Cytokine hypothesis of overtraining: a physiological adaptation to excessive stress?

Overtraining syndrome (OTS) is a condition wherein an athlete is training e xcessively, yet performance deteriorates. This is usually accompanied by mo od/behavior changes and a variety of biochemical and physiological alterati ons. Presently, there is no global hypothesis to account for OTS. The prese nt paper will attempt to provide a unifying paradigm that will integrate pr evious 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 monoc ytes are then activated by injury-related cytokines, and in turn produce la rge quantities of proinflammatory: IL-1 beta, and/or IL-6, and/or TNF-alpha , producing systemic inflammation. Elevated circulating cytokines then co-o rdinate the whole-body response by: a) communicating with the CNS and induc ing a set of behaviors referred to as "sickness" behavior, which involves m ood 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 h ypercatabolic state; and c) impacting on immune function. Theoretically, OT S 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.