Abstract
Our findings indicate that the participants of an 18 week intensive endurance exercise training program experienced significant (p < 0.001) reductions in resting testosterone (−25 to −45% decrease from pre-training), with some reaching the clinical criteria for androgen deficiency during the training regimen. Nonetheless, none of the participants displayed any running performance decrement, in fact, the opposite occurred (+18.6% improvement; p < 0.05). These preliminary findings suggest acute decreases in testosterone in and of itself may not be entirely indicative of a compromised exercise performance potential although elements of reproductive and bone health may still be compromised.
A recent publication in The Aging Male characterized endurance exercise training as impacting on the circulating testosterone levels in adult men, specifically that chronic endurance training leads to an increased risk of androgen deficiency (i.e. clinically low testosterone) development [Citation1]. Androgen deficiency in men is associated with compromised reproductive function, reduced bone mineral density, as well as compromised muscular capacity such as exercise performance [Citation2]. Anecdotal evidence from our laboratory had called into question this last point; therefore, we conducted a pilot study to examine the question of does endurance exercise training result in reductions in testosterone, and if so, is there an impact on exercise performance?
Initial participants (n = 15) were healthy adult men (age = 27.6 ± 2.5 years; mean ± SD) who regularly performed endurance exercise training (∼5 sessions/week; estimated aerobic capacity [VO2max] = 52.2 ± 5.5 mL/kg/min [good-excellent aerobic rating]) [Citation3]. They performed a monitored 18-week running program in which individual training volume (km/week) was increased at 25% increments over baseline (BL) levels (i.e. average weekly km run prior to study) at 4-week intervals throughout the first 12 weeks. After 12 weeks the training volume was reduced to the level of the first 4 weeks until the end of the study (week 18). On day 1 (Monday) of each week a morning resting, fasted blood sample was collected prior to daily training and after 24 h of complete rest. Blood specimens were obtained after a 30 min quiet rest at ∼08:00 h (±30 min). Also at BL and 4, 8, 12, and 16 weeks of the study, the participants were assessed for exercise performance capacity using the Cooper 12-min run which was carried out on a 400-m outdoor track and involved other individuals running to simulate a competition [Citation3]. The BL blood procedure was conducted twice under the same conditions during the 2 weeks prior to the study beginning and values pooled, to ensure a stable resting BL reference measurement. Throughout the study, participants ate a free-living diet and consumed food ad libitum. Collected serum was analyzed for total testosterone using a high-specificity radioimmunoassay procedure; assay sensitivity was 1 nmol/L and involved recommended quality-control procedures [Citation4]. Statistics involved ANOVA and Tukey HSD post-hoc analysis. Significance was set at p ≤ .05 with values reported as mean ± 95% confidence intervals (CI).
Testosterone was significantly and consistently (F-ratio = 2.11, degrees of freedom=17,136, p < .001) reduced from BL (21.6 nmol/L; CI = 18.7–23.9) at weeks 5 through 18 (i.e. −25 to −45% average decreases). The greatest reduction from BL was at week 13 (12.7 nmol/L; CI = 8.6–19.1), for ensuing time points (weeks 14–18) testosterone gradually returned toward BL, but remained significantly (p < .01) decreased. During weeks 13–18 approximately one-half of participants at some point reached the criteria to be classified as androgen deficient (≤10.4 nmol/L [Citation5]). Running performance improved significantly from BL at weeks 4, 8, 12, and 16 (p < .01; overall improvement= +18.6% [BL vs. week 16]), and each respective performance test was also improved from the respective prior performances (p < .05).
Our findings indicate the participants of the endurance exercise training experienced significant reductions in resting testosterone, with some reaching the clinical criteria for androgen deficiency classification during the training regimen. Nonetheless, none of the participants displayed any running performance decrement, in fact, the opposite occurred. These preliminary findings suggest acute decreases in testosterone in and of itself may not be entirely indicative of compromised exercise performance potential although elements of reproductive and bone health may still be compromised.
Disclosure statement
No potential conflict of interest was reported by the authors.
References
- Hackney AC, Lane AR. Increased prevalence of androgen deficiency in endurance-trained male runners across the life span. Aging Male. 2018;1.
- Hooper DR, Kraemer WJ, Focht BC, et al. Endocrinological roles for testosterone in resistance exercise responses and adaptations. Sports Med. 2017;47:1709–1720.
- Burke EJ. Validity of selected laboratory and field tests of physical working capacity. Res Q. 1976;47:95–104.
- Hackney AC, Viru A. Research methodology: issues with endocrinological measurements in exercise science and sports medicine. J Athl Train. 2008;43:631–639.
- Aversa A, Morgentaler A. The practical management of testosterone deficiency in men. Nat Rev Urol. 2015;12:641–650.