fatigue in athletes

Fatigue in Athletes: What’s Actually Causing It, and What the Evidence Says to Do About It

Key Takeaways: Fatigue in Athletes

  • Fatigue in athletes is a symptom, not a diagnosis. In athletes, it often results from multiple interacting factors rather than a single cause.
  • A detailed medical history is usually more informative than any individual laboratory test. Sleep, nutrition, training load, psychological stress, work, and recovery all need to be considered together.
  • Sleep deprivation is one of the most consistent performance impairments in sports science, affecting endurance, strength, power, speed, skill execution, and perceived effort.
  • Glycogen depletion remains an important cause of peripheral fatigue, particularly during prolonged or high-volume training, and usually responds well to appropriate carbohydrate intake and recovery.
  • Mental fatigue can impair endurance performance even when traditional physiological markers remain unchanged, making cognitive workload an often-overlooked contributor to poor performance.
  • Mild dehydration has a smaller effect on perceived exertion than is often assumed, but prolonged exercise, heat, and high sweat losses still make individualized hydration strategies important.
  • Overtraining syndrome remains a clinical diagnosis. No single blood test reliably confirms it, and other medical and psychological causes of fatigue should first be excluded.
  • Iron deficiency and thyroid dysfunction are among the most important treatable medical causes of persistent fatigue in athletes. Broader micronutrient abnormalities may be relevant, but their contribution to fatigue is often less specific and should be interpreted in clinical context.
  • The most effective treatment depends on identifying the underlying cause rather than assuming every fatigued athlete simply needs more sleep, more carbohydrates, or less training.

Introduction: Fatigue in Athletes

Fatigue is a common reason for consultation in my clinical practice, but it is also one of the least specific symptoms a patient can describe. “I just feel flat” may reflect a single poor night of sleep, accumulated training stress, inadequate energy intake, psychological strain, an underlying sleep disorder, or a medical condition that has not yet been identified. In many cases, several of these factors are present at the same time.

Patients often arrive with a particular explanation already in mind. At the moment, iron deficiency is a common concern, and many specifically ask for ferritin or other iron-related tests. At other times, thyroid dysfunction, subclinical hypothyroidism, or chronic Lyme disease have occupied a similar place in public discussion. These diagnoses can be relevant in selected cases, but in my experience, persistent fatigue is less often explained by one isolated abnormality than people may expect. Clear iron deficiency or clinically significant thyroid dysfunction may be found, but just as often the assessment reveals a more complex combination of sleep loss, stress, low energy availability, mood symptoms, excessive training load, or impaired recovery.

This is why I place so much emphasis on the medical history. Laboratory investigations can be useful for excluding relevant underlying disease, but they rarely replace the need to understand how the athlete is sleeping, eating, training, working, studying, and coping psychologically. From a clinical perspective, the central question is not simply whether one blood value is outside the reference range, but whether the overall pattern explains the athlete’s symptoms and decline in performance.

The same principle applies throughout sports medicine. Fatigue in athletes is not one condition with one universal solution. More sleep, more carbohydrate, better hydration, caffeine, or reduced training may each be appropriate in the right context, but none of them addresses every cause. This article examines the major physiological and clinical contributors to fatigue in athletes—including glycogen depletion, sleep loss, mental fatigue, dehydration, low energy availability, and the overreaching–overtraining spectrum—and explains what the available evidence can, and cannot, tell us about each of them.

Central vs. Peripheral: Two Different Types of Fatigue in Athletes

Exercise physiologists often distinguish between peripheral and central fatigue, although in practice the two can overlap. Peripheral fatigue arises primarily within the muscle itself and may involve depleted fuel stores, metabolite accumulation, or impaired excitation–contraction coupling. Central fatigue develops further upstream, when the brain and spinal cord become less able to sustain the neural drive required for continued performance.

From a clinical perspective, predominantly peripheral fatigue is often easier to interpret. The symptoms tend to follow a recognizable physical load, improve with adequate recovery and nutrition, and settle without further investigation in most cases. When an athlete reports heavy legs after a demanding training block, for example, the relationship between exertion and symptoms is usually relatively straightforward, provided there are no warning signs or an unexpectedly prolonged decline.

Central fatigue is considerably more difficult to define in clinical practice. There is no single laboratory test, imaging study, or physiological marker that can confirm it on its own. The assessment is therefore largely clinical and often depends on excluding other relevant causes of persistent fatigue. In my experience, the difficulty is that reduced motivation, impaired concentration, disturbed sleep, mood symptoms, psychological stress, and physical under-recovery may all appear together and may influence one another.

The serotonin–dopamine hypothesis is one proposed explanation for central fatigue during prolonged exercise. A rising ratio of brain serotonin to dopamine has been associated with greater tiredness and a reduced willingness to continue, whereas a lower ratio may favor sustained effort. However, a comprehensive review concluded that decades of nutritional and pharmacological attempts to manipulate serotonin have not provided robust evidence that serotonin alone plays a decisive role in the fatigue process [10]. This fits the clinical reality: central fatigue is unlikely to reflect one isolated neurotransmitter abnormality, and its mechanisms are often intertwined with sleep, stress, mood, training load, and recovery.

Fuel Depletion: Why Glycogen Still Matters

Muscle glycogen depletion is a well-documented peripheral driver of fatigue in athletes doing endurance exercise. Glycogen isn’t stored uniformly inside the muscle fiber — it sits in distinct subcellular pools, one of which is positioned right next to the machinery that releases calcium during muscle contraction. Depletion of this specific intramyofibrillar pool correlates closely with the onset of fatigue, and reduced glycogen in this location has been linked to impaired calcium release from the sarcoplasmic reticulum during prolonged exercise, which may help explain why total muscle glycogen alone does not fully capture the relationship between glycogen availability and contractile function [1].

Practically, this helps explain why carbohydrate availability remains an important consideration in endurance exercise. Muscle glycogen depletion is strongly associated with fatigue development, while training with low glycogen availability may be useful as part of a well-thought-out periodization program [2].

Glycogen-related fatigue is often relatively straightforward to recognize. In my experience, athletes can often connect unusually heavy legs or reduced endurance with demanding training and insufficient carbohydrate intake. When inadequate fueling is the main factor, appropriate nutrition and recovery may also resolve the symptoms fairly quickly.

Sleep Debt: The Most Underrated Fatigue Multiplier

A 2025 systematic review and meta-analysis pooling 45 controlled studies on sleep deprivation and athletic performance found that sleep loss significantly impaired aerobic endurance in athletes, reduced explosive power, reduced maximum force, slowed speed, degraded skill control, and increased ratings of perceived exertion (RPE) — with aerobic endurance and skill control showing the largest effects. Total sleep deprivation hit aerobic endurance hardest, while partial sleep deprivation at the end of the night was the type most damaging to explosive power, maximal force, and speed. Afternoon testing sessions showed larger performance losses than morning sessions across nearly every outcome measured [3].

The practical read for athletes: both the type of sleep loss and the timing of subsequent testing appear to matter — a single rough night before an early-morning session is a different risk profile than chronic partial sleep restriction heading into an afternoon competition, even though the meta-analysis doesn’t compare these two scenarios head-to-head.

In my clinical experience, athletes do not always give sleep the same priority as training or nutrition, and its effect on performance is often underestimated. Sometimes this is simply because work, school, stress, children, or family responsibilities take precedence. The result is not necessarily a complete lack of understanding, but a gradual acceptance of insufficient or poor-quality sleep as normal. This is why sleep history matters: an athlete may be highly disciplined with training while still carrying a significant recovery deficit from the rest of life.

Sleep Apnea: A Fatigue Cause That Sleep-Hygiene Advice Won’t Fix

Not all sleep-related fatigue can be explained by insufficient sleep duration. Obstructive sleep apnea may also warrant consideration in athletes with unexplained daytime sleepiness or poor sleep quality. In a survey of 175 elite and highly trained rugby and cricket athletes, 38% reported habitual snoring and 8% reported a witnessed apnoeic episode. These were questionnaire-based risk indicators rather than polysomnography-confirmed diagnoses, but the findings suggest that symptoms associated with possible OSA are not uncommon in athletic populations [8].

Repeated upper-airway obstruction during sleep can result in intermittent hypoxia, sleep fragmentation, and sympathetic hyperactivation. In athletes, these disturbances may be associated with impaired secretion of anabolic hormones such as growth hormone and testosterone and with prolonged or incomplete physical recovery. A recent systematic review of athletic populations found a substantial prevalence of OSA particularly in collision sports such as rugby and American football, with higher BMI and larger neck circumference associated with greater OSA risk. Across the included studies, OSA was also associated with reduced sleep quality, excessive daytime sleepiness, and slower reaction times [9].

An athlete who reports a “normal” eight hours of sleep but still wakes unrefreshed, snores heavily, or has witnessed breathing pauses may warrant assessment for an underlying sleep disorder rather than more generic sleep-hygiene advice. In my clinical experience, it is often the partner who first raises the concern: they may complain about loud snoring, describe apparent pauses in breathing, or eventually persuade the patient to seek medical evaluation. Occasionally, I have even heard that a neighbour has complained about the noise. This also means the diagnosis can be delayed in people who live alone, simply because no one is present to observe what happens during sleep. Obstructive sleep apnea can occur even in lean athletes when upper-airway anatomy, jaw structure, or enlarged tonsils contribute, while excess body weight may still be relevant in some sports. Restless legs syndrome and other sleep disorders may also contribute to persistent fatigue, particularly when the history suggests fragmented or poor-quality sleep despite apparently adequate sleep duration.

Mental Fatigue in Athletes: A Cause That Doesn’t Show Up in Blood Work

One of the more counterintuitive findings in this area comes from work on psychobiological (mental) fatigue — tiredness caused by prior demanding cognitive work rather than by physical exertion. In a controlled crossover trial, cyclists who completed 90 minutes of a demanding cognitive task before cycling to exhaustion reached exhaustion in 640 seconds on average, compared with 754 seconds after watching neutral documentaries — a reduction in time to exhaustion despite no meaningful difference in heart rate, oxygen consumption, or other cardiorespiratory measures between conditions [4]. The fatigue was real and it shortened performance, but it was not explained by the cardiorespiratory and metabolic variables measured in the study.

This matters for athletes juggling demanding jobs, exam periods, or heavy travel schedules on top of training — the cognitive load itself is a fatigue input that standard training-load monitoring (heart rate, HRV, session RPE for the training session alone) will typically miss entirely.

Dehydration: A Real Effect, But a Smaller Threshold Than Commonly Assumed

Dehydration is frequently blamed for fatigue in athletes at levels of fluid loss that a systematic review with meta-analysis suggests don’t move the needle much in practice. Pooling 16 controlled crossover studies (147 participants), the analysis found that each 1% increase in exercise-induced body mass loss raised RPE by 0.21 points on average — a real but small effect — and concluded that the impact on perceived exertion is unlikely to be practically meaningful until body mass loss reaches at least 3% [5].

This doesn’t mean hydration doesn’t matter — thermoregulatory and cardiovascular strain from fluid loss is well established, and higher body-mass losses are associated with measurably higher perceived effort. It means the RPE penalty from mild, typical in-session fluid losses is smaller than commonly assumed. That said, the meta-analysis studied endurance exercise generally rather than any specific session length, and it didn’t address heat, high sweat rates, or starting the session already underhydrated — factors that can matter well before 3% body-mass loss. Fluid needs should still be individualized to duration, environment, and sweat losses rather than chased to a fixed percentage.

From a practical perspective, this also depends heavily on the sport and the duration of exercise. In my clinical experience, dehydration is rarely the primary explanation for fatigue after shorter training sessions, including many combat-sport practices. It tends to become a much more relevant consideration during prolonged endurance events—such as marathons, ultramarathons, or long military marches—where fluid losses accumulate over many hours and environmental conditions may further increase the physiological strain.

When It’s Not a Single Bad Week: Overreaching and Overtraining Syndrome

Planned, short-term overload that produces temporary performance decline, and may be followed by improved performance after adequate recovery, is functional overreaching (FOR) — a normal and useful part of training. When the balance between training stress and recovery is chronically mismanaged, athletes can progress to non-functional overreaching (NFOR), and in more severe, prolonged cases, overtraining syndrome (OTS). The joint consensus statement from the European College of Sport Science and American College of Sports Medicine describes the defining feature of OTS as “prolonged maladaptation” — not just of the athlete’s subjective state, but of the underlying biological, neurochemical, and hormonal regulation systems, with fatigue, performance decline, and mood disturbance as the hallmark clinical picture [6].

The consensus statement is notably candid about the limits of objective diagnosis here: there is no single blood marker or hormone panel that reliably distinguishes NFOR from OTS, and a 2022 systematic review examining the literature found that zero included studies provided objective evidence of detailed performance changes from a healthy baseline through the onset of OTS with performance suppressed for more than 4 weeks alongside documented psychological symptoms [7] — meaning that despite decades of research interest, OTS remains largely a diagnosis of exclusion rather than a condition confirmed by a specific test.

At least for now, the diagnosis remains largely clinical, and distinguishing overtraining syndrome from burnout, depression, sleep disorders, or other medical causes can be extremely difficult. In my experience, athletes who are capable of pushing themselves into this state are often highly conscientious not only in training, but also in work, study, and other areas of life. The relevant question is therefore not just how much they train, but how much total stress they are carrying.

This is why the assessment usually combines a detailed history with investigations aimed at excluding other explanations. Laboratory tests may be useful, but they do not confirm overtraining syndrome on their own. The most important part is still understanding the timeline of symptoms, the change in performance, the athlete’s recovery, sleep, mood, workload, and whether another medical or psychological condition better explains the picture.

Other Causes Worth Ruling Out: Anemia, Thyroid, and Micronutrient Status

Everything above assumes training-related fatigue in an otherwise healthy athlete. Before attributing persistent fatigue to training load, sleep, or hydration, it’s worth ruling out three common medical contributors that present with the same complaint but need their own diagnostic workup:

  • Iron deficiency and sports anemia. Low ferritin — even without frank anemia — is a common and frequently missed cause of unexplained fatigue in athletes, particularly female endurance athletes. This deserves its own diagnostic approach rather than a quick mention here; see the dedicated guides on ferritin levels for athletes and dilutional pseudoanemia (sports anemia) for how to actually interpret these markers in an athletic population.
  • Thyroid dysfunction. Thyroid hormones regulate metabolic rate and mitochondrial function directly. TSH is generally an effective first-line screen for thyroid dysfunction, but it should be interpreted in clinical context — further testing (such as free T4) can be appropriate when symptoms, medication use, pituitary disease, or other specific findings make an isolated TSH difficult to interpret. See thyroid function in athletes for how to approach this in an athletic population.
  • Micronutrient status. Vitamin D deficiency and inadequate B-vitamin status (particularly B6, B12, and folate) are both common in athletic populations and both have fatigue as a presenting symptom; see the vitamin series on the site for markers worth testing.

Iron deficiency and thyroid dysfunction are among the clearest medical causes to exclude when persistent fatigue is affecting athletic performance. Both can have a relatively direct and clinically meaningful effect on exercise capacity, and this is why iron studies and thyroid markers often form part of the initial assessment when the history supports testing.

Micronutrient findings are usually less straightforward. A deficiency such as low vitamin D can be identified in laboratory testing, but unless it has produced a clear physiological consequence, its exact contribution to an individual athlete’s fatigue or performance decline may remain difficult to demonstrate. In my view, these abnormalities may still be relevant, but they should not automatically be treated as the complete explanation for a non-specific symptom.

For that reason, I do not usually find very broad laboratory panels helpful unless the history or clinical examination points toward a specific alternative diagnosis. A focused workup guided by the athlete’s symptoms, diet, medical history, training load, and other findings is generally more informative than screening an increasingly long list of biomarkers without a clear clinical question.

Conclusion: Fatigue in Athletes

Fatigue in athletes is rarely explained by a single mechanism. Glycogen depletion, sleep loss, mental strain, dehydration, low energy availability, excessive training load, and underlying medical conditions can all produce a similar subjective experience, and several of them may be present at the same time.

From a clinical perspective, this is why fatigue cannot be assessed reliably through one laboratory value, one wearable metric, or one favored diagnosis. The medical history remains the most important part of the evaluation: how the symptoms developed, whether performance has changed, how the athlete is sleeping and eating, what the total training and life stress look like, and whether there are signs pointing toward a specific medical or psychological cause.

In my experience, the most useful approach is usually a focused one. Clear and treatable contributors, such as iron deficiency, thyroid dysfunction, inadequate fueling, or an underlying sleep disorder, may warrant targeted investigation. At the same time, minor abnormalities in broad laboratory panels should not automatically be assumed to explain a non-specific symptom.

The practical lesson is that managing fatigue begins with identifying the most plausible cause rather than reaching immediately for more caffeine, more rest, or more testing. When fatigue is persistent, unexplained, or accompanied by a clear decline in performance or general functioning, a broader clinical assessment may become relevant.

References

[1] https://pubmed.ncbi.nlm.nih.gov/23652590/
[2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4687103/
[3] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11996801/
[4] https://journals.physiology.org/doi/full/10.1152/japplphysiol.91324.2008
[5] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9093000/
[6] https://pubmed.ncbi.nlm.nih.gov/23247672/
[7] https://pubmed.ncbi.nlm.nih.gov/35320774/
[8] https://pubmed.ncbi.nlm.nih.gov/26697921/
[9] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12843434/
[10] https://pubmed.ncbi.nlm.nih.gov/17004850/

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