Abstract

Sedentary lifestyle contributes to obesity. This study examined the effect of quantitative voluntary running on body adiposity and its associated inflammation in mice fed a high‐fat diet. Male C57BL/6 mice were assigned into six groups and fed the AIN93G (sedentary) or a high‐fat diet (sedentary, unrestricted running, or with 25%, 50%, or 75% restriction in running activity) for 12 weeks. The average daily running distance was 8.3, 6.3, 4.2, and 2.1 km for the unrestricted, 25%, 50%, and 75% restricted runners, respectively. The high‐fat diet increased body fat mass by 46% compared to the AIN93G diet in sedentary mice. Running reduced the fat mass in a dose dependent manner; there was no difference between sedentariness and running at 2.1 km/d. The high‐fat diet significantly increased blood glucose, plasma insulin, HOMA‐IR, and plasma and adipose concentrations of leptin and monocyte chemotactic protein‐1 (MCP‐1) in sedentary mice. Running, despite continued consumption of the high‐diet, reduced these variables in dose‐dependent manners. Running at 8.3 (unrestricted) and 6.3 km/d (25% restricted) had the greatest but similar reductions in, whereas running at 2.1 km/d did not affect (except MCP‐1), these measurements. Running, regardless of daily distance, significantly reduced MCP‐1 in both plasma and adipose tissues. In conclusion, voluntary running at 6.3 km/d is optimal to reduce body adiposity and its associated inflammation and metabolic disturbance in C57BL/6 mice. Results that running at 2.1 km/d reduced MCP‐1 without affecting body fat mass show the benefits of moderate amount of exercise in improving low‐grade inflammation. It suggests that different mechanisms, rather than reducing body adiposity, are responsible for this improvement.Support or Funding InformationThe U.S. Department of Agriculture, ARS, research project 5450‐51000‐045‐00D.

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