Abstract
Endothelial dysfunction is found both in patients with chronic heart failure and in patients with insulin-treated type 2 diabetes mellitus. This endothelial dysfunction leads to a significant reduction in endothelium-derived vasodilation. Physical exercise can have a positive effect on endothelial dysfunction in patients with coronary artery disease, chronic heart failure and diabetes mellitus. It is not clear, however, whether an exercise program influences endothelial function in diabetics with chronic heart failure. Our study was thus aimed at investigating whether a special exercise program would affect endothelial function. Comparisons were made with insulin-treated type 2 diabetics and with non-diabetics suffering from chronic heart failure. 42 patients with severe chronic heart failure (LVEF < or = 30%), insulin-dependent diabetics (n=20, mean age 67+/-6 yrs, 16 male, 4 female), non-diabetics (n=22, mean age 68+/-10 yrs, 20 male, 2 female) participated in a 4-week exercise program consisting of ergometer and special muscle strength training. Before (T1) and at the end (T2) of the training program endothelium-dependent and endothelium-independent vasodilatory capacity were assessed by brachial artery diameter measurement. At the end of the training program, there were no significant results within the two groups. The endothelium-dependent vasodilation changed between T1 and T2 as follows: In the diabetic group, the endothelium-dependent vasodilation at T1 and T2 was 5.1+/-3.6 and 4.9+/-2.5%, respectively. For the non-diabetics, the endothelium-dependent vasodilation was 6.8+/-4.5 and 7.6+/-4.0% at T1 and T2, respectively. The endothelium-independent vasodilation in the diabetics was 10.5+/-5.6 at T1 and dropped to 8.7+/-4.1% at T2. The results for the non-diabetics were 13.2+/-5.8 and 12.3+/-6.3% at T1 and T2, respectively. The LVEF in the diabetics was 24.2+/-3.4% at T1, increasing to 27.8+/-5.8% at T2. In the non-diabetics, the LVEF was 22.9+/-3.8 at T1 vs. 28.6+/-6.9% at T2. In the groups of diabetics, the maximum oxygen uptake (VO2-max) was 10.3+/-3.9 at T1 vs. 11.4+/-2.8 ml/kg/min at T2 and in the group of non-diabetics 10.0+/-3.1 vs. 13.5+/-5.0 ml/kg/min. No correlations were found between the change in endothelium-dependent vasodilation and the increase in oxygen uptake. In our study, a program of physical exercise had no influence on endothelium-dependent or endothelium-independent vasodilation in insulin-treated type 2 diabetics or in non-diabetics with considerably reduced ejection fraction. In both groups, however, an exercise-related influence on medical parameters and physical performance could be observed.
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