Aerobic exercise attenuates inducible TNF production in humans

Aerobic exercise attenuates inducible TNF production in humans Aerobic exercise reduces coronary heart disease risk, but the mechanisms of this protection are not fully understood. Atherosclerosis is an inflammatory disease mediated by monocyte-derived macrophages, which accumulate in arterial plaques and become activated to release factors, including cytokines, that cause damage. Here we studied the effects of aerobic training on monocyte production of tumor necrosis factor (TNF) in whole blood ex vivo. Healthy young sedentary adults ( n = 61, age 20–45 yr) were randomized to a moderate- (M) or a high- (H) intensity 12-wk training program. Whole blood was extracted before and after training, and then it was stimulated by addition of lipopolysaccharide (LPS); inducible TNF was measured in the plasma. Data were analyzed according to intention to treat principles using a random-effect model to determine the impact of training group on maximal aerobic capacity and LPS-stimulated TNF after correcting for covariates. Analyses revealed improvement in aerobic capacity in both the H (9%) and the M (7%) groups. However, aerobic training led to significant ( P < 0.001) decreases in TNF release only in the H group. These data suggest that in healthy young adults, a 12-wk high-intensity aerobic training program downregulates blood monocyte production of stimulated cytokine release. exercise; inflammation; laboratory study Address for reprint requests and other correspondence: R. P. Sloan, Columbia Univ., 1150 St. Nicholas Ave., Suite 121, New York, NY 10032 (e-mail: rps7@columbia.edu ) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Applied Physiology The American Physiological Society

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Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
8750-7587
eISSN
1522-1601
D.O.I.
10.1152/japplphysiol.00147.2007
Publisher site
See Article on Publisher Site

Abstract

Aerobic exercise reduces coronary heart disease risk, but the mechanisms of this protection are not fully understood. Atherosclerosis is an inflammatory disease mediated by monocyte-derived macrophages, which accumulate in arterial plaques and become activated to release factors, including cytokines, that cause damage. Here we studied the effects of aerobic training on monocyte production of tumor necrosis factor (TNF) in whole blood ex vivo. Healthy young sedentary adults ( n = 61, age 20–45 yr) were randomized to a moderate- (M) or a high- (H) intensity 12-wk training program. Whole blood was extracted before and after training, and then it was stimulated by addition of lipopolysaccharide (LPS); inducible TNF was measured in the plasma. Data were analyzed according to intention to treat principles using a random-effect model to determine the impact of training group on maximal aerobic capacity and LPS-stimulated TNF after correcting for covariates. Analyses revealed improvement in aerobic capacity in both the H (9%) and the M (7%) groups. However, aerobic training led to significant ( P < 0.001) decreases in TNF release only in the H group. These data suggest that in healthy young adults, a 12-wk high-intensity aerobic training program downregulates blood monocyte production of stimulated cytokine release. exercise; inflammation; laboratory study Address for reprint requests and other correspondence: R. P. Sloan, Columbia Univ., 1150 St. Nicholas Ave., Suite 121, New York, NY 10032 (e-mail: rps7@columbia.edu )

Journal

Journal of Applied PhysiologyThe American Physiological Society

Published: Sep 1, 2007

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