Abstract 14938: Exercise Improves Ventricular Function And Decreases Myocardial Oxygen Waste In Diet-induced Obese Mice.
Background: Diabetes/obesity is associated with left ventricular (LV) dysfunction, altered myocardial metabolism, decreased cardiac efficiency and impaired LV energetics. Exercise has been shown to influence myocardial calcium handling, oxidative stress and mitochondrial uncoupling, processes which are known to influence the progression of cardiomyopathy associated with diabetes/obesity. The aim of the present study was therefore to examine the effect of high intensity interval training (HIT) on LV function and energetics, using diet-induced obese (DIO) mice as experimental model.
Methods and Results: DIO mice (given a Western diet) were subjected to 8 weeks of HIT (1 h, 5 days a week). Hearts from sedate DIO mice (DIOSED) showed diastolic and systolic dysfunction (Fig. 1) and increased oxygen cost for basal metabolism (BM) and excitation-contraction (E-C) coupling (Fig. 2). DIO mice subjected to HIT (DIOHIT) showed increased aerobic capacity, reduced obesity and improved glucose tolerance. In addition, LV function (Fig. 1) and cardiac efficiency were normalized. Analysis of the relation between MVO2 and LV pressure-volume area revealed unaltered contractile efficiency, while unloaded MVO2 was normalized, due to reduced oxygen cost for BM and E-C coupling (Fig. 2). These changes were accompanied by attenuation of DIO-induced myocardial oxidative stress, and not by changes in energy substrate utilization.
Conclusion: Exercise-induced improvement of LV function and energetics are associated with attenuation of obesity-induced myocardial oxygen waste, most likely due to decreased ROS-induced impairments of mitochondrial function and Ca2+ handling.
- © 2011 by American Heart Association, Inc.