from the viewpoint of respiratory and cardiovascular functions. Bull Assoc Sci Study Judo 1972; 4: 43-52 78. Sugiyama M. Energy expenditure of throwing techniques in judo. IJF Judo Conference; 1999 Sep 1; Birmingham. Birmingham: International Judo Federation, 1999: 14 79. Oh JK, Han SC, Shin YO, et al. Genotypes of ACE and ApoE, cardiorespiratory fitness and blood lipid profile in elite judo players. In: Koskoulou M, Geladas N, Klissouras V, editors. Book of abstracts of the 7th Annual Congress of the European College of Sport Science 2002. Athens: European College of Sport Science, 2002: 366 80. Majean H, Gaillat ML. E´tude de l’acide lactique sanguin chez le judoka en fonction des me´thodes d’entraıˆ nement. Med Sport 1986; 60 (4): 194-203 81. Suay F, Salvador A, Gonza´lez-Bono E, et al. Effects of competition and its outcome on serum testosterone, cortisol and prolactin. Psychoneuroendocrinology 1999; 24 (5): 551-66 82. Salvador A, Suay F, Gonza´lez-Bono E, et al. Anticipatory cortisol, testosterone and psychological responses to judo competition in young men. Psychoneuroendocrinology 2003; 28 (3): 364-75 83. Degoutte F, Jouanel P, Filaire E. Mise em e´vidence de la sollicitation du cycle des purines nucle´otides lors d’un combat de judo. Sci Sports 2004; 19: 28-33 84. Cottin F, Durbin F, Papelier Y. E´tude comparative de l’analyse spectrale de la fre´quence cardiaque au cours de l’exercice sur ergocycle et de l’entraıˆ nement en judo. Sci Sports 2001; 16 (6): 295-305 85. Bonitch J, Ramirez J, Femia P, et al. Validating the relation between heart rate and perceived exertion in a judo competition. Med dello Sport 2005; 58: 23-8 86. Vidalin H, Dubreuil C, Coudert J. Judokas ceinture noire. Suivi physiologique: e´ tudes biome´trique et bioe´ nerge´tique – suvi de l’entraıˆ nement. Med Sport 1988; 62 (4): 184-9 87. Ahmaidi S, Portero P, Calmet M, et al. Oxygen uptake and cardiorespiratory responses during selected fighting techniques in judo and kendo. Sports Med Train Rehab 1999; 9 (2): 129-39 88. Franchini E, Yuri Takito M, Nakamura FY, et al. Effects of recovery type after a judo combat on blood lactate removal and on performance in an intermittent anaerobic task. J Sports Med Phys Fitness 2003; 43 (4): 424-31 89. Wilmore DL, Costill JH. Physiology of sport and exercise. 2nd edition. Champaign (IL): Human Kinetics, 1999

Correspondence: Dr Emerson Franchini, Av. Prof. Melo Morais, 65 – Cidade Universita´ria, Sa˜o Paulo (SP), 05508030, Brazil. E-mail: [email protected]

Sports Med 2011; 41 (2)

Sports Med 2011; 41 (2): 167-176 0112-1642/11/0002-0167/$49.95/0

REVIEW ARTICLE

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Should Performance-Enhancing Drugs in Sport be Legalized under Medical Supervision? Urban Wiesing University of Tuebingen, Tuebingen, Germany

Contents Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2. What Does Legalization of Performance-Enhancing Drugs under Medical Supervision Mean?. . . . . 3. Restrictions on Athlete Freedom through Doping Controls . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4. The Effectiveness of the Controls and the Credibility of Sport . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5. What Impact would Legalizing Performance-Enhancing Drugs in Competitive Sport Have? . . . . . . 6. The ‘Gentle’ Pressure to Use Performance-Enhancing Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7. Effects of Doping on Performance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8. The Meaning of Sport. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9. The Exemplary Role of Sport . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10. Children and Adolescents and the Legalization of Performance-Enhancing Drugs . . . . . . . . . . . . . . 11. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Abstract

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This review examines the question of whether performance-enhancing drugs should be permitted in sport under the control of physicians, and evaluates the expected outcomes of such a scenario. Such a change in regulation would need to be tightly controlled because of the risks involved. The results of legalizing performance-enhancing drugs in competitive sport would be either unhelpful or negative, and the unwanted aspects of doping control would not disappear. Athletes, including children and adolescents who wanted to pursue competitive sports, would be forced to take additional, avoidable health risks. The ‘natural lottery’ of athletic talents would be compensated for only partially by use of performance-enhancing agents. It would also be complemented by another ‘natural lottery’ of variable responses to doping measures, combined with the inventiveness of doping doctors. There would be no gain in ‘justice’ (i.e. fairer results that reflected efforts made) for athletes as a result of legalizing doping. Legalization would not reduce restrictions on athletes’ freedom; the control effort would remain the same, if not increased. Extremely complicated international regulations would have to be adopted. The game of the ‘tortoise and the hare’ between doping athletes and inspectors would remain because prohibited but not identifiable practices could still provide additional benefits from use of permissible drugs. Audience mistrust, particularly toward athletes who achieved outstanding feats, would remain

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because it would still be possible that these athletes were reliant on illegal doping practices. Doping entails exposing the athletes to avoidable risks that do not need to be taken to increase the appeal of a sport. Most importantly, the function of sport as a role model would definitely be damaged. It is not necessary to clarify the question of what constitutes the ‘spirit of sport’ and whether this may be changed. From a practical point of view, a legalization of performance-enhancing drugs in sport should not be considered for the simple reason that it has no advantages but many disadvantages.

1. Introduction The doping problem in sport has yet to be solved. One must continue to assume that controls do not identify all athletes who use performanceenhancing drugs.[1] As a result, a general suspicion has arisen that some of the most outstanding achievements in sport may have been achieved by doping. For this reason, several authors have claimed that controlled use of performance-enhancing drugs in sport should be permitted.[2-5] If that were to happen, the central argument against doping, i.e. the fairness argument, would immediately be rendered irrelevant (assuming that all athletes used performance-enhancing drugs within the permitted boundaries), and a ban on doping would be more difficult to justify. This review investigates whether a ban on doping should be included in the rules of sport and discusses the possible consequences of the legalization of performance-enhancing drugs under medical supervision. 2. What Does Legalization of Performance-Enhancing Drugs under Medical Supervision Mean? Any legalization of performance-enhancing drugs in sport, if it were to occur, would need to be subject to limitations. This is not disputed by either opponents or supporters,[2,3,6] for complete legalization would also sanction actions that introduced risks and possibly irreversible damage to an athlete’s health. That would certainly be unacceptable, even if the athlete were willing to accept the risks and damaging effects, because it is inconsistent with the favourable health requirements of sport. In extreme cases, the medicallyinduced, transient success achieved by doping ª 2011 Adis Data Information BV. All rights reserved.

would be paid for with definite and permanent damage to health or even loss of life. This is considered to be too high a price to pay in sport, even in a society that permits self-destructive behaviour. Thus, even if performance-enhancing drugs were to be legalized in sport, some possible doping activities would remain banned. Only those doping actions, which were considered to involve acceptable risks, would be permitted. How the appropriate limits of the use of performance-enhancing drugs can be determined is by no means self-evident and requires further investigation. The current lack of knowledge means deciding which doping activities lead to which unwanted effects is often difficult to determine, particularly with regard to the long-term perspective. This lack of knowledge is particularly problematic in relation to new substances. Theoretical considerations alone suggest that adverse effects should be anticipated if a substance actually enhances the athletic performance; indeed, as stated by the President’s Council on Bioethics, ‘‘y until proven otherwise, it makes sense to follow this prudent maxim: No biological agent powerful enough to achieve major changes in body or mind is likely to be entirely safe or without side effects.’’[7] This consideration should be kept in mind even in cases of doping in which unwanted side effects are supposed to be rare. Moreover, if a legalization of performanceenhancing drugs in sport were to be introduced, it would need to be clarified who should determine the permissible limits of use of such drugs. This could not be left to the discretion of an individual physician, as assessments of the acceptability of risks in doping may vary. Moreover, athletes who were willing to take risks would search for the most helpful doctor. This would mean that risks Sports Med 2011; 41 (2)

Legalization of Medically Supervised Performance-Enhancing Drugs

to athletes that many deemed unacceptable would be taken, and those athletes willing to take these risks would have an advantage over their opponents. Thus, the concept of equal opportunities for all athletes would be compromised by a physician factor. To avoid this, the limits of doping would need to be specified in advance and independent of the physician-patient relationship. However, doing this would need to have not only the necessary scientific expertise to evaluate the risks associated with specific doping activities but also to evaluate the level and nature of risks that are considered acceptable in sport. Furthermore, to ensure comparability of conditions for athletes, such rules would need to be established and ratified internationally. Thus, an international organization with the required expertise and authority to make such evaluations would be needed to determine the permissible limits of doping in sport. The mandated limitations on the use of performance-enhancing drugs could relate to particular methods of administration or substances, the dosages of agents used or the biological effects of doping, e.g. changes in hormone levels or blood parameters such as haemoglobin mass. In addition, the criteria would have to be specified when doping would need to be stopped because the ‘beneficial’ effects are outweighed by the adverse effects. All limits on doping would be based on whether the risk to the athlete was still considered acceptable. Indeed, this principle is confirmed by supporters of a legalization of performanceenhancing drugs;[2,3] as Savluescu et al.,[2] for instance, have noted, ‘‘There is one limit: safety.’’ Ensuring the safety of athletes in the event of a legalization of performance-enhancing drugs would require internationally coordinated, costly and complicated regulations that would require considerable effort and result in extensive controls. There might be rare instances of doping in sport that had acceptable side effects, but making these permissible would add further difficulties in terms of defining limits and introducing further controls. In short, even if performance-enhancing drugs were to be legalized in competitive sport, there would still be a specific portion of doping activity that would remain prohibited, and limits concerning what is allowed and not allowed, as ª 2011 Adis Data Information BV. All rights reserved.

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well as the responsibility for enforcing those limits, would need to be determined. Nothing would be gained in terms of eliminating the need for regulation of doping in sport. What role would be left for physicians if performance-enhancing drugs were to be legalized under medical supervision? Medical supervision would be concerned only with the development and, if necessary, production of performanceenhancing drugs, their use within the permissible boundaries and controlling their effects. Further responsibilities and, in particular, assessing which risks are acceptable for the athlete to take, should not, as noted earlier in this section, be assigned to the physician. Nevertheless, even with pre-determined limits on the permissibility of performance-enhancing drugs, physicians would always retain a degree of autonomy in terms of determining the optimal doping regimen for their athletes. 3. Restrictions on Athlete Freedom through Doping Controls Enforcement of the present ban on performanceenhancing drugs depends on extensive and logistically complex controls which, if they are effective at all, considerably limit the athlete’s freedom. However, would a legalization of performanceenhancing drugs change anything in the intensity of the control system or the limitations on the athlete’s freedom? No, because, as discussed in section 2, the legalization would not be without limits, mainly to avoid the risks to the athlete. Therefore, the doping control system would remain as complicated as it is now but with the different goal of detecting the use of illegal substances due to their risk. Supporters of a legalization of performanceenhancing drugs believe that concerns about athletes’ health would lead to more tests when the use of such drugs is permitted. For example, Savulescu et al.[2] have stated: ‘‘There would be more rigorous and regular evaluation of an athlete’s health and fitness to perform.’’ However, it is important to note that certain health problems manifest themselves only over the long term and cannot be detected by close medical inspection. In Sports Med 2011; 41 (2)

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this respect, the proposal to align limits on the use of doping agents with the damage they cause to athletes means that the long-term adverse effects are not controlled at all. This important consideration is overlooked by supporters of a limited legalization of performance-enhancing drugs.[2,4] Furthermore, if proponents of limited legalization advocate banning all doping practices with potential long-term risks, the great temptation remains for athletes to do these things illegally. In this respect, nothing would be gained. Thus, the key argument against limited legalization under medical supervision becomes clear, namely, that no advantage would be obtained in terms of reducing the current difficulties of implementing doping controls.[6] The controls would be just as extensive, all that would change is the limit of what needs to be controlled.1 4. The Effectiveness of the Controls and the Credibility of Sport Sport in general and the credibility of the doping control system in particular are suffering from the fact that not all doping activity can be verified because doping methods change.[8] In most cases, a certain amount of time elapses before new doping practices can be identified and verified. However, even this game of ‘the tortoise and the hare’ between athletes and doping control officers would persist if limited legalization of performanceenhancing agents became a reality. There would always be those who attempted to use new, performance-enhancing methods that are not permitted and have yet to be discovered. For these reasons, if limited legalization of performance-enhancing drugs did ensue, an unpleasant development in athletic sports, which has spoiled the relationship between the audience and the sport, would continue. This refers to the fact that when an athlete achieves outstanding results in sport, the suspicion is automatically raised that this was achieved by doping. In other

words, sports fans have become skeptical. This situation would probably not change with a limited legalization; there would still be the possibility that an excellent performance was achieved through the use of doping practices that are not within the rules. Thus, even the lack of trust in athletes would not disappear. 5. What Impact would Legalizing Performance-Enhancing Drugs in Competitive Sport Have? If there were a legalization of performanceenhancing drugs in competitive sports, the athletes would definitely take more risks, although, given the limits and medical supervision, the risks would be considered acceptable. The argument for legalization is usually based on the fact that athletes take risks in sport anyway, and banning doping therefore smacks of unacceptable paternalism.[2,3,5,9] However, this argument fails to observe an important distinction: the risks of doping in sport are additional and avoidable, whereas other risks in sport are unavoidable. It is impossible to play football or other kinds of sport without risk of injury. Furthermore, while in many other kinds of sport the precautions taken can lower the risks, they cannot eliminate them completely. Conversely, as noted, the risks of performanceenhancing drugs add to those that already exist in sport and can be completely avoided by doing without drugs all together. However, this raises the question of whether it is beneficial to take extra, avoidable risks in sport, e.g. to make the sport more attractive, an issue that is discussed further in the next section. Consideration of the risks of doping in sport also raises the question of whether the actions of physicians in this context would be consistent with their ethos of defining the health of the patient as their first concern. The question is raised similarly in other fields of medicine that have little to do with illness, e.g. cosmetic surgery. In

1 In this respect, the contention by Foddy and Savulescu is unconvincing. They state that it is ‘‘much easier to eliminate the anti-doping rules than to eliminate doping,’’[3] an assertion that appears to contradict their conclusion in another context that the amount of control needed would increase for safety reasons if legalization occurred.[2]

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Sports Med 2011; 41 (2)

Legalization of Medically Supervised Performance-Enhancing Drugs

these fields, it is considered acceptable to take measures that introduce a certain element of risk in order to fulfil a patient’s need, even though a disease is not being treated. Again, however, a distinction needs to be made. In cosmetic surgery, some risks are unavoidable if the individual wants to improve his/her appearance through surgical intervention. In contrast, the risks involved in using performance-enhancing drugs in sport are unnecessary, which means physicians would be needlessly exposing their patients to risks in an attempt to make the sport more appealing. If physicians were administering unauthorized doping agents, they would be involved in a violation of the rules of sport. 6. The ‘Gentle’ Pressure to Use Performance-Enhancing Drugs The concept of ‘inherent coerciveness’[10] would assume greater importance if limited legalization of performance-enhancing agents in sport were to come into effect. All competitive athletes have to make adjustments in many areas of their lives if they want to be successful in their given sports. Thus, the athlete has liberty to act but in the knowledge that his/her actions will have certain consequences. If the athlete were to forgo certain performance-enhancing behaviour, he/she would be less successful. The result is mentioned by Bette and Schimank:[11] ‘‘The only liberty one has is to avoid elite sports or leave.’’ If one allows the use of performance-enhancing drugs within certain boundaries, then all athletes who wished to be successful would have no choice but to use the substances that are allowed by the rules. They would have ‘‘free choice under pressure’’[10] in this respect. They would be forced to take actions that entail risks that are unnecessary in sport and confer no advantages upon their sport (see section 7). In this respect, a limited legalization of performance-enhancing drugs would unnecessarily put further pressure on athletes to do more risky things. Conversely, ‘‘an effective policy for eliminating performance-enhancing drug use would

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harm no one, except those who profit from it.’’[10] 7. Effects of Doping on Performance The fact that a legalization of performanceenhancing drugs would not be advantageous to sport can be seen by analysing how the use of these drugs would affect performance. The following possibilities arise: 1. All athletes respond to the approved doping measures in the same way and their performance improves in the same way. In that case, the finishing order of cyclists in the Tour de France, for example, would remain unchanged. The event would be slightly shorter in duration with the use of performance-enhancing drugs than without them. However, that would be of no benefit to the competition. All of the athletes would have put in considerably greater effort and would have been required to take more risks with no change in the result of the event. In terms of the ‘eternal competition’, i.e. the pursuit of records, the generations of athletes who were not entitled to use performance-enhancing drugs would be at a disadvantage. Indeed, many current records were probably established through the use of performance-enhancing drugs. (This generally accepted assumption is difficult to verify because athletes generally do not admit to the use of doping agents and, in most cases, it is impossible to subsequently prove that an athlete used performance-enhancing drugs.) Furthermore, the generations of athletes who were not allowed to use performance-enhancing substances would have more difficulty being included on lists of the ‘alltime best athletes’ based on absolute values of times, weights, lengths, etc. They would also have more difficulty being included on conditional ‘alltime best athletes’ lists if they were not illegally using performance-enhancing drugs.2 The world of sport has become more complicated, particularly in respect to doping. However, is the argument for justice in the ‘eternal competition’ sufficient to allow doping? No, because introducing limited

2 If it could be guaranteed that a sport was now free of the use of performance enhancers, the ‘old’ records could be accepted conditionally and all new records classified as unconditional.

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legalization of doping agents in sport will not change the possibility that records were obtained through practices that remained banned under that limited legalization; in other words, this injustice would remain. Thus, consideration of the ‘all-time best athletes’ lists does not provide a convincing argument to legalize performance-enhancing drugs under medical supervision. 2. The previous point explores the consequences of legalized doping in sport if the upshot is that all athletes respond in the same manner. However, it is improbable that all athletes will respond to doping options in the same way because (i) different measures would probably be used; and (ii) athletes respond differently to performance-enhancing drugs. The use of different doping measures is possible when there is flexibility in prescription (e.g. dosage) and enforcement of permissible doping practices. In such circumstances, athletes will strive, with the help of their physicians, to identify and use the best method for enhancing performance within the permitted limits. This would extend the competition among athletes beyond the actual event into the realm of who could find the best doping methods. Thus, the outcome would reflect not only the athletes’ performance, training methods, discipline and talent, but also the cleverness of their supervising physicians in finding and using the optimal doping aids within permissible boundaries. This technical extension of the competition in addition to current medical care in sport would become increasingly complicated and expensive as more substances were included on the permitted list. Different responses of athletes to performanceenhancing drugs would be expected to occur because of genotypic differences alone. Consideration of this point raises an interesting argument that has been put forward for the legalization of performance-enhancing drugs, which is that competitive sports are not fair anyway because some people are favoured on the basis of their talent alone, and that this unfairness could be compensated for with use of doping substances. This argument appeals to our sense of justice: sport would be fair with the use of performance-enhancing drugs because these would help offset the imbalance arising from the ‘natural lottery’ of talent among ª 2011 Adis Data Information BV. All rights reserved.

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athletes. According to Foddy and Savulescu,[3] ‘‘By allowing everyone to take performanceenhancing drugs, we level the playing field. We remove the effects of genetic inequality. Far from being unfair, allowing performance enhancement promotes equality.’’ However, is this argument convincing? No, it is not because if the use of performanceenhancing drugs were legalized, the natural lottery of various talents would only be compensated for to a limited extent. The fact is that certain biological advantages in sport cannot be leveled by medical interventions. Furthermore, the partial compensation of the natural lottery of talent would be thwarted by a new lottery of the different reactions to performance-enhancing drugs, which is also predetermined. While those who are biologically favoured because of their talent might not now have the advantage, they could be supplanted by a new group who, again because of biological factors, had an advantage because they obtained the largest increase in performance as a result of taking performance-enhancing drugs. Replacing one natural lottery with another would only change the nature of the inequality among athletes, it would not result in greater ‘justice’ for them in terms of ‘fair’ rewards for their efforts. In doping-free sport, the athlete’s genetic make-up introduces unequal chances in competitive sport; in doping-legalized sport, the ability to react to performance-enhancing drugs, which is just as randomly distributed, gives rise to another inequality.[5] In addition, there is an unequally distributed resourcefulness among physicians to optimize the use of doping agents within the permissible boundaries. In short, nothing would be gained. Foddy and Savulescu[3] contend that one advantage of a legalization of performance-enhancing drugs under strict health control is the fact that the difference in performance between athletes who use legal substances and those who continue to use additional illegal substances would narrow. Indeed, that would appear to be a possible effect of a limited legalization of performance-enhancing drugs. However, a (smaller) benefit from the use of prohibited substances would still be possible and, in elite sports, slight increases in performance are important. Furthermore, all the other Sports Med 2011; 41 (2)

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disadvantages of the use of the permitted drugs would remain. In this respect, the slight advantage in terms of narrowing the gap between legal and illegal doping agent users would not be of crucial significance in the overall evaluation. 8. The Meaning of Sport If a legalization of performance-enhancing drugs became a reality, the new lottery of differences in response to performance-enhancing drugs discussed in the previous section would be combined in most cases with the ingenuity of the particular sports physician and other existing factors (natural talent, discipline, training) to determine the outcomes of athletic events. It must be reiterated at this point that a limited legalization would not exclude continued use of prohibited doping methods, perhaps in addition to use of permitted agents. It also seems likely that the more the permitted drugs were limited to minimize risks, the greater the temptation would be to use prohibited doping measures. Crucially, a legalization of performanceenhancing drugs would have a massive impact on our perception of sport. It would ultimately compromise the currently, widely accepted ‘spirit of sport’. Sport is an artificial setting, created by human beings, in which the competitor is required to perform, at least according to current, widely prevalent belief, with a degree of ‘naturalness’. The sports-watching audience is interested in ‘‘athletic performance y not y biochemistry.’’[12] We associate the ‘spirit of sport’ with the notion that achievements come through hard work, discipline, training and natural talents, even when we do not recognize this in other areas of our lives. As has been recently noted, ‘‘The fascination of sports mainly comes from the demonstration of what people are able to do on their own. Doping destroys this fascination.’’[13] This culture of ‘naturalness’, to some extent at least, has previously been accepted as part of sport. These ideas have given rise to highly controversial discussions on what the ‘meaning of sport’ is, what is meant by the ‘spirit of sport’ and how important this is, and whether this ‘spirit of sport’ is immutable. Is the ‘spirit of sport’ a ‘‘key ª 2011 Adis Data Information BV. All rights reserved.

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constitutional quality’’[6] of sport, one that may never change or undergo ‘correction’, if necessary? Is doping ‘‘incompatible with the meaning of sports’’[13] or could it be considered consistent with the ‘spirit of sport’? For example, it has been suggested in a recent publication that ‘‘Performance enhancement [...] embodies the spirit of human sport.’’[11] Unfortunately, these questions cannot be answered at this point. It is not possible to determine what exactly constitutes the ‘spirit of sport’ and whether our views on this should change. However, and this is the central argument of this article, it is not necessary to settle these questions because a limited legalization of drugs in sports and the consequent change in the current perception of the ‘spirit of sport’ would have no advantages. Any other concept of the ‘spirit of sport’ should have to be proven to be advantageous in itself, and such advantages cannot be identified. There is no need to ponder whether the ‘spirit of sport’ is or should be subject to change because there is simply no good reason to make any such change in any case. However, it is important to clarify three aspects of ‘naturalness of performance’ in sport. The first is the difficulty of determining what constitutes a ‘natural’ measure of improving performance. Many permissible training methods and food supplements are in some ways less ‘natural’ than other things that athletes may do. However, the fact that defining an acceptable limit for such measures, particularly when the dividing line appears to be opinion-based and is established on a more or less continuous spectrum, does not necessarily mean that we should dispense with such limits. Furthermore, this is not the approach taken in other areas of life. The difficulties inherent in putting forward arguments as to why one substance or another should or should not be on the World Anti-Doping Agency list are not sufficient reasons to characterize this list as completely arbitrary and, therefore, irrelevant. Second, it must be clearly stated that ‘naturalness’ in sport is not considered as a value in itself, but only as a value in this specific context. In sport, great importance is attached to the ‘naturalness’ of achievements, whereas in other Sports Med 2011; 41 (2)

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areas of life this is not necessarily the case. Thus, there is no requirement in this context to argue that ‘naturalness’ is a value in itself. Third, according special attention and value on ‘naturalness’ of performance in sport means that sport is considered different to other areas of life, in which certain ‘artificial’ measures of obtaining improvement are allowed. A ‘‘premature (adjustment)’’[6] to this aspect of sport threatens destruction of the uniqueness of sport. Sport would no longer be a ‘‘special area,’’[13] a ‘‘counterworld of ‘personal achievement’.’’[6] 9. The Exemplary Role of Sport Another argument for the need to protect the ‘spirit of sport’ can be put forward. There can be no doubt that sport, playful in nature, but still in accordance with the rules, sets an example for society. As Albert Camus once said, ‘‘After many years during which I saw many things, what I know most surely about morality and the duty of man I owe to sport.’’[14] Sport shows, with its rules and requirement for fairness, how to deal with other problems in society. It conveys an attitude that acts as a role model in many other areas of human life and ‘‘in a sense, it can be a model for a better society.’’[6] The question then is: how would legalization of performance-enhancing drugs affect the exemplary character of sport? On this issue, three different facets of the functions of role models need to be distinguished. An aspect of society can take on the function of a role model if it (i) sets special, exemplary standards; (ii) respects certain standards in a special and exemplary way; or (iii) controls or ensures compliance with the standards in an exemplary way. First, it is useful to consider the ongoing impact of sport as a role model in these three areas if the ban on performance-enhancing drugs remained in place as follows:  With respect to setting standards, sport would remain a model at least for most citizens.  Continued violations of the norm (standard) would be anticipated and the function of sport as a role model in terms of respecting standards in a special and exemplary way would continue to be debatable. ª 2011 Adis Data Information BV. All rights reserved.

 The system of controlling or ensuring compliance with standards in sport is currently unconvincing, with many doping violations remaining undiscovered. Improving the control system would depend on further technical developments (e.g. in the collation of indirect evidence), which would make the system more convincing and therefore more able to act as a role model. Second, it is important to consider how the exemplary role of sport could change if doping were legalized as follows:  At least for a significant part of society, sport would lose its function as a role model because the model standard it exemplifies would be abolished.  With a limited legalization of performanceenhancing agents, continued violations of the new norm would be anticipated because the potential for the use of additional banned but performance-enhancing substances would remain. In terms of the exemplary role of strict adherence to standards, nothing would be gained from legalizing the use of performanceenhancing agents.  The cost of control would remain unchanged and the suspicion that the control system was not effective would remain. Again, therefore, nothing would be gained in these respects compared with the existing ban. The function of the role model would also still be dependent on further technical development. To summarize, a legalization of performanceenhancing drugs would definitely result in some lessening of the exemplary role of sport in terms of setting standards. The same challenges that exist at present would need to be faced with respect to the other facets of role model function. Overall, the function of sport as a role model would be reduced. 10. Children and Adolescents and the Legalization of Performance-Enhancing Drugs As discussed in the previous section, a legalization of performance-enhancing drugs would diminish the function of sport as a role model, and this would particularly be the case with reSports Med 2011; 41 (2)

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spect to children and adolescents. Self-restraint would be abandoned and the message would be that one must be willing to do anything for success. This ‘boundless willingness’ is not a preferred role model, especially for youth. As stated in a recent publication on doping in sport: ‘‘Also of concern is the will expressed when one takes performance enhancers [y] to force a specific peak output with all available means. It is doubtful whether one should raise children according to a life plan which links life satisfaction to the boundless willingness to provide peak performance.’’[13] Moreover, the consequences would be devastating for children and adolescents who are directly affected, i.e. training for a career as an athlete. A total ban on doping for children and adolescents when there is simultaneous legalization for adults is impracticable and would not seem to be feasible. Also, the manner in which children and adolescents under the age of 18 years (which is an advanced age in many sports) react to performance enhancers is not known. However, supporters of a legalization of performanceenhancing drugs do not exclude children and adolescents. Rather, they justify approval of doping in these age groups by pointing out that competitors at this stage are taking various other risks in sports anyway: ‘‘[y] if children are allowed to train as professional athletes, then they should be allowed to take the same drugs, provided that they are no more dangerous than their training is.’’[3] Why is this reasoning not convincing? First, the long-term consequences of even supposedly harmless drugs in children and adolescents cannot be determined on the basis of the available evidence. It is irresponsibly optimistic to believe that powerful biological interventions during childhood and adolescence do not have unwanted side effects over the longer term. Second, Savulescu et al.[2] again do not distinguish between unavoidable risks and additional, avoidable risks. The fact is that professional sports training for children and adolescents entails risks to both their health and their psychosocial development. These can be partly avoided (and should be avoided), but are not completely avoidable. However, this does not mean that further avoidable risks for children and adolescents thereª 2011 Adis Data Information BV. All rights reserved.

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fore need not be avoided! Trying to justify an additional, avoidable (and senseless) evil by pointing out the existence of another, unavoidable evil is not a persuasive argument. The only reasonable course of action for people who are concerned about the welfare of children and who wish to preserve the ‘‘educational credibility’’[15] of sport is to ensure that unavoidable risks are minimized as much as possible and avoid the clearly avoidable risks associated with professional sports training for children. The latter includes the risks associated with doping. 11. Conclusions The arguments for and against the legalization of performance-enhancing drugs in sport operate on two different levels. On one level, there are pragmatic arguments concerned with the effort required to establish and enforce controls, the quality and quantity of these controls, and the responsibility for and costs of regulations. Also on this level are arguments concerning the need to preserve the audience’s trust in sport, freedom of choice for athletes, the justification for introducing additional risks and the need to avoid risk, especially in children and adolescents. On another level, there are also arguments that touch on the ‘spirit of sport’ and the ‘naturalness’ of performance in sport. Whether this ‘spirit of sport’ has a ‘‘central constitutional quality’’[6] which one may not change under any circumstances, or whether in fact it can be modified, remain as controversial as the question of whether doping is consistent with the true ‘spirit of sport’ or not. However, these disputes do not have to be resolved in order to answer the question of whether drugs should be legalized under medical supervision. Even if it were thought acceptable to abolish normative behaviour consistent with the ‘spirit of sport’ and that it would be then still possible to perform with a degree of ‘naturalness’, this step should be taken only if advantages could be expected to ensue. However, this is not the case at all; a legalization of performance-enhancing drugs would confer no advantages and therefore would make no sense. The natural lottery of athletic talent would be only partially compensated for, and would also be Sports Med 2011; 41 (2)

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complemented by, the natural lottery of responsiveness to doping measures combined with the inventiveness of doping doctors. There would be no gains in terms of ‘justice’ for athletes from legalizing doping; at best, the benefits of doping misconduct would be reduced in the case of limited legalization, but a performance advantage from using non-permitted drugs could still be obtained. This is important, because in professional sport, even small advantages can be decisive. Doping also entails avoidable risks that are not necessary to increase the attractiveness of the sport. Furthermore, many risks, particularly over the long term, are difficult to anticipate. Legalization would not reduce the restrictions on athletes’ freedom; the control effort would remain the same, if not increased. Extremely complicated international regulations would have to be adopted. Athletes, including children and adolescents involved in competitive sport, would be forced to take additional, avoidable health risks. Audience mistrust, particularly in regard to athletes who had achieved outstanding feats, would remain because these athletes could still be relying on the use of illegal practices. The all-time best lists would remain unreliable. The game of the ‘tortoise and the hare’ between doping athletes and inspectors would continue because prohibited but not identifiable practices could provide additional benefits with respect to the use of permissible drugs. Above all, the function of sport as a role model would clearly be damaged. The legalization of drugs in sport is not desirable because it is ‘‘coercive, has significant potential for harm, and advances no social value.’’[10] Nothing would be gained, but a lot would be lost. The ‘spirit of sport’, exhibited in an artificial setting where performance with a certain degree of ‘naturalness’ is expected, would be abandoned without gain. These considerations suggest that the legalization of performance-enhancing drugs in sport, even under medical supervision, should not be entertained.

Bundesa¨rztekammer’ (Central Ethics Commission at the German Medical Association) for stimulating discussions on the topic. No funding was used to assist in the preparation of this review. The author has no conflicts of interest that are directly relevant to the content of this review.

References 1. Striegel H, Ulrich R, Simon P. Randomized response estimates for doping and illicit drug use in elite athletes. Drug Alcohol Depend 2010 Jan 15; 106 (2-3): 230-2 2. Savulescu J, Foddy B, Clayton M. Why we should allow performance enhancing drugs in sport. Br J Sport Med 2004; 38: 666-70 3. Foddy B, Savulescu J. Ethics of performance enhancement in sport: drugs and gene doping. In: Ashcroft RE, Dawson A, Draper H, et al., editors. Principles of health care ethics. 2nd ed. London: Wiley, 2007: 511-20 4. Savulescu J, Foddy B. Sports ethics: an anthology. Br J Sports Med 2005; 39: 686-7B 5. Fost N. Banning drugs in sports: a sceptical view. Hastings Center Report 1986 Aug; 16 (4): 5-10 6. Digel H. Warum doping niemals erlaubt sein darf. Edition Ethik Kontrovers 2001; 9: 63-7 7. President’s Council on Bioethics. Beyond therapy: biotechnology and the pursuit of happiness. Washington, DC: President’s Council on Bioethics, 2003 8. Scha¨nzer W, Thevis M. Doping im sport. Medizinische Klinik 2007; 102: 631-46 9. Maiworm H. Doping geho¨rt zum Leistungssport [online]. Available from URL: http://wandern-philosophieren.blog spot.com/2008/10/doping.html, (12.7.2009) 2008 [Accessed 2010 Oct 27] 10. Murray TH. The coercive power of drugs in sports. The Hastings Center Report 1983; 13 (4): 24-30 11. Bette KH, Schimank U. Doping: der entfesselte Leistungssport. Aus Politik und Zeitgeschichte: Beilage zur Wochenzeitung Das Parlament 29, 2008 [online]. Available from URL: http://www.bpb.de/files/OUQAYB.pdf [Accessed 2010 Dec 1] 12. Luhmann N. Die Ehrlichkeit der Politiker und die ho¨here Amoralita¨t der Politik. In: Luhmann N, editor. Die Moral der Gesellschaft. Frankfurt am Main: Suhrkamp, 2008: 163-74 13. ZEKO. Zentrale Kommission zur Wahrung ethischer Grundsa¨tze in der Medizin und ihren Grenzgebieten (Zentrale Ethikkommission) bei der Bundesa¨rztekammer. Doping und a¨rztliche Ethik. Deutsches A¨rzteblatt 2009; 106: A 360-4 14. The Albert Camus Society of the UK. Albert Camus and football [online]. Available from URL: http://www.camussociety.com/camus-football.htm [Accessed 2010 Oct 27] 15. Grupe O. Doping und Leistungsmanipulation aus sportethischer Sicht. In: Digel H, Dickhuth HH, editors. Doping im Sport. Tu¨bingen: Attempto, 2002: 58-76

Acknowledgements The author would like to thank Professor Andreas NieX for his helpful suggestions, and members of the Working Group ‘Doping’ of the ‘Zentrale Ethik-Kommission bei der

ª 2011 Adis Data Information BV. All rights reserved.

Correspondence: Prof. Dr Urban Wiesing, Institute for Ethics and History of Medicine, University of Tuebingen, Gartenstrasse 47, 72074 Tuebingen, Germany. E-mail: [email protected]

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