title: Physical exercise as a human model of limited inflammatory response.
abstract: An inflammatory response represents a fundamental series of humoral and cellular reaction cascades in response to infection, tissue injury, and related insults. An excessive response is commonly seen under the pathological conditions of trauma, sepsis, and burns. It is becoming increasingly evident that most, if not all, of the distinguishing features of a classical inflammatory response are detectable in an exercising individual, namely mobilization and activation of granulocytes, lymphocytes, and monocytes; release of inflammatory factors and soluble mediators; involvement of active phase reactants; and activation of the complement and other reactive humoral cascade systems. While the manifestation of many exercise-induced immune and related changes has been reported and confirmed repeatedly, the underlying mechanisms triggering and modulating the elicited immune responses are, at best, poorly understood. Unlike the exaggerated and sometimes uncontrollable inflammatory response in septic and trauma patients resulting in morbidity and mortality, strenuous and severe exercise normally elicits an inflammatory response of a subclinical nature to facilitate the repairing process for site-specific tissue damage. Regardless of the inciting event, for example trauma, infection, or exercise, and given an appropriate triggering signal, a remarkably similar sequence of inflammatory reactions can be reproduced in the affected host. Therefore, physical exercise and training represent an acceptable and good model for the study of limited inflammatory responses in humans.
authors.affiliation: Defence and Civil Institute of Environmental Medicine, Department of Laboratory Medicine and Pathobiology, Toronto, Ontario, Canada. pang.shek@dciem.dnd.ca
authors.forename: P N
authors.initials: PN
authors.lastname: Shek
authors.forename: R J
authors.initials: RJ
authors.lastname: Shephard
mesh_terms: D016207:Cytokines / Q000276:immunology; D015444:Exercise / Q000502:physiology*; D006801:Humans; D007109:Immunity; D007239:Infections / Q000276:immunology*; D007249:Inflammation / Q000276:immunology*; D018836:Inflammation Mediators / Q000276:immunology; D007375:Interleukin-1 / Q000276:immunology; D015850:Interleukin-6 / Q000276:immunology; D008954:Models, Biological; D018805:Sepsis / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology; D014947:Wounds and Injuries / Q000276:immunology*
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D007375:Interleukin-1; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha