Overtraining Syndrome: a practical guide
Jeffrey B. Kreher, MD,
Jennifer B. Schwartz, MD
Department of Orthopaedic Surgery—Pediatric Orthopaedics, Massachusetts
General Hospital for Children, Boston, Massachusetts and
Department of Family
Medicine, Tufts University Family Medicine Residency at Cambridge Health Alliance,
*Address correspondence to Jeffrey B. Kreher, MD, Department of Orthopaedic
Surgery—Pediatric Orthopaedics, Massachusetts General Hospital for Children, Yawkey
Center for Outpatient Care, Suite 3400, 55 Fruit Street, Boston, MA 02114 (e-mail:
Context: Fatigue and underperformance are common in athletes. Understanding
overtraining syndrome is helpful in the evaluation, management, and education of
Evidence Acquisition: Relevant articles in English were searched with OVID (1948-
2011) and PubMed using keywords below and bibliographies were reviewed for
Results: OTS appears to be a maladapted response to excessive exercise without
adequate rest resulting in perturbations of multiple body systems (neurologic,
endocrinologic, immunologic) coupled with mood changes. Many hypotheses of OTS
pathogenesis are reviewed and a clinical approach to athletes with possible OTS
(including history, testing, and prevention) is presented.
Conclusions: Overtraining syndrome remains a clinical diagnosis with arbitrary
definitions per the European College of Sports Science (ECSS) Position Statement.
History and, in most situations, limited serologies are helpful. However, much remains
to be learned given most past research has been on athletes with overreaching rather than
overtraining syndrome (OTS), overtraining, overreaching, unexplained
underperformance, staleness, pathophysiology, management, treatment, evaluation
Generally speaking, athletes train to increase performance. Performance
increases are achieved through increased training loads. Increased loads are tolerated
only through interspersed periods of rest and recovery—training periodization.
Overreaching is considered an accumulation of training load that leads to performance
decrements requiring days to weeks for recovery.
Overreaching followed by
appropriate rest can ultimately lead to performance increases.
overreaching is extreme and combined with an additional stressor, overtraining syndrome
(OTS) may result.
OTS may be caused by systemic inflammation and subsequent
effects on the central nervous system including depressed mood, central fatigue, and
resultant neurohormonal changes.
This article summarizes previous literature and
updates the European College of Sport Science (ECSS) Position Statement.
Definitions from the ECSS Position Statement on OTS will be used.
Symptoms of nonfunctional overreaching (NFO) and OTS are varied, nonspecific,
anecdotal, and numerous. (Table 2)
Past terminology includes burnout, staleness, failure adaptation, underrecovery,
training stress syndrome, and chronic fatigue. Some researchers refer to overtraining as
unexplained underperformance syndrome (UUPS).
Differentiation of NFO and OTS
is clinically difficult and can often only be made after a period of complete rest. The
difference between the two is based on time to recovery and not necessarily the degree or
type of symptoms.
Many consider overreaching and overtraining as a continuum.
anecdotal evidence suggesting NFO precedes OTS. Unfortunately, much of the
literature has been done on overreached rather than overtrained athletes by current
terminology. Some studies used “overtrained athletes” but failed to show these athletes
suffered from performance impairment.
Recent reports highlight the importance of
psychological and/or social stressors in addition to physiologic stress in the development
An individual’s stress capacity plays a role in the development of
Epidemiologic studies use varied terminology. It appears that OTS is extremely
rare, but exact prevalence and incidence data are lacking.
One study found
a NFO lifetime prevalence of ~60% in elite male and female runners compared with 33%
in non-elite female runners.
A multi-center, multi-country survey found 35% of
adolescent swimmers had been “overtrained” at least once.
Estimates of “staleness”
were reported in 5-30% of swimmers over a season
and 15% of British elite
In the most recent survey of elite adolescent athletes ~30% reported NFO at
least once in their career—they averaged two episodes lasting four weeks. The risk was
significantly increased in individual sports, low physically demanding sports such as golf,
females, and elite athletes.
Numerous hypotheses have been proposed for OTS, each with strengths and
weaknesses. (Table 3) When attempting to understand OTS mechanistically and
clinically it is crucial to seek an explanation that accounts for the many symptoms of this
Low muscle glycogen can impair performance due to inadequate fuel for the work
Low muscle glycogen also results in increased oxidation and decreased
concentrations of branched chain amino acids (BCAA). This can alter synthesis of
central neurotransmitters involved in fatigue.
Because decrements in performance and
fatigue are hallmarks of OTS, decreased muscle glycogen may cause OTS.
While this association seems plausible, it has not been substantiated in the
literature. Swimmers who consume inadequate carbohydrates have more fatigue during
training, but do not necessarily suffer a performance decrement needed to diagnose OTS.
Even athletes who consume increased amounts of carbohydrates and maintain normal
glycogen levels can still become overtrained.
While low muscle glycogen levels may
be associated with exercise-induced fatigue, the link with OTS appears weak.
Central Fatigue Hypothesis:
OTS nearly always has disrupted mood, sleep, and behavior.
neurotransmitter serotonin (5-HT) is implicated in regulation of these functions;
therefore, alterations in 5-HT could lead to OTS.
5-HT is derived from
tryptophan. With exercise there is increased unbound tryptophan, which competes with
BCAAs for entry into the brain.
Exercise decreases levels of BCAAs due to
increased oxidation, favoring tryptophan entry in to the brain and conversion to 5-HT.
Increases in unbound tryptophan have been positively correlated with fatigue,
presumably due to increased serotonin synthesis in the brain.
reuptake inhibitors to athletes artificially increases 5-HT in the brain and reduces
Conversely, marathon runners receiving BCAA supplementation felt more
energized and mentally clear, possibly due to dampened 5-HT synthesis.
Fatigue in overtrained athletes may be due to increased sensitivity to 5-HT rather
than increased 5-HT.
Increased neurological sensitivity to a 5-HT agonist has been
reported in overtrained athletes.
Well trained athletes usually are less sensitive to 5-HT;
this adaptation may be lost in OTS.
There is fairly consistent evidence that concentrations of 5-HT precursors and
prolactin, an indirect measure of central 5-HT activity, are altered in excessive exercise,
but few studies have actually measured 5-HT activity in overtrained athletes. Mood
changes and fatigue are subjective, difficult to measure, and influenced by many
confounding factors. Therefore, 5-HT activity requires cautious interpretation.
Glutamine is integral for immune cell function.
It also plays a role in
DNA/RNA synthesis, nitrogen transport, gluconeogenesis and acid-base balance.
Decreased glutamine after exercise may be responsible for increased incidences of upper
respiratory tract infections (URTIs) in overtrained athletes.
Prolonged exercise (>2 hours) or repeated bouts of high intensity exercise can
transiently decrease plasma glutamine concentrations.
Low plasma glutamine
concentrations have been reported specifically in overtrained athletes.
represent overutilization and/or a decreased production by over-worked muscles.
It is unclear whether decreased glutamine influences immune cell function. In
vitro, immune cell function can be compromised when glutamine concentrations are
below physiological levels.
Despite decreased glutamine concentrations after exercise,
the amount of glutamine available to immune cells does not necessarily change.
Glutamine supplementation can restore physiological levels, but does not improve post
exercise impairment of immune cells.
Nevertheless, glutamine supplementation may
decrease early rates of infection amongst athletes.
Epidemiological data has shown athletes may be more susceptible to URTIs after
but there is no evidence that immunosuppression is greater in
athletes with NFO/OTS. In one study, 13% of overreached athletes compared with 56%
of non-overreached athletes reported URTIs.
Low plasma glutamine has been seen in
athletes with URTIs while others demonstrate the opposite.
Finally, glutamine levels
can be influenced by nutritional state, trauma, and infection.
Oxidative Stress Hypothesis:
Some oxidative stress is desired during exercise because reactive oxygen species
released from damaged muscles regulate cellular repair.
When oxidative stress
becomes pathologic, however, reactive oxygen species (i.e. superoxide, hydrogen
peroxide, and hydroxyl radical) can cause inflammation, muscle fatigue and soreness
with resultant inhibition of athletic performance.
Resting markers of oxidative stress are higher in overtrained athletes compared
Moreover, oxidative stress markers increase with exercise in the
Citrate synthase reflects oxidative capacity and is expected to
increase during endurance training. In an overreached rat model, citrate synthase activity
OTS athletes may have diminished responses to exercise-induced
stress and be more susceptible to oxidative damage.
It is unclear if the increased oxidative stress state is a trigger or result of OTS.
Clinically relevant research is limited. Moreover, confounding factors such as menstrual
cycles and estrogen’s anti-oxidative properties are unknown.
Autonomic Nervous System Hypothesis:
An imbalance in the autonomic nervous system can explain some symptoms of
OTS. Specifically, decreased sympathetic activation and parasympathetic dominance,
can lead to performance inhibition, fatigue, depression and bradycardia.
Reduced sympathetic activation in overtrained athletes is supported in some
studies by decreased nocturnal urinary catecholamine excretion.
excretion decreases with increasing fatigue and returns to baseline during recovery.
However, not all studies find this trend.
A decreased organ sensitivity to
catecholamines may also be responsible for symptoms of decreased sympathetic
Heart rate variability (HRV) has also been used as an indicator of autonomic
One study showed no difference in HRV between overtrained and control
athletes during sleep. However, a reduced HRV was seen soon after awakening in
overtrained athletes suggesting increased sympathetic tone.
Using HRV, studies have
indicated that the effects of intense training on automatic control may be reversible.
Balance between sympathetic and parasympathetic forces maybe restored after a week of
Alterations in the hypothalamic-pituitary-adrenal (HPA) and gonadal (HPG) axes
may be responsible for OTS. Endurance athletes may show subtle changes in function of
the HPA axis, and overtrained athletes can have alterations in cortisol, ACTH,
testosterone and other hormone levels.
Unfortunately, the current data is
contradictory as to patterns of these hormonal changes.
Alterations in the HPA and
HPG axes are individualized and depend on other factors including exercise capacity,
inherent vulnerability to stressors, and other hormonal levels.
No single hypothesis explains all aspects of OTS. The cytokine hypothesis
suggests OTS is a physiological (mal)adaptation to excess stress initiated by an
imbalance between training and recovery.
Muscle contraction and repetitive joint action cause microtrauma to tissues.
Adaptation through tissue healing and strengthening occurs via activation of a local
inflammatory response and recruitment of cytokines.
With continued intense training
and absence of adequate rest, this inflammatory response can become amplified, chronic,
. Eventually a systemic inflammatory response can result with
negative consequences throughout the body.
Implicated cytokines in OTS include IL-
1b, IL-6, and TNF-
Reduced muscle glycogen levels are frequently observed in overtrained athletes.
Decreased glycogen may be a consequence of OTS through cytokine mediated effects.
Cytokines acting on hunger centers in the hypothalamus induce anorexia resulting in
decreased glycogen stores.
Cytokines themselves may interfere with glucose transport
into muscle cells for glycogen synthesis. Studies have shown decreased concentrations
of GLUT-4 transporters in stressed muscles due to down regulation of protein synthesis
Decreased glycogen stores may account for feelings of heavy legs and
muscular fatigue in overtrained athletes.
Increased uptake of tryptophan into the brain and enhanced sensitivity to
serotonin have been postulated to induce fatigue and depression. The cytokine
hypothesis argues that serum tryptophan levels are actually decreased with systemic
inflammation like that seen in OTS. This is because tryptophan is used for the synthesis
of inflammatory related proteins. Reduced tryptophan levels have actually been
associated in many studies with depressive symptoms.
Behavioral and psychological changes seen in OTS can also be attributed to
cytokines. Pro-inflammatory IL-1b and TNF-
act on the brain to cause decreased
appetite, sleep disturbance and depression, referred to as “sickness” behavior. Cytokines
may act directly on central receptors, or they may activate the HPA axis and release of
stress hormones with similar peripheral effects.
There is evidence of elevated cytokine
levels in depressed patients and a precipitation of depressed mood with cytokine
administration to normal subjects offering credibility to the notion of cytokine-induced
mood changes in OTS.
Alterations in the HPA and HPG axes with a resultant decrease in
testosterone:cortisol ratios have been implicated in OTS. Pro-inflammatory cytokines are
potent activators of the HPA system which cause release of CRH, ACTH and cortisol.
These cytokines suppress testosterone through central inhibition.
Although patterns of
hormonal changes in OTS are varied, cytokine mediators may be responsible for some of
Plasma glutamine is decreased in overtrained athletes and this can be attributed to
its increased utilization for various cytokine-controlled processes. Glutamine is a
precursor for synthesis of inflammatory proteins which are up-regulated with
overtraining. IL-6 and TNF-
actually stimulate glutamine uptake into hepatocytes for
In addition, systemic inflammation induces a catabolic state with a
necessary increase in glucose and protein metabolism. Glutamine is a crucial element for
gluconeogenesis, and also essential in aiding renal nitrogen excretion with increased
As previously mentioned, increased susceptibility to infection in overtrained
athletes has previously been blamed on decreased glutamine without much support.
There are two subsets of T helper cells: TH1 lymphocytes associated with cell mediated
immunity and TH2 lymphocytes linked to humoral immunity. Which subset
predominates depends on the prevailing cytokine milieu. OTS causes activation of
cytokines which favor a TH2 lymphocyte profile. Indeed, multiple studies show
increases in TH2-favoring cytokines (IL-6, TNF-
, IL-10) after a marathon and no
detectable levels of TH1-related cytokines.
TH2 predominance causes increased
humoral immunity, but with a concomitant down-regulation of TH1 sponsored cell
mediated immunity and reduced protection against URTI.
The cytokine theory does provide a comprehensive paradigm to explain many
features of OTS. It views systemic inflammation as the underlying basis for overtraining
and draws parallels between overtraining and other stress conditions. Unlike many other
theories, it proposes to answer “why” OTS develops. It presents a primary stimulus that
causes activation of many biochemical pathways and correlates activation of these
pathways with symptoms observed in overtrained athletes.
Although mechanistically sophisticated, the theory does have some concerning
limitations. Despite a plausible correlation between cytokines and symptoms of
overtraining, there is scant evidence showing elevated cytokine levels in overtrained
Some studies have demonstrated acute increases in IL-2 and IL-6
following exercise, but long term responses to training were not explored.
specifically looked at overtrained cyclists, but found no changes in IL-6 or TNF-
It argued that because muscle contraction during cycling is largely
concentric, perhaps there is not a great enough degree of microtrauma to induce an
inflammatory cascade. This seems reasonable, but other studies have found increased IL-
6 levels in cyclists.
Athletes in many of the cytokine studies were quite fit at baseline
and so it is questionable whether conclusions drawn are similarly applicable to a general
population of athletes.
These are justifiable concerns, but it is uncertain whether they are enough to
discredit the mounting body of evidence linking cytokines with OTS. Once a definitive
correlation is demonstrated between elevated cytokine levels and overtrained athletes,
this could become the gold standard in explaining OTS. For now, patience is key as we
wait for new studies to reconcile theory and findings in athletes.
Patients will primarily present with unexplained underperformance. Diagnosis of
OTS is clinical and accomplished through history, which should demonstrate the
following: 1) decreased performance persisting despite weeks to months of recovery, 2)
disturbances in mood and 3) lack of signs/symptoms or diagnosis of other possible causes
The list of organic diseases that can result in underperformance
is extensive and not limited to the following: undiagnosed asthma/bronchial
hyperreactivity, thyroid disease, adrenal disease, diabetes mellitus or insipidus, iron
deficiency with or without anemia, infection (i.e. myocarditis, hepatitis, HIV, etc.), and
malnutrition (due to eating disorders, celiac sprue, etc.). An extensive nutrition history
should be obtained along with an assessment of caloric expenditure.
If an athlete presents with underperformance without a period of rest and
recovery, OTS can not be diagnosed. By definition, such patient has FO versus NFO
with possible OTS. The diagnosis from history can only be made in retrospect given the
definitions of NFO and OTS. If less than 14-21 days of rest are required for return to
previous performance, NFO would be diagnosed. If it has been greater than 14-21 days
of rest, OTS is diagnosed by some.
Often underperformance will be met with an increase in training volume and
intensity to improve results. History should include assessment of possible triggers
(Table 4). In addition, certain historical clues should raise suspicion of NFO/OTS over
organic diseases. These clues include the ability to start training session but inability to
complete and/or a loss of finishing kick.
While mood symptoms can coexist with
organic processes, the presence of pervasive mood changes in the proper setting may
signal NFO/OTS versus a primary mood disorder.
Ruling out organic diseases leading to underperformance is driven by history.
The sports medicine provider may consider screening tests to include: CMP (including
kidney function, potassium, magnesium, and glucose), CBC, ESR, CRP, iron studies,
creatine kinase (CK), and TSH. Metabolic issues (i.e. mitochondrial, glycogen storage,
and lipid peroxidation diseases) and cardiovascular disease should be considered in
athletes new to higher intensities and volumes.
Cardiovascular disease should be
investigated in master athletes or someone with a positive family history.
In one of the few studies describing evaluation of underperforming athletes, a
cause for repeated infections and/or fatigue was found in 68% of regional- or higher-level
athletes. Ninety-three percent of the athletes reported decreases in performance. Their
evaluation was significant for a more extensive and costly laboratory evaluation
including: B12, folate, serology for viral hepatitis, toxoplasmosis, CMV/EBV titers, EBV
DNA in saliva, serum and salivary immunoglobulins (serum IgG subclasses and specific
serum IgE to aeroallergens), and ANA.
Such extensive testing should be considered
only in the appropriate setting. In those athletes with atopic complaints (allergic rhinitis,
dyspnea and/or exertional cough, eczema), pulmonary function tests should be
Biochemical markers have been studied in a variety of athlete populations. There
have been no specific or sensitive levels defined for CK, urea, or iron.
oxidative stress biomarkers have been found to correlate well with training load and
but such markers remain impractical in standard laboratories.
Hematologic markers have also been disappointing. Recently plasma viscosity > 1.44
was found to be specific but not sensitive for NFO.
Immunologic markers have also been studied with variable results. Two studies
have found increased levels of T cell activation but such testing lacks practicality.
Most recent studies focus on salivary IgA. In endurance athletes, lower levels of salivary
IgA have been correlated with increased incidence of URTI symptoms.
showed 18-32% lower levels in athletes with symptoms of overtraining but no
performance measures were reported.
However, another study did not find a
statistically significant decrease of salivary IgA after intensified training in cyclists.
Most would agree that excessive exercise, FO, NFO, and OTS can result in impairment in
cell mediated immunity, but there does not appear to be an immunologic marker that
Hormonal markers have shown some promising results, but have a multitude of
confounding variables (i.e. diurnal and seasonal timing, phase of menstrual cycle,
nutritional status, etc.). Resting cortisol levels have not differentiated between athletes
with and without NFO/OTS. Testosterone results have been contradictory. Some have
suggested that a decreased testosterone:cortisol ratio can be diagnostic of NFO and/or
OTS. However, the ratio represents the physiologic strain of training rather than the
athlete’s maladaption to that stress. The utility of testosterone:cortisol ratio has not been
supported by the literature.
Cortisol has a peak during the day with nadir during night. AM cortisol does not
accurately reflect levels of free cortisol. Free cortisol is filtered by the kidney at a
constant rate and therefore 24-hour and overnight urinary free cortisol have been more
studied. However, even overnight excretion shows high interindividual variability.
Cortisol (catabolic and anti-inflammatory) is converted to inactive cortisone by 11
HSD2. A prospective study found a clinically significant increase in overnight urinary
cortisol:cortisone ratio during a high training load period in triathletes, who subsequently
underperformed and reported fatigue. It is proposed that cytokines may inhibit 11
HSD2 activity and result in relative increases in cortisol and hence catabolism.
However, overnight urinary cortisol:cortisone ratio remains in the research realm and
Clinically it would be helpful to know what level of training signals the change
from FO to NFO and from NFO to OTS. However, there are no specific and validated
blood markers for NFO or OTS.
Therefore, some have focused on physiologic tests. A
couple recent studies show promise for discriminating NFO from OTS. A two-bout
maximal exercise protocol reportedly diagnoses FO, NFO, and OTS by investigating the
HPA axis response.
The bouts of maximal exercise are separated by four hours. It is
believed FO, NFO, and OTS represent a disturbance, an adaptation and eventual
maladaption of the HPA axis. In an early study FO athletes had a less pronounced
hormonal response to a second bout of maximal exercise in comparison to the extremely
exaggerated response in NFO athletes.
These findings were in contrast to the extreme
response to the first bout of exercise and absence of response to the second bout in OTS
This first study displayed great utility in picking up FO before NFO.
most recent study of two-bout maximal exercise protocol, reliable differentiation of NFO
from OTS was achieved. However, the diagnosis of NFO and OTS was made
retrospectively and arbitrarily defined OTS as greater than one year of symptoms.
Athletes were tested after having symptoms ranging from two weeks to one year and
prospectively followed for resolution of symptoms. After a second bout, NFO athletes
showed very large increases in ACTH and prolactin whereas OTS athletes showed absent
or very limited increases. They propose the different responses are due to
hypersensitivity of glucocorticoid receptors in NFO compared to insensitivity in OTS.
This would seem to confirm a disturbance in the HPA and give credence to the close
relationship between OTS and other stress related syndromes such as major depression
and post traumatic stress disorder.
If findings can be replicated, two-bout maximal
exercise protocol may have prognostic value by identifying athletes requiring greater than
one year to recover.
Physiologic testing with resting heart rate, maximal heart rate, and HRV do not
show consistent results nor do they allow differentiation of FO, NFO, and OTS.
Researchers have argued that use of performance tests for diagnosis is “polluted” by the
underperformance inherent to NFO and OTS.
However, the most consistent finding is a
diminished maximal lactate in OTS, but it was not sensitive enough to rule out NFO.
an analysis of the literature, greater performance decreases were found in studies that
report time to fatigue versus studies that report more functional performance measures
(i.e. 100 or 400 meter swim, 15 minute time trial).
Most agree that psychological distress is required for diagnosis of OTS. The best
studied measure is Profile of Mood States (POMS) scores. In two studies, 81% of “stale”
swimmers were identified with the POMS questionnaire.
However, increased scores
can be seen in athletes with increased training without FO/NFO
and have not always
been reported with performance measures.
Regardless, mood questionnaires can be
prospectively followed, are cheap, and are quickly available. Variables such as timing of
testing in relation to training must be standardized. In a case study of an NFO athlete, it
was suggested that decreased POMS vigor score may be more specific to overreaching
than the POMS fatigue score. It is suggested that fatigue is a “normal experience” in
athletes whereas decreased vigor can be viewed as maladaptive.
Treatment varies based on the etiology for the underperformance. First, any
organic disease should be treated appropriately. No treatment is required for FO other
than balancing overload training with appropriate recovery. Treatment of NFO and OTS
is rest; however, some propose that relative rest is more appropriate.
suggest a management strategy focused on cross training to avoid the desire to increase
intensity too quickly. It is recommended to build up volume prior to intensity starting
from 5-10 minutes daily till one hour is tolerated.
It is unclear which strategy is best so
the motivation for exercise, internal versus external, should be considered when
recommending complete versus relative rest. Given the significant psychological
overlay, one may consider involving a sports psychologist or other mental health expert
in multidisciplinary management. If stress, depression, and/or anxiety are increased with
full rest, relative rest with well defined expectations should be provided.
Treatment with selective serotonin reuptake inhibitor (SSRI) is suggested by some
based on similarities between neuroendocrinologic changes between depression and
However, one should be cautious of increased heat stress and possible
decreased performance with antidepressant treatment in athletes. In addition, if sleep
complaints are prominent, treatment with trazodone or amitriptyline could be
Given the unethical nature of inducing OTS in athletes and uncertain
pathogenesis, there are no evidence-based means of preventing OTS. However,
observation of training load, performance measures, and mood questionnaires can help
interrupt the progression from FO to NFO/OTS. A study has shown a decrease in
“burnout” in collegiate swimmers from 10% to zero when altering training load in
response to POMS questionnaire. When the mood state decreased, training load was also
Major components of prevention are screening and education. One should
educate athletes at risk for overtraining that one of the initial signs of overreaching is
increased rating of perceived exertion (RPE) for a given work load.
In addition, sports
medicine providers may consider preemptively asking if training has increased to
compensate for decreases in performance. History of athletes should include inquiry
about training (monotony, excessive load, sudden increase, caloric/hydration needs in
relation to load) and personal (interpersonal, family, sleep, travel) stressors. (Tables 4 &
Some hope that a recently developed animal model of overtraining may help
guide further hypothesis testing of NFO and OTS.
A very promising technology being
studied in elite athletes is Fourier Transform Infrared (FT-IR) Spectroscopy. A group of
researchers are monitoring athletes prospectively and propose changes in metabolism can
be appreciated by FT-IR before symptoms and objective performance decrements are
Their results are very thought provoking but require
Others are suggesting further investigation of psychomotor speed testing as a
means of diagnosing OTS. In a survey of the literature, psychomotor speed is known to
be decreased in many different pathologies most notably major depression and chronic
fatigue syndrome, which share many characteristics with NFO/OTS. One study showed
differences in psychomotor speed between NFO/OTS athletes compared with control
athletes; therefore. However, a decrease in psychomotor speed was also found in
overload training without FO and in a second group that did show FO.
Overtraining syndrome remains a clinical diagnosis with arbitrary definitions per
the European College of Sports Science Position Statement.
History and, in most
situations, limited serologies are paramount. Many pathophysiologic hypotheses have
been proposed. Currently, it appears OTS represents a systemic inflammatory process
with diffuse effects on the neurohormonal axis affecting host immunology and mood.
OTS is a maladapted response to exercise when excessive and not matched with
Terminology from the European College of Sports Science Position
Statement on OTS should be used when appropriate.
But one may chose
to use “unexplained underperformance syndrome” (UUPS) to describe the
clinical presentation of many athletes.
Extensive history with minimal and focused laboratory evaluation (CMP,
CBC, ESR, CRP, iron studies, CK, and TSH) is most helpful in diagnosis
of overtraining syndrome, overreaching, or other potential etiologies.
Neither biochemical, hematologic, immunologic, and hormonal markers
nor physiologic tests can reliably differentiate overtraining syndrome from
However, a two-bout maximal exercise protocol may
prove helpful in certain situations.
The best treatment of overtraining syndrome is prevention and (relative)
If an organic disease is discovered it should be treated
Monitoring the Profile of Mood States (POMS) score and altering
workload in training may decrease risk of overreaching and overtraining
Table 1. Terminology from Position Statement on Overtraining by European College of
Synonym Definition Performance
Increased training leading to a
temporary (day to weeks)
performance decrement and
with improved performance
Days to weeks
Intense training leading to a
longer performance decrement
(weeks to months) but with
full recovery after rest.
Accompanied by increased
Negative due to
loss of training
Consistent with extreme NFO
a) longer performance
decrement (>2 months)
b) more severe
c) accompanied by an
d) not explained by other
Negative due to
possible end to
Table 2. Summary of symptoms of OTS.
(more common in aerobic sports)
(more common in anaerobic sports)
Fatigue Insomnia Anorexia
Depression Irritability Weight loss
Bradycardia Agitation Lack of mental
Loss of motivation Tachycardia Heavy, sore, stiff
Table 3. Common hypotheses of OTS etiology (arranged in order of complexity).
THEORY STRENGTHS WEAKNESSES
• Low glycogen can be correlated
with decreased performance and
• No proven correlation in the literature
between low glycogen and overtrained
• Athletes with normal glycogen levels
still became overtrained
• Doesn’t account for all symptoms
in the brain leads
to increased 5-HT
• Exercise correlated with increased
tryptophan, 5-HT, and fatigue
• Rats undergoing intense training
have increased 5-HT
• SSRIs decrease performance
• Athletes getting BCAA supplement
had less fatigue
• Few studies measure 5-HT directly
• Mood changes/fatigue subjective and
difficult to study
• Mood/fatigue influenced by many
• Doesn’t account for all symptoms
• Glutamine does decrease after
• In vitro, immune cell function is
compromised with decreased
• Athletes are more susceptible to
URTIs after “intense” exercise
• In vivo, decreased plasma glutamine
not necessarily correlated with
decreased bio available glutamine
• Glutamine supplementation does not
improve post exercise impairment of
• Some studies show low glutamine in
athletes with URTIs and some do not
• Glutamine can be influenced by many
• Increased URTIs are seen in most
athletes after intense exercise and not
just overtrained ones
• Doesn’t account for all symptoms
• Resting markers of oxidative stress
higher in overtrained athletes and
further increase with exercise
• Citrate synthase (marker of
oxidative capacity) decrease in
overreached rats so more
susceptible to oxidative stress
• Studies have been small
• Lack of clinically relevant research
• Doesn’t account for all symptoms
• A study showed variability in ANS
forces (through HRV) with exercise
• Decreased HRV with awakening in
overtrained athletes suggests
disruption of ANS modulation
• Decreased nocturnal catecholamines
in overtrained athletes in some studies,
no change or increased in other studies
• Studies looking at catecholamine
excretion with methodological
differences and hard to compare
• No difference in HRV/ANS influence
between overtrained and control
athletes during sleep, when free of
• Doesn’t account for all symptoms
axes cause many
• Endurance athletes have activation
of the HPA axis compared to
• Contradictory data in terms of
activation of HPA/HPG axes in
overtrained athletes and levels of
ACTH, cortisol, testosterone
• Other factors can influence HPA/HPG
• Doesn’t account for all symptoms
causes most of
the above effects
and symptoms of
• Unified theory accounting for many
symptoms of OTS and “why” it
• Cytokines may act on hypothalamic
centers to regulate “sickness”
behavior, causing mood changes
• Little evidence actually verifying
increased cytokines in overtrained
• No studies looked at long term
responses to (over)training
• One study showed no change in
• Subacute muscle injury and
cytokines decreases glucose
transport into muscles, decreases
glycogen, causes fatigue
• Tryptophan used to synthesize
inflammatory proteins and
decreases with systemic
• Decreased tryptophan associated
with depressive symptoms
• Increased cytokine levels found in
• Giving normal subjects cytokines
caused depressive symptoms
• Cytokines activate the HPA system
(increase cortisol) and inhibit the
HPG system (decrease testosterone)
• Inflammation causes activation of
glucose/protein metabolism and
• Increased cytokines that favor TH2
lymphocyte activation lead to
increased humoral/decreased cell
mediated immunity and more URTI
cytokine levels in overtrained cyclists
• Cytokine studies to date look
predominantly at very fit athletes with
questionable application to the general
Table 4. Potential (anecdotal) triggers of OTS.
Increased training load without adequate recovery
Monotony of training
Excessive number of competitions
Stressors including personal life (family, relationships) and occupational
Heat injury episode
Table 5. Preventative measures for NFO/OTS.
Periodization of training
Tapering for competition
Adjust training volume and intensity based on performance and mood
Ensure adequate calories for training load
Ensure adequate hydration
Ensure adequate carbohydrate ingestion during exercise
Ensure adequate sleep
Promoting mental toughness or resilience as buffer
Rest period of greater than 6 hours between exercise bouts
Abstinence of training following infection, heat stroke/stress, periods of high stress
Avoid extreme environmental conditions
Utilize POMS (or stress level) and alter training load
Concentric Muscle Action
(Repetitive Motion Injury)
Local Acute Inflammation
Local Chronic Inflammation
Systemic Inflammatory Response
IL-6 (pro- and anti-inflammatory)
Figure 1. Proposed etiology of OTS through exercise and resultant inflammation. There is
a time-dependant sensitization with amplification at each step to repeated intermittent
stimuli over time.
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