The experimental literature of the foregoing decade has furnished an assemblage of mechanisms explaining the metabolic perturbations and overall decline in cardiac performance implicated in the pathogenesis of diabetes mellitus. Particularly, the experimentally-induced diabetic rat model has been indispensable in the examination of diabetic cardiomyopathy, an entity distinctly separable from atherosclerosis, hypertension, coronary artery disease and valvular dysfunction, yet convincingly attributable to the increase in cardiac-associated mortality commonly observed in the diabetic patient. The widespread epidemic of diabetes mellitus in developed societies has elicited considerable attention and the role of exercise as an adjuvant therapy in diabetes management has been increasingly emphasized. However, the evidence endorsing the beneficial attributes of exercise in the diabetic state is indeterminate despite markedly observed increases in myocardial and skeletal muscle glucose homeostasis, endothelial and autonomic function, insulin sensitivity and amelioration of diabetes pathogenesis. As evidenced by review of the experimental literature, a mild to moderately intense exercise regime may be a reliably implicated insulin-sensitizing therapy for the experimentally-diabetic rat model as well as the human diabetic patient. Notably, the cardio-protective and metabolic benefits of aerobic exercise are seemingly more pronounced in those individuals most susceptible to diabetes progression.
Keywords: Diabetes, Streptozotocin, Exercise, GLUT, Cardiac, Metabolism
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