Testicular Atrophy in Athletes: Causes and the Link to Pharmacology
Shrinking testicles are one of the best-known — and least discussed — consequences of hormonal drug use in sport. But atrophy can also have medical causes unrelated to doping. Our editorial team explains how testicular size is regulated, why outside androgens disrupt it, which other conditions to consider, and what the risks are for fertility.
What testicular atrophy means
Testicular atrophy is a reduction in the size of one or both testicles, usually accompanied by a decline in their function. The testes have two jobs: Leydig cells produce testosterone, and the seminiferous tubules — which make up most of the testicular volume — produce sperm. When sperm production slows, the tubules shrink, and the testicle becomes smaller and often softer.
Clinicians estimate testicular volume with a Prader orchidometer, a string of beads of known volume, or more precisely with scrotal ultrasound. Adult volumes vary considerably between individuals, so a single measurement means less than a change over time or a clear difference between the two sides.
Atrophy itself is a sign, not a diagnosis. It points toward an underlying problem with the hormonal signals that drive the testes, or with the testicular tissue itself. Identifying which one is involved determines both prognosis and treatment.
Men often notice the change themselves, sometimes along with reduced libido, erectile difficulties, fatigue or mood changes. In athletes, the context of training, diet and substance use is essential for making sense of these symptoms.
How the hormonal axis controls the testes
Testicular function is governed by the hypothalamic–pituitary–gonadal (HPG) axis. The hypothalamus releases gonadotropin-releasing hormone (GnRH) in pulses, prompting the pituitary to secrete luteinizing hormone (LH) and follicle-stimulating hormone (FSH). LH stimulates Leydig cells to make testosterone; FSH, together with high local testosterone levels, supports sperm production.
The system runs on negative feedback. When circulating testosterone or estradiol is high, the hypothalamus and pituitary reduce GnRH, LH and FSH output. This keeps hormone levels within a stable range under normal conditions.
The key point is that testosterone inside the testes is many times higher than in the blood, and that local concentration depends on LH. If LH falls, intratesticular testosterone collapses even if blood testosterone is high from an outside source — which is why exogenous androgens suppress sperm production and cause the testes to shrink.
Anything that disrupts this chain — at the level of the brain, the pituitary or the testes — can lead to reduced testicular size and function.
Causes in athletes: pharmacological and non-pharmacological
In athletes, the most common identifiable pharmacological cause is the use of anabolic-androgenic steroids (AAS). A systematic review and meta-analysis by Christou and colleagues (2017) found that AAS use was consistently associated with suppressed LH and FSH, reduced testicular volume and impaired sperm parameters. Other substances that act on the same axis — testosterone itself, many SARMs, some prohormones and hCG misuse patterns — carry related risks.
Atrophy is, however, not always drug-related. Several medical conditions can cause it, and athletes are not immune to them.
| Category | Examples |
|---|---|
| Exogenous hormones | Anabolic steroids, testosterone, SARMs, prohormones, some estrogen-related drugs |
| Other medications | Opioids (long-term), high-dose glucocorticoids, some anti-androgens |
| Energy deficiency | Very low body fat, chronic undereating, high endurance volume (RED-S) |
| Local conditions | Varicocele, testicular torsion, trauma, mumps orchitis |
| Genetic and endocrine disorders | Klinefelter syndrome, pituitary disease, hemochromatosis |
Endurance athletes with chronically low energy availability can develop functional hypogonadism with lower testosterone, a pattern Hackney has called the "exercise-hypogonadal male condition." This is usually milder than drug-induced suppression, but it can be clinically significant.
Testicular torsion is a surgical emergency: sudden severe scrotal pain needs immediate care, as delay can result in loss of the testicle. Direct blows in contact sports can also cause injury that later leads to atrophy.
Consequences: fertility, hormones and recovery
The most important consequence of drug-induced atrophy is impaired fertility. Sperm counts can fall to very low levels or to zero during AAS use. In many men the axis recovers after stopping, but recovery may take months, and in some cases it is incomplete.
Kanayama and colleagues (2015) described prolonged hypogonadism in men after withdrawal from AAS, with symptoms such as low libido, fatigue and depressed mood persisting long after cessation. Rahnema and colleagues reviewed anabolic steroid-induced hypogonadism and noted that duration and intensity of use influence the likelihood of recovery.
- Reduced or absent sperm production (oligospermia or azoospermia)
- Low natural testosterone after discontinuation, with fatigue and low mood
- Decreased libido and erectile dysfunction
- Possible loss of muscle and bone density during the hypogonadal phase
- Psychological distress related to body image and sexual function
The clinical picture varies widely, and there is no reliable way to predict individual recovery time. This uncertainty is one of the strongest reasons medical guidelines advise against non-medical androgen use, especially for men who plan to have children.
Diagnosis and medical management
A physician evaluating testicular atrophy will typically take a detailed history — including supplements and any hormonal substances, which should be disclosed honestly — and perform a physical exam. Blood tests usually include morning total testosterone, LH, FSH, estradiol, prolactin and sometimes SHBG. A semen analysis assesses fertility directly.
Low testosterone with low or "inappropriately normal" LH and FSH suggests a central (pituitary or hypothalamic) cause, including suppression by outside hormones. Low testosterone with high LH and FSH points to primary testicular failure. Scrotal ultrasound can identify varicocele, masses or structural problems.
Management depends on the cause and the patient's goals, especially regarding fertility. Treatment of drug-induced hypogonadism is a specialist decision made by an endocrinologist, urologist or andrologist; it is not something to self-manage based on online protocols, which carry their own risks and frequently delay proper care.
For non-drug causes, interventions may include correcting energy deficiency, treating a varicocele or addressing an underlying endocrine disorder. Early evaluation generally improves outcomes.
Editorial Team Conclusions
Testicular atrophy is a visible sign of disrupted testicular function. In athletes it is most often linked to exogenous androgens, which shut down LH and FSH and collapse intratesticular testosterone.
Non-pharmacological causes — energy deficiency, varicocele, trauma, infections and genetic conditions — must also be considered, and torsion requires emergency care.
The biggest long-term concern is fertility, and recovery after stopping hormonal drugs is variable and sometimes incomplete. Medical evaluation, honest disclosure and specialist-guided treatment are the safest path.
Related reading: which hormone tests athletes should monitor, how relative energy deficiency affects male hormones, and what is known about recovery of natural testosterone after steroid use.
References
- Christou MA, Christou PA, Markozannes G, Tsatsoulis A, Mastorakos G, Tigas S. Effects of anabolic androgenic steroids on the reproductive system of athletes and recreational users: a systematic review and meta-analysis. Sports Med. 2017;47(9):1869–1883.
- Rahnema CD, Lipshultz LI, Crosnoe LE, Kovac JR, Kim ED. Anabolic steroid-induced hypogonadism: diagnosis and treatment. Fertil Steril. 2014;101(5):1271–1279.
- Kanayama G, Hudson JI, DeLuca J, et al. Prolonged hypogonadism in males following withdrawal from anabolic-androgenic steroids: an under-recognized problem. Addiction. 2015;110(5):823–831.
- Pope HG Jr, Wood RI, Rogol A, Nyberg F, Bowers L, Bhasin S. Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Endocr Rev. 2014;35(3):341–375.
- Hackney AC. Hypogonadism in exercising males: dysfunction or adaptive-regulatory adjustment? Front Endocrinol (Lausanne). 2020;11:11.
- Bhasin S, Brito JP, Cunningham GR, et al. Testosterone therapy in men with hypogonadism: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2018;103(5):1715–1744.
