We evaluated structural microvascular alterations in the skeletal muscle and left ventricle, as well as endothelium-dependent microvascular reactivity in the skeletal muscle, of diabetic rats subjected to long-term aerobic exercise training.
Methods:
Diabetes was experimentally induced by a combination of a high-fat diet with a single low dose of streptozotocin (35 mg/kg, i.p.). Animals with diabetes were divided into sedentary (DM+SED) and training groups (DM+TR) and compared with rats without diabetes (CON). We then measured maximal exercise capacity, fasting glucose and insulin, endothelium-dependent microvascular reactivity in skeletal muscle, and structural alterations of microvasculature in the skeletal and cardiac muscles.
Results:
Diabetes induced microvascular rarefaction and reduced endothelium-dependent microvascular reactivity. Physical exercise completely reversed microvascular rarefaction in the skeletal muscle (1.85 ± 0.05 vs. 1.17 ± 0.03 capillary/fiber ratio, P < 0.05) and in the left ventricle (0.48 ± 0.66 vs. 0.25 ± 0.01 Vv[cap]/Vv[fib] ratio, P < 0.05) compared with the DM+SED group and normalized the microcirculatory responses to acetylcholine in skeletal muscle (CON 38.76 ± 5.60 vs. DM+TR 30.47% ± 5.77%). As expected, exercise training increased the maximal velocity and exercise tolerance compared with the DM+SED (P < 0.05) and CON (P < 0.05) groups. Exercise training also reduced fasting glucose (P < 0.05) compared with DM+SED and normalized insulin levels compared with CON.
Conclusions:
Our results suggest that long-term physical exercise reverses skeletal and cardiac muscle microvascular rarefaction, as well as impaired endothelium-dependent microvascular reactivity, induced by diabetes in rats.
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