Physical activity and diabetic cardiomyopathy: myocardial adaptation depending on exercise load.

Diabetes mellitus (DM), an increasing health problem worldwide, is associated with severe cardiovascular complications. To date, the beneficial effects of physical activity in both prevention and treatment of DM and its complications are well established. Nevertheless, it appears that exercise training, depending on the load, exerts differential effects on the myocardium. Hence, in this review, the impact of exercise training, focusing on exercise modalities and adaptations in response to load, on diabetic cardiovascular function, are discussed. Molecular mechanisms that may be involved in these adaptions to exercise training are also addressed.

Effects of exercise training combined with insulin treatment on cardiac NOS1 signaling pathways in type 1 diabetic rats.

This study examined the effects of a dual treatment combining insulin treatment and exercise training on basal cardiac function and signaling pathways involving ß3-AR, NOS1, and RyR2 in type 1 diabetic rats. Male Wistar rats were assigned into a diabetic group receiving no treatment (D), an insulin-treated diabetic (Ins), a trained diabetic (TD), and a trained insulin-treated diabetic (TIns) group. Control group (C) was included in order to confirm the deleterious effects of diabetes. Insulin treatment and/or treadmill exercise training were conducted for 8 weeks. Basal cardiac function was evaluated by Langendorff technique. Cardiac protein expression of ß3-AR, NOS1, and RyR2 was assessed using Western blots. Diabetes induced a decrease of both basal diastolic and systolic (±dP/dt) cardiac function (P < 0.05). Moreover, diabetes was associated with an increase of ß3-AR and NOS1 and a decrease of RyR2 expression (P < 0.05). Although combined treatment was not able to normalize -dP/dt, it succeeded to normalize +dP/dt of diabetic rats. Combined treatment led to an overexpression of RyR2. Effects of this combined treatment on +dP/dt and RyR2 were greater than the effects of insulin and exercise training, applied solely. Treatments, applied solely or in combination, resulted in a complete normalization of ß3-AR and in a down-regulation of NOS1 because this protein expression in all treated diabetic rats became lower than control values (P < 0.01). Our study shows that unlike single treatments, dual treatment combining insulin treatment and exercise training was able to normalize basal systolic function of diabetic rats by a specific regulation of ß3-AR-NOS1-RyR2 signaling pathways.

Intense exercise training induces adaptation in expression and responsiveness of cardiac ß-adrenoceptors in diabetic rats.

BACKGROUND: Informations about the effects of intense exercise training on diabetes-induced myocardial dysfunctions are lacking. We have examined the effects of intense exercise training on the cardiac function of diabetic rats, especially focusing on the Langendorff ß-adrenergic responsiveness and on the ß-adrenoceptors protein expression. METHODS: Control or Streptozotocin induced-diabetic male Wistar rats were randomly assigned to sedentary or trained groups. The training program consisted of 8 weeks running on a treadmill (10° incline, up to 25 m/min, 60 min/day) and was considered to be intense for diabetic rats. RESULTS: This intense exercise training amplified the in vivo diabetes-induced bradycardia. It had no effect on Langendorff basal cardiac contraction and relaxation performances in control and diabetic rats. In diabetic rats, it accentuated the Langendorff reduced responsiveness to ß-adrenergic stimulation. It did not blunt the diabetes-induced decrease of ß1-adrenoceptors protein expression, displayed a significant decrease in the ß2-adrenoceptors protein expression and normalized the ß3-adrenoceptors protein expression. CONCLUSIONS: Intense exercise training accentuated the decrease in the myocardial responsiveness to ß-adrenergic stimulation induced by diabetes. This defect stems principally from the ß2-adrenoceptors protein expression reduction. Thus, these results demonstrate that intense exercise training induces specific effects on the ß-adrenergic system in diabetes.