Effects of Low Intensity Exercise Against Apoptosis and Oxidative Stress in Streptozotocin-induced Diabetic Rat Heart

Abstract

The aim of this study was to investigate the effects of low intensity exercise on heart of streptozotocin (STZ)-induced diabetic rats. The rats were randomly divided into 3 experimental groups: A (control), B (diabetic untreated), and C (diabetic treated with low intensity exercise); each group contains 8 animals. B and C groups received STZ. Diabetes was induced in 2 groups by a single intraperitoneal (i.p) injection of STZ (40 mg/kg, freshly dissolved in 0,1 M citrate buffer, pH 4.2). 2 days after STZ treatment, diabetes in 2 experimental groups was confirmed by measuring blood glucose levels. Rats with blood glucose levels of 250 mg/dl or higher were considered to be diabetic. Animals in the exercise group were made to run the treadmill once a day for 4 consecutive weeks. Exercise started 3 days prior to STZ administration. After induction of diabetes, histological abnormalities were observed, including myofibrillar loss, vacuolization of cytoplasm and irregularity of myofibrils. These alterations were attenuated by low intensity exercise. Our data indicates a significant reduction of oxidative stress and apoptosis in cardiomyocytes after exercise. Treatment of diabetic animals with low intensity exercise, decreased the elevated tissue malondialdehyde (MDA) levels and increased the reduced activities of the enzymatic antioxidants superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in cardiac tissue. These findings suggest that low intensity exercise has a therapeutic protective effect in diabetes by decreasing oxidative stress and apoptosis, and by preservation of myocardial integrity.

High‐Intensity Exercise Reduces Cardiac Fibrosis and Hypertrophy but Does Not Restore the Nitroso‐Redox Imbalance in Diabetic Cardiomyopathy

“…Interestingly, the high-intensity training increased the degree of apoptosis. This is contrary to what has been observed in rats under low-intensity exercise [18], which reduced the apoptotic index associated with a recovery in the level of antioxidant enzymes glutathione peroxidase, catalase, and superoxide dismutase. Nevertheless, in that study, plasma levels of glucose reached about 300 mg/dL in the diabetic animals, much lower compared to those in our study (around 600 mg/dL in the diabetic rats).…”

“…A recent report indicates that intense exercise is associated to reduction in the risk of cardiovascular events in type 1 diabetes patients [16]. In animal models of type 1 diabetes, low-to-moderate exercise training has been found to improve cardiac glucose metabolism [17], reduce apoptosis [18], and improve ventricular function [19]. …”

“…As mentioned before, in animal models of type 1 diabetes, low- and moderate-intensity exercise have been reported to reverse or prevent some of the cardiac maladaptations of diabetic cardiomyopathy [18, 24]. Nevertheless, the information regarding high-intensity exercise in diabetic cardiomyopathy is less abundant.…”

Aerobic exercise protects against pressure overload-induced cardiac dysfunction and hypertrophy via β3-AR-nNOS-NO activation

“…SOD levels may reflect the ability to scavenge free radicals. In accordance with previous study [51], our results suggest that SOD activity was increased by aerobic exercise training. Furthermore, the decrease in MDA and the increase in SOD induced by aerobic exercise was abolished by treatment with SR59230A.…”

Enhancement of beta-catenin in cardiomyocytes suppresses survival protein expression but promotes apoptosis and fibrosis

“…Streptozotocin (STZ) was previously shown to induce diabetes in rats [29][30][31][32]; therefore, it was administered in the animal model. All animals were acclimatized to the lab conditions for 1 week after their arrival prior to the experiment.…”