Overtraining syndrome (OTS) is an entity which is poorly understood in sports medicine. One challenge is that it goes by the muse of multiple entities including burnout, chronic fatigue, training stress syndrome, staleness, and unexplained underperformance syndrome (Budgett et al). The European College of Sports Medicine defines OTS as a spectrum of issues that start as something called functional overreaching, then develop to nonfunctional overreaching and, in extreme cases, turn into full blown overtraining syndrome (Meeusen et al). See Table 1 for definitions of functional overreaching, nonfunctional overreaching, and overtraining syndrome as per the European Society of Sports Science (ECSS).
One of the current challenges in defining OTS is that a majority of the research was done on athletes in the functional overreaching category. Studies show that OTS is almost certainly multifactorial including social stressors, psychological diseases, and possibly the individual’s ability to deal with stress (Kentta et al, Meehan et al). Prior studies have shown varying degrees of this disease prevalence but it is classified as rare. Risk is increased in individual sports and studies have shown a range from 15-60% prevalence in studies done in runners and swimmers (Kentta et al, Matos et al, Morgan et al). Additionally, the pathophysiology is poorly understood; however, there are many hypotheses as to why these issues occur in athletes. These include the most widely accepted cytokine hypothesis as well as the less accepted glycogen, central fatigue, glutamine, oxidative stress, autonomic nervous system, and Hypothalamic/Hypopituitary (HPA/HPG) axis hypothesis (Kreher and Schwartz).
Low muscle glycogen can most certainly impair athletic performance by decreasing the amount of amino acids synthesized by the body and has been shown to have a deleterious effect on central neurotransmitters. Swimmers who took in lower amounts of carbohydrates showed signs of more fatigue and training issues; however, evidence has been shown that increasing intake to an appropriate amount of carbohydrates prior to training can still experience OTS (Costill et al, Snyder et al).
Researchers also postulated that serotonin sensitivity plays a role in overtraining syndrome. The glutamine theory involves similar physiology as the serotonin theory and it is involved in various other bodily physiological efforts, mainly immune function (Makinon et al). Studies have shown mixed results, however, there is some evidence that athletes have lowered glutamine levels and this has been associated with increased respiratory infections (Smith et al, Makinon et al). Additionally, athletes in general have been found to be at increased risk for respiratory infections after “excessive exercise”(Walsh et al). The oxidative stress, autonomic nervous system, and hypothalamic hypothesis all have some reasonable physiological evidence as possible causes of OTS; however, the majority of evidence points towards the cytokine hypothesis as the cause for the disease.
The cytokine theory states that OTS is a “physiologic adaptation/maladaption to excess stress initiated by imbalance between training and recovery” (Robson et al, Smith et al). Exercise requires violent muscular contraction that causes microtrauma to the muscles which heals through local inflammatory responses which are mainly mediated by cytokines (Robson et al). If continued for a long time without adequate rest, this is thought to transform from a local to a systemic inflammation in which research has implicated cytokines interleukin-1 beta, interleukin 6, and tumor necrosis factor alpha (Smith et al). Cytokines have been implicated to have effects on decreasing glycogen, decreased levels of trypotophan which is a precursor for serotonin, and alterations in the Hypothalamic axis (Smith et al).
The only lab work or imaging that would be required for this entity would be that to rule out organic causes which are vast and can include infections such as URI, EBV, or HIV, liver disease, anemia, malnutrition, among others such as C-reactive protein as a sign of systemic inflammatory response (Smith et al). In athletes with atopic or allergic symptoms, it is recommended to test pulmonary function (Pichot et al). In past years, studies have been done on ways to further evaluate this disease by evaluating biochemical and immunologic markers. Of these, none have been found to definitively diagnosis overtraining syndrome; however, various trends have been observed (Smith et al). Cytokines such as interleukin 1 beta, interleukin 6, and tumor necrosis facor alpha have been noted to be implicated in OTS (Robson et al).
In treating an athlete with overtraining syndrome, the most utilized strategy is prevention of the disorder. This has been shown to be effective in the literature. One study showed a decrease in “burnout” in college swimmers from 10% to 0% when implementing questionnaires on the mood of the athlete and altering training schedules based on survey results. This was done by decreasing training load with poor mood scores on the questionnaires (Mogan et al). Along with training monitoring, preemptive questioning of athletes with decreased performance could be done to evaluate the myriad of factors involved in this disease state. Identification of the athlete with functional overreaching or early stage nonfunctional overreaching is key to make changes to prevent full blown overtraining syndrome. Education is also important for the athletes who can help identify signs in themselves or teammates to hopefully decrease poor outcomes. Additionally management of associated issues like insomnia, psychological disease, nutritional deficits, or other organic causes should be treated appropriately (Smith et al, Pearce et al). It is not within the scope of this article to discuss all the various organic causes and treatments for these given the wide array of causes and management options for said ailments.