Infertility in athletes: causes and the link with pharmacology
Fertility problems in athletes rarely have a single cause. Heavy training loads, low energy availability, injuries, certain medicines and, above all, the non-medical use of anabolic steroids can all disrupt the reproductive system. Our editorial team looks at what the research shows, which factors are reversible and when it is time to see a specialist.
How common is infertility in sport
Infertility is usually defined as the failure to conceive after twelve months of regular unprotected intercourse. In the UK, the NHS estimates that around one in seven couples experiences difficulty conceiving, and in roughly half of cases a male factor contributes. There are no reliable national figures specifically for athletes, so any claim that sport "causes" infertility in a fixed proportion of people should be treated with caution.
What we do know is that several conditions linked to sport are well documented. In women, menstrual disturbances associated with low energy availability are common in endurance, aesthetic and weight-category sports. In men, prolonged high-volume endurance training has been associated with lower resting testosterone, and the use of anabolic-androgenic steroids (AAS) is one of the most frequent causes of acquired hypogonadism in young men seen at fertility clinics.
It is important to separate recreational exercise from extreme loads. Moderate physical activity generally supports reproductive health by improving insulin sensitivity, body composition and mood. Problems tend to appear at the edges: very high training volumes combined with inadequate food intake, or the use of hormones and other drugs outside medical supervision.
Fertility also depends on factors that have nothing to do with sport: age, smoking, alcohol, sexually transmitted infections, varicocele, genetic conditions and chronic illness. An athlete with fertility problems therefore needs the same full assessment as anyone else, rather than an assumption that training or a particular substance must be to blame.
Training load, energy availability and hormones
The concept of Relative Energy Deficiency in Sport (RED-S), introduced in the 2014 IOC consensus statement, describes what happens when dietary intake does not cover the energy cost of training plus basic physiological functions. The body responds by downregulating "non-essential" systems, and reproduction is one of the first to be affected. The hypothalamus reduces the pulsatile release of gonadotrophin-releasing hormone, which in turn lowers luteinising hormone (LH) and follicle-stimulating hormone (FSH).
In women this can present as irregular cycles, missed periods or functional hypothalamic amenorrhoea. The earlier "Female Athlete Triad" model linked these changes with low bone mineral density, and later consensus work stressed that the problem lies on a spectrum: subtle cycle disturbances, such as a shortened luteal phase, may reduce fertility long before periods stop completely.
Men are not immune. Studies of male endurance athletes have described lower resting testosterone and, in some cases, altered semen parameters with very high weekly training volumes. Hackney and colleagues coined the term "exercise-hypogonadal male condition" for this pattern. The changes are usually modest and often reverse with reduced load and better nutrition, but they can be clinically relevant for a couple trying to conceive.
Other training-related factors may contribute: repeated scrotal heat exposure (for example long hours of cycling in tight clothing), chronic sleep restriction, overtraining syndrome and rapid weight cutting before competition. The evidence for each of these individually is mixed, but together they form a plausible picture of cumulative physiological stress.
Anabolic steroids and the male reproductive axis
The single strongest pharmacological link between sport and infertility is the use of anabolic-androgenic steroids. Exogenous testosterone and its derivatives act on the hypothalamus and pituitary through negative feedback. When circulating androgen levels are high, the brain reduces LH and FSH secretion. Without LH the testes produce little testosterone of their own, and without FSH and high intratesticular testosterone, sperm production slows or stops.
This is not a theoretical concern. Testosterone was once studied as a male contraceptive precisely because it reliably suppresses sperm counts, often to very low levels, in most men within a few months. In people who use AAS outside medicine, doses typically exceed those used in such trials, and multiple compounds are frequently combined, so suppression is usually profound.
Recovery after stopping is variable. Reviews by Rahnema and colleagues, and by Nieschlag and Vorona, describe men whose sperm production returned within months, but also others with persistent hypogonadism lasting a year or longer. Kanayama and co-workers highlighted prolonged post-withdrawal hypogonadism as an under-recognised problem. Longer duration of use, higher doses and older age appear to be associated with slower recovery, although individual outcomes cannot be predicted reliably.
Women who use AAS face a different set of reproductive consequences: menstrual irregularity, anovulation, clitoral enlargement and voice changes, some of which are irreversible. Data on long-term fertility in female AAS users are limited, which is itself a reason for caution.
| Factor | Main mechanism | Typical reversibility |
|---|---|---|
| Low energy availability | Reduced GnRH pulsatility, low LH/FSH | Usually reversible with adequate intake |
| Very high endurance volume (men) | Lower resting testosterone, possible semen changes | Often reversible with reduced load |
| Anabolic-androgenic steroids | Negative feedback, suppressed spermatogenesis | Variable; may persist for months or longer |
| Opioid analgesics (long-term) | Central suppression of gonadotrophins | Generally improves after stopping |
| Heavy alcohol use | Direct testicular toxicity, hormonal disruption | Partly reversible |
Other substances and medicines that matter
Beyond AAS, a range of substances can affect fertility. Human chorionic gonadotrophin, aromatase inhibitors and selective oestrogen receptor modulators are sometimes misused in sport; all of them are prescription-only medicines in the UK, are prohibited by the World Anti-Doping Agency in various categories, and alter the hormonal axis in ways that require medical monitoring. Self-directed use can mask underlying problems and delay proper diagnosis.
Some commonly prescribed medicines also have reproductive effects. Long-term opioid painkillers, taken for example after serious injury, can suppress testosterone. Certain antidepressants and antipsychotics may affect libido, ejaculation or prolactin levels. 5-alpha-reductase inhibitors, such as finasteride, have been associated with changes in semen volume in some men. Any athlete planning a family should review their regular medicines with a GP rather than stopping them abruptly.
Lifestyle substances deserve a mention too. Heavy alcohol intake, smoking, cannabis and anabolic "pro-hormone" products sold online have all been linked with poorer sperm quality or hormonal disruption. Contaminated supplements are a separate concern: products marketed for muscle gain have been found to contain undeclared steroids, meaning that an athlete may be exposed without knowing it.
Ordinary dietary supplements such as creatine, whey protein, caffeine or vitamin D have not been shown to impair fertility at usual intakes. The practical message is not to fear legitimate nutrition, but to choose batch-tested products and be sceptical of anything promising hormonal effects.
- Red flags in men: shrinking testicles, low libido, erectile problems, breast tenderness, or a history of AAS use.
- Red flags in women: periods absent for three months or more, very irregular cycles, recurrent stress fractures.
- For both: no conception after 12 months of trying (6 months if the woman is over 35), or known risk factors at any time.
Assessment, recovery and treatment
The first step is an honest conversation with a GP, who can refer to a fertility service or an endocrinologist. Being open about training, diet and any use of hormones or other drugs is essential: clinicians are bound by confidentiality, and the information directly shapes which tests are ordered and how results are interpreted.
For men, assessment usually includes a semen analysis, morning testosterone, LH, FSH, prolactin and sometimes oestradiol, along with a physical examination. For women, it typically involves hormone profiling in relation to the cycle, assessment of ovulation, thyroid function and, where relevant, a pelvic ultrasound. In athletes with suspected RED-S, a dietitian experienced in sport is a valuable part of the team.
When energy deficiency is the cause, the most effective treatment is restoring energy availability, often combined with a temporary reduction in training. Recovery of menstrual function may take several months. When AAS use is involved, the first measure is stopping the drugs; specialists may then consider medical treatment to support recovery of the hormonal axis, but such treatment is individualised, prescription-only and should never be self-administered on the basis of internet protocols.
Couples should also remember that sperm take roughly ten weeks to develop, so any improvement in lifestyle or hormonal status will show up in semen analysis only after that delay. Patience and repeat testing are part of the process.
Editorial team's conclusions
Infertility in athletes is usually the result of several interacting factors rather than sport itself. Low energy availability and extreme training loads can suppress reproductive hormones in both sexes, but these effects are generally reversible.
The clearest pharmacological risk is the use of anabolic-androgenic steroids, which suppress sperm production in most male users and may leave some with long-lasting hypogonadism. Other medicines and lifestyle factors also play a role and deserve review.
Early, candid medical assessment gives the best chance of identifying the cause and restoring fertility. Self-treatment with hormonal drugs is risky and can delay an accurate diagnosis.
Readers may also find our articles on RED-S in female athletes, on recovering hormonal health after steroid use, and on semen analysis explained useful.
References
- Mountjoy M, Sundgot-Borgen J, Burke L, et al. The IOC consensus statement: beyond the Female Athlete Triad—Relative Energy Deficiency in Sport (RED-S). Br J Sports Med. 2014;48(7):491–497.
- Hackney AC. Endurance exercise training and reproductive endocrine dysfunction in men: alterations in the hypothalamic-pituitary-testicular axis. Curr Pharm Des. 2001;7(4):261–273.
- Rahnema CD, Lipshultz LI, Crosnoe LE, et al. Anabolic steroid-induced hypogonadism: diagnosis and treatment. Fertil Steril. 2014;101(5):1271–1279.
- Nieschlag E, Vorona E. Mechanisms in endocrinology: medical consequences of doping with anabolic androgenic steroids: effects on reproductive functions. Eur J Endocrinol. 2015;173(2):R47–R58.
- 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, et al. Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Endocr Rev. 2014;35(3):341–375.
- De Souza MJ, Nattiv A, Joy E, et al. 2014 Female Athlete Triad Coalition consensus statement on treatment and return to play of the female athlete triad. Br J Sports Med. 2014;48(4):289.
