Aims: 

Diabetes / obesity is associated with left ventricular (LV) dysfunction, altered myocardial metabolism and impaired LV energetics. Exercise has been shown to influence myocardial Ca²⁺ handling, oxidative stress and mitochondrial uncoupling, processes known to influence the progression of cardiomyopathy associated with diabetes/obesity. The aim of the present study was 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: 

DIO mice (given a Western diet) were subjected to 8 weeks of HIT (1 h, 5 days a week). Aerobic capacity, glucose tolerance, myocardial oxidative stress and LV function, energetics and metabolism were determined.

Results: 

Hearts from sedentary DIO mice exhibited diastolic and systolic dysfunction and reduced cardiac efficiency. HIT increased aerobic capacity, reduced obesity and improved glucose tolerance in DIO mice. In addition, the adverse effects of obesity on LV function and cardiac efficiency were normalized by HIT. Analysis of the relation between myocardial oxygen consumption (MVO2) and LV pressure-volume area revealed unaltered contractile efficiency, while unloaded MVO2 (oxygen costs for non-contractile work) was normalized, due to reduced oxygen cost for basal metabolism and excitation-contraction coupling. 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.