Select cardiovascular and metabolic responses of diabetic rats to moderate exercise training

Cardiovascular control in experimental diabetes

“…Studies from our laboratory have shown reduction in vagal tonus and maintenance of sympathetic tonus to the heart evaluated by pharmacological blockade with propranolol and methylatropine, respectively (14,16) (Figure 1), as previously demonstrated by Wegner et al (17), suggesting the presence of cardiac vagal neuropathy. Resting bradycardia in STZ-diabetic rats has been attributed to changes in the sinoatrial node with a consequent reduction in intrinsic HR (14,16,18), although functional alterations in the cholinergic mechanism cannot be excluded as a causal factor.…”

“…In STZ-induced diabetic rats we did not observe changes in sympathetic tonus between sedentary and trained groups, suggesting that the increase in resting HR in trained diabetic rats may be related to the improvement of intrinsic pacemaker regulation (16) (Figure 1). In contrast to the impairment of vagal function observed in normal rats after exercise training by the reduced bradycardia in response to electrical vagal stimulation (55), exercise training did not modify the reduced parasympathetic function observed in diabetic rats (16,17) (Figure 1). Therefore, changes in reflex control of the circulation related to parasympathetic function may persist after exercise training, as demonstrated previously in trained nitric oxide blockade hypertensive rats (54).…”

Exercise training improves cardiac performance in diabetes: in vivo demonstration with quantitative cine-MRI analyses

“…Confirmation of identical effect on this parameter with a drug (captopril) in diabetes, and the possibility of a shared therapeutic mechanism between drug and training in the form of reduced interstitial fibrosis (1,34) suggest that the trained group in this study might have benefited from the improvements in the passive components of cardiac pump function. Meanwhile, the exercise-induced conditioning effect might be speculated for the improvement in active components of cardiac pump function in diabetes, chiefly due to the benefits of training in improving the contractility of LV in diabetic animals (26,42). Exercise training in our study improved the systolic volume dysfunction that occurred with sedentary lifestyle in diabetes.…”

Angiotensin II-NADPH oxidase-derived superoxide mediates diabetes-attenuated cell excitability of aortic baroreceptor neurons

“…Arterial baroreflex dysfunction is a frequent complication of diabetes associated with high morbidity and mortality in symptomatic diabetic patients (17). The function of the baroreflex is decreased in Type 1 diabetic patients (3,20,31) and animals (6,8,34,47). The mechanisms concerning the impairment of the baroreflex are still unclear.…”

“…These findings suggest that endogenous angiotensin II-NADPH oxidase-superoxide signaling contributes to the enhanced HCN currents and the depressed cell excitation in the aortic baroreceptor neurons of diabetic rats. baroreflex; ion channels CLINICAL TRIALS and animal models of type 1 diabetes have demonstrated pathophysiological alterations in the arterial baroreflex control of the cardiovascular function and blood pressure (3,6,8,20,31,34,47), contributing to the overall increased morbidity and mortality in diabetic patients (17, 44). The arterial baroreflex normally minimizes short-term oscillations in blood pressure and maintains a homeostatic state, acting on both the sympathetic and parasympathetic limbs of the autonomic nervous system (22, 33).…”