Submitted on February 5, 2007
Accepted on July 9, 2007
Aerobic Exercise Attenuates Inducible TNF Production in Humans
Richard P Sloan1*, Peter A Shapiro1, Ronald E. De Meersman2, Paula S McKinley1, Kevin J Tracey3, Iordan Slavov1, Yixin Fang1, and Pamela D Flood4
1 Psychiatry, Columbia University, New York, New York, United States
2 Dept of Rehabilitation Medicine, Columbia University, New York, New York, United States
3 Surgery, North Shore University Hospital, Manhasset, New York, United States
4 Anesthesiology, Columbia, New York, New Jersey, United States
* To whom correspondence should be addressed. E-mail: rps7{at}columbia.edu.
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 TNF in whole blood ex vivo. Healthy young sedentary adults (n=61, age 20-45 y) were randomized to a moderate (M) or a high (H) intensity 12-week training program. Whole blood was extracted before and after training, and then stimulated by addition of lipopolysaccharide; 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 aerobic capacity (VO2max) 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 < .001) decreases in TNF release only in the H group. These data suggest that in healthy young adults, a 12-week high intensity aerobic training program downregulates blood monocyte production of stimulated cytokine release.
