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1Division of Behavioral Medicine, Department of Psychiatry, Columbia University, 2New York State Psychiatric Institute, 3Division of Consultation Liaison Psychiatry, Department of Psychiatry, Columbia University Medical Center, 4Department of Rehabilitation Medicine, Columbia University Medical Center, 5The Feinstein Institute for Medical Research at North Shore-LIJ Health System, and 6Department of Anesthesiology, Columbia University Medical Center, New York, New York
Submitted 5 February 2007 ; accepted in final form 9 July 2007
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
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