INTRODUCTION

Over the past 3 decades, our understanding of the Female Athlete Triad has evolved in response to research advances over time, such as the establishment of prevalence data, the expansion of the spectra to include the subclinical expressions of each of the 3 conditions, and, most importantly, the causal role of energy deficiency/low energy availability (EA) on reproductive dysfunction as determined through short-term and long-term laboratory experiments including randomized controlled trials (RCTs). In male athletes, a Triad-like syndrome has been frequently noted in the literature. With increasing awareness, there has been a recent uptick in Triad-like research in men. Because the causal role of low EA in the modulation of reproductive function has been established in the female and male literature1–7 and because the observations thus far in men, like women, reinforce the notion that skeletal health and reproductive outcomes are the primary clinical concerns, the authors believe that the science in men is best built on the scaffolding of the Female Athlete Triad model. This point is reinforced given that most of the scientific evidence that forms the foundation for the emerging concept of Relative Energy Deficiency in Sport is limited to the scientific evidence supporting the Triad model in both women and men. As such, the Female and Male Athlete Triad Coalition present a model for the Male Athlete Triad with the scientific evidence available to date. Because of the comprehensive nature of each topic, we have elected to publish 2 articles focused on the Male Athlete Triad. The first article, “The Male Athlete Triad: Definition and Scientific Basis,” will present the scientific evidence to support the model, and the second article, “The Male Athlete Triad: Diagnosis, Treatment and Return-to-Play,” will present the clinical diagnostic criteria and the risk assessment criteria for a clearance and return-to-play model.

The Female and Male Athlete Triad Coalition convened an expert panel in conjunction with the American College of Sports Medicine (ACSM) 64th Annual Meeting in Denver, Colorado, May 30, 2017, to consolidate evidence-based data and develop recommendations for the Male Athlete Triad and this consensus statement. We drew on emerging data developments and the experience of a diverse group of clinicians and basic scientists. The meeting began with an introduction of the problem and case presentations, followed by selected presentations from invited expert panel members and a panel discussion on various clinical questions and recommendations for team physicians and other sports medicine professionals in preparation for a consensus article.

Invitees to the expert panel included recognized national and international representatives, including expert clinical and basic scientists who have published extensively on the Triad and related topics, particularly as it relates to the male athlete. The panel included participants from a variety of medical and scientific experts in applied physiology, kinesiology, nutrition, women's and men's health, exercise physiology, pediatric and adult medical endocrinology, bone health, reproductive medicine, clinical sports medicine, and epidemiology.

We aimed to examine, consolidate, and implement practical, sport-specific strategies for diagnosing, managing, and preventing the manifestations of the Triad in male athletes guided by evidence-based science and expert opinion. The 2-part Female and Male Athlete Triad Coalition Consensus Statement on the Male Athlete Triad and accompanying figures represent the key themes discussed at the meeting, with scientific support and summary of vital clinical implications for male athletes.

DEFINITION OF THE MALE ATHLETE TRIAD

The Male Athlete Triad is a syndrome of 3 interrelated conditions, including energy deficiency/low EA, impaired bone health, and suppression of the hypothalamic–pituitary–gonadal (HPG) axis (Figure 1). Energy deficiency/low EA refers to the level of energetic status where one or more of the following compensatory metabolic adaptations have occurred: suppression of resting metabolic rate (RMR) normalized for body size or fat-free mass (FFM),8 a loss of body weight that is associated with a new chronically low set point,8,9 low body mass index (BMI),10,11 and/or suppression of metabolic hormones, such as triiodothyronine (T3) and leptin,6,7,12 reflecting the prolonged failure to consume adequate energy to support energy expenditure. At the optimal, “healthy,” end of the continuum, energy intake (EI) is sufficient to meet the combined needs of exercise and all physiological processes; bone health is appropriate for age, sex, and exercise exposure; and the HPG axis is functioning normally. As energy deficiency ensues and EA is reduced, there is a progressive deterioration in reproductive health and bone outcomes. At the extreme, “unhealthy,” end of the continuum, clinical outcomes include energy deficiency/low EA associated with or without eating disorders or disordered eating, hypogonadotropic hypogonadism, oligospermia, decreased libido, and osteoporosis with or without bone stress injury (BSI). At present, and in contrast to the Female Athlete Triad model, the specific intermediate subclinical outcomes are less clearly defined in men and are represented as subtle alterations in the HPG axis and increased risk for BSI. The degree of energy deficiency/low EA associated with such alterations remains unclear. However, the available data suggest a more severe energy deficiency/low EA state is needed to affect reproductive and skeletal health in the Male Athlete Triad than in the Female Athlete Triad,7,12–15 although additional research is needed to further clarify and quantify this association. The bidirectional arrows indicate that the outcomes associated with energy deficiency/low EA can be reversed, with the exception of bone outcomes, for which additional research is needed to clarify.

Figure 1.:

Model of the Male Athlete Triad. The unidirectional arrows from energetic status/EA toward bone health and the HPG axis indicate the causal role of EA on both bone health and HPG axis function. Similarly, the unidirectional arrow from HPG toward bone health indicates the causal effect of reproductive hormones on bone health. Furthermore, the bidirectional arrows along each continuum of severity represent the “reversibility” of the condition such that an individual can improve or worsen over time. The line showing reversal of bone health outcomes is dashed with a question mark because the reversal of BMD is less known, and more research is needed. Notably, with the Male Athlete Triad, the subclinical and clinical sequelae present at lower EA levels than what is often required for the development of health consequences in exercising women.

The data available to date are presented below and include summary statements regarding the strength of scientific evidence. Because of challenges associated with evidence being drawn from studies using a variety of methodologies, we have used a taxonomy in which both RCT and observational data are considered important and that has been used in ACSM position stands and by the Agency for Healthcare Research and Quality.16,17 The specific evidence scoring criteria are as follows:

Evidence Level A: Consistent pattern of findings on the basis of substantial data from RCTs and/or observational studies. Evidence Level B: Strong evidence from RCT and/or observational studies but with some inconsistent results from the overall conclusion. Evidence Level C: Evidence from a smaller number of observational and/or uncontrolled or nonrandomized trials, which is generally suggestive of an overall conclusion. Evidence Level D: Insufficient evidence for categories A to C; panel consensus judgment. ENERGY DEFICIENCY/LOW ENERGY AVAILABILITY IN MALE ATHLETES What Is the Evidence for Chronic Energy Deficiency/Low Energy Availability in Male Athletes?

Objective indicators of compensatory adaptations to chronic energy deficiency include changes in body weight and body composition,8–11 the suppression of RMR normalized for body size or FFM,8 and changes in circulating metabolic hormones, such as suppressed T3 and leptin concentrations.6,7,12 In addition to these measures, EA has been used by many investigators and is conceptually described as the energy remaining for bodily processes after the energy cost of exercise training is accounted for.7,18 This expression of EA from Loucks4,7,18,19 has persisted in the Triad literature despite the lack of consideration of nonpurposeful energy expenditure, which can be quite variable (and significant in many cases), concerns regarding the accuracy with which it can be determined in free living athletes, and the reliance of this measure on self-reported variables, especially dietary EI.20 Similarly, assessments of FFM may be specific to laboratory settings but may be calculated based on the weight of the athlete in kilograms, as well as the percent body fat, which may be estimated by dual X-ray absorptiometry, air displacement plethysmography, skinfold measurements, Bod Pod, or bioelectrical impedance.21,22

In this consensus article, we provide an operational definition of the concept of “low” EA. We shall use the terminology of low EA to refer to a level of EA that reflects energy deficiency such that there is evidence that compensatory metabolic adaptations are present that reflect the failure to consume adequate energy to support energy expenditure. The compensatory adaptations include the suppression of RMR normalized for body size or FFM,8 a loss of body weight that is associated with a new chronically low set point,8,9 low BMI,10,11 and or suppressed metabolic hormones, such as T3 and leptin.6,7,12 These changes occur over weeks to months and are therefore reflective of adaptations to chronic energy deficiency.

Causal evidence that energy deficiency impairs reproductive function is available.5–7,23 In women, Loucks and Thuma7 identified an EA threshold of 30 kcal/kg FFM/d, below which changes in menstrual function ensued. Although more research is necessary, this particular EA threshold of 30 kcal/kg FFM/d failed to predict the onset of menstrual disturbances with energy deficiency/low EA-associated exercise training for 3 months in young, untrained, ovulatory women12 and, in cross-sectional reports of menstrual status, it failed to discriminate menstrual status of varying categories.24 As such, recent data do not support the idea that there is a particular threshold below which reproductive outcomes are impaired.25 However, data do support a strong relationship between EA and menstrual suppression, such that as EA decreases, the likelihood of menstrual disruption increases.24 In men, the literature to date has not identified a clear threshold of EA below which reproductive function impairment is observed. Therefore, at this point in the development of the Male Athlete Triad model, there are not sufficient data to provide a quantitative definition of low EA in male athletes. Thus, this article will use the term “chronic energy deficiency/low EA” to refer to the compensatory metabolic adaptations that occur during prolonged periods of inadequate dietary EI relative to total energy expenditure.

Currently, no standard protocol exists for the measurement of EA among athletes in the field. Although we recommend that EA is a measure best reserved for laboratory assessment, it can be useful for the nutritionist or healthcare professional working with an athlete in a clinical setting because treatment goals based on improving EA may be more acceptable to the athlete than goals based on increasing body weight. The challenges faced by investigators and clinicians aiming to measure EA are described in detail in a recent review and include the lack of a universal protocol, the resources needed to estimate each component of the EA equation, and error associated with estimating each component, particularly dietary EI.20 The limitations of assessing EA notwithstanding, investigations that estimate EA in male athletes can nonetheless provide some initial insights into the subpopulations at risk, and if low EA is referred to, it is presumably referring to an EA level that reflects an energy deficiency. In the clinical article “The Male Athlete Triad: Diagnosis, Treatment, and Return-to-Play,” we will address the usefulness of EA assessments when counseling athletes and suggest communication strategies.

Cross-sectional data identifying EA below 30 kcal/kg FFM/d in male athletes have been reported, particularly for athletes who participate in sports that have a leanness component such as weight class26,27 and endurance sports,28–31 although an exact definition for “low” EA is still to be determined in male athletes. The prevalence of EA below 30 kcal/kg FFM/d in exercising men is similar to what has been reported in women.26,29,31 For example, the prevalence of EA below 30 kcal/kg FFM/d is 56% versus 51% in adolescent male and female athletes across a variety of sports,26 25% versus 31% in male and female endurance runners/race walkers,29 and 42% versus 29% in male and female cross-country runners.31 Notably, the methods used to assess EA vary greatly among published studies making direct comparisons difficult and underscoring the inherent problems in the assessment of EA, which is dependent on several self-report measures, that is, EI and exercise energy expenditure (EEE).

Other investigators do not report EA specifically, but rather have included concurrent assessments of EI and EEE in athletes. Male athletes, particularly those participating in leanness sports, often have low EI according to the Institute of Medicine Daily Recommended Intakes or Food and Agriculture Organization of the United Nations/World Health Organization recommendations.32 Although it is recognized that accurate recording of food intake is challenging,33 estimates available among male athletes, especially in sports requiring leanness or with weight limitations, often suggest EI of 500 to 1000 kcal/d lower than that required for EEE32,34–36 or the recommended EI.37 For example, in a systematic review, it was reported that among studies that measured EI and EEE (n = 55; 1195 athletes) male endurance athletes exhibited, on average, an energy deficit of 577 kcal/d.34 Lower EI relative to EEE has also specifically been reported in professional male endurance athletes including runners (2987 ± 293 kcal/d intake vs 3605 ± 119 kcal/d expenditure),35 and cyclists (3224 ± 358 kcal/d intake vs 4562 ± 979 kcal/d expenditure).36 Furthermore, after a 54-hour 1230-km ultra-endurance cycling event, male athletes averaged an energy deficit of 2468 kcal/24 hours.38

Energy deficiency and EA below 30 kcal/kg FFM/d have been documented in exercising men.39 The results from 2 investigators13,14 who manipulated EI and EEE in men to test a low level of EA (15 kcal/kg FFM/d) and an adequate level of EA (40-45 kcal/kg FFM/d) did not report many of the metabolic hormone perturbations that have been previously reported by Loucks et al4,7,18 in women with an EA of 30, 20, and 10 kcal/kg FFM/d (ie, reductions in T3, leptin, and insulin). For example, Papageorgiou et al13 manipulated exercise and EI for 4 to 5 days in exercise-trained men, as was performed in the study by Loucks et al in sedentary women. The low set point of 15 kcal/kg FFM/d failed to induce any significant reductions in T3, leptin, insulin-like growth factor 1 (IGF-1), or insulin.13 In a very similar study, Koehler et al14 manipulated both EI and EEE and failed to report any significant reductions in T3, IGF-1, or testosterone concentrations after exposure for 4 days to 15 kcal/kg FFM/d (vs 40 kcal/kg FFM/d), but insulin and leptin concentrations were significantly reduced at an EA of 15 kcal/kg FFM/d. As such, if an appropriate definition of “low” EA in men is to be considered, more rigorous scientific evidence of the magnitude of energy deficiency/low EA associated with indices of metabolic compensation (ie, inducing metabolic and hormonal adaptations) will be required. Similarly, understanding the influence of time spent in varying degrees of energy deficiency/low EA on indices of metabolic compensation is needed as well. The data available to date are very limited but are in contrast to similar studies in women. In both the Papageorgiou et al13 and the Koehler et al14 studies in men, study participants were exercise-trained men, whereas in the studies by Loucks,4,7,18 the participants were sedentary women. The extent to which this fact affected the outcomes remains unclear, and more research is necessary to clarify these issues.

Other data that demonstrate better evidence of energy deficiency affecting metabolic hormones in men include the multistressor studies in Army Rangers during an 8-week training period of exposure to desert, swamp, mountain, and forest conditions during severe energy restriction.40 After the severe energy restriction (∼1100 kcal/d) and extreme environments, dramatic reductions in concentrations of IGF-1 (−57%) and T3 (−15%) were observed.40 Although Rangers were exposed to multiple stressors simultaneously, the specific effects of energy restriction are highlighted by the findings that, within a subgroup of Rangers who were fed a supplemental ∼400 kcal/d, declines in IGF-1 and T3 were attenuated.40 Finally, in all Army Rangers, metabolic hormone concentrations were restored to pre-exposure concentrations rapidly within 1 to 4 weeks, after cessation of the 8-week training.40 As such, these data provide evidence that energy deficiency/low EA in men induces metabolic perturbations, although the energy deficits required to induce metabolic hormone perturbations need to be quantified and men seem to require more severe energy deficits than women before decrements to metabolism are observed.

Evidence Level B. Severe energy deficit (∼1100 kcal/d) in men is associated with alterations in metabolic hormones indicative of metabolic compensation. Data are not consistent for alterations in these hormones in states of low EA (defined as <15 kcal/kg FFM/day).

What Are the Pathways to Energy Deficiency/Low Energy Availability in Male Athletes?

The psychological and behavioral underpinnings of inadequate EI and/or excessive exercise that contribute to energy deficiency/low EA also warrant discussion. As with female athletes, male athletes may exhibit multiple pathways, that is, intentional weight loss, inadvertent undereating, disordered eating, and clinical eating disorders, that contribute to their failure to consume adequate volume of calories to meet the needs of EEE. However, the underlying motivations that contribute to undereating may differ between men and women, and particularly male and female athletes; therefore, relying on the same criteria that have been applied to exercising women may not be appropriate for male athletes. For example, high cognitive dietary restraint,41–43 as measured by the Three-Factor Eating Questionnaire,44 and high drive for thinness,45,46 as measured by the Eating Disorders Inventory,47 have both been used as surrogate measures of energy deficiency and as screening tools to identify women at-risk for disordered eating. Currently, scarce information is available regarding how cognitive restraint and drive for thinness may relate to disordered eating and energy deficiency in exercising men, and what little information is available suggests that men have lower drive for thinness subscale scores than women.48,49 Furthermore, because of differing societal and cultural body ideals between the sexes, such as men wanting to improve muscularity50 or striving for a combination of muscularity and thinness,51 disordered eating behaviors may manifest differently in men versus women.52 Notably, both muscularity and thinness were independently and positively associated with disordered eating in college-aged men.51 A tool has been developed to identify the interaction between muscularity and thinness, which has been referred to as a “drive for leanness”—this may be relevant to a Triad-like condition in men.53 Much additional work must be conducted to better understand disordered eating behaviors in men.

To date, the most comprehensive information available regarding the prevalence of eating disorders in male athletes identified that 8% of athletes (55/687) were at-risk and subsequently met the diagnostic criteria for an eating disorder.54 Sports with the highest prevalence of male athletes who met the criteria for an eating disorder were those categorized as antigravitation sports (ie, high/long/triple jump, pole vault, and rock climbing, 22%, n = 8/37) and weight-class sports (ie, wrestling, martial arts, and weight lifting, 18%, n = 14/79).54 Similarly, a high prevalence of disordered eating or extreme body weight-cutting behaviors has been reported in cycling and in weight-class and leanness sports.54–60

Evidence Level C. Exercising men, particularly those in leanness sports, are at risk for developing disordered eating/eating disorders; however, the specific eating behaviors may differ from those observed in exercising women.

HYPOGONADOTROPIC HYPOGONADISM IN MALE ATHLETES

Several levels of evidence are available to demonstrate that acute exercise and high-volume endurance exercise have suppressive effects on the HPG axis resulting in hypogonadotropic hypogonadism. This is demonstrated by (1) suppressed testosterone (T) and luteinizing hormone (LH) concentrations and pulse frequency, particularly in athletes engaged in lean sports,61–65 after acute bouts of prolonged exercise38,66–68 with T concentrations often, but not always, observed within the subclinical to clinical range; (2) decreased T and responsiveness of gonadotropins to gonadotropin-releasing hormone (GnRH) stimulation in male athletes after exercise training40,69,70; (3) negative changes in spermatogenesis in high-volume male athletes and in men after exercise training69,71–74; and (4) self-report data of decreased libido and sexual desire in men participating in high-volume exercise training.61,75 The levels of evidence available to support the occurrence of hypogonadotropic hypogonadism in male athletes include (1) acute responses to prolonged exercise, (2) cross-sectional reports, and (3) RCTs. This evidence is summarized in Tables 1 and 2.

TABLE 1. - Testosterone Concentrations in Exercising Men Study Pre Post Recovery Control Significance Short-term restricted EA  Koehler et al14   Caloric restriction only 18.72 ± 1.42 17.44 ± 2.95 None   Caloric restriction + exercise 18.27 ± 1.59 15.46 ± 3.33 None Acute exercise bouts  Kraemer et al64   Runners 12.32 ± 1.41 6.96 ± 1.01 Pre vs post   Cyclists 13.81 ± 1.30 5.59 ± 1.53 Pre vs post  Kupchak et al65,* 14.9 10.9 13.5 Pre vs post
Post vs recovery  Hooper et al66,* 14 15 10 Pre vs recovery Multistressor environment  Friedl et al38,† 16.3 ± 1.6 2.2 ± 0.9 19.3 ± 3.2 Pre vs post
Post vs recovery Cross-sectional  McColl et al60,* 17.3 ± 1.0 13.8 ± 1.0 29.4 ± 1.0 Pre vs post  MacConnie et al68 21.5 ± 1.1 20.8 ± 1.2 None  Wheeler et al63,* 24.0 28.0 Runners vs controls  Hooper et al59 9.2 ± 0.8 16.2 ± 1.2 Runners vs controls RCT  Safarinejad et al67   High intensity 13.2 ± 0.4 8.6 ± 0.4 13.8 ± 0.4 Pre vs post   Moderate intensity 13.4 ± 0.4 11.4 ± 0.4 13.7 ± 0.4 None

Data presented as mean ± SEM or mean. The units of total testosterone are expressed as nmol/L.

*Approximations of concentrations based on available data and figures; SEM not available.

†Subset of completers who had a follow-up visit during recovery.

TABLE 2. - Semen Characteristics in a Subset of Studies of Exercising Men Study Volume (mL) Concentration (106/mL) Total No. (106) Normal Forms (%) Vaamonde et al72  Active controls 3.2 ± 0.9 61.0 ± 23.0 191.8 ± 73.4 15.2 ± 1.2  Water Polo 3.4 ± 1.3 58.0 ± 24.4 196.6 ± 85.4 9.7 ± 3.0*  Triathletes 2.9 ± 0.9 48.2 ± 14.7* 141.3 ± 58.0* 4.7 ± 2.2* De Souza et al69  High-mileage runners 4.1 ± 01.7 88.5 ± 49.0* 352.0 ± 230.4 40.9 ± 6.6  Low-mileage runners 3.5 ± 1.8 127.2 ± 96.6 317.8 ± 249.9 46.4 ± 13.2  Controls 2.5 ± 1.6 175.5 ± 78.7 375.9 ± 186.1 47.0 ± 10.4 Safarinejad et al67  High intensity   Pre 2.7 ± 1.4 66.2 ± 14.6 196 ± 32.6 19.2 ± 2.6   Running 2.7 ± 1.6 35.4 ± 4.2* 106 ± 20.8* 14.6 ± 2.4*   Recovery 2.7 ± 1.7 64.8 ± 4.2 188 ± 31.2 18.8 ± 2.1  Moderate intensity   Pre 2.8 ± 1.3 64.4 ± 14.4 197 ± 32.4 19.3 ± 2.7   Running 2.8 ± 1.1 56.8 ± 3.6*† 161 ± 31.4*† 16.2 ± 2.1   Recovery 2.7 ± 1.4 62.8 ± 3.4 191 ± 30.4 18.4 ± 1.8

Data presented as mean ± SD.

*Significantly different from controls/pre.

†Significantly different from high-intensity group at same time point.

Which Specific Reproductive Hormones Are Suppressed in Male Athletes?

Ironman events (ultra-endurance running and cycling races of ∼160-1200 km) provide evidence for the effects of acute responses to prolonged, strenuous exercise on the suppression of the HPG axis in men, as characterized by reduced serum total T concentrations,38,66–68 often in the subclinical67 and clinically low range,38,66 and reduced LH.62,67 In cross-sectional reports where athletes, primarily runners, are compared with controls, suppression of total T and mean LH is also observed, although T is often still within the normal range. For example, runners training >80 km/wk had lower total T and lower LH mean pulse amplitude and mean area under the 6 hours LH curve compared with controls.62 However, male marathoners (running 125-200 km/wk) demonstrated decreased LH pulse frequency and amplitude and suppressed LH responsiveness to GnRH, but no difference in T levels compared with healthy controls.70 In other studies of male runners with a lower training load of ∼80 km/wk, no changes in LH pulse frequency were observed when compared with controls.62,76 Other cross-sectional reports observe similar findings,63,65 except for 1 study in endurance-trained men averaging >450 min/wk of training (in running, swimming, and cycling) that failed to observe any differences in LH pulse frequency or amplitude compared with sedentary controls.64

A limitation to the interpretation of these studies is that energy status and/or EA is not typically quantified in studies of reproductive function. Presumably, the effects of the acute prolonged bouts of exercise and cross-sectional comparisons of male athletes and nonathletes were associated with energy deficiency/reductions in EA, subsequently translated to suppression of the HPG axis. One such example in long-distance runners reported that EA of runners (27.2 kcal/kg lean body mass [LBM]/d) was lower than that observed in controls (45.4 kcal/kg LBM/d) in concert with subclinically low T.61 In another study of a 54-hour 1230-km ultra-endurance cycling event, athletes averaged an energy deficit of 2468 kcal/24-hour and demonstrated severe reductions in serum T in the clinically low range.38 Further research that carefully documents EA changes after acute exercise and chronic training is necessary to clearly identify whether prolonged endurance exercise has suppressive effects on the male reproductive axis in the absence of energy deficiency/low EA.

Other prospective data supporting a link between energy status and reproductive function in men are the aforementioned 8-week multistressor studies of Army Rangers.40 As a reminder, 1 group of Rangers was exposed to extreme energy restriction with deficits averaging ∼1100 kcal/d and experienced reduced mean LH concentration and severely reduced concentrations of T (4.5 ± 3.9 nmol/L), which fell below the normative range and within a clinically low range (see Table 3 for normal to clinically low T concentrations in men77–83) at the completion of the 8-week training regimen.40 However, in the group of Rangers receiving supplemental calories (400 kcal), suppression of both T and LH was avoided. Moreover, at completion of the training, recovery of both T and LH concentrations was observed within 1 week in the group who did not receive supplemental calories,40 providing strong support for the notion that reproductive hormone concentrations are dependent on energy status.1,2

TABLE 3. - Classification of Testosterone Concentrations in Men* Total Testosterone Concentration Classification <8 nmol/L (<230 ng/dL) Clinical testosterone deficiency 8-12 nmol/L (230-350 ng/dL) Subclinical gray zone >12 (>350 ng/dL) Likely normal *These ranges are found in multiple guidelines, including those from the International Society for Sexual Medicine, the British Society for Sexual Medicine, and the European Association of Urology, and are widely referenced in the literature.75–79 However, the Endocrine Society and the American Urological Association recommend a single cutoff value of 80,81

Evidence in support of hypogonadotropic hypogonadism also comes from RCTs, including both short-term and long-term training studies. To date, 1 long-term RCT of 286 previously sedentary men consisted of exercise training at either moderate-intensity (60% maximal oxygen uptake [V̇o2max]) or high-intensity (80% V̇o2max) treadmill running 5 d/wk for 120 minutes each session for 60 weeks, followed by a period of 36 we