Exercise training improves insulin stimulated skeletal muscle glucose uptake independent of changes in perfusion in patients with dilated cardiomyopathy

Objective: The purpose of the present study was to investigate the effects of a 5-month exercise training program on skeletal Muscle perfusion and insulin sensitivity at rest and during exercise in patients with idiopathic dilative cardiomyopathy (DCM). Background: Patients with chronic heart failure are characterized by impaired insulin sensitivity and endothelial function. It is hypothesized that exercise training improves metabolism by enhancing perfusion in patients with heart failure. Methods: Fifteen DCM patients (New York Heart Association I-III) on stable medical therapy participated in the study. Patients were divided to receive either supervised strength and aerobic training (n = 9, left ventricular ejection fraction [LVEF] = 34 +/- 8%) for 5 months (3 times per week at an intensity of 70% of peak oxygen uptake [VO2]) or standard care (n = 7, LVEF = 36 +/- 6%) based on their living proximity to the exercise training site. Muscle blood flow, oxygen consumption, and glucose uptake were quantified using [O-15]-water, [O-15]-oxygen, [F-18]FDG, and positron emission tomography (PET) during euglycemic hyperinsulinemia and 1-legged isometric exercise. PET studies were performed twice for each patient at the same individual workloads. Results: Exercise training improved exercise capacity by 27% (P < .001). Whole body insulin-stimulated glucose uptake enhanced by 23% (P < .05) and muscle glucose uptake by 53% (P < .05) in the trained group but tended to decrease in the untrained group. When studied using identical workloads, muscle glucose uptake in exercising muscles was enhanced by 55% (P < .05), whereas no chancres were observed in muscle blood flow and oxygen uptake. Conclusions: Exercise training counteracts the impaired insulin sensitivity caused by DCM. Training improves exercise capacity with a concomitant enhancement in whole body, resting., and exercising skeletal muscle glucose uptake. The improved insulin sensitivity is not explained by changes in muscle perfusion suggesting enhanced cellular glucose extraction.