Adipokine Responses to Acute Resistance Exercise in Trained and Untrained Men

VARADY, KRISTA A.1; BHUTANI, SURABHI1; CHURCH, EMILY C.2; PHILLIPS, SHANE A.2,3

Medicine & Science in Sports & Exercise:
doi: 10.1249/MSS.0b013e3181ba6dd3
Basic Sciences
Abstract

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.

Author Information

1Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL; 2Department of Physical Therapy, University of Illinois at Chicago, Chicago, IL; and 3Department of Medicine, University of Illinois at Chicago, Chicago, IL

Address for correspondence: Krista A. Varady, Ph.D., Department of Kinesiology and Nutrition, University of Illinois at Chicago, 1919 W Taylor St, Room 506F, Chicago, IL 60612; E-mail: varady@uic.edu.

Submitted for publication June 2009.

Accepted for publication August 2009.

©2010The American College of Sports Medicine