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A patient asks for your help with fatigue, which she has been experiencing for the past several weeks. She says she is having increasing difficulty carrying out her daily responsibilities, lacks motivation and energy, and is irritable and discouraged. She reports trouble sleeping, is often late to her scheduled responsibilities, is not performing as well as previously in her job and other roles, and has had several minor injuries and mild headache and back pain.
If you are a family doctor or general practitioner, you would suspect that this woman has a major depressive disorder (MDD), although the likelihood that a depressed patient would actually present her symptoms in such a clear and obvious fashion is extraordinarily low. However, if you are a sports doctor and the patient is a competitive athlete, you may label her as being burned out, overtrained or stale, depending on your personal nomenclature for this problem. You may carry out a routine battery of laboratory tests, often including measuring a variety of immunological, hormonal, and haematological variables, consult with the athlete's coach about a modified training schedule, and suggest the athlete consider a trial of rest which may even include cessation of all training and competition. On the other hand, the primary care doctor would recommend some combination of counselling and/or medication for the non-athlete patient, with an active treatment programme designed to maintain the patient's roles and responsibilities.
Why the dramatic difference in approach to labelling, diagnosing, and treating what appears to be the same disease? Three issues stand out when attempting to answer this question.
Despite the known beneficial and protective effect of exercise on mental illness,1 athletes are still susceptible to depression and other mental illness, although perhaps at a lower prevalence than the general population.2
Athletes may be even more susceptible to underdiagnosis and inadequate treatment of depression and other mental illness than are non-athletes,3 particularly for problems that are related to athletic training and performance and are viewed from a narrow physiological rather than a broader biopsychosocial perspective.
The current conceptualisation of and approach to mental illness in athletes is fraught with stigmatisation, denial, and dichotomous paradigms of “psychological” versus “physical” disease, which are inaccurate, unhelpful, and deprive the athlete of effective care.
The similarities between “depression”, as a psychiatric disease, and “overtraining”, as a consequence of overly intense athletic training, are remarkable both for their number and strength, as well as for their denial by many sports doctors and psychologists. Current nomenclature defines overreaching as a short term decrement in performance in which recovery may take a few days to weeks, usually through a temporary and modest decrease in training load.4 Overreaching is the athletic equivalent of an adjustment reaction, grieving, or a more minor depression in which psychosocial loss or stressors lead to a temporary decrement in social or work function. Overtraining (OT) is defined as a long term decrement in performance,4 usually with various physiological, immunological, hormonal, and metabolic changes that are remarkably similar to those in MDD, the only difference being the nature of the role dysfunction: athletic performance in the case of the overtrained athlete, social, cognitive, and work in the case of the depressed patients.
The similarities between OT and MDD extend to immunological effects, in which natural killer cell and humoral immunological parameters are suppressed in both, leading to an increased risk of upper respiratory infection. In fact, the J shaped curve relating exercise to immunological function5 is equally appropriate to describe the relation between exercise and mood, in which both too little and too much exercise correlate with increased levels of irritability and depression, and moderate exercise is associated with the lowest level of mood disturbance.
Both OT and MDD are related to central fatigue, with similar alterations in neurotransmitter levels and function.6 Elevated and unsuppressed cortisol secretion are found in both OT and MDD.7 Both depressed patients and overtrained athletes have decreased sensitivity to noradrenaline (norepinephrine) and dopamine, decreased levels of growth hormone, lutrophin, β-endorphins, and thyrotrophin, and increased levels of corticotrophin-releasing hormone leading to hypercortisolism. Similar changes may also occur in both MDD and OT in brain monoamines, including tryptophan and serotonin.6 These intriguing similarities are enhanced by the highly anecdotal, but common and often successful, use of serotonergic antidepressants in overtrained athletes. These athletes report both early and delayed benefits in their energy, motivation, and training similar to those reported by depressed patients in mood, energy, and role function.
Perhaps the most telling comparison of OT and MDD is in the denial and avoidance of each diagnosis by the respective patient groups. There is a common response that the disease represents a personal failure, a loss of willpower, and a defect in character, and is a problem of which one is ashamed and hides.8 Patients reject the implications of loss of control, diminished vitality, and inadequate coping skills that both diagnoses carry, and often vow to work harder so as to overcome their inadequacies, which usually leads to even more severe symptoms and dysfunction. Athletes with OT are particularly susceptible to harm from these myths because of their heightened levels of goal orientation and task mastery.
In summary, competitive athletes are special in many ways, including a high level of goal orientation, a commitment to intense physical training and competition, and a decreased risk of depression and possibly other mental illnesses. But the risk of depression is not eliminated, and may be reflected, at its most severe level, in what sports doctors and scientists currently call OT. MDD as a neuropsychiatric disorder causes profound chemical and role dysfunction that is remarkably similar to the effects of OT in athletes, the major difference being that the role dysfunction in athletes relates to the major role in their life—athletic training and performance. Most importantly, the stigmatisation of and denial by athletes with OT, similar to the behaviour of patients with MDD, are preventing sports doctors and scientists from a proper study and treatment of overtrained athletes. OT deserves a broader, more enlightened, biopsychosocial approach if we are to help athletes with this devastating problem.