Why Is My Performance Declining?
Table of Contents
Key Takeaways: Why Is My Performance Declining?
- Declining athletic performance is a symptom, not a diagnosis, and the cause is often best understood by looking at the full clinical picture rather than a single metric.
- Overreaching and overtraining are possible explanations, but there is no single blood test, cortisol value, testosterone level, or HRV reading that can confirm the diagnosis on its own.
- Iron deficiency can affect physical performance even when hemoglobin remains normal, but low iron stores should not automatically be assumed to explain every case of fatigue.
- Low energy availability and RED-S are especially relevant when training demands are high relative to energy intake, including in sports where body weight or body composition is important.
- Sleep loss can meaningfully impair performance, and in practice the problem is not always a primary sleep disorder — sometimes the athlete is simply not getting enough opportunity to sleep.
- Recent infection can affect training and performance, but persistent fatigue after illness still warrants a broader differential diagnosis rather than being attributed automatically to the infection.
- Thyroid-hormone changes can occur in athletes, particularly with low energy availability, but thyroid tests still need to be interpreted using the same basic clinical principles as in non-athletic patients.
- In my clinical approach, the most useful assessment combines training load, recovery, sleep, nutrition, mental wellbeing, symptoms, and appropriate medical evaluation rather than forcing the problem into a single explanation.
Introduction: Why Is My Performance Declining?
From time to time, an athlete comes to my clinic because their performance has started to drift in the wrong direction and they want to know why. These cases are often more complicated than they first appear. Athletes rarely have training as their only source of load: many are also studying, working, managing relationships and other responsibilities, and quite a few are highly conscientious and ambitious in several areas of life at the same time.
They may also arrive with a surprising amount of data. Oura rings, sports watches and other wearables can provide weeks or months of information on sleep, recovery, resting heart rate and HRV. That data can be useful, but it does not automatically tell you what the underlying problem is. Fatigue and declining performance can sit at the intersection of several different issues — overreaching or overtraining, psychological stress, depression or anxiety, sleep problems, medical conditions, nutritional deficiencies or thyroid dysfunction can all produce overlapping symptoms.
This is one reason I tend to approach unexplained performance decline as a differential diagnosis rather than assuming the athlete is simply “overtrained.” Even the evidence base for overtraining syndrome itself is less straightforward than the term might suggest. A 2022 systematic review looking specifically for objective evidence behind overtraining syndrome diagnoses found zero included studies that objectively documented both a performance decrement lasting four weeks or longer and corroborated psychological symptoms together — many studies described athletes as having declined, but none met the review’s criteria for demonstrating it rigorously [1].
In practice, making sense of declining performance often means looking at the whole picture: training load, recovery, sleep, everyday stress, mental wellbeing, symptoms and possible medical contributors, rather than letting a single metric or a single label explain everything.
Overtraining and functional overreaching
The overtraining spectrum runs from functional overreaching (a short, deliberate dip in performance followed by a stronger rebound) through non-functional overreaching to full overtraining syndrome, with recovery time generally increasing along that spectrum and psychological symptoms forming part of the overtraining syndrome picture [2]. The distinction matters because functional overreaching is often a normal, even useful, part of periodized training, while non-functional overreaching and overtraining syndrome are not — for the full breakdown of how the two are told apart in practice, including typical recovery timeframes, see my functional overreaching vs. non-functional overreaching guide.
The endocrine picture is messier than most summaries suggest. A systematic review of hormonal findings across overtraining, functional overreaching, and non-functional overreaching concluded that resting hormone levels generally cannot distinguish athletes who are adapting normally from those heading toward overtraining syndrome — the more useful signal appears to be a blunted hormonal response to a stimulation test, specifically growth hormone and ACTH, rather than any single resting blood value [2]. A dedicated hypothalamic-pituitary-adrenal axis study in overtrained athletes versus healthy athletes and non-athletes found no difference in cortisol response to a standard cosyntropin stimulation test across the three groups, but did identify specific cortisol and ACTH cutoffs on a separate insulin tolerance test that could help exclude or support an overtraining diagnosis — the study’s authors concluded that the hormonal conditioning healthy athletes typically show under this more demanding stress test was at least partially lost in the overtrained group [7].
Athletes often ask whether there is a blood test that can confirm overreaching, overtraining syndrome, or something along that spectrum. Cortisol and testosterone are common examples, and some athletes arrive having already tracked or tested these markers themselves.
In practice, I usually have to explain that there is no single laboratory value that can establish the diagnosis. Blood tests can still be very useful, but mainly for looking for other medical explanations for declining performance or fatigue rather than for “proving” overtraining itself.
This is an important distinction. At least for now, overtraining syndrome remains primarily a clinical diagnosis based on the overall picture rather than a single biomarker. Measures such as HRV can add context and may support the assessment, especially when viewed as a trend over time, but I would not treat HRV alone as diagnostic either.
Iron deficiency — with or without anemia
This is a cause I flag often, because a normal hemoglobin does not exclude it. Iron deficiency progresses through three stages: in the first (prelatent), iron stores fall but serum iron stays normal; in the second (latent), ferritin and serum iron both drop while hemoglobin is still normal; only in the third stage does hemoglobin itself fall, marking true anemia [15]. A case report on a collegiate athlete with unexplained exercise intolerance concluded that ferritin below 50 µg/L is a reasonable threshold for detecting deficiency that matters physiologically in athletes, and argued iron deficiency should be considered early in athletes with unexplained reduced exercise capacity, even without anemia [3].
Prevalence data varies by population and threshold used, which is exactly why a single “normal” lab report can be misleading. In a small case study of internationally competitive, non-professional female endurance athletes using a ferritin cutoff of 30 µg/L, 46% were classified as iron deficient [4]. A cohort study of Japanese university athletes using the same 30 µg/L threshold cited a comparable finding of 46% deficiency in another internationally competitive female endurance cohort [5].
The practical issue is that iron deficiency without anemia produces a fairly generic symptom list — fatigue, reduced exercise capacity, presyncope — that overlaps heavily with several other items on this list, which is precisely why guessing rather than testing tends to waste time [3]. For a deeper breakdown of interpreting the full panel, see iron panel interpretation for athletes and, for sex-specific considerations, female athlete bloodwork.
Athletes often ask whether there is a blood test that can confirm overreaching, overtraining syndrome, or something along that spectrum. Cortisol and testosterone are common examples, and some athletes arrive having already tracked or tested these markers themselves.
In practice, I usually have to explain that there is no single laboratory value that can establish the diagnosis. Blood tests can still be very useful, but mainly for looking for other medical explanations for declining performance or fatigue rather than for “proving” overtraining itself.
This is an important distinction. At least for now, overtraining syndrome remains primarily a clinical diagnosis based on the overall picture rather than a single biomarker. Measures such as HRV can add context and may support the assessment, especially when viewed as a trend over time, but I would not treat HRV alone as diagnostic either.
Low energy availability and RED-S
Relative Energy Deficiency in Sport is defined by the International Olympic Committee’s 2023 consensus statement as a syndrome of impaired physiological and/or psychological functioning caused by exposure to problematic, prolonged and/or severe low energy availability, with detrimental outcomes that include impaired musculoskeletal and haematological health and can lead to increased injury risk and decreased sports performance [12]. A separate review of its performance and health consequences lists impaired metabolic rate, hormonal disruption, menstrual dysfunction, reduced bone health, impaired immunity, and cardiovascular effects among the documented consequences [6].
A case series tracking seven Division I collegiate female runners across a full cross-country season found that vitamin D declined significantly over the season, while ferritin showed a downward trend that didn’t reach statistical significance (p=0.07) — body composition and resting metabolic rate, notably, did not change significantly within that single competitive season, though RMR did rise significantly once the athletes moved into the following track season [16]. That’s a useful reminder on its own: even in a population being actively monitored for RED-S, not every marker moves together, or on the timeline you’d expect.
Low energy availability can be particularly relevant in sports where body weight or body composition plays a major role. In my own case, I experienced this myself when I was training and competing in a weight-class sport, which is one reason I take the issue seriously when assessing athletes with declining performance or persistent fatigue.
The same concern can become relevant in other sports where athletes may feel pressure to stay light, make a weight category, or maintain a certain physique, including combat sports, wrestling, gymnastics, and figure skating. From a clinical perspective, the underlying issue is not the sport itself but whether energy intake is sufficient relative to training demands.
Dietary pattern can also matter. For example, some athletes follow vegetarian diets, which does not automatically mean low energy availability, but it can become relevant when looking at the overall picture of energy and nutrient intake.
Sleep debt
Sleep loss has substantial quantitative meta-analytic evidence behind it. A meta-analysis covering 27 studies and 75 performance indicators found an overall negative effect of acute sleep deprivation on athletic performance, with a notably larger effect for partial sleep deprivation occurring specifically toward the end of the night compared with a full night of lost sleep, and found that affected athletes’ afternoon performance was worse than their morning performance following sleep loss [8]. A separate 2025 systematic review and meta-analysis spanning 45 studies broke this down further by performance type — aerobic endurance, anaerobic endurance, explosive power, and maximal strength were all assessed — and, notably, found the evidence on endurance specifically has been inconsistent across prior meta-analyses, with some concluding sleep deprivation meaningfully impairs endurance and others finding no significant effect [9].
The practical takeaway is that the type and timing of sleep-deprivation protocol appear to matter. In the same meta-analysis, partial sleep deprivation specifically at the end of the night carried a substantially larger performance cost (effect size −1.17) than whole-night sleep deprivation (−0.23) or partial deprivation at the beginning of the night (−0.25, not statistically significant) — these are separate deprivation protocols the meta-analysis compared, not the same total hours of lost sleep redistributed [8].
Sleep problems in athletes are not always caused by a primary sleep disorder. Conditions such as sleep apnea can still be relevant, but in practice there are often more immediate explanations to consider as well. Iron deficiency, for example, may contribute to restless legs, which can in turn interfere with sleep. Psychological stress, competition schedules, travel, and the general demands of training can also make adequate sleep harder to achieve.
What I also see, however, is a more straightforward problem: some athletes simply do not give sleep the same priority they give training, work, or studying. They may stay up too late, compress their sleep around other commitments, or assume that they can compensate for insufficient recovery by being disciplined in every other part of their routine.
From a clinical perspective, that distinction matters. An athlete can feel profoundly fatigued and perform worse without there being a complicated underlying sleep disorder. Sometimes the broader assessment points back to something much simpler — they are consistently not getting enough opportunity to sleep. In other cases, a contributing medical factor such as iron deficiency may also be part of the picture.
Recent illness and immune suppression
Even a seemingly minor respiratory infection can affect training and performance. A systematic review by a subgroup of the IOC consensus group on acute respiratory illness in athletes found that self-reported training ability and capacity can be reduced during an upper respiratory infection, that infections accompanied by fever can alter running mechanics, and that training mileage and overall training load can remain affected for a period afterward, even though cardiorespiratory endurance itself is largely unaffected in milder infections [10].
For guidance on deciding whether to train through a specific illness or rest, see my exercise when sick guide. There’s also a training-load side to this that runs in both directions. A review of upper respiratory tract infections in athletes describes elevated infection risk in the one-to-two-week window following heavy exertion — citing a two- to six-fold increase in infection risk after marathon participation in normal or hot conditions, and roughly 13% of runners reporting illness in the week after a Los Angeles marathon compared with about 2% of non-running controls — alongside evidence that performance itself can stay measurably reduced for two to four days after a respiratory infection [11]. In other words: heavy training raises infection risk in the following days, and the infection itself then further suppresses performance — a cycle that’s easy to misread as “just overtraining” if illness isn’t specifically considered.
Since the COVID-19 pandemic, I have also seen patients who wonder whether a previous infection could explain a persistent decline in energy or performance. That possibility can be relevant in some cases, but in practice I try not to let the assessment stop at COVID alone.
When symptoms are persistent or otherwise warrant further investigation, the laboratory work-up may be broader and guided by the overall clinical picture. Depending on the presentation, this can include basic blood tests as well as selected investigations for other infectious causes, such as EBV or borreliosis, and in some cases tests related to HIV, autoimmune disease, or rheumatological conditions.
From a clinical perspective, the important point is that post-infectious fatigue is a differential diagnosis rather than an automatic explanation. If an athlete remains unusually fatigued after an infection, I find it more useful to assess the wider medical context than to assume that the previous infection must explain everything.
Suppressed thyroid function
Thyroid-hormone changes are another consideration worth ruling in or out — see my full guide on thyroid function in athletes for more on interpreting thyroid markers in athletes, including why a standard panel doesn’t always tell the full story. A controlled study in regularly menstruating women found that four days of low energy availability — independent of how much exercise was actually performed — reduced T3 by 15% and free T3 by 18%, while reverse T3 rose by 24%; exercise volume and intensity on their own, with adequate energy intake, produced none of these changes [13]. That’s a fairly direct demonstration that it’s the energy deficit, not the training itself, driving these low-T3 thyroid-hormone changes in this experimental model — a plausible physiological link to the thyroid changes sometimes seen alongside RED-S, though this particular study didn’t measure how often the two co-occur.
Population data points in a similar direction: an NHANES-based analysis found daily physical activity was negatively associated with T4 levels [14]. Separately, a small study of collegiate female endurance runners found that season-long percentage change in T3 correlated with end-of-season running performance, even though average TSH, T3, and T4 levels didn’t change significantly across the season [17]. In my own clinical view, low T3 without an accompanying rise in TSH is easy to write off as “within normal range” on a standard panel, since it doesn’t look like classical hypothyroidism — but for an athlete relying on a normal metabolic rate to support training adaptation, it’s worth taking seriously.
In practice, the main reason I assess thyroid function in an athlete with fatigue or declining performance is still the same as in other patients: to look for genuine thyroid disease, particularly hypothyroidism and, when relevant, hyperthyroidism. Being an athlete does not create a separate set of diagnostic criteria for primary thyroid disease.
That distinction is clinically useful. Training status and energy availability may affect thyroid physiology, but the basic interpretation of TSH and free T4 still follows the same medical principles used in non-athletic patients. I therefore try to separate potentially adaptive or energy-related hormonal changes from findings that may warrant evaluation as thyroid disease in their own right.
Conclusion: Why Is My Performance Declining?
Declining performance is a symptom, not a diagnosis. In my clinical experience, the most useful approach is rarely to search for one perfect biomarker or to assume that the athlete is simply overtrained. Training load matters, but so do sleep, energy availability, iron status, recent illness, thyroid function, psychological stress, and everything else happening outside sport.
The real value of the assessment comes from putting those pieces together. A mildly abnormal laboratory value, a poor HRV trend, or a difficult training block may provide useful context, but none of them necessarily explains the whole picture on its own. When performance continues to drift in the wrong direction, I find it more useful to step back, look at the athlete as a whole, and work through the plausible contributors systematically rather than forcing the symptoms into a single explanation.
References
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