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Microsoft word - transitioned athletes project final sci lit review_1_rw _2_.doc
Do Transitioned Athletes Compete at an Advantage or Disadvantage
as compared with Physically Born Men and Women:
Prepared for the Promising Practices: Working with Transitioning/Transitioned
Table of Contents
Sex Differences in Performance, Anthropometrics and Metabolism
Metabolic Effects of Testosterone and Estrogen
Hormone Levels in Transitioned Men and Women Compared with
5.1 Acceptable limits for testosterone and estrogen in
sport and how this pertains to transitioned athletes
Effects of Cross-Sex Hormones on Parameters that may Influence Performance 11
6.1 Testosterone administration to transitioned men
6.2 Estrogen administration to transitioned women
6.3 Based on the evidence presented above, would either
transitioned men or women compete at an advantage against
6.4 How do the findings to date compare with the IOC Stockholm
7.1 Is there a performance advantage or disadvantage?
Transitioned athletes present a unique challenge to sport governing bodies with respect to
determining the eligibility of such athletes to compete against physically born men and women. The IOC Stockholm consensus on sex reassignment in sports allows transitioned men and women to compete against members of their new sex provided that sex reassignment surgery is complete, the individuals are legally recognized as a member of their new sex and proper cross-sex hormone administration has been ongoing for at least two years. The basis behind this statement is to minimize the effects of previous sex hormone exposure on athletic performance. The purpose of the current review is to examine the scientific evidence that exists to determine if transitioned athletes compete at an advantage or disadvantage as compared with physically born men and women. Men outperform women in athletic events by approximately 11-18%, potentially as a result of well known sex differences including that men are taller, have a greater maximal aerobic and anaerobic capacity, muscle mass and strength and altered substrate utilization characteristics. The observed sex differences are the result of differences in testosterone and estrogen. Testosterone increases muscle mass and strength, bone size and mineral content and haemoglobin content. Estrogen has a profound effect on substrate metabolism during exercise, increasing the reliance on lipid stores. As both testosterone and estrogen can influence performance measures it is important to ensure that transitioned athletes have sex hormone levels within the normal physiological range for their new sex. While hormone concentrations in transitioned women fall in line with those of physically born women, transitioned men spend the majority of time with supraphysiological levels of testosterone and higher estrogen as compared with physically born men. Cross-sex hormone administration to transitioned individuals results in haemoglobin and subcutaneous fat content and muscle cross-sectional areas similar to those values in physically born men and women. To date, no study has examined the effects of cross-sex hormones on any objective measures of athletic performance (maximal aerobic capacity, time trials). Additionally, no trial has been conducted in transitioned athletes as compared with physically born men and women athletes. As such, there is no concrete evidence to support or refute the position that transitioned athletes compete at an advantage or disadvantage as compared with physically born men and women athletes.
Transitioned athletes present a unique challenge to sport governing bodies in determining
the eligibility of such athletes to compete against physically born men and women. Many
differences exist between men and women; however, whether these differences persist upon
transition or whether they impact performance is yet to be determined. The purpose of the
current review is to examine the scientific literature in an attempt to determine if enough
information is currently available to address the question of whether transitioned athletes
compete at an advantage/disadvantage as compared with physically born men and women. For
the purpose of this review the genotypic definition of man and woman will be used. Specifically,
an XY genotype will denote men and an XX genotype will denote women. Throughout the
course of this report the differences between men and women, the metabolic effects of sex
hormones, the hormone levels in transitioned men and women as compared with physically born
men and women and future research will be discussed.
3.0 Sex Differences in Performance, Anthropometrics and Metabolism
Typically, men outperform women by 11-18% depending on the type of activity
(Comben, 1996). Additionally, there is a 5-37% difference in world record times between men and women for a variety of sporting events, as summarized in Table 1. Additionally, for any given training status men have a higher maximal aerobic capacity (VO2peak) relative to body
weight as compared with women (26, 27). The differences in performance observed between men and women are likely the result of numerous factors that are different between the sexes. Anthropometrically, men are taller by approximately 12-15 cm (26, 27, 93), have greater muscle mass and less body fat (26, 27, 57, 93) and greater bone thickness (45, 56, 57) and bone mineral density (12, 56, 93).
Table 1: World records by sporting event for men and women as at May 18, 2008 and the percent difference in performance between men and women in each event.
* % difference in distance for high jump, pole vault, long jump and javelin world records, and in speed for all other world records. Data obtained from the International Association of Athletics Federations (www.iaaf.org) and the Official Site of the Olympics Movement (www.olympic.org). Being leaner can be a performance benefit because for a given body weight more muscle mass indicates increased metabolically active tissue as well as increased capacity to generate force. Additionally, thicker/denser bones can increase stability and decrease risk of injury. Additionally, fat distribution differs between men and women with women having a more gynoid (gluteal-femoral region) fat distribution and men having a more android (abdominal region) fat distribution (11, 93), resulting in a lower centre of gravity in women. Increased body fat and body fat distribution can influence performance because increased body fat is additional weight that needs to be carried during athletic events and body fat distribution may influence performance biomechanics. Interestingly, at birth sex differences in anthropometrics already exist with boys being longer and having greater fat-free mass than girls (93).
In accordance with an increased muscle mass and muscle cross-sectional area (57), men
also have increased muscle strength (57, 58). However, even when muscle cross-sectional area is accounted for, men have greater knee flexor and extensor muscle strength (57), while no sex differences in muscle strength was observed in elbow flexor and extensor muscles when determined relative to muscle cross-sectional area (57). The disproportionately higher leg muscle strength in men may be the result of a greater percentage of type II (fast twitch) muscle fibres (68, 79, 81). Type II muscle fibres, as compared with type I (slow twitch) muscle fibres, are larger allowing for greater contraction strength and power (41); whereas type I muscle fibres have a greater mitochondrial content allowing for greater muscle endurance (41). Thus, a greater proportion of type II muscle fibres would suggest a greater ability in sports requiring high force and explosive movements; whereas an individual with a greater proportion of type I fibres would be better suited for endurance events. Additionally, greater muscle mass in men also results in a higher anaerobic capacity (63, 92). However, in trained men and women, sex differences in anaerobic capacity are no longer found when relative to lean body mass (63). In untrained men and women, the sex difference in anaerobic capacity persists despite controlling for lean body mass (92). Again the sex difference in anaerobic capacity may be the result of differing muscle fibre type between men and women (68, 79, 81) and may disappear with training when muscle fibre type shifts (48, 78, 82) to meet the metabolic demands imposed on it by the athlete. A greater anaerobic capacity would allow an athlete to continue to perform at levels beyond the
anaerobic threshold (beyond the VO2peak) for a greater period of time; thus allowing the athlete to
perform at a higher intensity for a longer period of time.
Men and women also differ in that the Q angle (the angle of the quadriceps to the knee) is
greater in women, the result of a wider pelvis (2, 39). The Q angle is a determinant of patellar tracking and is determined by measuring the angle that is formed at the knee when a line is drawn from the anterior superior iliac spine to the centre of the patella and from the centre of the patella to the centre of the tibial tuberosity (39). The greater Q angle in women results in a greater valgus orientation of the knee extensor mechanism (35), which can increase risk of knee injury (35) and may influence sport performance, specifically running efficiency (3). Indeed, elite women runners typically have narrower pelvises than age-matched controls (95). However, recently the anatomical importance of the sex difference in Q angle (~2.30 difference between men and women) has been questioned (39).
Lung capacity is also greater in men as compared with women. Specifically men have a
greater lung volume (64, 65) and larger airways (76) as compared with height-matched women. As summarized by Harms (42), the smaller airways in women can lead to greater limitations to expiratory flow, which may result in early fatigue of the respiratory muscles (i.e. diaphragm) during heavy exercise in women. Additionally, women have lower resting lung diffusing capacity, which is the result of fewer alveoli and smaller airway diameter (46). Together these findings suggest that gas exchange, and ventilation may be limiting in women during exercise; however, a lower oxygen demand due to lower body weight may nullify the effect of these differences on exercise performance (46). However, if gas exchange is limited in women during exercise then oxygen delivery to active muscles would also be limited and would lower maximal aerobic metabolism.
Oxygen delivery to the muscles may also be limited in women as a result of lower
haemoglobin levels (37). Haemoglobin is the oxygen carrying metalloprotein in red blood cells, allowing for delivery of oxygen from the lungs to the tissues (41). During exercise, oxygen is delivered to the active muscles via haemoglobin; thus lower haemoglobin content in women limits oxygen delivery to the active muscles and would lower maximal aerobic capacity. Importantly, there is a positive correlation between blood testosterone concentrations and haemoglobin levels (37). Additionally, absolute heart mass and volume is greater in men as compared with women (72, 73). When normalized to body surface area, to control for differences in body weight and height between men and women, sex differences in left ventricular volume, but not right ventricular volume or left and right ventricular function, disappeared (73). However, cardiac output (a function of heart rate and stroke volume) is not different between the sexes (73).
From a metabolic standpoint women rely to a greater extent on lipid stores to fuel
exercise as compared with men as evidenced by a lower respiratory exchange ratio (RER) (17, 26, 34, 47, 69, 86, 88, 90). It has been consistently shown that women use less liver glycogen/glucose (lower glucose rate of appearance, rate of disappearance and metabolic clearance rate) (26, 34), have a higher rate of lipolysis (greater glycerol turnover) (17), higher plasma free fatty acid concentration (9, 66) and depending on the type of exercise performed and the menstrual cycle phase in which women are tested, lower muscle glycogen utilization (26,
86), with no difference in intramyocellular lipid (IMCL) utilization (27, 94) during endurance exercise. Additionally, skeletal muscle and myocardial glycogen depletion is lower in female, as compared with male, rats following exercise (36, 51). It has been suggested that these sex differences during exercise are due to differences in estrogen concentration/activity (15, 61). In fact, estrogen supplementation studies in animals and humans have supported the aforementioned findings of higher fat oxidation for women during endurance exercise (17, 25, 71).
While there is no difference in IMCL utilization during exercise between men and
women, it has been consistently shown that women have a greater IMCL content as compared with men (26, 33, 68, 83). Increased IMCL content may influence exercise performance as it is a readily available fuel source within the muscle. Additionally, using electron microscopy it has been shown that prior to and following a period of endurance training women have a higher number of IMCL in a given area of muscle, but not a greater lipid size, as compared with men, and this greater number of IMCL contributed to the increased IMCL content in women (26). Thus, women have an increased availability of IMCL to use as a substrate source during exercise; however, IMCL utilization is not different between the sexes.
Intriguingly, while there are sex differences in IMCL storage and not IMCL utilization
during exercise it appears the opposite is true with regards to muscle glycogen storage and utilization. Depending on the type of exercise performed (during running women spare muscle glycogen as compared with men (86)) or the menstrual cycle in which women are tested (in the luteal phase women spare muscle glycogen as compared with men (26)) women utilized less muscle glycogen during exercise as compared with men. However, there is no sex difference in muscle glycogen storage between the sexes (26, 53, 86, 87). Overall the increased reliance on lipid and decreased reliance on carbohydrate stores during exercise in women can influence endurance exercise performance by slowing carbohydrate depletion. The attenuated carbohydrate depletion in women allows women to exercise at a higher intensity for a longer period of time since carbohydrates are necessary to maintain exercise intensities greater than approximately 65-70% (90).
The extent to which, if any, the aforementioned sex differences influence sport
performance is yet to be determined. Additionally, whether differences in hormone levels
between men and women mediate these differences, with several exceptions, is also unknown.
4.0 Metabolic Effects of Testosterone and Estrogen
One of the main elements differentiating men and women is the differences in hormonal
milieu. The average concentrations of testosterone and estrogen in men and mid-follicular and mid-luteal women are presented in Table 2.
Table 2: Normal hormone concentrations in physically born men and women. Testosterone
Data are means + standard area of the mean (SEM), where SEM is a measure of variance within the study population. Data from Devries, MC et al. Am J Physiol Regul Integr Comp Physiol,
Aside from the obvious role sex hormones play in primary and secondary sexual characteristics, these hormones also influence numerous other metabolic systems. 4.1 Metabolic effects of testosterone
Testosterone is well known as an anabolic agent regulating muscle mass (6, 44, 75, 85)
and strength (6, 31, 75, 85). In fact, testosterone supplementation can increase strength by ~5-20% and lean body mass by ~2-5 kg (43). Additionally, the effect of testosterone on muscle mass and strength are dose dependent; however, its effects to increase strength are typically only found when testosterone levels are at high end normal or supraphysiological levels (7). In fact, when given at levels that mimic normal physiological concentrations, no change in muscle strength is found, despite increases in muscle mass (80). When testosterone levels are ablated via orchidectomy in mice, there is a decrease in type I and II muscle fibre cross-sectional area and this effect is attenuated by testosterone administration (5). Specifically, slow twitch (type I) muscle fibres are the most sensitive to testosterone removal and supplementation (5). Following orchidectomy, maximal force generation decreased in mice; whereas in testosterone treated orchidectomized mice, maximal force generation was not different from control mice (5). However, while maximal force generation is enhanced following testosterone administration in orchidectomized mice, there is no difference in contraction speed (5).
Testosterone is also thought to play a role in fatigue resistance and muscle recovery. In
mice, testosterone administration following orchidectomy enhanced fatigue resistance in slow twitch (type I), but not fast twitch (type II) muscle fibres (5). However, in humans, a wide range of testosterone doses did not influence muscle fatigability (85). Additionally, muscle specific tension, a measure of muscle quality, did not change in response to any testosterone dose (85). The role of testosterone on muscle recovery is not compelling. Despite higher testosterone concentrations following resistance exercise when repetitions were performed slowly, as compared with when repetitions were performed at regular speed, no difference was found in recovery of maximal strength or jump performance in humans (38).
The sex differences in bone size and mineral content and haemoglobin content are the
direct result of differences in testosterone concentrations between the sexes. During puberty in boys, the anabolic effects of testosterone increase the total quantity of bone and increase calcium retention within the bone, resulting in larger, stronger bones (41). Testosterone also influences the shape of the pelvis by narrowing the pelvic inlet and lengthening it, as well as, increasing the strength of the pelvis for load-bearing (41). If no testosterone is present, the male pelvis resembles that of the female (41). Testosterone also stimulates red blood cell production, which, as described in detail above, contains haemoglobin, which carries oxygen to the working muscles. Testosterone administration to a castrated man to mimic physiological testosterone levels increases red blood cell count by 15-20% (41).
The observed sex differences in metabolism between men and women during exercise are
not mediated by differences in testosterone. In fact, a recent study investigated substrate utilization during exercise in men with physiological testosterone levels, ablated testosterone and supraphysiological concentrations of testosterone and found no differences in lipid or carbohydrate oxidation during exercise (13). Thus, while testosterone does appear to regulate some of the differences between the sexes, substrate metabolism during exercise is not one of them. 4.2 Metabolic effects of estrogen
The observed sex difference in metabolism during exercise is mediated by differences in
estrogen concentration between the sexes. 17-β-estradiol (E2) supplementation trials in animals (16, 60, 61), and humans (18, 25, 71, 89), have shown that short term administration of E2 can modify fuel selection during endurance exercise. In animals, E2 supplementation to oophorectomized female or male rats spared skeletal muscle, hepatic and myocardial glycogen during exhaustive and submaximal exercise, resulting in improved performance (16, 60, 61, 70). In ammenorrheic women, 100 μg/d E2 supplementation for 3 days increased free fatty acid concentration, decreased liver glucose utilization, with no effect on whole body lipolysis and no change in RER, carbohydrate or fat oxidation (71). However, there was no effect of E2 supplementation on performance during a run to exhaustion at 85% VO2peak that was preceded by
a 90 min run at 65% VO2peak (71). E2 supplementation trials in men have yielded similar findings
(18, 25, 89). Low dose E2 (100-300 μg/d) supplementation to men for 11 days, resulting in serum estradiol concentrations similar to the level seen in the follicular phase of the menstrual cycle in women, had no effect on performance or muscle glycogen utilization during a 90 min cycling bout at 60% VO2peak; however, there was a trend towards higher lipid and lower
carbohydrate oxidation during the exercise bout (89). When the E2 dose administered to men was increased (1-3 mg/d, 8 days) RER and carbohydrate oxidation were decreased and lipid oxidation increased (25). Additionally, high dose E2 lowered liver glucose utilization (18, 25) and resting muscle glycogen content with no effect on muscle glycogen utilization (25). Lastly, similar to the findings of Ruby et al
(71), there was no effect of high dose E2 supplementation on whole body lipolysis in men (18). To date, only one E2 supplementation trial has found an effect of E2 on whole body substrate utilization by lowering RER and CHO oxidation and increasing lipid oxidation (25). It is possible that a dose response relationship exists with respect to E2 and RER as there was no effect of low dose E2 on RER (71, 89). However, in the study conducted by Carter et al
(18), serum estradiol concentrations were higher than those in the Devries et al
(25) study, and yet no effect of E2 on RER was observed. One possible explanation could be the smaller sample size used in the study by Carter et al
(18) resulting in a type II error. Alternatively, as E2 is known to increase IMCL content and lipoprotein lipase activity in rats (22, 67, 96), and given that there is simultaneous FFA esterification and IMCL hydrolysis during exercise (40), and that increased IMCL synthesis would elevate RER, it is possible that the RER could be falsely elevated with E2. Therefore, it is possible that in the study conducted by Carter et al
(18), that the dosing regime was so high that the effects of E2 on lipid synthesis exceeded those on lipid mobilization leading to an inability to detect an effect of E2 on lowering RER. Collectively these data suggest that E2 has a primary action on liver glycogenolysis and glucose release, while muscle glycogenolysis is not affected by short term E2 supplementation. However, as E2 lowered muscle glycogen content (25), perhaps with time an effect of E2 on muscle
glycogen utilization will be seen. Additionally, these studies suggest that at the level of substrate utilization E2 has a greater impact on CHO, as opposed to lipid, metabolism.
Estrogen also acts as an anti-oxidant, attenuating exercise-induced oxidative stress and
inflammation (54, 84). Acute bouts of exercise increase reactive oxygen species production in
humans (1, 24, 74). Increases in reactive oxygen species production leads to oxidative stress and
can result in oxidative damage in muscle and blood (1, 10, 55, 74, 97). Oxidant induced muscle
damage can decrease muscle function and result in muscle soreness (24, 62) and may also result
in muscle fatigue (4), decreasing performance capacity. In various cell lines, E2 inhibits reactive
oxygen species generation by inhibiting NADPH oxidase enzyme activity (50, 91). Similar
effects of E2 to inhibit reactive oxygen species production have been found in animal models as
well (21, 32, 50, 54). However, acute increases in reactive oxygen species production during
exercise stimulate gene transcription to increase antioxidant enzyme content (77). In fact, despite
acute bouts of exercise increasing reactive oxygen species production, trained individuals have
lower levels of oxidative stress and higher levels of antioxidant enzymes (14, 23, 59) as
compared with their sedentary counterparts. These findings can be interpreted in two ways. First,
if estrogen acts to attenuate reactive oxygen species production, perhaps the oxidant effect of an
acute bout of exercise is lower in women, as compared with men, resulting in lower muscle
damage and soreness. On the other hand, the effect of estrogen to attenuate reactive oxygen
species production during exercise may result in a smaller adaptation to repeated bouts of
exercise (i.e. endurance training) in women. Thus, estrogen plays an important role in the
regulation of substrate metabolism during exercise as well as the oxidative stress response to
5.0 Hormone Levels in Transitioned Men and Women Compared with Physically Born Men
The typical sex hormone concentrations in transitioned men and women, as well as those
from physically born men and women are presented in table 3. When comparing the values, physically born women and transitioned women have very similar concentrations of both testosterone and estrogen. However, transitioned men appear to have higher estrogen and Table 3: Testosterone and estrogen concentrations in transitioned men and women as compared with physically born men and women. Testosterone
Data are means + SEM. Data from Elbers et al. Am J Physiol Endocrinol Metab
, 1999; 276:E317-E325. testosterone concentrations as compared with physically born men. This is intriguing as it suggests that transitioned men may experience performance benefits from higher levels of both testosterone (muscle strength and mass) and estrogen (increased reliance on lipid stores during
exercise). Traditionally, testosterone is administered to transitioned men once every 14 days, resulting in supraphysiological testosterone concentrations that remain elevated for at least 5-9 days after testosterone administration (8) and then drop to subnormal levels during the last few days before the next scheduled injection (52). However, recently a long-acting testosterone, testosterone undecanoate, dosing regime has been developed. This dosing regime requires female-to-male transitioned individuals to undergo two initial injections separated by 6 weeks, followed by one injection every 12 weeks thereafter (52). Thus, using this regime transitioned men only require 4 doses per year. This dosing regime is advantageous because the testosterone concentrations that result immediately following injection are within the physiological range and remained stable between doses (52). Additionally, at the end of one year of dosing with testosterone undecanoate, testosterone levels in transitioned men were mid-range of normal physiological values for physically born men (52). As testosterone has a multitude of performance-enhancing effects (see above), transitioned men who wish to compete at the elite level should strive to minimize the large variation in testosterone concentrations (peaks and troughs) that result with traditional testosterone injection regimes and should utilize the testosterone undecanoate regime, as described above. The reasons for this recommendation are two-fold. First, as described above, traditional testosterone dosing regimes result in supraphysiological testosterone levels for at least 5-9 days following testosterone injection. As transitioned men undergo testosterone dosing every 14 days, they spend a large proportion of time with supraphysiological testosterone concentrations, which may enhance athletic performance, resulting in an unfair advantage as compared with physically born men. Second, as drug testing is common practice in elite sport, the traditional dosing regime may result in a failed drug-test as testosterone levels are elevated for at least 36-64% of the time during the two week period after a single testosterone dose. Using the new long-acting testosterone ensures that transitioned men are not competing at an unfair advantage, as compared with physically born men and prevents the transitioned male athlete from failing a drug test as testosterone levels do not reach supraphysiological levels using this dosing method. 5.1 Acceptable limits for testosterone and estrogen in sport and how this pertains to transitioned athletes
The Canadian Centre for Ethics in Sport is the regulating body in Canadian Sport for
doping infractions (19). There is no acceptable level of synthetic or exogenous testosterone or
estrogen in competing athletes (19). Thus, transitioned athletes taking cross-sex hormones would
be required to complete a Therapeutic Use Exemption (TUE) to permit the use of synthetic
testosterone or estrogen (i.e. testosterone undecanoate, ethinyl estradiol) (19). If a TUE has not
been obtained by a transitioned athlete and exogenous sources of testosterone or estrogen are
found within the athlete’s sample, a doping infraction would be charged against the athlete (19).
In this case, the transitioned athlete would be able to present his/her case to the review board to
explain why the endogenous hormone was found (19).
6.0 Effects of Cross-sex Hormones on Parameters that may Influence Performance
Data on the effects of cross-sex hormone administration on factors that may influence
6.1 Testosterone administration to transitioned men
Testosterone administration to transitioned men increased haemoglobin and hematocrit
content within one year of hormone supplementation (37, 52), with no further increase beyond one year (37), thus perhaps increasing oxygen delivery to the muscle during exercise. Importantly, there was no difference in haemoglobin levels between transitioned men and physically born men (37). Testosterone administration to transitioned men also increased muscle cross-sectional area; however, muscle cross-sectional area was still smaller than that of transitioned women prior to testosterone deprivation (i.e. physically born men) (28, 29, 37). However, of note, while average muscle cross-sectional area was greater in physically born men, there was a large range in muscle cross-sectional area within both groups of men (37). Further examination of the data shows that at the average muscle cross-sectional area was only greater in physically born men because they had a larger minimum muscle cross-sectional area, as compared with transitioned men (37). At the high end of the spectrum, muscle cross-sectional area was not different between transitioned and physically born men (37). These findings suggest that since an athletic population would have greater muscle mass and the maximal muscle cross-sectional area did not differ between transitioned and physically born men, differences in muscle mass between physically born and transitioned men may not be an issue when comparing athletic performance. However, as the above-mentioned study was not conducted in athletes, this hypothesis warrants further investigation.
Testosterone administration to transitioned men also decreased fat content at the triceps,
biceps, suprailiac and paraumbilical regions, with no change at the subscapular region (28). Specifically, there was an overall decrease in subcutaneous fat content with testosterone administration (28, 29), despite an increase in body weight (28). The decrease in body fat content was the greatest in the gynoid region resulting in a decrease in the waist-to-hip ratio (28). Additionally, the lower subcutaneous fat content following testosterone treatment was the result of smaller fat cell size (30). However, subcutaneous fat content was still greater in transitioned men as compared with physically born men (28). On the other hand testosterone administration increased visceral fat content within 1 year of treatment (28, 29), which was further increased at 3 years of treatment (29). There was also an increased basal, but not stimulated, lipolytic activity in abdominal, but not gluteal, adipocytes following 1 year of testosterone supplementation (30). 6.2 Estrogen administration to transitioned women
Estrogen and anti-androgen administration to transitioned women decreased haemoglobin
content in transitioned women and these levels were comparable to values in physically born women (37). Again these changes were observed in transitioned women within one year of cross-sex hormone administration and no further change in haemoglobin content was found after three years of hormone administration (37). To date no study has investigated the effect of estrogen administration on hematocrit content in transitioned women. Estrogen and anti-androgen supplementation to transitioned women decreased muscle cross-sectional area (28, 37); however, muscle cross-sectional area was still greater than that of transitioned men prior to testosterone administration (i.e. physically born women). Importantly, although the average muscle cross-sectional area was greater in transitioned women, there was a dramatic range in muscle cross-sectional area within both groups (37). Specifically, while at the low end of the
spectrum, physically born women had smaller muscle cross-sectional area; at the high end of the spectrum muscle cross-sectional area was equal between transitioned women and physically born women (37). This finding is of importance as individuals (both transitioned and physically born women) taking part in sport would likely have greater muscle mass than the average population, thus as difference did not exist at the upper end of the muscle cross-sectional area spectrum, differences in muscle cross-sectional area may not exist between transitioned women and physically born women athletes. However, as the aforementioned trial did not compare muscle cross-sectional area in transitioned and physically born women athletes, this premise remains unsubstantiated.
Estrogen and anti-androgen administration also alters body fat content and distribution
(28, 30). Specifically, in transitioned women estrogen supplementation increased both subcutaneous (28, 30) and visceral fat (28) content, resulting in an overall increase in percent body fat. Additionally, the increase in subcutaneous fat was most prominent in the gynoid region (66% vs 57% increase); however, the waist-to-hip ratio did not change in transitioned women (28). Additionally, total subcutaneous fat content still appeared to be lower in transitioned women following one year of estrogen treatment as compared with physically born women (28). Looking at individual anatomical locations, estrogen and anti-androgen administration increased percent body fat at the triceps, biceps, subscapula, suprailiac and para-umbilical regions (28). Estrogen and anti-androgen supplementation also increased individual adipocyte size and decreased basal lipolytic activity of gluteal and abdominal fat cells (30). However, similar to the effect of testosterone supplementation to transitioned men, estrogen and anti-androgen supplementation to transitioned women did not alter rates of stimulated lipolysis (30).
Despite women generally being lighter than men (26, 27), total body weight increased in
response to estrogen and anti-androgen supplementation in transitioned women, despite a decrease in muscle mass (28). Thus, for sporting events where an athlete would have to carry their own body weight (i.e. running) an increase in body weight following estrogen and anti-androgen treatment may be detrimental to performance. However, again, to date no study has been conducted investigating the effect of estrogen supplementation on body weight in transitioned women athletes. As athletes are very active and proper nutrition plays an important role in athletic performance, it is likely that body weight would decrease in this subset of transitioned women. Additionally, the body weight decrease would likely be due to the effect of estrogen to decrease muscle mass, while body fat stores would not increase as dramatically as that found in non-athletic transitioned women. However, this theory needs to be tested.
To date no study has been conducted investigating the long term effects of estrogen
supplementation on carbohydrate or lipid metabolism during endurance exercise. However, as described in detail above (see “metabolic effects of estrogen), E2 supplementation to men can spare liver glucose/glycogen utilization (17, 25), resulting in lower carbohydrate and higher lipid oxidation during a bout of endurance exercise (25). However, these E2 supplementation trials have used dosing periods of 72h to 11 days (18, 25, 71, 89), thus their applicability to metabolism during exercise in transitioned women needs further investigation.
6.3 Based on the evidence presented above, would either transitioned men or women compete at an advantage against physically born men and women?
Based on the evidence above, to date there is really no concrete evidence to support or
refute that transitioned men or women would compete at an advantage as compared with physically born men and women. Testosterone administration to transitioned men resulted in haemoglobin levels similar to those in physically born men (37). Additionally, at the upper level, muscle cross-sectional area was not different between physically born and transitioned men (37). In fact, the only sex difference that persisted following one year of testosterone administration was a higher amount of subcutaneous fat in transitioned men, as compared with physically born men (28). Thus, if this factor was an important determinant of performance it may result in a performance detriment when transitioned men competed against physically born men. However, importantly as discussed in the sex difference section above, absolute muscle mass is not necessarily indicative of muscle quality (57), as evidenced by the finding that when absolute muscle mass is controlled for, men still have greater leg muscle strength (57). Estrogen and anti-androgen treatment to transitioned women resulted in haemoglobin levels similar to those found in physically born women (37). Anthropometrically, at the higher end muscle cross-sectional area was equal between transitioned and physically born women (37); whereas subcutaneous fat content remained lower and total body weight higher in transitioned women, as compared with physically born women (28). Importantly, none of the studies that have been conducted to date have specifically looked at performance variables in transitioned versus physically born men and women. The only study written to address the issue of transitioned individuals in competitive sport (37) did so using a retrospective design in a non-athletic population. Additionally, no study has recorded whether height has changed in response to cross-sex hormone administration. Thus, based on the currently available information there is not enough evidence to support or refute a claim that transitioned athletes compete at an unfair advantage or disadvantage as compared with physically born men and women. 6.4 How do the findings to date compare with the IOC Stockholm Consensus?
In 2003 the International Olympic Committee (IOC) Medical Commissioner convened a
group of individuals to issue recommendations on sex reassignment in sports (49). The group issued the following recommendations (49):
1) Individuals undergoing sex reassignment of male to female (and vice versa) prior to
puberty should be regarded as girls and women (and vice versa) and no restrictions should be made with regards to participation in sport.
2) Individuals undergoing sex reassignment of male to female (and vice versa) after puberty
are eligible for participation in sport in their new sex category provided the following conditions are met:
a. Sex-reassignment surgery has been completed, including external genitalia
b. The athlete is legally recognized as a member of their new sex c. Cross-sex hormone therapy appropriate for the new sex has been administered in
a verifiable manner and for a sufficient length of time to minimize sex-related advantages in sport competition.
d. In the opinion of the review board, competition against one’s new sex should
commence no sooner than 2 years after gonadectomy.
However, the data presented above suggests that fewer than 2 years may be required to minimize
the effects of sex hormone exposure prior to transition on sport performance. Testosterone
administration to transitioned men increased haemoglobin content and muscle cross-sectional
area within one year with no further change after three years (37). Estrogen administration to
transitioned women decreased haemoglobin content within one year with no further decrease
after three years (37). Additionally, estrogen supplementation decreased muscle cross-sectional
area within one year with only a slight further decrease after three years (37). Thus, these
preliminary findings suggest that one year of cross-sex hormone supplementation may be
sufficient to minimize the effects of prior hormone exposure on performance in transitioned men
and women. However, again these results are taken from average transitioned individuals, not
transitioned athletes, thus the applicability of these results to an athletic population is yet to be
7.1 Is there a performance advantage or disadvantage?
To date there are limited data with regards to the effects cross-sex hormone
administration have on factors that influence performance. No study has been conducted in transitioned athletes and no study has performed any objective performance testing (i.e. VO2peak,
time trial performance or strength). We do know the effects of testosterone and estrogen
administration on body composition and muscle mass; however, these factors themselves do not
necessarily dictate performance. Until specific research is conducted comparing performance
measures in transitioned and physically born men and women no conclusive statement can be
made with regards to competitive advantage/disadvantage. One factor that does stand out with
regards to fair play in sporting competition is the finding that depending on the type of
testosterone that is used by transitioned men, supraphysiological concentrations of testosterone
persist for 5-9 days following injection. As dosing periods using traditional injection regimes are
every 14 days, transitioned men spend the majority of their time with an elevated testosterone
level (8). As testosterone is a known anabolic agent increasing muscle mass and improving
strength (6, 31, 75, 85), care must be taken to ensure that testosterone levels in transitioned men
match those of physically born men. One recommendation that can be made is the use of
testosterone undecanoate in transitioned men wanting to compete in sporting events, as this
dosing regime produces long-term stable testosterone levels (52). However, again, further
research is likely needed before this recommendation can be conclusive.
Overall there is a paucity of data regarding the effect of transitioning on athletic
performance. What performance data does exist was not taken from transitioned athletes; thus its applicability within an athletic population is uncertain. To date no study has conducted any sort of exercise test to assess athletic performance. The only study to have addressed transitioned athletes in competitive sport used a retrospective study design and considered muscle mass and
haemoglobin content to be predictors of athletic prowess. Undoubtedly these factors do influence performance; however, in athletics the whole is greater than its parts and as such, performance during athletic events needs to be assessed. While to date the data available does not appear to suggest that transitioned athletes would compete at an advantage or disadvantage as compared with physically born men and women, there is not enough data available to fully substantiate this claim. Much more research needs to be conducted before a consensus can be made. However, due to the low prevalence of transitioned individuals in the population, conducting these studies will be challenging. Due to these complications we may never truly know whether transitioned athletes compete at an advantage or disadvantage as compared with physically born men and women.
. Exercise-induced oxidative stress. Med Sci Sports Exerc
25: 218-224, 1993.
. The quadriceps angle and its relation to femoral tension. Acta Orthop
. Biomechanics and running economy. Sports Med
22: 76-89, 1996.
Anguilo A, Tauler P, Sureda A, Cases N, Tur J, and Pons A
. Antioxidant diet
supplementation enhances aerobic performance in amateur sportsmen. J Sports Sci
25: 1203-1210, 2007. 5.
Axell A, MacLean H, Plant D, Harcourt L, Davis J, Jimenez M, Handelsman D,
Lynch G, and Zajac J
. Continuous testosterone administration prevents skeletal muscle atrophy
and enhances resistance to fatigue in orchidectomized male mice. Am J Physiol Endocrinol
291: E506-E516, 2006.
Bhasin S, Storer T, Berman N, Callegari C, Clevenger R, Phillips J, Bunnell T,
Tricker R, Shirazi A, and Casaburi R
. The effects of supraphysiologic doses of testosterone
on muscle size and strength in normal men. N Engl J Med
335: 1-7, 1996.
Bhasin S, Woodhouse L, Casaburi R, Singh A, Bhasin D, Berman N, Chen X,
Yarasheski K, Magliano L, Dzekov C, Dzekov J, Bross R, Phillips J, Sinha-Hikim I, Shen
R, and Storer T
. Testosterone dose-response relationships in healthy young men. Am J Physiol
Bisschop P, Toorians A, Endert E, Wiersinga W, Gooren L, and Fliers E
. The effects
of sex-steroid administration on the pituitary-thyroid axis in transsexuals. Eur J Endocrinol
155: 11-16, 2006. 9.
Blatchford F, Knowlton R, and Schneider D
. Plasma FFA responses to prolonged
walking in untrained men and women. Eur J Appl Physiol Occup Physiol
53: 343-347, 1985. 10.
Bloomer R, and Goldfarb A
. Anaerobic exercise and oxidative stress: A review. Can J
29: 245-263, 2004. 11.
Blouin K, Boivin A, and Tchernof A
. Androgens and body fat distribution. J Steroid
Biochem Mol Biol
103: 272-280, 2008. 12.
Bottcher J, Pfeil A, Shafer M, Petrovitch A, Seidl B, Mentzel H, Lehmann G, Malich
A, Heyne J, Hein G, Wolf G, and Kaiser W
. Normative data for digital X-ray radiogrammetry
from a single female and male German cohort. J Clin Densitom
9: 341-350, 2006.
Braun B, Gerson L, Hagobian T, Grow D, and Chipkin S
. No effect of short-term
testosterone manipulation on exercise substrate metabolism in men. J Appl Physiol
99: 1930-1937, 2005. 14.
Brites F, Zago V, Verona J, Muzzio M, Wikinski R, and Schreier L
. HDL capacity to
inhibit LDL oxidation in well-trained triathletes. Life Sci
78: 3074-3081, 2006. 15.
. Metabolic actions of estradiol: significance for acute and chronic exercise
responses. Med Sci Sports Exerc
22: 286-290, 1990. 16.
Campbell SE, and Febbraio MA
. Effect of the ovarian hormones on GLUT 4 expression
and contraction-stimulated glucose uptake. Am J Physiol
282: E1139-E1146, 2002. 17.
Carter S, McKenzie S, Mourtzakis M, Mahoney D, and Tarnopolsky MA
17-beta-estradiol decreases glucose Ra but not whole body metabolism during endurance exercise. J Appl Physiol
90: 139-146, 2001.
Carter SL, McKenzie S, Mourtzakis M, Mahoney DJ, and Tarnopolsky MA
term 17-beta-estradiol decreases glucose Ra but not whole body metabolism during endurance exercise. J Appl Physiol
90: 139-146, 2001. 19.
. Canadian Centre for Ethics in Sport. www.cces.ca.
. Transgender issues in sport. Problems, solutions and the future. Research
Paper, Master of Laws, University of Melbourne, 1996. 21.
Dantas A, Tostes R, Fortes Z, Costa S, Nigro D, and Carvalho M
. In vivo evidence
for antioxidant potential of estrogen in microvessels of female spontaneously hypertensive rats. Hypertension
39: 405-411, 2002. 22.
De Bellis M, Keshavan M, Beers S, Hall J, Frustaci K, Masalehdan A, Noll J, and
. Sex differences in brain maturation during childhood and adolescence. Cerebral
11: 552-557, 2001.
Dekany M, Nemeskeri V, Gyare I, Harbula J, Malomsoki J, and Pucsok J
Antioxidant status of interval-trained athletes in various sports. Int J Sports Medicine
27: 112-116, 2006. 24.
Dekkers JvD, LJ, and Kemper H
. The role of antioxidant vitamins and enzymes in the
prevention of exercise-induced muscle damage. Sports Med
21: 216-238, 1996. 25.
Devries M, Hamadeh M, Graham T, and Tarnopolsky MA
supplementation decreases glucose Ra and Rd with no effect on muscle glycogen utilization during moderate intensity exercise in men. J Clin Endocrinol Metab
90: 6218-6225, 2005. 26.
Devries M, Hamadeh MJ, Phillips SA, and Tarnopolsky MA
. Menstrual cycle phase
and sex influence muscle glycogen utilization and glucose turnover during moderate-intensity endurance exercise. Am J Physiol Regul Intergr Comp Physiol
291: R1120-R1128, 2006. 27.
Devries M, Lowther S, Glover A, Hamadeh M, and Tarnopolsky M
. IMCL area
density, but not IMCL utilization, is higher in women during moderate-intensity endurance exercise, compared with men. Am J Physiol Regul Comp Physiol
293: R2336-R2342, 2007. 28.
Elbers J, Asscheman H, Seidell J, and Gooren L
. Effects of sex steroid hormones on
regional fat depots as assessed my magnetic resonance imaging in transsexuals. Am J Physiol
276: E317-E325, 1999. 29.
Elbers J, Asscheman H, Seidell J, Megens J, and Gooren L
. Long-term testosterone
administration increases visceral fat in female to male transsexuals. J Clin Endocrinol Metab
82: 2044-2047, 1997. 30.
Elbers J, de Jong S, Teerlink T, Asscheman H, Seidell J, and Gooren L
. Changes in
fat cell size and in vitro lipolytic activity of abdominal and gluteal adipocytes after a one-year cross-sex hormone administration in transsexuals. Metabolism
48: 1371-1377, 1999. 31.
Ferrando A, Sheffield-Moore M, Yeckel C, Gilkison C, Jiang J, Achacosa A,
Lieberman SA, Tipton K, Wolfe R, and Urban R
. Testosterone administration to older men
improves muscle function: molecular and physiological mechanisms. Am J Physiol Endocrinol
Florian M, Freiman A, and Magder S
. Treatment with 17-beta-estradiol reduces
superoxide production in aorta of ovariectomized rats. Steroids
69: 779-787, 2004. 33.
Forsberg A, Nilsson E, Werneman J, Bergstrom J, and Hultman E
composition in relation to age and sex. Clin Sci
81: 549-256, 1991. 34.
Friedlander AL, Casazza GA, Horning MA, Huie MJ, Piacentini MF, Trimmer JK,
and Brooks GA
. Training-induced alterations of carbohydrate metabolism in women: women
respond differently from men. J Appl Physiol
85: 1175-1186, 1998.
Fulkerson J, and Arendt E
. Anterior knee pain in females. Clin Orthop Relat Res
Goldberg D, Palmer W, Rumsey W, and Kendrick Z
. Effect of sexual maturation and
exhaustive exercise on myocardial glycogen metabolism. Proc Soc Exp Biol Med
174: 53-58, 1983. 37.
Gooren L, and Bunck M
. Transsexuals and competitive sports. European Journal of
151: 425-429, 2004. 38.
Goto K, Takahashi K, Yamamoto M, and Takamatsu K
. Hormone and recovery
responses to resistance exercise with slow movement. J Physiol Sci
58: 7-14, 2008. 39.
Grelsamer R, Dubey A, and Weinstein C
. Men and women have similar Q angles. A
clinical and trigonometric evaluation. J Bone Joint Surg (Br)
87: 1498-1501, 2005. 40.
Guo Z, Burguera B, and Jensen MD
. Kinetics of intramuscular triglyceride fatty acids
in exercising humans. J Appl Physiol
89: 2057-2064, 2000. 41.
Guyton A, and Hall J
. Textbook of Medical Physiology
. Philadelphia, PA: W.B.
. Does gender affect pulmonary function and exercise capacity. Respiratory
Physiology and Neurobiology
151: 124-131, 2005. 43.
Hartgens F, and Kuipers H
. Effects of androgenic-anabolic steroids in athletes. Sports
Herbst K, and Bhasin S
. Testosterone action on skeletal muscle. Curr Opin Clin Nutr
Hogler W, Blimkie C, Cowell C, Inglis D, Rauch F, Kemp A, Wiebe P, Duncan C,
Farpour-Lambert N, and Woodhead H
. Sex-specific developmental changes in muscle size
and bone geometry at the femoral shaft. Bone
Jan 26 Epub ahead of print: 2008.
Hopkins S, and Harms C
. Gender and pulmonary gas exchange during exercise. Med
Sci Sports Exerc
32: 50-56, 2004. 47.
Horton TJ, Pagliassotti MJ, Hobbs K, and Hill JO
. Fuel metabolism in men and
women during and after long-duration exercise. J Appl Physiol
85: 1823-1832, 1998. 48.
Hostler D, Schwirian C, Campos G, Toma K, Crill M, Hagerman G, Hagerman F,
and Staron R
. Skeletal muscle adaptations in elastic resistance-trained young men and women. Eur J Appl Physiol
86: 112-118, 2001.
. Stockholm Consensus on sex reassignment in sports.
Itagaki T, Shimizu I, Cheng X, Yuan Y, Oshio A, Tamaki K, Fukuno H, Honda H,
Okamura Y, and Ito S
. Opposing effects of oestradiol and progesterone on intracellular
pathways and activation processes in the oxidative stress induced activation of cultured rat
hepatic stellate cells. Gut
54: 1782-1789, 2005.
Ivey P, and Gaesser G
. Postexercise muscle and liver glycogen metabolism in male and
female rats. J Appl Physiol
62: 1250-1254, 1987. 52.
Jacobeit J, Gooren L, and Schulte H
. Long-acting intramuscular testosterone
undecanoate for treatment of female-to-male transgender individuals. J Sex Med
4: 1479-1484, 2007. 53.
James A, Lorraine M, Cullen D, Goodman C, Dawson B, Palmer T, and Fournier P
Muscle glycogen supercompensation: absence of a gender-related difference. Eur J Appl Physiol
85: 533-538, 2001.
Ji H, Zheng W, Menini S, Pesce C, Kim J, Wu X, Mulroney S, and Sandberg K
Female protection in progressive renal disease is associated with estradiol attenuation of superoxide production. Gender Medicine
4: 56-70, 2007. 55.
Ji L, and Fu R
. Responses of glutathione system and antioxidant enzymes to exhaustive
exercise and hydroperoxide. J Appl Physiol
72: 549-554, 1992. 56.
Kaji H, Kosaka R, Yamauchi M, Kuno K, Chihara K, and Sugimoto T
. Effects of
age, grip strength and smoking on forearm volumetric bone mineral density and bone geometry by peripheral quantitative computed tomography: comparisons between female and male. Endocr J
52: 659-666, 2006. 57.
Kanehisa H, Ikegawa S, and Fukunaga T
. Comparison of muscle cross-sectional area
and strength between untrained women and men. Eur J Appl Physiol Occup Physiol
68: 148-154, 1994. 58.
Kanehisa H, Okuyama H, Ikegawa S, and Fukunaga T
. Sex difference in force
generation capacity during repeated maximal knee extensions. Eur J Appl Physiol Occup Physiol
73: 557-562, 1996. 59.
Karolkiewicz J, Szczesniak L, Deskur-Smielecko E, Nowak A, Stemplewski R, and
. Oxidative stress and antioxidant defense system in healthy, elderly men:
relationship to physical activity. Aging Male
6: 100-105, 2003.
Kendrick ZV, and Ellis GS
. Effect of estradiol on tissue glycogen metabolism and lipid
availability in exercised male rats. J Appl Physiol
71: 1694-1699, 1991. 61.
Kendrick ZV, Steffen CA, Rumsey WL, and Goldberg DI
. Effect of estradiol on
tissue glycogen metabolism in exercised oophorectomized rats. J Appl Physiol
63: 492-496, 1987. 62.
. Exercise-induced muscle damage. Int J Sports Med
15: 132-135, 1994.
Maud P, and Schultz B
. Gender comparisons in anaerobic power and anaerobic capacity
test. Br J Sports Med
20: 51-54, 1986. 64.
McClaran S, Harms C, Pegelow D, and Dempsey J
. Smaller lungs in women affect
exercise hyperpnea. J Appl Physiol
84: 1872-1881, 1998. 65.
. Dysanapsis in normal lungs assessed by the relationship between maximal flow,
static recoil, and vital capacity. Am Rev Respir Dis
121: 339-343, 1980. 66.
Mittendorfer B, Horowitz JF, and Klein S
. Effect of gender on lipid kinetics during
endurance exercise of moderate intensity in untrained subjects. Am J Physiol Endocrinol Metab
283: E58-65, 2002. 67.
. Estradiol-induced changes in lipoprotein lipase, eating, and body weight in
rats. Am J Physiol (Endocrinol Metab)
240: E533-E538, 1981. 68.
Roepstorff C, Thiele M, Hillig T, Pilegaard H, and Richter E
. Higher skeletal muscle
alpha-2-AMPK activation and lower energy charge and fat oxidation in men than women during submaximal exercise. J Physiol
574: 2006. 69.
Romijn JA, Coyle EF, Sidossis LS, Rosenblatt J, and Wolfe RR
metabolism during different exercise intensities in endurance-trained women. J Appl Physiol
88: 1701-1714, 2000. 70.
Rooney TP, Kendrick ZV, Carlson J, Ellis GS, Matakevich B, Lorusso SM, and
. Effect of estradiol on the temporal pattern of exercise-induced tissue glycogen
depletion in male rats. J Appl Physiol
75: 1502-1506, 1993.
Ruby B, Robergs R, Waters D, Burge M, Mermier C, and Stolarczyk L
. Effects of
estradiol on substrate turnover during exercise in amenorrheic females. Med Sci Sports Exerc
29: 1160-1169, 1997. 72.
Salton C, Chuang M, O'Donnell C, Kupka M, Larson M, Kissinger K, Edelman R,
Levy D, and Manning W
. Gender differences and normal left ventricular anatomy in an adult
population free of hypertension. A cardiovascular magnetic resonance study of the Framingham
Heart Study Offspring cohort. J Am Coll Cardiol
39: 1055-1060, 2002.
Sandstede J, Lipke C, Beer M, Hofmann S, Pabst T, Kenn W, Neubauer S, and
. Age- and gender-specific differences in left and right ventricular cardiac function and
mass determined by cine magnetic resonance imaging. Eur Radiol
10: 438-442, 2000.
Sastre J, Asensi M, Gasco E, Pallardo F, Ferrero J, and Furukawa T
physical exercise causes oxidation of glutathione status in blood: Prevention by antioxidant administration. Am J Physiol
263: R992-R995, 1992. 75.
Schroeder E, Terk M, and Sattler F
. Androgen therapy improves muscle mass and
strength but not muscle quality: results from two studies. Am J Physiol Endocrinol Metab
285: 2003. 76.
Schwartz J, Katz S, Fegley R, and Tockman M
. Sex and race differences in the
development of lung function. Am Rev Respir Dis
138: 1415-1421, 1988. 77.
Sen C, and Packer L
. Antioxidant and redox regulation of gene transcription. FASEB J
Simoneau J, Lortie G, Boulay M, Marcotte M, Thibault M, and Bouchard C
skeletal muscle fiber type alteration with high-intensity intermittent training. Eur J Appl Physiol Occup Physiol
54: 250-253, 1985. 79.
Simoneau J, Lortie G, Boulay M, Thibault M, Theriault G, and Bouchard C
Skeletal muscle histochemical and biochemical characteristics in sedentary male and female subjects. Can J Physiol Pharmacol
63: 30-35, 1985. 80.
Snyder P, Peachey H, Hannoush P, Berlin J, Loh L, Lenrow D, Holmes J, Dlewati
A, Santanna J, Rosen C, and Strom B
. Effect of testosterone treatment on body composition
and muscle strength in men over 65 years of age. J Clin Endocrinol Metab
88: 2647-2653, 1999.
Staron R, Hagerman F, Hikida R, Murray T, Hostler D, Crill M, Ragg K, and Toma
. Fiber type composition of the vastus lateralis muscle of young men and women. J Histochem
48: 623-629, 2000.
Staron R, Karapondo D, Kraemer W, Fry A, Gordon S, Falkel J, Hagerman F, and
. Skeletal muscle adaptations during early phase of heavy-resistance training in men
and women. J Appl Physiol
76: 1247-1255, 1994.
Steffensen CH, Roepstorff C, Madsen M, and Kiens B
. Myocellular triacylglycerol
breakdown in females but not in males during exercise. Am J Physiol Endocrinol Metab
282: E634-642, 2002. 84.
Stirone C, Duckles S, Krause D, and Procaccio V
. Estrogen increases mitochondrial
efficiency and reduces oxidative stress in cerebral blood vessels. Mol Pharmacol
68: 2005. 85.
Storer T, Magliano L, Woodhouse L, Lee M, Dzekov C, Dzekov J, Casaburi R, and
. Testosterone dose-dependently increases maximal voluntary strength and leg power,
but does not affect fatigability or specific tension. J Clin Endocrinol Metab
88: 1478-1485, 2003.
Tarnopolsky L, MacDougall J, Atkinson ST, Tarnopolsky MA, and Sutton J
differences in substrate for endurance exercise. J Appl Physiol
68: 302-308, 1990.
Tarnopolsky M, Zawada C, Richmond L, Carter S, Shearer J, Graham T, and
. Gender differences in carbohydrate loading are related to energy intake. J Appl
91: 225-230, 2001.
Tarnopolsky MA, Atkinson SA, Phillips SA, and MacDougall JD
loading and metabolism during exercise in men and women. J Appl Physiol
78: 1360-1368, 1995. 89.
Tarnopolsky MA, Roy BD, MacDougall JD, McKenzie S, Martin J, and Ettinger S
Short-term 17-beta-estradiol administration does not affect metabolism in young males. Int J of Sports Med
22: 175-180, 2001. 90.
Venables MC, Achten J, and Jeukendrup AE
. Determinants of fat oxidation during
exercise in healthy men and women: a cross-sectional study. J Appl Physiol
98: 160-167, 2005. 91.
Wagner A, Schroeter M, and Hecker M
. 17beta-estradiol inhibition of NADPH
oxidase expression in human endothelial cells. FASEB J
15: 2121-2130, 2001. 92.
Weber C, and Schneider D
. Maximal accumulated oxygen deficit expressed relative to
the active muscle mass for cycling in untrained male and female subjects. Eur J APpl Physiol
82: 255-261, 2000. 93.
. Sexual dimorphism of body composition. Best Pract Res Clin Endocrinol Metab
White L, Ferguson M, McCoy S, and Kim H
. Intramyocellular lipid changes in men
and women during aerobic exercise: a (1)H-magnetic resonance spectroscopy study. J Clin Endocrinol Metab
88: 5638-5643, 2003. 95.
Williams K, Cavanagh P, and Ziff J
. Biomechanical studies of elite female distance
runners. Int J Sports Med
8: 107-118, 1987. 96.
Wilson D, Flowers C, Carlile S, and Udall K
. Estrogen treatment and gonadal function
in the regulation of lipoprotein lipase. Atherosclerosis
24: 491-499, 1976. 97.
Witt E, Reznick A, Viguie C, Starke-Reed P, and Packer L
. Exercise, oxidative
damage and effects of antioxidant manipulation. J Nutr
122: 766-773, 1992.
Science Fair Topics 2. Determining the Empirical Formula of Potassium Chlorate through Thermal Decomposition 6. How effective are natural mosquito repellents? 7. Does light affect the rates at which foods spoil? 8. Do all dishwashing detergents produce the same amount of bubbles? Clean the same 9. Is bottled water more pure than tap water? 10. How does the pH of juice ch
401 Mass. 812 (1988) 520 N.E.2d 134 COMMONWEALTH JOHN K. MULICA, JR. Supreme Judicial Court of Massachusetts, Essex. Present: WILKINS, LIACOS, NOLAN, & LYNCH, JJ Thomas G. Shapiro for the defendant. Robert J. Bender, Assistant District Attorney, for the Commonwealth. The defendant was convicted of embezzlement from the Newburyport Five Cents Savings Bank (bank), of p