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G
enerally speaking, athletes train to increa
performance. Performance increas are achieved through incread training loads. Incread loads
are tolerated only through intersperd 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.14,30 Overreaching followed by appropriate rest can ultimately lead to performance increas.14,30 However, if overreaching is extreme and combined with an additional stressor, overtraining syndrome (OTS) may result.30 OTS may be caud by systemic inflammation and subquent effects on the central nervous system, including depresd mood, central fatigue, and resultant neurohormonal changes.2,45,46 This article summarizes previous literature and updates the European College of Sport Science’s position statement.30
Terminology
Definitions from the European College of Sport Science position statement on OTS are ud 30 (Table 1). 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 rearchers refer to overtraining as
unexplained underperformance syndrome.5,44 Differentiation of NFO and OTS is clinically difficult and can be made often only after a period of complete rest.30,36 The difference between the 2 is bad on time to recovery and not necessarily the degree or type of symptoms.30,36
Many consider overreaching and overtraining as a
continuum.10 Others question anecdotal evidence suggesting that NFO precedes OTS.14 Unfortunately, much of the literature has been done on overreached rather than overtrained athletes by current terminology. Some studies ud overtrained athletes but failed to show that the athlete
s suffered from performance impairment.14 Recent reports highlight the importance of
psychological and/or social stressors in addition to physiologic stress in the development of NFO/OTS.20,28,49 An individual’s stress capacity plays a role in the development of NFO/OTS.20
epidemiology
Epidemiologic studies u varied terminology. It appears that OTS is extremely rare, but exact prevalence and incidence data are lacking. *One study found a NFO lifetime prevalence
Overtraining Syndrome: A Practical Guide
Jeffrey B. Kreher, MD,*† and Jennifer B. Schwartz, MD ‡
Context: Fatigue and underperformance are common in athletes. Understanding overtraining syndrome (OTS) is helpful in the evaluation, management, and education of athletes.
Evidence Acquisition: Relevant articles in English were arched with OVID (1948-2011) and PubMed using the following keywords: overtraining syndrome , overtraining , overreaching , unexplained underperformance , staleness , pathophysiology , management , treatment , evaluation . Bibliographies were reviewed for additional resources.
Results: OTS appears to be a maladapted respon to excessive exerci without adequate rest, resulting in perturbations of multiple body systems (neurologic, endocrinologic, immunologic) coupled with mood changes. Many hypothes of OTS pathogenesis are reviewed, and a clinical approach to athletes with possible OTS (including history, testing, and prevention) is prented.
Conclusions: OTS remains a clinical diagnosis with arbitrary definitions per the European College of Sports Science’s position statement. History and, in most situations, limited rologies are helpful. However, much remains to be learned given that most past rearch has been on athletes with overreaching rather than OTS.
Keywords: overtraining syndrome; overtraining; overreaching; unexplained underperformance; staleness; pathophysiology; man-agement; treatment; evaluation
[ Athletic T raining ]
From †Department of Orthopaedic Surgery–Pediatric Orthopaedics, Massachutts General Hospital for Children, Boston, Massachutts, and ‡Department of Family Medicine, Tufts University Family Medicine Residency at Cambridge Health Alliance, Malden, Massachutts.
*Address correspondence to Jeffrey B. Kreher, MD, Department of Orthopaedic Surgery–Pediatric Orthopaedics, Massachutts General Hospital for Children, Yawkey Center for Outpatient Care, Suite 3400, 55 Fruit Street, Boston, MA 02114 (e-mail:).DOI: 10.1177/1941738111434406© 2012 The Author(s)*References 18, 21, 27-33, 35, 37, 42.
vol. 4 • no. 2SPORTS HEALTH
of ~60% in elite male and female runners, compared with 33% in nonelite female runners.35 A multicenter, multicountry survey found that 35% of adolescent swimmers had been “overtrained” at least once.42 Estimates of “staleness” were reported in 5% to 30% of swimmers over a ason18,33,37 and in 15% of British elite athletes.21 In the most recent survey of elite adolescent athletes, ~30% reported NFO at least once in their careers—they averaged 2 episodes lasting 4 weeks. The risk was significantly incread in individual sports, low physically demanding sports (such as golf), females, and elite athletes.27 paThophysiology
Numerous hypothes have been propod for OTS, each with strengths and weakness (Table 3). In attempting to understand OTS mechanistically and clinically, it is crucial to
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奥数比赛ek an explanation that accounts for the many symptoms of this complicated entity.
户外帐篷品牌Glycogen Hypothesis
Low muscle glycogen can impair performance becau of inadequate fuel for the workload.47 Low muscle glycogen also results in incread oxidation and decread concentrations of branched chain amino acids. This can alter synthesis of central neurotransmitters involved in fatigue.7 Becau decrements
in performance and fatigue are hallmarks of OTS, decread muscle glycogen may cau OTS.
铁甲犀牛While this association ems 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 diagno OTS.7 Even athletes who consume incread amounts of carbohydrates and maintain normal glycogen levels can still become overtrained.47 While low muscle glycogen levels may be associated with exerci-induced fatigue, the link with OT
S appears weak.
Central Fatigue Hypothesis
饼的做法大全OTS nearly always includes disrupted mood, sleep, and behavior.2,18,22,33,45 The neurotransmitter rotonin (5-HT)
is implicated in regulation of the functions; therefore, alterations in 5-HT could lead to OTS.2-4,22,30,45 5-HT is derived from tryptophan. With exerci, there is incread unbound tryptophan, which competes with branched chain amino acids for entry into the brain.2-4,45 Exerci decreas levels of branched chain amino acids due to incread oxidation, favoring tryptophan entry into the brain and conversion to 5-HT.5 Increas in unbound tryptophan have been positively correlated with fatigue, presumably due to incread rotonin synthesis in the brain.3,4,45 Giving rotonin reuptake inhibitors to athletes artificially increas 5-HT in the brain and reduces performance.5 Converly, marathon runners receiving branched chain amino acids supplementation felt more energized and mentally clear, possibly due to dampened 5-HT synthesis.6 Fatigue in overtrained athletes may be due to incread nsitivity to 5-HT rather than incread 5-HT.4 Incread neurologic nsitivity to a 5-HT agonist has been reported
in overtrained athletes.4 Well-trained athletes usually are less nsitive to 5-HT; this adaptation may be lost in OTS.4
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 exerci,4 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.4 Therefore, 5-HT activity requires cautious interpretation.
Glutamine Hypothesis
Glutamine is integral for immune cell function.14,16,45 It also plays a role in DNA/RNA synthesis, nitrogen transport, gluconeogenesis and acid-ba balance.14,16,53 Decread glutamine after exerci may be responsible for incread incidences of upper respiratory tract infections in overtrained athletes.14,25,46
Prolonged exerci (> 2 hours) or repeated bouts of high-intensity exerci can transiently decrea plasma glutamine concentrations.16,53 Low plasma glutamine concentrations have been reported s
pecifically in overtrained athletes.14,25 This may reprent overutilization and/or a decread production by overworked muscles.16
It is unclear whether decread glutamine influences immune cell function. In vitro, immune cell function can
be compromid when glutamine concentrations are
below physiologic levels.16 Despite decread glutamine concentrations after exerci, the amount of glutamine available to immune cells does not necessarily change.16 Glutamine supplementation can restore physiologic levels but does not improve postexerci impairment of immune cells.16 Nevertheless, glutamine supplementation may decrea early rates of infection among athletes.6
Epidemiologic data have shown that athletes may be more susceptible to upper respiratory tract infections after “excessive exerci,”53 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 nonoverreached athletes reported upper respiratory tract infections.25 Low plasma glutamine has been en in athletes with upper respiratory tract infections, while others demonstrate the opposite.53 Finally, glutamine levels can be influenced by nutritional state, trauma, and infection.16
Oxidative Stress Hypothesis
Some oxidative stress is desired during exerci becau reactive oxygen species relead from damaged muscles regulate cellular repair.50 When oxidative stress becomes pathologic, however, reactive oxygen species (ie, superoxide, hydrogen peroxide, and hydroxyl radical) can cau inflammation, muscle fatigue, and soreness with resultant inhibition of athletic performance.48
Resting markers of oxidative stress are higher in overtrained athletes compared with controls.17,26,48 Moreover, oxidative stress markers increa with exerci in the overtrained athletes.26,48 Citrate syntha reflects oxidative capacity and is expected
to increa during endurance training. In an overreached
rat model, citrate syntha activity actually decreas.17 OTS athletes may have diminished respons to exerci-induced stress and be more susceptible to oxidative damage.17
It is unclear if the incread oxidative stress state is a trigger or result of OTS. Clinically relevant rearch is limited. Moreover, confounding factors such as menstrual cycles and estrogen’s antioxidative properties are unknown.48 Autonomic Nervous System Hypothesis
An imbalance in the autonomic nervous system can
explain some symptoms of OTS. Specifically, decread
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vol. 4 • no. 2SPORTS HEALTH sympathetic activation and parasympathetic dominance can
lead to performance inhibition, fatigue, depression, and
bradycardia.14,22,45
Reduced sympathetic activation in overtrained athletes is
supported in some studies by decread nocturnal urinary
catecholamine excretion.14 Catecholamine excretion decreas
with increasing fatigue and returns to baline during
recovery.14,20,45 However, not all studies find this trend.12,20
A decread organ nsitivity to catecholamines may also
be responsible for symptoms of decread sympathetic
activation.22
Heart rate variability (HRV) has also been ud as an
indicator of autonomic function.9,14,51 One study showed no
difference in HRV between overtrained and control athletes
during sleep.19 However, a reduced HRV was en soon after
awakening in overtrained athletes, suggesting incread
sympathetic tone.19 Using HRV, studies have indicated that
the effects of inten training on automatic control may be
reversible. Balance between sympathetic and parasympathetic
forces may be restored after a week of rest.41
Hypothalamic Hypothesis
Alterations in the hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-gonadal 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, adrenocorticotropic hormone, testosterone, and other hormone levels.1,14,22,45,51 Unfortunately, the current
data are contradictory as to patterns of the hormonal changes.14,22,51 Alterations in the HPA and hypothalamic-pituitary-gonadal axes are individualized and depend on other factors, including exerci capacity, inherent vulnerability to stressors, and other hormonal levels.14,51
Cytokine Hypothesis
曲线玲珑
No single hypothesis explains all aspects of OTS. The cytokine hypothesis suggests that OTS is a physiologic adaptation/ maladaptation to excess stress initiated by an imbalance between training and recovery.44-46
Muscle contraction and repetitive joint action cau microtrauma to tissues.44,45 Adaptation through 山阴公主刘楚玉
tissue healing and strengthening occurs via activation of a local inflammatory respon and recruitment of cytokines.44,45 With continued inten training and abnce of adequate rest, this inflammatory respon can become amplified, chronic, and pathologic.44-46 Eventually a systemic inflammatory respon can result with negative conquences throughout the body.44,45 Implicated cytokines in OTS include interleukin 1 beta (IL-1b), IL-6, and tumor necrosis factor α (TNF-α)45 (Figure 1). Reduced muscle glycogen levels are frequently obrved
in overtrained athletes.7,47 Decread glycogen may be a conquence of OTS through cytokine-mediated effects.45 Cytokines acting on hunger centers in the hypothalamus induce anorexia, resulting in decread glycogen stores.45Cytokines themlves may interfere with gluco transport
into muscle cells for glycogen synthesis. Studies have shown decread concentrations of GLUT-4 transporters in stresd muscles due to downregulation of protein synthesis by TNF-
α.45 Decread glycogen stores may account for feelings of
短暂heavy legs and muscular fatigue in overtrained athletes.45 Incread uptake of tryptophan into the brain and enhanced nsitivity to rotonin have been postulated to induce
fatigue and depression.45 The cytokine hypothesis argues
that rum tryptophan levels are actually decread with systemic inflammation like that en in OTS.45 The reason
虚心学习
is that tryptophan is ud for the synthesis of inflammatory-related proteins. Reduced tryptophan levels have actually been associated in many studies with depressive symptoms.45 Behavioral and psychological changes en in OTS can also
be attributed to cytokines. Proinflammatory IL-1b and TNF-α
act on the brain to cau decread 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 relea of stress hormones with similar peripheral effects.45 There is evidence of elevated cytokine
levels in depresd patients and a precipitation of depresd mood with cytokine administration to participants, offering credibility to the notion of cytokine-induced mood changes in OTS.45
Alterations in the HPA and hypothalamic-pituitary-gonadal axes with a resultant decrea in testosterone:cortisol ratios
have been implicated in OTS. Proinflammatory cytokines are potent activators of the HPA system, which cau relea of corticotropin-releasing hormone, adrenocorticotropic hormone, and cortisol. The cytokines suppress testosterone through central inhibition.45 Although patterns of hormonal changes
in OTS are varied, cytokine mediators may be responsible for some of the changes.
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