Introduction
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Overtraining syndrome (OTS) is a medical disorder occurring in athletes, and it is complicated by several diagnostic and therapeutic challenges. Current research in this area is limited by a small number of studies and inconsistent results. Several researchers have concluded the following: there are poorly established diagnostic criteria; there are significant confounding influencers, including illness, injury, menstruation, and unique training methods for different sports, and it is difficult, if not impossible, to establish controls and/or laboratory models to study the illness.
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This chapter will review the epidemiology and key terminology as well as describe the proposed pathophysiology of OTS. In particular, we will discuss the clinical presentation, diagnosis, management, and prevention of this disorder.
Epidemiology
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OTS is an issue that has plagued athletes, trainers, coaches, and clinicians for generations. As evidenced by this quote from Dr. D. C. Parmenter, this ailment is not new to the medical literature:
“Overtraining or staleness is the bug-a-boo of every experienced trainer…a condition difficult to detect and still more difficult to describe…evaluation should focus on training load, nutrition, sleep and rest, competition stress and psychological state.” Parmenter
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The current literature on OTS has limited insight into the incidence and prevalence of this disorder. However, observational data and clinical experience suggest that OTS is not rare. An early study reported that 65% of elite competitive swimmers had experienced staleness at some time in their career. A subsequent survey study of endurance runners described a prevalence rate of 10% during one training cycle and a lifetime risk of 64% and 60% among male and female runners, respectively. Athletes who have experienced OTS appear more likely to relapse: a study of college swimmers reported that 91% of swimmers who experienced OTS in their freshman year suffered a repeat episode during the subsequent year as opposed to 34% of those who did not experience an initial episode.
Terminology
Training: A series of stimuli used to stress or displace homeostasis to provide stimulation for adaptation. Training involves progressive overload in an effort to improve performance in a sport or activity. Training for success involves a balance between achieving peak performance and avoiding negative consequences of overtraining.
Adaptation: Physiologic response to stress that results in an adjustment in function or dimension of an organism
Recovery: The period of time following a training stimulus when work capacity returns to prestimulus levels. If recovery time is optimal, supercompensation results, whereas excessive training, without rest, can result in a decline in performance ( Fig. 28.1 ). Available literature describes four components of recovery: hydration and nutrition, sleep and rest, relaxation and emotional support, and stretching and active rest. Recovery that is inadequate results in fatigue. Fatigue may be classified as either pathologic or physiologic.
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Physiologic fatigue includes categories such as insufficient sleep, nutritional, jet lag, pregnancy, and training-induced (from either excessive competition or overreaching).
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Pathologic fatigue includes the following categories: medical, including infectious, neoplastic, hematologic, endocrine, toxic, iatrogenic, and psychiatric; chronic fatigue syndrome; and OTS.
Figure 28.1
Hypothetical overtraining syndrome model.
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Periodization: Planned sequencing of increased training loads and recovery periods within a training program
Acute Fatigue (AF): The immediate response to overload training; although fatigued, the athlete experiences no perceivable decline in performance
Functional Overreaching (FOR): Short-term decrement in performance after a period of overload training usually lasting <2 weeks after a period of overload training
Non-functional Overreaching (NFOR): A longer period of performance decline (2 weeks to 2 months) following a period of overload training
Overtraining Syndrome (OTS): Maladaptive response to training from an extended period of overload (usually 2 months or more); the result of too severe or a prolonged period of overreaching (see Fig. 28.1 ). Overtraining is manifested by decreased sport-specific performance and enhanced fatigability, pronounced vegetative complaints, sleep disorder, emotional instability, organ-related complaints without organic disease, overuse injuries, blood chemistry changes, and immune dysfunction.
Pathophysiology
Overview
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The pathophysiology of OTS has not been fully elucidated. There are multiple models/hypotheses that attempt to explain the signs and symptoms of this disorder, including the autonomic imbalance hypothesis, the central fatigue hypothesis, the glycogen depletion hypotheses, and the cytokine hypothesis.
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Fig. 28.2 summarizes the various hypotheses to explain the complexity of this disorder.
Figure 28.2
Genesis of overtraining syndrome. 5-HT , Serotonin; DA , dopamine.
(Modified from Foster C, Lehmann M. Overtraining syndrome. In Guten GN, ed: Running Injuries . Philadelphia: W.B. Saunders; 1997.)
Autonomic Imbalance Hypothesis
The autonomic imbalance hypothesis proposes that underlying imbalances in the autonomic nervous system cause OTS. The initial stage of this proposed mechanism involves negative feedback caused by a surge of catecholamine release during periods of heavy training. This causes a decrease in baseline catecholamine secretion. Second, an increase in metabolism during exercise causes an imbalance among plasma amino acids and alterations in brain neurotransmitter metabolism leading to an increase in the concentrations of aromatic amino acids (phenylalanine, tryptophan, and tyrosine). The resulting increases in hypothalamic tryptophan and cerebral dopamine concentrations cause “metabolic error signals” with inhibitory effects on the sympathetic nervous system. In addition, the increase in core temperature associated with high-intensity training (HIT) may exert inhibitory effects on the sympathetic centers of the hypothalamus. Third, a neuronal negative feedback system results in down-regulation of catecholamine receptors in the exercising muscles.
Central Fatigue Theory
The central fatigue theory hypothesizes that OTS is caused by an increase in the synthesis of 5-hydroxytryptomine (5-HT) in the central nervous system (CNS). Extensive exercise results in glycogen depletion in muscles, leading to the use of secondary energy sources by these muscles. The branched-chain amino acids (BCAAs: leucine, isoleucine, and valine) are oxidized to glucose. Concurrently, levels of fatty acids increase as well. Fatty acids compete with tryptophan for albumin-binding sites, leading to an increase in plasma tryptophan. Since both BCAAs and tryptophan use the same transporter to pass through the blood–brain barrier, a decrease in plasma BCAAs and an increase in plasma tryptophan leads to an increase in tryptophan passing through into the CNS. In the brain, tryptophan is converted into the neurotransmitter 5-HT. 5-HT is known to play a role in various neuroendocrine and emotional functions, all of which can be seen with OTS. This connection between OTS and an increase in the free tryptophan/BCAA ratio forms the basis for this hypothesis.
Glycogen Depletion Hypothesis
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Glycogen is the predominant energy source for moderate to intense exercise.
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According to the glycogen hypothesis, glycogen depletion may lead to overtraining through following three mechanisms.
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Direct effects of glycogen depletion: low levels of muscle glycogen stores may cause muscular fatigue and poor performance.
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Glycogen depletion may also cause increased oxidation of BCAAs, which eventually leads to central fatigue.
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Glycogen depletion may lead to a net negative caloric state, which induces a catabolic state and multiple neuroendocrine changes.
Cytokine Hypothesis
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The cytokine hypothesis theorizes that chronic tissue injury without regenerative healing leads to a systemic inflammatory and immune response. This systemic inflammatory response leads to increased concentration of interleukins, interferons, tumor necrosis factor, and other proinflammatory factors.
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These factors are thought to act centrally, promoting central fatigue, anorexia, depression, a catabolic state, and changes in the hypothalamic–pituitary–adrenal and hypothalamic–pituitary–gonadal axes.
Clinical Presentation
Overview
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Although a universal feature of OTS is decreased performance, it may include a broad array of psychiatric, musculoskeletal, cardiovascular, and immunologic symptoms ( Table 28.1 ). However, on account of individual variation, few (if any) athletes exhibit all features of overtraining.
TABLE 28.1
CLINICAL PRESENTATION OF OVERTRAINING SYNDROME
Sport-Specific Performance Complaints
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Inability to meet prior performance standards
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Prolonged recovery time
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Decreased coordination
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Decreased muscular strength
Physiologic Findings
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Blood pressure changes
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Increased resting heart rate
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Weight loss
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Increased incidence of injuries
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Increased incidence of infections
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Amenorrhea
Subjective Complaints
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Fatigue
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Feeling of depression
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Anorexia
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Hypersomnia/disturbed sleep
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Myalgias
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Gastrointestinal disturbances
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Headaches
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Increased irritability
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Concentration difficulties
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Apathy
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