Abstract We analyzed adaptation mechanisms regulating systemic inflammatory response of the stressed body by using an experimental challenge of repeated exercise bouts and accompanying muscle inflammation. Eight untrained men bicycled at 90 W for 90 min, 3 days in a row. Exercise induced peripheral neutrophilia with a leftward shift of neutrophil nucleus and neutrophil priming for oxidative activity determined by luminol-dependent chemiluminescence. Plasma growth hormone and interleukin-6 rose significantly after exercise and were closely correlated with the neutrophil responses. Serum creatine kinase and myoglobin levels as muscle damage markers rose after exercise in “delayed onset” and were closely correlated with the preceding neutrophil responses. These exercise-induced responses were strongest on day 1 , but the magnitude gradually decreased with progressive daily exercise. In contrast, the magnitude of catecholamine responses to exercise sessions gradually rose, possibly suppressing neutrophil oxidative responses. These results indicate that stress-induced systemic release of bioactive substances may determine neutrophil mobilization and functional status, which then may affect local tissue damage of susceptible organs. growth hormone interleukin-6 catecholamine reactive oxygen species systemic inflammatory response syndrome Footnotes Address for reprint requests and other correspondence: S. Nakaji, Dept. of Hygiene, Hirosaki Univ. School of Medicine, 5 Zaifu-cho, Hirosaki, Aomori 036-8562, Japan. The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. §1734 solely to indicate this fact. Copyright © 1999 the American Physiological Society
Journal of Applied Physiology – The American Physiological Society
Published: Oct 1, 1999
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