Abstract
Indices of cardiovascular autonomic neuropathy (CAN) in experimental models of Type 1 diabetes mellitus (T1DM) are often contrary to clinical data. Here, we investigated whether a relatable insulin-treated model of T1DM would induce deficits in cardiovascular (CV) autonomic function more reflective of clinical results and if exercise training could prevent those deficits. Sixty-four rats were divided into four groups: sedentary control (C), sedentary T1DM (D), control exercise (CX), or T1DM exercise (DX). Diabetes was induced via multiple low-dose injections of streptozotocin and blood glucose was maintained at moderate hyperglycemia (9–17 mM) through insulin supplementation. Exercise training consisted of daily treadmill running for 10 weeks. Compared to C, D had blunted baroreflex sensitivity, increased vascular sympathetic tone, increased serum neuropeptide Y (NPY), and decreased intrinsic heart rate. In contrast, DX differed from D in all measures of CAN (except NPY), including heart rate variability. These findings demonstrate that this T1DM model elicits deficits and exercise-mediated improvements to CV autonomic function which are reflective of clinical T1DM.
Highlights
A common and serious complication of Type 1 diabetes mellitus (T1DM) is diabetic autonomic neuropathy [1, 2]
At the end of the study, the body weights of the T1DM groups (D and Exercised T1DM high frequency (HF) (DX)) were lower than non-T1DM groups (C and control exercise (CX)), and exercised groups (CX and DX) weighed less than their nonexercised counterparts (C and D; p < 0.05)
This study showed that high intensity aerobic exercise training can prevent deficits of cardiovascular autonomic function caused by T1DM
Summary
A common and serious complication of Type 1 diabetes mellitus (T1DM) is diabetic autonomic neuropathy [1, 2]. CAN has been reported to increase the mortality of diabetic patients by a factor of 3.45 [4]. The most common methods for assessing CAN are heart rate variability (HRV) analysis and baroreflex sensitivity (BRS) [3, 5, 6]. Autonomic efferents, primarily of the parasympathetic nervous system (PSNS), have decreased activity, reduced responsiveness, and decreased neurochemical activity in the heart [10, 11]. Impairment of central nervous system regions has been reported as the limiting factor of BRS [12, 13]. Reduced heart rate variability (HRV) is often the earliest symptom of CAN [14].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
