Adipokine Responses to Acute Resistance Exercise in Trained and Untrained Men

VARADY, K. A., S. BHUTANI, E. C. CHURCH, and S. A. PHILLIPS. Adipokine Responses to Acute Resistance Exercise in Trained and Untrained Men. Med. Sci. Sports Exerc., Vol. 42, No. 3, pp. 456-462, 2010. Introduction: Adipose tissue-derived hormones act as key mediators that may link active lifestyles to improved cardiovascular function. This study tested the hypothesis that a single weight training session would beneficially modulate adipokine profile in a way that would exert protection against endothelial dysfunction, in trained but not sedentary subjects. Methods: Male subjects (n = 43) were categorized into four separate groups based on exercise history: 1) sedentary, 2) weight trainers, 3) runners, or 4) weight trainer + runners. All subjects underwent a single progressive leg press weight training session (low weight for two sets of 8-12 repetitions each and then near-maximal exertion for three sets of 8-12 repetitions each). Results: There were no differences between groups for age, body weight, BMI, waist circumference, or percent body fat. Adiponectin increased (P < 0.05) by 30% and 37%, whereas resistin decreased (P < 0.05) by 35% and 34% in the weight trainers and weight trainer + runners, respectively, after training. Flow-mediated dilation (FMD) was impaired (P < 0.05) in sedentary subjects (-1.1 +/- 0.3%) but not in the athletic groups (1.7 +/- 0.4%). Improvements in FMD were associated with increased adiponectin (r = 0.61, P = 0.01), and decreased resistin (r = -0.56, P = 0.01) in weight trainers only. Leptin was not altered by acute resistance training in any group. There were no differences after training for total, LDL, HDL cholesterol, triglycerides, C-reactive protein levels, and systolic or diastolic blood pressure. Increased adiponectin was related to higher levels of HDL cholesterol after intervention (r = 0.71, P = 0.001). Conclusions: These findings suggest that habitual resistance training may modulate adipokine profiles in a way that is protective against endothelial dysfunction.