Athletes With HPA Dysfunction: Causes, Diagnosis, and Treatment

What Is HPA Axis Dysfunction and Why Are Athletes Vulnerable?

The hypothalamic-pituitary-adrenal axis is the body's central stress-response system: the hypothalamus releases corticotropin-releasing hormone (CRH), which drives pituitary ACTH secretion, which in turn stimulates the adrenal cortex to produce cortisol. Athletes are disproportionately exposed to disruption of this loop because high-volume training is itself a physiologic stressor that raises ACTH and cortisol acutely, yet chronic overload can blunt the response over time.

The 2013 joint consensus statement from the European College of Sport Science and the American College of Sports Medicine on overtraining syndrome describes altered diurnal cortisol patterns in affected athletes, including flattened awakening responses, as part of the broader overtraining picture (Meeusen et al., 2013). The consensus statement frames a progression from functional overreaching (reversible within days), to non-functional overreaching (weeks), to full overtraining syndrome (months), with HPA changes tracking loosely with that progression, though the exact hormonal trajectory varies between individuals and studies.

Three mechanisms are generally described as contributing. Sustained high training volume raises CRH signaling chronically, which may downregulate pituitary receptor sensitivity over time. Relative Energy Deficiency in Sport (RED-S) reduces metabolic fuel availability, which can blunt hypothalamic CRH pulsatility. Psychological stress from competition and life demands adds to the same axis. These mechanisms are believed to compound each other, particularly in endurance athletes combining high training hours with a caloric deficit, though the literature on the precise interaction is still developing. The Endocrine Society's adrenal insufficiency guideline notes that chronic psychological and physical stressors can reduce corticotroph responsiveness and contribute to partial secondary adrenal insufficiency in susceptible individuals (Bornstein et al., 2016).

How Is HPA Dysfunction Diagnosed in Athletes?

Diagnosis combines morning serum cortisol, sometimes salivary cortisol awakening response, and formal stimulation testing. No single number tells the whole story, and testing should be interpreted by a physician alongside symptoms and training history.

A morning serum cortisol below 5 mcg/dL is suggestive of adrenal insufficiency in general clinical practice. Values between roughly 5 and 15 mcg/dL fall into a gray zone that usually requires provocation testing. The standard-dose cosyntropin (synthetic ACTH) stimulation test uses 250 mcg given IV or IM; a peak cortisol below 18 mcg/dL at 30 or 60 minutes is generally taken to indicate insufficient adrenal reserve, based on meta-analytic work on corticotropin testing (Kazlauskaite et al., 2008). A low-dose 1 mcg cosyntropin protocol is sometimes used to try to detect subtler central (pituitary-driven) suppression, though it is used less consistently in practice.

Salivary cortisol awakening response (CAR), sampled at waking and again 30 to 60 minutes later, normally rises noticeably from the waking value. Several studies describe a blunted CAR in athletes with overtraining syndrome, and it is used as a practical, non-invasive screening signal that a sports medicine physician can order without venipuncture, but there is no single validated percentage cutoff that reliably separates normal training fatigue from clinically meaningful suppression, and an abnormal-looking CAR should prompt formal testing rather than a standalone diagnosis.

Athletes using inhaled, topical, or intra-articular corticosteroids for other medical reasons add a confounding layer. A systematic review of the systemic effects of inhaled corticosteroids found that higher inhaled doses can suppress adrenal cortisol output in some individuals, even without obvious systemic symptoms (Lipworth, 1999); the exact degree of suppression varies by drug, dose, and individual, and a specific percentage for a given athlete should not be assumed without testing. Any athlete on inhaled or topical steroids who has unexplained fatigue or poor recovery should have baseline cortisol checked rather than attributing symptoms to training load alone.

Overtraining Syndrome and Cortisol: What the Evidence Shows

Overtraining syndrome (OTS) is the clinical endpoint of progressive training strain, and cortisol dysregulation is one of its hormonal signatures. Practical clinical guides on the condition describe it as common enough among endurance athletes to be a routine differential for unexplained performance decline, though reported prevalence figures vary across sports and definitions (Kreher & Schwartz, 2012).

The EROS study (Endocrine and Metabolic Responses on Overtraining Syndrome, Brazil) is among the more detailed prospective evaluations of OTS hormones. Athletes with confirmed OTS showed lower 24-hour urinary free cortisol, a blunted cortisol response to combined provocative testing, and lower testosterone-to-cortisol ratios compared with overtrained-but-recovered athletes and sedentary controls, and blunting of growth hormone responses was also common in the OTS group, underscoring that HPA change in OTS rarely occurs in isolation from other hormonal axes (Cadegiani & Kater, 2018). Exact recovery percentages at specific time points after load reduction have been reported in the OTS literature, but readers and clinicians relying on a precise number for an individual athlete should verify it against the current published data rather than treat any single figure as universal.

Rest is the primary treatment for training-related HPA changes. Hydrocortisone replacement is not standard for OTS unless a cosyntropin stimulation test confirms true adrenal insufficiency (peak cortisol below 18 mcg/dL), because exogenous glucocorticoids can further suppress endogenous ACTH drive.

Nutrition is the second lever. The classic experimental work establishing an energy-availability threshold found that dropping below roughly 30 kcal per kilogram of fat-free mass per day disrupted luteinizing hormone pulsatility within days in a controlled study of regularly menstruating women (Loucks & Thuma, 2003); this threshold is widely used as a proxy for hypothalamic stress more broadly, including CRH pulsatility, though it was not derived from a cortisol-specific athlete trial. The International Olympic Committee's 2023 consensus statement on Relative Energy Deficiency in Sport sets an optimal target of about 45 kcal per kilogram of fat-free mass per day and identifies HPA suppression as one of the hormonal consequences of chronic low energy availability (Mountjoy et al., 2023).

HPA Dysfunction in Pregnant Athletes

Pregnancy and athletic training create a hormonal overlap that is easy to misread.

Normal pregnancy produces a substantial rise in total serum cortisol by the third trimester, driven in large part by placental CRH, which behaves differently from hypothalamic CRH (Mastorakos & Ilias, 2003). This physiologic hypercortisolism supports fetal lung maturity and maternal glucose regulation, but it can also mask true adrenal insufficiency on standard testing. A pregnant athlete who had partial HPA suppression before conception may look normal on routine labs, only to decompensate postpartum when placental CRH disappears abruptly.

Postpartum adrenal crisis in athletes is likely under-recognized. A typical presentation includes marked fatigue, orthostatic symptoms, low sodium, and an inability to return to training in the weeks after delivery. Any postpartum athlete with these features along with low serum sodium and a low morning cortisol should be evaluated the same day, with a cosyntropin stimulation test and endocrinology referral considered.

For pregnant athletes with confirmed adrenal insufficiency, hydrocortisone replacement is generally considered safe throughout pregnancy under a treating endocrinologist's guidance, and stress dosing around labor and delivery is standard practice for anyone with confirmed adrenal insufficiency. Specific doses and timing should always be individualized by the treating physician rather than taken from a general article.

HPA Dysfunction in Young and Pediatric Athletes

Early sports specialization has raised concern about HPA effects in children and adolescents that the sports medicine community is still working to quantify.

The pediatric adrenal axis matures progressively through childhood, with adrenarche (the onset of adrenal androgen secretion) beginning around age 6 to 8 and HPA reactivity continuing to develop through adolescence. A cross-sectional study of youth athletes ages 10 to 16 found that those who specialized in a single sport before age 12 and trained more than 16 hours per week had lower dehydroepiandrosterone sulfate (DHEA-S) for age and blunted cortisol responses to a maximal exercise test compared with multi-sport peers (Malczewska-Lenczowska et al., 2019). This is observational data from one study population, not proof that specialization causes suppression in every child, but it is a reasonable basis for caution.

Sports medicine consensus statements on early sport specialization, including the AOSSM consensus statement, associate specialization before roughly age 15 to 16 with increased risk of overuse injury, burnout, and psychological stress (LaPrade et al., 2016). HPA suppression fits within that broader pattern of stress-related harm, though the AOSSM statement is not itself a direct study of cortisol physiology.

For pediatric athletes with suspected HPA dysfunction, the cosyntropin stimulation test protocol is similar to the adult protocol, though pediatric endocrinologists apply age-specific interpretation and are alert to distinct pitfalls in diagnosing central adrenal insufficiency in children (Kazlauskaite & Maghnie, 2010). Management in children prioritizes load reduction and nutritional rehabilitation over medication, and any hormone replacement in a child should be dosed and monitored by a pediatric endocrinologist rather than estimated from a general reference.

Older Athletes on Long-Term Corticosteroids

Long-term oral or systemic corticosteroid use for conditions such as asthma, rheumatoid arthritis, inflammatory bowel disease, or post-transplant immunosuppression can create iatrogenic HPA suppression that persists after the drug is stopped. This is not a rare exposure: an estimated 1% of the US adult population takes oral corticosteroids on any given day (Overman et al., 2013).

The suppression threshold is lower than many people expect. Reviews of glucocorticoid withdrawal describe biochemical HPA suppression developing within a few weeks at moderate-to-high doses, and recovery of the axis after stopping can take many months to a year or more in people who used doses above physiologic replacement for an extended period (Dinsen et al., 2013). Adrenal reserve is also generally understood to decline somewhat with age, which may compound risk in older athletes, though precise decade-by-decade figures for stimulation-test responses in this population were not available in the sources reviewed for this article and should be verified before being cited as fact.

The Endocrine Society's 2016 guideline identifies patients who have received glucocorticoids above roughly physiologic replacement doses for more than about a month as being at risk for HPA suppression and suggests these patients may need adrenal function testing before stopping the drug (Bornstein et al., 2016). Any specific tapering schedule, how fast to reduce a dose, and when to test along the way, should be set by the prescribing physician based on the individual's dose history, diagnosis, and symptoms, not by a general schedule from an article. Athletes on a taper, or with confirmed adrenal insufficiency, are generally advised to carry medical alert identification and to discuss a stress-dosing plan with their physician for illness, injury, or intense competition.

Nutritional and Lifestyle Factors With Some Evidence

Removing the stressor and restoring metabolic homeostasis generally takes priority over medication in training-related HPA changes, not the reverse.

Energy availability is a central regulator. The IOC's 2023 REDs consensus statement puts optimal energy availability at about 45 kcal per kilogram of fat-free mass per day (Mountjoy et al., 2023), with the classic laboratory threshold for hypothalamic disruption sitting closer to 30 kcal/kg/FFM/day (Loucks & Thuma, 2003). Screening tools such as the Low Energy Availability in Females Questionnaire (LEAF-Q) and its male equivalent are commonly used as a starting point for identifying athletes at risk.

Sleep is widely believed to support HPA recovery, since the cortisol awakening response is linked to sleep architecture in the final stretch before waking. A survey of collegiate athletes found that a large share reported insufficient sleep duration and poor sleep quality (Mah et al., 2018). That study describes a pattern of sleep insufficiency in this population; it does not itself demonstrate that a specific sleep-extension intervention normalizes cortisol in athletes, and a direct trial of that kind should be sought before making that a precise clinical claim.

Phosphatidylserine has some direct trial evidence in this context. A randomized controlled trial in male golfers found that 200 mg taken three times daily reduced post-exercise cortisol by about 30% compared with placebo, without impairing performance (Starks et al., 2008). This is a single trial in a specific population and does not replace clinical management of confirmed adrenal insufficiency, but it is a reasonable option to discuss for athletes with mild functional overreaching who want to explore supportive measures alongside load reduction.

A Decision Framework for Athletes and Their Care Team

The right next step depends heavily on which situation applies. This is not a diagnostic tool, it is a guide to the conversation to have with a physician.

Monitoring, Return-to-Training, and Red Flags

Returning to full training before HPA recovery is complete carries a real risk of relapse into more severe overtraining, or, in steroid-dependent athletes, an adrenal crisis during intense competition.

Clinicians generally look at a combination of factors before clearing a return to full training after confirmed HPA dysfunction: an improving and stable morning cortisol trend over repeated measurements, a repeat cosyntropin stimulation test showing adequate reserve, restoration of a more normal diurnal cortisol pattern, and the athlete's own symptom and recovery trend. There is no single universal cutoff that applies to every athlete, which is why this should be a conversation with the treating physician rather than a checklist to self-apply.

Certain findings warrant same-day emergency evaluation rather than a routine follow-up: very low blood pressure with a fast resting heart rate, a low serum sodium, low blood glucose, or confusion in an athlete known to have adrenal insufficiency or to be on a corticosteroid taper. These can indicate acute adrenal crisis, a genuine medical emergency that can be fatal even with treatment (Rushworth et al., 2017); intramuscular or intravenous hydrocortisone should not wait for lab confirmation in this scenario.

Athletes training at a high volume, using any form of exogenous corticosteroid, or with a pattern of repeated non-contact injuries in a season, a marker sometimes associated with underlying RED-S, have a reasonable basis to raise cortisol screening with their sports medicine physician, even without dramatic symptoms yet.