Stress-associated testosterone suppression: central adaptation or hypogonadism?
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic and physiological literature without systematic methodology
PubMed 42044038 · doi:10.1210/clinem/dgag181
What was done
This narrative review synthesized findings from military field studies, endurance athletes, resistance-trained cohorts, and competitive stress models to evaluate whether stress-induced testosterone suppression represents intrinsic hypogonadism or a functional central neuroendocrine adaptation.
What was found
The abstract reports qualitative neuroendocrine mechanisms without numerical data. Sustained stress—driven by severe energy deficits, sleep disruption, and psychogenic strain—suppresses hypothalamic GnRH and LH pulsatility, reduces testicular androgen production, and frequently elevates sex hormone-binding globulin (SHBG), leading to marked reductions in free testosterone. Intact Leydig cell responsiveness during hCG stimulation confirmed central inhibition rather than primary testicular dysfunction. Basal testosterone was preserved during heavy mechanical loading when energy availability was maintained, and androgen suppression reversed upon restoration of energy balance and recovery.
Why it matters
Distinguishing functional central suppression from pathological hypogonadism helps clinicians avoid misdiagnosis and inappropriate testosterone replacement therapy in physically or psychologically stressed individuals.
Limits
The abstract provides no quantitative effect sizes, specific sample sizes, or formal systematic search protocol. Exact physiological thresholds for energy availability, sleep deprivation, and time-to-recovery are not detailed.