Despite more than 20 years of research into mechanisms which could result in the increased predisposition of athletes to ‘infection' incidence following excessive and prolonged exercise, definitive explanations are not yet available. A strong temporal relationship between the incidence of upper respiratory tract infection symptoms and immune system changes following excessive exercise load (EEL) have not been shown. T-helper cells are functionally polarised according to the cytokines which they produce. While exercise-induced upregulation of T-helper- 2 (TH2) cells and type 2 cytokines is indicative of enhanced activation of allergic responses, downregulation of T-helper-1 (TH1) cells and type 1 cytokines confirms suppression of cellular immune functions. The current knowledge regarding the exercise-induced kinetics of interleukin (IL)-4, a cytokine that is crucial in the activation of the TH2 cells, does, however, not appear to provide sufficient support for an upregulation of a type 2 response. Lowered or unchanged circulating concentrations of type1 cytokines (IL12, IL-2 and interferon γ) and short-term suppression of lymphocyte, natural killer cell and neutrophil function following EEL, reflect a transient, post-exercise suppression of cellular immunity. Despite a partial dampening thereof by the anti-inflammatory actions of IL-10, IL-1ra and IL-6, the evidence supporting a pro-inflammatory response to prolonged exercise and overtraining is unequivocal. At present, the data appear to support the theory that symptoms of ‘infection' experienced by athletes are the manifestation of a significant pro-inflammatory response, combined with a modest, transient suppression of cellular immune functions which may be clinically insignificant.
South African Journal of Sports Medicine Vol.16(1) 2004: 3-9