The glucoregulatory response to high-intensity aerobic exercise following training in rats with insulin-treated type 1 diabetes mellitus

Abstract

An acute bout of exercise elicits a rapid, potentially deleterious, reduction in blood glucose in patients with type 1 diabetes mellitus (T1DM). In the current study, we examined whether a 10-week aerobic training program could alleviate the rapid exercise-associated reduction in blood glucose through changes in the glucoregulatory hormonal response or increased hepatic glycogen storage in an insulin-treated rat model of T1DM. Thirty-two male Sprague-Dawley rats were divided evenly into 4 groups: non-T1DM sedentary (C) (n = 8), non-T1DM exercised (CX) (n = 8), T1DM sedentary (D) (n = 8), and T1DM exercised (DX) (n = 8). Exercise training consisted of treadmill running for 5 days/week (1 h, 27 m/min, 6% grade) for 10 weeks. T1DM was induced by multiple streptozotocin injections (20 mg/kg) followed by implantation of subcutaneous insulin pellets. At week 1, an acute exercise bout led to a significant reduction in blood glucose in DX (p < 0.05), whereas CX exhibited an increase in blood glucose (p < 0.05). During acute exercise, serum epinephrine was increased in both DX and CX (p < 0.05), whereas serum glucagon was increased during recovery only in CX (p < 0.01). Following aerobic training in DX, the exercise-mediated reduction in blood glucose remained; however, serum glucagon increased to the same extent as in CX (p < 0.05). DX exhibited significantly less hepatic glycogen (p < 0.001) despite elevations in glycogenic proteins in the liver (p < 0.05). Elevated serum epinephrine and decreased hepatic adrenergic receptor expression were also evident in DX (p < 0.05). In summary, despite aerobic training in DX, abrupt blood glucose reductions and hepatic glycogen deficiencies were evident. These data suggest that sympathetic overactivity may contribute to deficiencies in hepatic glycogen storage.

Effect of moderate and high intensity chronic exercise on the pancreatic islet morphometry in healthy rats: BDNF receptor participation

“…Furthermore, previous authors reported that the high intensity training in rats increases the epinephrine levels in the plasma, 29 Although, at the moment, only has been reported the negative effect of the epinephrine on the b cell function, 30,31 we not discard the negative epinephrine effect on the b cell survival, thus the epinephrine could modify the b cells percentage after the high intensity training (Fig. 3).…”

Aerobic exercise regulates blood lipid and insulin resistance via the toll‑like receptor 4‑mediated extracellular signal‑regulated kinases/AMP‑activated protein kinases signaling pathway

“…Currently, exercise treatments combined with diets have been analyzed in patients with diabetes mellitus by kerberos authentication protocol and data mining. In addition, studies have evidenced that exercise treatments may improve diabetes mellitus-induced myocardial ischemia and failure in patients in the clinical setting (46). Currently, oxidative stress followed by excessive apoptosis frequently occurs in the liver of patients with type-ІІ diabetes mellitus (47).…”

Exercise Training Induced Cardioprotection with Moderate Hyperglycemia versus Sedentary Intensive Glycemic Control in Type 1 Diabetic Rats

“…The measure of insulin resistance was considered the AUC of the IVGTT multiplied by exogenous insulin concentration. We have previously reported that when using this T1DM model, sedentary rats can become insulin resistant and require substantial more exogenous insulin in order to maintain the desired blood glucose concentrations [ 15 , 24 ]. Accordingly, when determining the insulin resistance measure, the amount of circulating insulin present in the rat during the IVGTT was factored into the calculation.…”

“…Additionally, it has been established both experimentally [ 15 ] and clinically [ 16 ] that poor glycemic control leads to hepatic glycogen deficiencies. Restoration of hepatic glycogen content could represent a mechanism for combatting hypoglycemia, as hepatic glycogen is the predominant source of blood glucose during exercise [ 17 ] and insulin overcorrection [ 18 ].…”

“…Restoration of hepatic glycogen content could represent a mechanism for combatting hypoglycemia, as hepatic glycogen is the predominant source of blood glucose during exercise [ 17 ] and insulin overcorrection [ 18 ]. Our laboratory has recently shown that ten weeks of AT high fails to normalize hepatic glycogen in T1DM rats despite significantly elevated levels of hepatic glycogenic storage enzymes [ 15 ]. In contrast, resistance training (RT) has been shown to increase hepatic glycogen content in rats [ 19 ], while also alleviating the risk of exercise-induced hypoglycemia in T1DM [ 4 , 20 ].…”