Cytokine hypothesis of overtraining: a physiological adaptation to excessive stress?
Overtraining syndrome (OTS) is a condition wherein an athlete is training excessively, yet performance deteriorates. This is usually accompanied by mood/behavior changes and a variety of biochemical and physiological alterations. Presently, there is no global hypothesis to account for OTS. The present paper will attempt to provide a unifying paradigm that will integrate previous research under the rubric of the cytokine hypothesis of overtraining. It is argued that high volume/intensity training, with insufficient rest, will produce muscle and/or skeletal and/or joint trauma. Circulating monocytes are then activated by injury-related cytokines, and in turn produce large quantities of proinflammatory IL-1beta, and/or IL-6, and/or TNF-alpha, producing systemic inflammation. Elevated circulating cytokines then co-ordinate the whole-body response by: a) communicating with the CNS and inducing a set of behaviors referred to as "sickness" behavior, which involves mood and behavior changes that support resolution of systemic inflammation: b) adjusting liver function, to support the up-regulation of gluconeogenesis, as well as de novo synthesis of acute phase proteins, and a concomitant hypercatabolic state; and c) impacting on immune function. Theoretically, OTS is viewed as the third stage of Selye's general adaptation syndrome, with the focus being on recovery/survival, and not adaptation, and is deemed to be "protective," occurring in response to excessive physical/physiological stress. Recommendations are made for potential markers of OTS, based on a systemic inflammatory condition.
Smith
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Department of Health, Leisure, and Exercise Science, Appalachian State University, Boone, NC 28608, USA.
D000209:Acute-Phase Proteins / Q000494:pharmacology; D000222:Adaptation, Physiological; D000339:Affect; D016207:Cytokines / Q000494:pharmacology*; D017079:Exercise Tolerance / Q000502:physiology*; D006801:Humans; D007596:Joints / Q000293:injuries / Q000473:pathology / Q000502:physiology; D018482:Muscle, Skeletal / Q000293:injuries / Q000473:pathology / Q000502:physiology*; D013177:Sports; D013312:Stress, Physiological / Q000503:physiopathology*; D018746:Systemic Inflammatory Response Syndrome / Q000503:physiopathology
D000209:Acute-Phase Proteins; D016207:Cytokines