Before you call it overtraining, rule these out
"Overtraining" is a comfortable word because it puts you in charge. It says the problem is your training load, which is a thing you control, and that the fix is rest, which is free. That comfort is exactly what makes it dangerous. Three serious things present as a tired athlete whose performance is falling, and all three are treatable when they are found.
A note on who this page is for. If you lift four times a week, run a club 10k, do CrossFit, or came back to sport at 45, you count. Nothing below requires you to think of yourself as an athlete, and none of these conditions checks your race results before it arrives.
1. Anything cardiac. This is the one that kills athletes.
Stop training and get assessed the same day if you have any of the following, and treat them as more urgent still in the weeks after a viral illness, when inflammation of the heart muscle (myocarditis) is a live possibility:
- Chest pain, pressure or tightness during or after exercise.
- Fainting or near-fainting during exertion. The cardiology literature describes exercise-induced syncope as an alarming symptom of underlying cardiac disease that predisposes to cardiac arrest, and says every athlete with syncope needs a focused cardiac workup. It is not dehydration until a doctor has said it is dehydration.
- Breathlessness out of proportion to the effort, or a racing or thumping heartbeat at easy intensities.
Here is why this box sits at the top of an article about training load. A review of sudden cardiac death in athletes reports that roughly 30% of the athletes who died had symptoms in the lead-up, and the list of those symptoms reads: chest pain, shortness of breath, performance decline, palpitations, near-fainting and fainting. Performance decline is the reason you opened this page. It is also on that list.
What the absence of these signs does not rule out. The same figure means most athletes who died had no warning at all, so feeling fine between sessions proves nothing. A clean pre-participation screen or a normal resting ECG in the past does not close the question either. This red flag is only useful in one direction: if you have these symptoms, act on them. If you do not have them, you have learned nothing about your heart.
The exit, not just the warning. Do not "test it" with another session, and do not wait for it to happen twice. Book an urgent assessment, and use the exact words: chest pain on exertion, or I fainted while exercising. Those phrases change what happens next in a way that "I think I am overtrained" does not.
2. Rhabdomyolysis, after an unusually hard or unaccustomed session
Muscle breaks down, its contents spill into the blood, and the kidneys take the damage. Strenuous exercise, especially in people untrained for it and especially in heat, is a recognised cause. StatPearls puts the risk of acute kidney injury at 10% to 50% once creatine kinase passes 1,000 U/L. This is an emergency, and it does not announce itself as one.
Go to an emergency department or urgent care today if, after a hard session, you have:
- Severe muscle pain, well beyond ordinary soreness, often with visible swelling of the muscle.
- Weakness out of proportion to the soreness. Not "sore to move", but "cannot straighten my arms".
- Dark, tea-coloured or cola-coloured urine, or passing much less urine than usual.
What the absence of dark urine does not rule out, and this is the part that hurts people. The classic triad of muscle pain, weakness and dark urine is present in fewer than half of patients. Muscle pain is reported in about 50% of adults. Dark urine appears in only 30% to 40%. Clear urine therefore does not mean you are safe, and it is not a screening test you can run in your own bathroom.
We are not going to hand you a rule for telling this apart from ordinary soreness, because there is not an honest one. Both hurt, both follow hard sessions, and the thing that separates them is a blood test, not a judgment you make while wincing. The exit: ask for creatine kinase and kidney function by name, keep drinking water, and do not train again until you have the result. Training on top of rhabdomyolysis is how the kidney injury gets worse.
3. Under-fuelling: REDs, the female athlete triad, and eating disorders
This is not a footnote to overtraining. In a great many cases it is what the overtraining actually was. A 2021 review in Sports Medicine went back through the training-overload and overtraining studies that had also measured what the athletes ate. 18 of the 21 studies that qualified (86%) showed a fall in energy availability or in carbohydrate availability during the overload period. The authors' stated aim is to help clinicians exclude low energy availability and REDs from an overtraining diagnosis, because from the outside the two are the same picture.
Relative Energy Deficiency in Sport (REDs) is defined by the International Olympic Committee as a syndrome of harmful health and performance outcomes in female and male athletes exposed to low energy availability. It also loops straight back to this page's subject: an underfed body raises cortisol. In functional hypothalamic amenorrhea, the brain-adrenal axis goes into overdrive and cortisol release increases. A high cortisol reading in a lean, hard-training athlete is at least as likely to be telling you about food as about training volume.
Talk to a doctor, and ask for a sports dietitian, if any of these are true:
- Your periods have stopped or become irregular. This is not a badge of hard training and it is not harmless. Amenorrheic athletes carry 10% to 20% lower lumbar spine bone density and 2 to 4 times the stress fracture risk of athletes with normal cycles.
- Repeated bone stress injuries, or a first stress fracture in someone who has never had one.
- In men: loss of libido, loss of morning erections, unplanned weight loss. REDs is not a women's condition, and framing it as one is precisely why men go undiagnosed.
- You are eating less to stay light, training to earn food, weighing yourself daily, or treating a missed session as a debt to be repaid.
What a normal body weight does not rule out. Low energy availability happens at completely ordinary weights and ordinary BMIs, and you do not need a diagnosed eating disorder to have it. Eating disorders do sit inside this cluster, and they are common in sport: across 1,620 Norwegian elite athletes and 1,696 controls, 13.5% of athletes had a subclinical or clinical eating disorder against 4.6% of controls. Among female athletes the figure reached 42% in aesthetic sports and 24% in endurance sports. Among male athletes it reached 22% in antigravitation sports. Being male, or being a normal weight, or having a fast 10k, rules out none of it.
The exit. REDs is treated by eating more, not by resting more, so a deload aimed at "overtraining" can leave the real problem running underneath it. Say the words low energy availability to your doctor and ask for a referral to a sports dietitian. And if your mood has gone down with your performance, say that out loud too. If you are having thoughts of ending your life, that is not a training-load problem and it does not wait for a blood test. In Canada and the United States, call or text 988, at any hour, or contact emergency services.
Does overtraining raise your cortisol?
Not reliably, and the popular version of this story has the mechanism backwards. Start with the uncontroversial half. Hard exercise raises cortisol while you are doing it, and intensity is the lever. In a controlled study of 12 trained men, 30 minutes at 60% and at 80% of maximal oxygen uptake raised circulating cortisol, while 30 minutes at 40% lowered it once the researchers corrected for the drop in plasma volume. That is a normal, useful response to a hard session, and it is not what "overtraining" means.
The real question is what happens to cortisol in athletes who are already in trouble. A 2017 systematic review of 38 articles in BMC Sports Science, Medicine and Rehabilitation pooled what the literature had found, and the answer is less tidy than the supplement ads suggest. Resting cortisol was normal in most of the studies that measured it. Among the studies that used a stimulation test instead of a resting draw, the split was exactly even: half found a normal cortisol response, half found a blunted one. The authors' own conclusion is worth quoting rather than paraphrasing:
"Acute hormone responses to stimulation tests, such as ACTH, GH and prolactin, tend to be blunted in OTS/NFOR/FOR, whereas cortisol and plasma catecholamines presented conflicting results." The same review states that basal levels of hormones are not a good predictor.
Cadegiani and Kater, systematic review, 2017.The shape of the finding: a smaller response, not a bigger number
The most detailed look at this comes from the same group's EROS study, which put 14 athletes with overtraining syndrome, 25 healthy athletes and 12 healthy sedentary people through identical challenges. It is small and single-centre, and it deserves to be read as a strong hypothesis rather than a settled fact. But the pattern is the one worth carrying around.
| Test | Healthy athletes | Overtraining syndrome | Sedentary controls |
|---|---|---|---|
| Cortisol response to an insulin tolerance test | 21.7 µg/dL (a rise of 9.2) | 17.9 µg/dL (a rise of 6.3) | 16.9 µg/dL (a rise of 6.0) |
| ACTH response to the same test (median) | 91.4 pg/mL (a rise of 45.1) | 30.3 pg/mL (a rise of 9.7) | 51.4 pg/mL (a rise of 38.0) |
| Saliva cortisol 30 minutes after waking | 500 ng/dL | 323 ng/dL | 393 ng/dL |
| Cortisol response to direct adrenal stimulation | Normal | Normal | Normal |
Read the columns in order and the story tells itself. The healthy athletes had the biggest responses, not the calmest ones. Training had raised their capacity to mount a stress response, including a larger cortisol rise after waking. The overtrained athletes had lost that, and on several measures they had landed back at or below people who do not train at all. The last row is the one that closes off a popular myth: give the adrenal glands a direct chemical order and they answer perfectly well. Nothing is exhausted in these athletes. What changed is upstream, in the signalling, which is the same point made at length in why adrenal fatigue is not a diagnosis.
So the honest headline is not "overtraining raises cortisol." It is closer to this: hard training sharpens the stress response, and overtraining flattens it. A resting number cannot see that, because the finding is not in the resting number. It is in what the number does when something is asked of it.
What about the testosterone-to-cortisol ratio?
It is a real research variable with a real history, and it is not a test result. Adlercreutz and colleagues proposed it in the 1980s as an index of the balance between building tissue up and breaking it down. The threshold that became famous: a fall of more than 30% in the ratio, or an absolute fall to 0.35 × 10⁻³ or below.
Two details go missing every time that number is repeated, and both of them matter:
- The original threshold used free testosterone, not total testosterone. Hackney and Walz note that the distinction "seems to have been lost to some researchers who have calculated the ratio using the alternative testosterone value." A 30% drop in one is not a 30% drop in the other, and a lab panel will hand you the wrong one by default.
- It was derived from overreaching, not from overtraining syndrome, and has since been applied extensively to the condition it was not built for.
And in practice it does not sort athletes cleanly. Across the 10 studies that reported the ratio in the 2017 systematic review, it was reduced in 50%, normal in 40% and increased in 10%. A marker that comes back normal or high in half of affected athletes is not a gate you can put a training decision behind, and it is certainly not one to put a race behind.
Overreaching, or overtraining syndrome?
The vocabulary is worth getting right, because the three terms describe different outcomes and because the consensus statement is far more candid about its own uncertainty than the people who quote it.
| What it is | What the consensus actually says | |
|---|---|---|
| Functional overreaching | A short-term drop in performance from a hard block, then recovery | It "will eventually lead to an improvement in performance after recovery." This is the intended result of training, not a failure of it |
| Non-functional overreaching | Performance stays down. The rebound does not arrive | It occurs "when athletes do not sufficiently respect the balance between training and recovery" |
| Overtraining syndrome | A prolonged failure to adapt, across several regulatory systems at once | The keyword is "prolonged maladaptation." Telling it apart from non-functional overreaching "is very difficult and will depend on the clinical outcome and exclusion diagnosis" |
| Is overtraining syndrome the more severe one? | Everyone assumes so | "There is no scientific evidence to either confirm or refute this suggestion." The consensus declines to claim it, and so do we |
If it is not overtraining, what is it?
Overtraining syndrome is a diagnosis of exclusion. That is not a technicality, it is the whole clinical protocol. The consensus statement describes the approach as excluding organic disease and infection, along with caloric restriction, insufficient carbohydrate or protein, iron deficiency, magnesium deficiency and allergies, before the label goes on. Every row below is more common than overtraining syndrome, and every row below is treatable.
| What it can be instead | How it presents | What to do about it |
|---|---|---|
| Low energy availability and REDs | Identical to overtraining, which is the whole problem. Fatigue, stalled performance, illness, injury | Ask for it by name. Rest does not fix a calorie deficit, and 86% of the qualifying overtraining studies showed one |
| Iron deficiency, with or without anemia | Breathlessness, heavy legs, a collapsed ceiling on hard efforts | Blood test: ferritin and a full blood count. Common in endurance athletes and in menstruating athletes |
| Thyroid disease | Fatigue, weight change, cold intolerance, low mood | Blood test: thyroid function. Cheap, and routinely missed because the symptoms had already been explained by something else |
| Adrenal insufficiency (Addison's disease) | Fatigue and falling performance, plus weight loss, nausea, salt craving, dizziness on standing, or darkening of the skin. This is genuine low cortisol, not "adrenal fatigue" | Blood test: morning cortisol and electrolytes. The physical stress of exercise or illness can tip it into a life-threatening adrenal crisis, so raise it early if these signs are present |
| Infection, including glandular fever and myocarditis | Profound fatigue and a collapsed exercise capacity, usually dating from a virus | Myocarditis is the dangerous one. Chest pain, palpitations or breathlessness after a viral illness is an urgent assessment, not a rest week |
| Depression | Loss of drive, broken sleep, nothing feels worth doing, and yes, worse training | It shares most of its symptom list with overtraining syndrome. It is treatable, and it does not resolve on a deload |
| A sleep disorder, including sleep apnea | Unrefreshing sleep, daytime fatigue, snoring, morning headache | Raise it specifically. Start with how sleep and cortisol drive each other |
Get the bloods first. Ferritin, full blood count, thyroid function, and, if you also have weight loss, nausea, salt craving, dizziness on standing or darkening skin, morning cortisol and electrolytes to rule out adrenal insufficiency. Add an honest accounting of what you have been eating. If any of them come back abnormal, you were never overtrained. You were undertreated.
So what can cortisol actually tell an athlete?
Less than you want it to, and we are not going to pretend otherwise on our own website. The limit, stated as plainly as we can put it: there is no validated cortisol criterion for overtraining at any sampling rate. Not from a morning blood draw, not from a saliva kit, and not from a continuous sensor. Measuring the hormone more often does not conjure a threshold that the science has never established. The ECSS and the ACSM reviewed every marker in use and found that none of them meet all the criteria to be generally accepted. That finding is a limit on us exactly as much as it is a limit on a lab, and any company that tells you otherwise is selling you a number that does not exist yet.
What cortisol is, is a real hormone with a real daily shape, and that shape moves in response to things you can name: intensity above a threshold, short sleep, a calorie deficit, alcohol, a hard week at work. Watching your own rhythm move against inputs you control is a legitimate thing to be curious about. Reading a training verdict off it is not, and nobody has earned the right to sell you one.
The Auromone Curve is designed to read cortisol from a trace of sweat on your wrist, continuously. It ships Q4 2026. To be explicit about what it is not: it is a general wellness device. It does not diagnose overtraining syndrome, REDs, myocarditis or anything else named on this page, it cannot tell you whether to train tomorrow, and it is not a substitute for the blood tests and the clinical assessment that this article has spent most of its length telling you to go and get. If you want the hormone itself explained first, start with Cortisol 101, then read what actually moves your cortisol and why heart-rate variability is a proxy rather than the hormone.
This guide is for general education only. The Auromone Curve is a general wellness device, not a diagnostic, and does not replace medical advice or clinical testing. Persistent fatigue and declining performance deserve a proper medical assessment. Please talk to a healthcare provider.
References
- Meeusen R, Duclos M, Foster C, et al. Prevention, diagnosis, and treatment of the overtraining syndrome: joint consensus statement of the ECSS and the ACSM. Med Sci Sports Exerc. 2013;45(1):186-205. (Source for "none of them meet all the criteria", "prolonged maladaptation", the exclusion-diagnosis approach and its list, and "no scientific evidence to either confirm or refute".)
- Cadegiani FA, Kater CE. Hormonal aspects of overtraining syndrome: a systematic review. BMC Sports Sci Med Rehabil. 2017;9:14. (38 articles. Source for resting cortisol being normal in most studies, the even split on stimulated cortisol, the testosterone-to-cortisol ratio at 50% reduced / 40% normal / 10% increased, and both quoted conclusions.)
- Cadegiani FA, Kater CE. Hypothalamic-pituitary-adrenal (HPA) axis functioning in overtraining syndrome: EROS-HPA axis. Sports Med Open. 2017;3(1):45. (Source for every figure in the EROS table: n = 14 / 25 / 12, the insulin-tolerance-test cortisol and ACTH responses, saliva cortisol 30 minutes after waking, and the normal cosyntropin response.)
- Hill EE, Zack E, Battaglini C, Viru M, Viru A, Hackney AC. Exercise and circulating cortisol levels: the intensity threshold effect. J Endocrinol Invest. 2008;31:587-591. (12 trained men, 30 minutes at 40%, 60% and 80% of maximal oxygen uptake.)
- Hackney AC, Walz EA. Hormonal adaptation and the stress of exercise training: the role of glucocorticoids. Trends Sport Sci. 2013;20(4):165-171. (Source for the Adlercreutz threshold, a free-testosterone-to-cortisol fall of more than 30% or to 0.35 × 10⁻³ or below, and for both criticisms of it.)
- Stellingwerff T, Heikura IA, Meeusen R, et al. Overtraining syndrome (OTS) and relative energy deficiency in sport (RED-S): shared pathways, symptoms and complexities. Sports Med. 2021;51(11):2251-2280. (Source for 18 of 21 studies, 86%, and for the call to exclude low energy availability and RED-S from an overtraining diagnosis.)
- Mountjoy M, Ackerman KE, Bailey DM, et al. 2023 International Olympic Committee consensus statement on Relative Energy Deficiency in Sport (REDs). Br J Sports Med. 2023;57(17):1073-1097. (Source for the definition of REDs and low energy availability, and for REDs affecting male as well as female athletes.)
- Nazem TG, Ackerman KE. The female athlete triad. Sports Health. 2012;4(4):302-311. (Source for HPA overactivity increasing cortisol release in functional hypothalamic amenorrhea, for 10% to 20% lower lumbar-spine bone density, and for the 2-to-4-times stress fracture risk.)
- Sundgot-Borgen J, Torstveit MK. Prevalence of eating disorders in elite athletes is higher than in the general population. Clin J Sport Med. 2004;14(1):25-32. (1,620 athletes and 1,696 controls. Source for 13.5% versus 4.6%, for 42% in female aesthetic sports and 24% in endurance, and for 22% in male antigravitation sports.)
- Rout P, Chippa V, Adigun R. Rhabdomyolysis. StatPearls, NCBI Bookshelf. (Source for the classic triad appearing in fewer than half of patients, muscle pain in about 50%, dark urine in 30% to 40%, acute kidney injury in 10% to 50% once creatine kinase exceeds 1,000 U/L, and strenuous exercise in the untrained as a recognised cause.)
- Wasfy MM, Hutter AM, Weiner RB. Sudden cardiac death in athletes. Methodist Debakey Cardiovasc J. 2016;12(2):76-80. (Source for approximately 30% of athletes having prodromal symptoms, and for performance decline appearing on that symptom list.)
- Syncope as a warning symptom of sudden cardiac death in athletes. Cardiol Clin. 2015. (Exercise-induced syncope is an alarming symptom of underlying cardiac disease predisposing to arrhythmic cardiac arrest, and every athlete with syncope needs a focused cardiac workup.)
- 9-8-8 Suicide Crisis Helpline. Call or text 988 anywhere in Canada, 24 hours a day, in English or French. The same number reaches the 988 Suicide and Crisis Lifeline in the United States.