What is overtraining syndrome
Overtraining syndrome appears to be a maladapted response to excessive exercise without adequate rest, resulting in disturbances of multiple body systems (neurologic, endocrinologic, immunologic) coupled with mood changes 1). Past terminology includes burnout, “staleness”, failure adaptation, under-recovery, training stress syndrome, and chronic fatigue. Some researchers refer to overtraining as unexplained underperformance syndrome 2). However, overtraining syndrome remains a clinical diagnosis with arbitrary definitions per the European College of Sports Science’s position statement 3).
Table 1. Terminology from position statement on overtraining by European College of Sport Science
|Functional overreaching (FO)||Short-term overreaching||Increased training leading to a temporary performance decrement and with improved performance after rest||Days to weeks||Positive (super- compensation)|
|Nonfunctional overreaching (NFO)||Long-term overreaching||Intense training leading to a longer performance decrement but with full recovery after rest; accompanied by increased psychologic and/or neuroendocrinologic symptoms||Weeks to months||Negative due to symptoms and loss of training time|
|Overtraining syndrome||Consistent with extreme nonfunctional overreaching but with (1) longer performance decrement (> 2 months), (2) more severe symptomatology and maladapted physiology (psychologic, neurologic, endocrinologic, immunologic systems), (3) and an additional stressor not explained by other disease||Months||Negative due to symptoms and possible end to athletic career|
Differentiation of nonfunctional overreaching (NFO) and overtraining syndrome is clinically difficult and can be made often only after a period of complete rest 5). The difference between the 2 is based on time to recovery and not necessarily the degree or type of symptoms 6).
Many consider overreaching and overtraining as a continuum 7). Others question anecdotal evidence suggesting that nonfunctional overreaching (NFO) precedes overtraining syndrome 8). 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 that these athletes suffered from performance impairment 9). Recent reports highlight the importance of psychological and/or social stressors in addition to physiologic stress in the development of nonfunctional overreaching/overtraining syndrome 10). An individual’s stress capacity plays a role in the development of nonfunctional overreaching/overtraining syndrome 11).
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 12). Overreaching followed by appropriate rest can ultimately lead to performance increases 13). However, if overreaching is extreme and combined with an additional stressor, overtraining syndrome (OTS) may result 14). Overtraining syndrome may be caused by systemic inflammation and subsequent effects on the central nervous system, including depressed mood, central fatigue, and resultant neurohormonal changes 15).
Table 2. Symptoms of overtraining syndrome
|Parasympathetic Alterationsa||Sympathetic Alterationsb||Other|
|Bradycardia||Agitation||Lack of mental concentration|
|Loss of motivation||Tachycardia||Heavy, sore, stiff muscles|
Epidemiologic studies use varied terminology. It appears that Overtraining Syndrome is extremely rare, but exact prevalence and incidence data are lacking. *One study found a nonfunctional overreaching (NFO) lifetime prevalence of ~60% in elite male and female runners, compared with 33% in nonelite female runners 17). A multicenter, multicountry survey found that 35% of adolescent swimmers had been “overtrained” at least once 18). Estimates of “staleness” were reported in 5% to 30% of swimmers over a season 19) and in 15% of British elite athletes 20). In the most recent survey of elite adolescent athletes, ~30% reported nonfunctional overreaching (NFO) at least once in their careers—they averaged 2 episodes lasting 4 weeks. The risk was significantly increased in individual sports, low physically demanding sports (such as golf), females, and elite athletes 21).
Causes of Overtraining Syndrome
Numerous hypotheses have been proposed for Overtraining Syndrome, each with strengths and weaknesses (Table 3). In attempting to understand Overtraining Syndrome mechanistically and clinically, it is crucial to seek an explanation that accounts for the many symptoms of this complicated entity.
Table 3. Common hypotheses of overtraining syndrome etiology (arranged in order of complexity)
|Glycogen hypothesis||Decreased glycogen causes fatigue and decreased performance||Low glycogen can be correlated with decreased performance and exercise-induced fatigue||No proven correlation in the literature between low glycogen and overtrained athletes|
Athletes with normal glycogen levels still become overtrained
Does not account for all symptoms
|Central fatigue hypothesis||Increased tryptophan uptake in the brain leads to increased 5-HT centrally and mood symptoms||Exercise correlated with increased tryptophan, 5-HT, and fatigue|
Rats undergoing intense training have increased 5-HT
Selective serotonin reuptake inhibitors decrease performance
Athletes getting branched chain amino acids supplement had less fatigue
|Few studies measure 5-HT directly|
Mood changes/fatigue subjective and difficult to study
Mood/fatigue influenced by many other factors
Does not account for all symptoms
|Glutamine hypothesis||Decreased glutamine causes immune dysfunction and increased susceptibility to infection||Glutamine does decrease after prolonged exercise|
In vitro immune cell function is compromised with decreased glutamine
Athletes are more susceptible to upper respiratory tract infections after “intense” exercise
|In vivo, decreased plasma glutamine not necessarily correlated with decreased bioavailable glutamine|
Glutamine supplementation does not improve postexercise impairment of immune cells
Some studies show low glutamine in athletes with upper respiratory tract infections, and some do not
Glutamine can be influenced by many other factors
Increased upper respiratory tract infections are seen in most athletes after intense exercise, not just overtrained ones
Does not account for all symptoms
|Oxidative stress hypothesis||Excessive oxidative stress causes muscle damage and fatigue||Resting markers of oxidative stress are higher in overtrained athletes and increase with exercise|
Citrate synthase (marker of oxidative capacity) decreases in overreached rats, so they are more susceptible to oxidative stress
|Studies have been small|
Lack of clinically relevant research
Does not account for all symptoms
|Autonomic nervous system hypothesis||Parasympathetic predominance causes many symptoms of overtraining syndrome||A study showed variability in autonomic nervous system forces (through heart rate variability) with exercise versus rest|
Decreased heart rate variability with awakening in overtrained athletes suggests disruption of autonomic nervous system modulation
|Decreased nocturnal catecholamines in overtrained athletes in some studies; no change or increased in others|
Studies looking at catecholamine excretion with methodological differences are hard to compare
No difference in heart rate variability/autonomic nervous system influence between overtrained and control athletes during sleep, when free of external influences
Does not account for all symptoms
|Hypothalamic hypothesis||Dysregulation of the hypothalamus and hormonal axes cause many symptoms of overtraining syndrome||Endurance athletes have activation of the hypothalamic-pituitary-adrenal axis compared with controls||Contradictory data in terms of activation of hypothalamic-pituitary-adrenal/hypothalamic-pituitary-gonadal axes in overtrained athletes and levels of ACTH, cortisol, testosterone|
Other factors can influence hypothalamic-pituitary-adrenal/hypothalamic-pituitary-gonadal axis activation
Does not account for all symptoms
|Cytokine hypothesis||Inflammation and cytokine release causes most of the above effects and symptoms of overtraining syndrome||Unified theory accounting for many symptoms of overtraining syndrome and “why” it develops|
Cytokines may act on hypothalamic centers to regulate “sickness” behavior, causing mood changes and fatigue
Subacute muscle injury and cytokines decreases glucose transport into muscles, decreases glycogen, and causes fatigue
Tryptophan is used to synthesize inflammatory proteins and decreases with systemic inflammation
Decreased tryptophan is associated with depressive symptoms
Increased cytokine levels are found in depressed patients
Giving participants cytokines caused depressive symptoms
Cytokines activate the hypothalamic-pituitary-adrenal system (increasing cortisol) and inhibit the hypothalamic-pituitary-gonadal system (decreasing testosterone)
Inflammation causes activation of glucose/protein metabolism and decreased glutamine
Increased cytokines that favor TH2 lymphocyte activation lead to increased humoral/decreased cell-mediated immunity and more upper respiratory tract infection
|Little evidence actually verifying increased cytokines in overtrained athletes|
No studies looked at long-term responses to training/overtraining
One study showed no change in cytokine levels in overtrained cyclists
Cytokine studies to date look predominantly at very fit athletes with questionable application to the general population
Diagnosis of Overtraining Syndrome
Patients will primarily present with unexplained underperformance. Diagnosis of Overtraining Syndrome is clinical and accomplished through history, which should demonstrate the following 23):
- Decreased performance persisting despite weeks to months of recovery,
- Disturbances in mood, and
- Lack of signs/symptoms or diagnosis of other possible causes of underperformance.
The list of organic diseases that can result in underperformance is extensive and not limited to the following 24):
- undiagnosed asthma/bronchial hyperreactivity,
- thyroid disease,
- adrenal disease,
- diabetes mellitus
- diabetes insipidus,
- iron deficiency with or without anemia,
- infection (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, Overtraining Syndrome cannot be diagnosed. By definition, such patient has functional overreaching (FO) versus nonfunctional overreaching (NFO) with possible Overtraining Syndrome 25). The diagnosis from history can be made only in retrospect given the definitions of nonfunctional overreaching (NFO) and overtraining syndrome. If less than 14 to 21 days of rest are required for return to previous performance, nonfunctional overreaching (NFO) would be diagnosed. If it has been greater than 14 to 21 days of rest, Overtraining Syndrome is diagnosed by some 26).
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) 27). In addition, certain historical clues should raise suspicion of nonfunctional overreaching (NFO)/overtraining syndrome over organic diseases. These clues include the ability to start a training session but the inability to complete and/or a loss of finishing kick 28). While mood symptoms can coexist with organic processes, the presence of pervasive mood changes in the proper setting may signal nonfunctional overreaching (NFO)/overtraining syndrome versus a primary mood disorder 29).
Table 4. Potential triggers of overtraining syndrome
|Increased training load without adequate recovery|
|Monotony of training|
|Excessive number of competitions|
|Stressors including personal life (family, relationships) and occupational|
|Heat injury episode|
Testing for overtraining syndrome
Ruling out organic diseases leading to underperformance is driven by history 31). The sports medicine provider may consider screening tests to include comprehensive metabolic panel (including kidney function, potassium, magnesium, and glucose), complete blood count, erythrocyte sedimentation rate, C-reactive protein, iron studies, creatine kinase, and thyroid stimulating hormone. Metabolic issues (ie, mitochondrial, glycogen storage, and lipid peroxidation diseases) and cardiovascular disease should be considered in athletes new to higher intensities and volumes 32). 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 33). Ninety-three percent of the athletes reported decreases in performance. This evaluation was significant for a more extensive and costly laboratory evaluation, including B12, folate, serology for viral hepatitis, toxoplasmosis, cytomegalovirus/Epstein-Barr virus titers, Epstein-Barr virus DNA in saliva, serum and salivary immunoglobulins (serum immunoglobulin G subclasses and specific serum immunoglobulin E to aeroallergens), and antinuclear antibodies 34). 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 considered 35).
Biochemical markers have been studied in a variety of athlete populations. There have been no specific or sensitive levels defined for creatine kinase, urea, or iron 36). Recently, oxidative stress biomarkers have been found to correlate well with training load and overreached status,26 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 37).
Immunologic markers have also been studied with variable results. Two studies have found increased levels of T cell activation, but such testing lacks practicality 38). Most recent studies focus on salivary immunoglobulin A. In endurance athletes, lower levels of salivary immunoglobulin A have been correlated with increased incidence of upper respiratory tract infection symptoms 39). One study showed 18% to 32% lower levels in athletes with symptoms of overtraining, but no performance measures were reported 40). However, another study did not find a statistically significant decrease of salivary immunoglobulin A after intensified training in cyclists 41). Most would agree that excessive exercise, functional overreaching (FO), nonfunctional overreaching (NFO) and Overtraining Syndrome can result in impairment in cell-mediated immunity, but there does not appear to be an immunologic marker that differentiates them 42).
Hormonal markers have shown some promising results but have a multitude of confounding variables (ie, diurnal and seasonal timing, phase of menstrual cycle, nutritional status) 43). Resting cortisol levels have not differentiated between athletes with and without nonfunctional overreaching (NFO) or Overtraining Syndrome. Testosterone results have been contradictory. Some have suggested that a decreased testosterone:cortisol ratio can be diagnostic of nonfunctional overreaching (NFO) and/or Overtraining Syndrome. 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 44).
Cortisol has a peak during the day with nadir during night 45). Morning cortisol does not accurately reflect levels of free cortisol 46). Free cortisol is filtered by the kidney at a constant rate; therefore, 24-hour and overnight urinary-free cortisol have been more studied 47). However, even overnight excretion shows high interindividual variability 48). Cortisol (catabolic and anti-inflammatory) is converted to inactive cortisone by 11β-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 49). It is proposed that cytokines may inhibit 11β-HSD2 activity and result in relative increases in cortisol and, hence, catabolism 50). However, overnight urinary cortisol:cortisone ratio remains in the research realm and awaits validation.
Clinically, it would be helpful to know what level of training signals the change from functional overreaching (FO) to nonfunctional overreaching (NFO) and from nonfunctional overreaching (NFO) to overtraining syndrome. However, there are no specific and validated blood markers for nonfunctional overreaching (NFO) or overtraining syndrome 51). Therefore, some have focused on physiologic tests. A couple recent studies show promise for discriminating nonfunctional overreaching (NFO) from overtraining syndrome. A 2-bout maximal exercise protocol reportedly diagnoses functional overreaching (FO), nonfunctional overreaching (NFO) and overtraining syndrome by investigating the HPA (hypothalamic-pituitary-adrenal) axis response 52). The bouts of maximal exercise are separated by 4 hours. It is believed that functional overreaching (FO), nonfunctional overreaching (NFO) and overtraining syndrome represent a disturbance, an adaptation, and eventual maladaption of the HPA (hypothalamic-pituitary-adrenal) axis. In an early study, functional overreaching (FO) athletes had a less pronounced hormonal response to a second bout of maximal exercise in comparison with the extremely exaggerated response in nonfunctional overreaching (NFO) athletes 53). These findings were in contrast to the extreme response to the first bout of exercise and absence of response to the second bout in overtraining syndrome athletes 54). This first study displayed great utility in picking up functional overreaching (FO) before nonfunctional overreaching (NFO) 55). In the most recent study of 2-bout maximal exercise protocol, reliable differentiation of nonfunctional overreaching (NFO) from overtraining syndrome was achieved. However, the diagnosis of nonfunctional overreaching (NFO) and overtraining syndrome was made retrospectively and arbitrarily defined overtraining syndrome as greater than 1 year of symptoms. Athletes were tested after having symptoms ranging from 2 weeks to 1 year and prospectively followed for resolution of symptoms. After a second bout, nonfunctional overreaching (NFO) athletes showed very large increases in adrenocorticotropic hormone and prolactin, whereas overtraining syndrome athletes showed absent or very limited increases. The study’s authors propose that the different responses are due to hypersensitivity of glucocorticoid receptors in nonfunctional overreaching (NFO) compared with insensitivity in overtraining syndrome. This would seem to confirm a disturbance in the HPA (hypothalamic-pituitary-adrenal) axis and give credence to the close relationship between overtraining syndrome and other stress-related syndromes, such as major depression and posttraumatic stress disorder 56). If findings can be replicated, 2-bout maximal exercise protocol may have prognostic value by identifying athletes requiring greater than 1 year to recover.
Physiologic testing with resting heart rate, maximal heart rate, and heart rate variability do not show consistent results, nor do they allow differentiation of FO, NFO, and overtraining syndrome. Researchers have argued that use of performance tests for diagnosis is “polluted” by the underperformance inherent to NFO and overtraining syndrome 57). However, the most consistent finding is a diminished maximal lactate in overtraining syndrome, but it was not sensitive enough to rule out NFO 58). In 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 (ie, 100- or 400-m swim, 15-minute time trial) 59).
Most agree that psychological distress is required for diagnosis of overtraining syndrome. The best-studied measure is Profile of Mood States scores. In 2 studies, 81% of “stale” swimmers were identified with the Profile of Mood States questionnaire 60). However, increased scores can be seen in athletes with increased training without FO/NFO 61) and have not always been reported with performance measures 62). 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 Profile of Mood States vigor score may be more specific to overreaching than the Profile of Mood States fatigue score. It is suggested that fatigue is a “normal experience” in athletes, whereas decreased vigor can be viewed as maladaptive 63).
Treatment of overtraining syndrome
Treatment varies based on the etiology for the underperformance 64), and any organic disease should be treated appropriately. No treatment is required for FO other than balancing overload training with appropriate recovery 65). Treatment of NFO and overtraining syndrome is rest; however, some propose that relative rest is more appropriate 66). It is recommended to build up volume prior to intensity, starting from 5 to 10 minutes daily until 1 hour is tolerated 67). 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 68). If stress, depression, and/or anxiety are increased with full rest, relative rest with well-defined expectations should be provided 69).
Treatment with selective serotonin reuptake inhibitor is suggested by some based on similarities between neuroendocrinologic changes between depression and overtraining syndrome 70). 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 considered 71).
Prevention of overtraining syndrome
Given the unethical nature of inducing overtraining syndrome in athletes and uncertain pathogenesis, there are no evidence-based means of preventing overtraining syndrome. However, observation of training load, performance measures, and mood questionnaires can help interrupt the progression from FO to NFO/overtraining syndrome 72). A study has shown a decrease in “burnout” in collegiate swimmers from 10% to zero when altering training load in response to the Profile of Mood States questionnaire. When the mood state decreased, training load was also decreased 73).
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 for a given workload 74). 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 stressors (interpersonal, family, sleep, travel) (Tables 5).
Table 5. Preventative measures for nonfunctional overreaching/overtraining syndrome
|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 Profile of Mood States (or stress level) and alter training load|
References [ + ]
|1, 16, 22.||↵||Kreher JB, Schwartz JB. Overtraining Syndrome: A Practical Guide. Sports Health. 2012;4(2):128-138. doi:10.1177/1941738111434406. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3435910/|
|2.||↵||Elucidating the unexplained underperformance syndrome in endurance athletes : the interleukin-6 hypothesis. Robson P. Sports Med. 2003; 33(10):771-81. https://www.ncbi.nlm.nih.gov/pubmed/12895132/|
|3, 4, 12, 14, 23, 24, 25, 26, 27, 30, 31, 42, 43, 58, 64, 65, 68, 69, 72.||↵||Meeusen R, Duclos M, Gleeson M, et al. Prevention, diagnosis and treatment of the overtraining syndrome: ECSS Position Statement Task Force. Eur J Sport Sci. 2006;6(1):1-14|
|5, 6.||↵||Psychomotor speed: possibly a new marker for overtraining syndrome. Nederhof E, Lemmink KA, Visscher C, Meeusen R, Mulder T. Sports Med. 2006; 36(10):817-28.|
|7.||↵||Overtraining in athletes. An update. Fry RW, Morton AR, Keast D. Sports Med. 1991 Jul; 12(1):32-65.|
|8, 9, 13.||↵||Does overtraining exist? An analysis of overreaching and overtraining research. Halson SL, Jeukendrup AE. Sports Med. 2004; 34(14):967-81.|
|10.||↵||Tenenbaum G, Jones CM, Kitsantas A, et al. Failure adaptation: psychological conceptualization of the stress response process in sport. Int J Sport Psychol. 2003;34:1-26|
|11.||↵||Overtraining and recovery. A conceptual model. Kenttä G, Hassmén P. Sports Med. 1998 Jul; 26(1):1-16.|
|15.||↵||Overtraining, excessive exercise, and altered immunity: is this a T helper-1 versus T helper-2 lymphocyte response? Lakier Smith L. Sports Med. 2003; 33(5):347-64.|
|17.||↵||Psychological characterization of the elite female distance runner. Morgan WP, O’Connor PJ, Sparling PB, Pate RR. Int J Sports Med. 1987 Nov; 8 Suppl 2():124-31.|
|18.||↵||Raglin J, Sawamura S, Alexiou S, et al. Training practice and staleness in 13-18-year-old swimmers: a cross-cultural study. Pediatr Exerc Sci. 2000;12:61-70|
|19.||↵||Hooper S, MacKinnon LT, Hanrahan S. Mood states as an indication of staleness and recovery. Int J Sport Psychol. 1997;28:1-12|
|20.||↵||Seasonal variations of injury and overtraining in elite athletes. Koutedakis Y, Sharp NC. Clin J Sport Med. 1998 Jan; 8(1):18-21.|
|21.||↵||Prevalence of nonfunctional overreaching/overtraining in young English athletes. Matos NF, Winsley RJ, Williams CA. Med Sci Sports Exerc. 2011 Jul; 43(7):1287-94.|
|28.||↵||Fatigue and underperformance in athletes: the overtraining syndrome. Budgett R. Br J Sports Med. 1998 Jun; 32(2):107-10.|
|29.||↵||The unknown mechanism of the overtraining syndrome: clues from depression and psychoneuroimmunology. Armstrong LE, VanHeest JL. Sports Med. 2002; 32(3):185-209.|
|32.||↵||Pichot V, Roche F, Gaspoz FE. Relation between heart rate variability and training load in middle-distance runners. Med Sci Sports Exerc. 2000;32:1729-1736|
|33, 34, 35.||↵||Reid VL, Gleeson M, Williams N, et al. Clinical investigation of athletes with persistent fatigue and/or recurrent infections. Br J Sports Med. 2004;38:42-45|
|36, 51.||↵||Urhausen A, Kindermann W. Diagnosis of overtraining: what tools do we have? Sports Med. 2002:32;95-102|
|37.||↵||Varelet-Marie E, Mercier J, Brun J. Is plasma viscosity a predictor of overtraining in athletes? Clin Hemorheol Microcirc. 2006;35:329-332|
|38.||↵||Gabriel H, Kindermann W. The acute immune response to exercise: what does it mean? Int J Sports Med. 1997;18(1)(suppl):S28-S45|
|39.||↵||Mackinnon LT. Chronic exercise training effects on immune function. Med Sci Sports Exerc. 2000;32(7)(suppl):S369-S376|
|40.||↵||Mackinnon LT, Hooper SL. Mucosal (secretory) immune system responses to exercise of varying intensity and during overtraining. Int J Sports Med. 1994;15(3)(suppl):S179-S183|
|41.||↵||Halson SL, Lancaster GI, Jeukendrup AE, et al. Immunological responses to overreaching in cyclists. Med Sci Sports Exerc. 2003;35(5):854-861|
|44, 59.||↵||Halson SL, Jeukendrup AE. Does overtraining exist? An analysis of overreaching and overtraining research. Sports Med. 2004;34(14):967-981|
|45.||↵||Gouarne C, Groussard C, Gratas-Delamarche A, et al. Overnight urinary cortisol and cortisone add new insights into adaptation to training. Med Sci Sports Exerc. 2005;37:1157-1167. https://www.ncbi.nlm.nih.gov/pubmed/16015133|
|46, 47, 48, 49, 50.||↵||Gouarne C, Groussard C, Gratas-Delamarche A, et al. Overnight urinary cortisol and cortisone add new insights into adaptation to training. Med Sci Sports Exerc. 2005;37:1157-1167. https://www.ncbi.nlm.nih.gov/pubmed/16015133|
|52, 54, 56.||↵||Meeusen R, Nederhof E, Buyse L, et al. Diagnosing overtraining in athletes using the two-bout exercise protocol. Br J Sports Med. 2010;44:642-648|
|53, 55.||↵||Meeusen R, Piacentini MF, Busschaert B, et al. Hormonal response in athletes: the use of a two bout exercise protocol to detect subtle differences in (over)training status. Eur J Appl Physiol. 2004;91:140-146|
|57.||↵||Meeusen R, Duclos M, Gleeson M, et al. The overtraining syndrome: facts and fiction. Eur J Sport Sci. 2006;6(4):263|
|60, 62.||↵||O’Connor PJ, Morgan WP, Raglin JS, et al. Mood state and salivary cortisol levels following overtraining in female swimmers. Psychoneuroendocrinology. 1989;14(4):303-310|
|61, 73, 74.||↵||Morgan WP, Costill DL, Flynn MG, et al. Mood disturbance following increased training in swimmers. Med Sci Sports Exerc. 1988;20(4):408-414|
|63.||↵||Gustafsson H, Holmberg H, Hassmen P. An elite endurance athlete’s recovery from underperformance aided by a multidisciplinary sport science support team. Eur J Sport Sci. 2008;8(5):267-276|
|66, 67.||↵||Budgett R. Fatigue and underperformance in athletes: the overtraining syndrome. Br J Sports Med. 1998;32:107-110|
|70, 71.||↵||Pearce PZ. A practical approach to the overtraining syndrome. Curr Sports Med Rep. 2002;1:179-183|
|75.||↵||Armstrong LE, VanHeest JL. The unknown mechanism of the overtraining syndrome: clues from depression and psychoneuroimmunology. Sports Med. 2002;32:185-209|
|76.||↵||Robson PJ. Elucidating the unexplained underperformance syndrome in endurance athletes: the interleukin-6 hypothesis. Sports Med. 2003;33:771-781|