Cortisol and Overtraining: Understanding the Hidden Stress-Response Failure
Table of Contents
Introduction
Cortisol and overtraining present a frequent clinical interpretation challenge in athletes. In real-world practice, athletes with clear performance decline and fatigue often undergo cortisol testing that appears reassuring at rest, despite ongoing functional impairment related to overtraining. This disconnect between symptoms, training load, and standard hormonal markers complicates decision-making and can delay appropriate recognition of cortisol dysregulation in overtraining syndrome. Understanding how cortisol behaves under stress—rather than at baseline—is therefore central to accurately interpreting cortisol and overtraining and guiding management.
Patients often come to my office and ask for a check of laboratory tests. Usually patients, especially women, suspect iron deficiency as the primary cause. In my experience, that is often a contributing factor, so it is good to emphasize that in the first line. That is why I wrote a guide female athlete iron markers.
The Scope of the Problem
Overtraining states affect an estimated 30–60% of high-level athletes at some point, although the prevalence of strictly defined overtraining syndrome is likely lower and remains difficult to quantify [7]. Unlike simple fatigue, OTS manifests as a prolonged decrease in sport-specific performance coupled with persistent exhaustion, mood disturbances, disturbed sleep, and hormonal dysregulation, with cortisol and overtraining playing a central role in this maladaptive stress response [1].
Many of my patients already live a disciplined life and in addition to sports they have a hard and complicated everyday life. A large part of them study and many also work at the same time. In these situations, in practice it is often difficult to distinguish which symptom is caused by which. OTS seems to occur simultaneously with ordinary fatigue in my experience, which is understandable.
The syndrome exists on a spectrum. Functional overreaching (FOR) causes brief performance decrements lasting days to weeks with subsequent supercompensation. Non-functional overreaching (NFOR) produces longer-term performance declines spanning weeks to months. OTS itself represents the severe end—performance deficits persist for months or longer, often accompanied by significant psychological symptoms [1].
Cortisol Levels in Overtraining: A More Complex Relationship Than Expected
Cortisol’s role in overtraining proves far more nuanced than early theories suggested. A comprehensive systematic review of 38 studies examining hormonal aspects of OTS revealed a striking pattern: basal (resting) cortisol levels typically remain normal in overtrained athletes [1]. Among studies measuring basal cortisol, roughly 72.7% found normal levels, with only 22.7% showing reduced levels and 4.6% showing elevated levels [1].
This finding challenges the intuitive assumption that overtrained athletes would display obviously abnormal baseline hormone levels. The reality is more subtle—and potentially more revealing about the underlying mechanisms.
Some of my patients know how to request cortisol testing as part of a battery of tests. Because cortisol typically does not increase much in the long term, testing it rarely shows anything. In addition, many of my patients are occupational health clients, and few occupational health contracts cover cortisol testing. In practice, cortisol testing is often limited to testing by internal medicine physicians, at least in Finland, to detect other endocrinological diseases (Cushing’s syndrome, Addison’s disease, pituitary or adrenal problems). In addition, in practice, many athletes have stressful lives, so often an elevated cortisol level does not necessarily indicate OTS.
In clinical practice, this manifests as athletes presenting with clear performance decrements and fatigue despite routine blood work appearing normal. This disconnect between symptoms, training load, and objective markers may delay recognition of overtraining and appropriate intervention. The shortened duration of ACTH and cortisol responses may help explain why overtrained athletes experience premature fatigue during training sessions.
The critical differences emerge not at rest, but under stress. Research using gold-standard testing protocols demonstrates that overtrained athletes exhibit blunted cortisol responses to acute stressors compared to healthy athletes [2]. During insulin tolerance testing—which directly evaluates hypothalamic-pituitary-adrenal (HPA) axis integrity—healthy athletes showed mean cortisol responses of 21.7 μg/dL compared to only 17.9 μg/dL in overtrained athletes [2].
However, this type of cortisol testing has often been limited to research settings, and in everyday clinical work, such a detailed analysis is often not possible. In practice, this would require several measurements, at different stages of the season, as well as information about the patient’s baseline cortisol levels. At least in Finland, athletes rarely have the resources to have their cortisol levels measured repeatedly, and there would often be no need. In addition, the daily and diurnal variation in cortisol makes interpretation at the individual level almost impossible, and differences are often only seen in large statistical samples. In practical clinical work, cortisol testing rarely provides any definitive diagnosis, at least in the diagnosis of OTS.
The HPA Axis Dysfunction: Where the Breakdown Occurs
The hypothalamic-pituitary-adrenal axis governs the body’s stress response system through coordinated hormone release. In healthy athletes, this system shows remarkable conditioning—cortisol and ACTH responses to stress become exaggerated compared to sedentary individuals, representing an adaptive enhancement that supports performance [2].
Overtraining appears to strip away this conditioning. While adrenal glands themselves function normally in overtrained athletes—as demonstrated by normal responses to direct ACTH stimulation—the central components (hypothalamus and pituitary) show impaired responsiveness [2].
Research reveals that ACTH responses to stress are particularly blunted in OTS. Median ACTH response during insulin tolerance testing was higher in healthy athletes (91.4 pg/mL) than in overtrained athletes (30.3 pg/mL) [2]. This represents a marked reduction in pituitary ACTH responsiveness in overtrained athletes
The implications extend beyond laboratory values. The shortened duration of adequate ACTH and cortisol responses may directly explain why overtrained athletes experience premature fatigue during training sessions—they can start strong but cannot sustain performance as the workout progresses [2].
I have a similar experience from my own sports career, when I myself suffered from OTS. I was able to start the workout strong, but very quickly as the strain increased, the stress levels seemed to rise very high. My heart rate rose very quickly, and my endurance quickly felt insufficient. As if there was a throttle in the machine that was slowing down my performance. I was mentally fighting to get through the workout to the end.
However, hormonal findings in OTS are not uniform across studies. Systematic reviews demonstrate mixed findings: approximately half of studies report blunted cortisol responses to stimulation tests, while the remainder report normal responses, with similar variability observed in ACTH findings. This inconsistency likely reflects differences in diagnostic precision, testing protocols, and athlete populations rather than a true absence of HPA-axis involvement. Taken together, the evidence suggests that impaired stress regulation is common in OTS, but its hormonal expression varies between individuals and study settings [1].
The Cortisol Awakening Response: A Practical Marker
One promising avenue for assessment involves the cortisol awakening response (CAR)—the natural surge in cortisol that occurs within 30 minutes of waking. Research demonstrates that healthy athletes show significantly elevated cortisol levels 30 minutes after awakening (mean 500 ng/dL) compared to overtrained athletes (323 ng/dL) [2].
A salivary cortisol level above 530 ng/dL at 30 minutes post-awakening showed 93.9% accuracy in excluding OTS, while levels below 370 ng/dL increased the likelihood of the condition [2]. This relatively simple, non-invasive test may offer practical utility for monitoring athletes.
Accurate assessment of the CAR requires standardized sampling conditions, including precise timing and avoidance of confounding factors. CAR is not yet widely available in practical clinical work, at least in Finland, but it may become a useful tool in sports physiology in the future. It would also be a much easier and potentially more easily standardized measurement method than measuring purely cortisol levels or cortisol exercise response. Furthermore, unlike cortisol response measurement, CAR does not require information on basal cortisol levels measured prior to the OTS condition.
Exercise-Induced Cortisol Surges: Temporary Elevation
Acute exercise triggers substantial cortisol elevation, with intense prolonged exercise (approximately 85 minutes at 75% VO2max) capable of raising cortisol levels to magnitudes approaching those seen in Cushing’s syndrome patients. However, these elevations are transient, generally declining toward baseline during the recovery period following exercise cessation [5].
Following short-term intensified training (11 days), research shows blunted cortisol responses to high-intensity exercise stress tests, a characteristic finding in cortisol and overtraining states [7]. This finding, replicated across multiple studies, suggests that during overtraining periods, both ACTH and cortisol concentrations decrease in response to exercise stress [7].
The mechanism likely involves protective desensitization—when repeatedly exposed to elevated cortisol from daily training sessions, the system dampens its responsiveness, possibly through receptor downregulation or altered feedback loops at the hypothalamic-pituitary level [7].
My own first-hand experience with overtraining supports this hypothesis. The feeling in the body is similar to driving a car one or two gears too low. The engine is running hot, but you can’t get the power out. There is a similar analogy going on in the body, where the lack of a proper stress response means that the body is not able to mobilize the necessary metabolic resources that the situation would require.
The Bigger Picture: HPA Axis as Part of a Complex System
1. Neuroendocrine and Immune Interactions
While cortisol dysregulation represents an important component of overtraining syndrome, it likely occurs within a broader neuroendocrine–immune disturbance. The cytokine hypothesis proposes that excessive training may increase pro-inflammatory cytokines such as IL-6 and TNF-α, which could influence HPA-axis activity and anabolic hormone regulation. However, evidence for a consistent inflammatory pattern in OTS remains limited, and these mechanisms are best understood as proposed rather than definitive [6][8].
Such systemic interactions may help explain why cortisol changes are not uniformly present or predictive, suggesting that they represent only one manifestation of a complex physiological state. Some models propose that athletes may move through phases of altered HPA-axis sensitivity, initially showing heightened responses that later transition toward blunted reactivity, although this temporal pattern remains incompletely established [6].
Mechanistically, prolonged psychosocial stress may blunt HPA responsiveness through persistent central activation and feedback inhibition, resulting in reduced hormonal reactivity despite ongoing stress exposure.
2. Burnout as a Parallel State
Burnout may represent a psychologically driven parallel to overtraining syndrome. While the triggers differ, systematic reviews indicate that burnout is also associated with altered stress physiology, including changes in cortisol regulation, yet no single biomarker consistently identifies the condition. This mirrors OTS, where dysfunction emerges not from one abnormal value but from reduced adaptive capacity of the stress system, reinforcing the view that chronic overload—physical or psychological—can lead to similar patterns of stress dysregulation [9].
Mechanistically, prolonged psychosocial stress may blunt HPA responsiveness through persistent central activation and feedback inhibition, resulting in reduced hormonal reactivity despite ongoing stress exposure.
3. Overlapping Features with Depression
The resemblance between OTS and major depression is notable, as both conditions involve HPA-axis dysregulation, sleep disturbance, mood changes, and performance or cognitive decline. This parallel supports the possibility that psychological and physical overload states may share overlapping regulatory pathways [8].
Mechanistically, chronic stress exposure in depression is thought to alter glucocorticoid receptor sensitivity and feedback control, leading to sustained or poorly regulated activation of the stress system in at least a subgroup of patients.
However, depression is biologically heterogeneous, and some chronic stress–related or exhaustion-type presentations may instead show reduced cortisol responsiveness, bringing their physiological profile closer to burnout or OTS.
4. A Unified Psychological State
An overtrained athlete doesn’t experience separately a hormonal problem, an immune problem, a mood problem, and a performance problem—these represent different expressions of a unified physiological state. Similarly, the athlete who dismisses early warning signs as “just mental weakness” or “needing to push harder” fails to recognize that mental resilience itself depends on intact neuroendocrine function. Recovery requires addressing the whole system, not isolated symptoms
For this reason, many of my patients find it difficult to distinguish whether they are suffering from OTS, burnout, or a combination of both. In general, my elite athlete patients are conscientious in other areas of life as well and often also work and study in conjunction with training with the same diligence, and clinically, many also have overlapping clinical symptoms of burnout and OTS. Therefore, these often occur hand in hand in my patients. As mentioned above, the clinical symptoms of both typically include a blunting of the HPA-axis response, which may partly explain their similar clinical presentation.
Table 1. Typical HPA-axis response patterns in different overload states
| Condition | Typical HPA-axis pattern |
| Overtraining syndrome (OTS) | Often reduced or blunted response during physical stress |
| Burnout | Altered stress regulation; findings inconsistent |
| Major depression | Often sustained or dysregulated activation (in at least a subgroup of patients) |
Recovery and Prevention: Hormonal Perspectives
Addressing cortisol dysregulation in overtraining requires a fundamentally different approach than treating primary endocrine disorders. The hormonal changes represent consequences rather than causes—attempting to “fix” cortisol levels misses the point entirely.
Recovery centers on restoring balance between training stress and recovery capacity. Research indicates this requires sustained periods—often months—of reduced training volume and intensity. During this time, the HPA axis gradually regains its conditioned responsiveness [2].
Training periodization
Systematic variation in training intensity and volume, with planned recovery periods, appears protective. Periodization allows systematic variation in volume and intensity to prevent the continuous accumulation of fatigue while still driving adaptation [3]. Athletes showing early signs of excessive training stress may benefit from temporarily reducing load before OTS develops [1].
Block periodization can be particularly effective, as it concentrates demanding work into focused phases while reducing load in other areas, thereby preserving recovery capacity. Just as importantly, scheduled reductions in overall training stress are essential for long-term progress.
In my own preparation for World Championships, I structured training into distinct blocks:
- Basic fitness block (6 weeks): high training volume at lower intensity to build general capacity
- Intensified fitness block (4 weeks): elevated intensity combined with substantial volume, intentionally approaching functional overreaching, followed by a one-week deload to facilitate supercompensation
- Competition-specific block (4 weeks): maintained intensity with reduced total volume, prioritizing sport-specific performance qualities
- Competition block (4–6 weeks): moderate intensity with carefully managed volume to sustain readiness
- Recovery block (4 weeks): active recovery and physiological regeneration
This structured fluctuation allowed adaptation while limiting cumulative stress on the neuroendocrine system.
Sleep and Nutrition Optimization
Sleep optimization. Some athletic patients may sleep too little, as excessive sleep can feel unproductive to highly driven individuals. Direct research examining “sleep prioritization” as an independent predictor of overtraining syndrome is limited. However, we know that overtraining states are frequently associated with impaired sleep quality, including increased sleep fragmentation and subjective sleep disturbance. In other words, sleep disruption is commonly observed once maladaptation has begun [4].
Nutrition adequacy. Low calorie intake relative to energy expenditure represents a key trigger for OTS. Ensuring sufficient total energy intake and particularly carbohydrate availability helps maintain hormonal balance [1]. Athletes, especially those competing in a certain weight class, may have restrictive diets that can impair recovery. I noticed this myself in my athletic career when I had to lose weight to fit into a certain weight class. The calorie deficit clearly slowed my recovery and also increased my risk of injury.
Recovery from OTS
Progressive return to training. Following recovery from OTS, training must be reintroduced gradually. The loss of hormonal conditioning means athletes temporarily have reduced capacity to handle stress, necessitating a conservative rebuilding approach [2].
Clinically, one of the greatest challenges is persuading athletes to reduce training load. Traits that drive high performance—discipline, tolerance for discomfort, and persistence—often impede recovery once overtraining develops. For many athletes, this is a difficult situation. Often it means that the rest of the season is over for the athlete. I often advise athletes to take a break, then slowly transition into a base season when the next season is about to start and implement block periodization in the next season to avoid overloading the next season. It often helps if you encourage the patient to approach the situation in the same way they would approach an injury.
Conclusion: Cortisol, Stress Regulation, and Systemic Adaptation
Overtraining syndrome presents a clinical paradox: athletes may experience clear performance decline, fatigue, mood disturbance, and sleep disruption while routine laboratory tests—including resting cortisol—remain normal.
The key dysfunction in OTS does not typically lie in baseline hormone levels but in impaired stress responsiveness, particularly blunted ACTH and cortisol reactions under physiological challenge. This loss of conditioned HPA-axis adaptability helps explain why affected athletes can initiate effort but struggle to sustain performance. At the same time, hormonal findings are heterogeneous and no single biomarker reliably defines the condition.
OTS exists within a broader neuroendocrine–immune context and shares physiological overlap with burnout and certain subtypes of depression, all of which may reflect reduced stress-system flexibility after prolonged overload. Effective management therefore focuses not on correcting isolated hormone values but on restoring balance between training stress and recovery capacity through structured periodization, adequate nutrition, sufficient sleep, and gradual return to load. Ultimately, OTS represents a systemic failure of adaptive regulation rather than a discrete endocrine disorder.
References
1 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5541747/
2 https://pmc.ncbi.nlm.nih.gov/articles/PMC5722782/
3 https://pubmed.ncbi.nlm.nih.gov/23247672/
4 https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2018.00436/full
5 https://pubmed.ncbi.nlm.nih.gov/31371847/
6 https://pmc.ncbi.nlm.nih.gov/articles/PMC3435910/
8 https://www.frontiersin.org/journals/network-physiology/articles/10.3389/fnetp.2021.794392/full
