Document Type : Research Paper I Open Access I Released under CC BY-NC 4.0 license

Authors

1 . Ph.D. Student of Exercise Physiology, Faculty of Sport Sciences, Shahid Chamran University of Ahvaz, Ahvaz, Iran

2 Professor, Faculty of Physical Education and Sport Sciences, University of Tehran, Tehran, Iran

3 professor Faculty of Physical Education and Sport Sciences, University of Tehran, Tehran,Iran.

4 Assistant Professor, Faculty of Physical Education and Sport Sciences, Alzahra University, Tehran, Iran

Abstract

Diabetic cardiomyopathy (DCM) is one of the most important complications of diabetes and is one of the major causes of death in diabetic patients. DCM at the molecular level is rooted in down regulation of expression or activity of those various proteins involved in maintenance or regulation of intracellular calcium homeostasis. The aim of this study was to investigate the effect of 4 weeks of high intensity interval training (HIIT) on gene expression of calcium channel of ryanodine receptors (RyR2), SERCA2a and phospholamban (PLB) in the heart of diabetic male rats. In this experimental study, 24 male Wistar rats were divided into two groups: sedentary control and HIIT. Diabetes was induced in both groups by intraperitoneal injection of Streptozotocin (STZ) solution. 24 hours after the last training session, the rats were euthanized and their left ventricle was extracted. Real Time-PCR technique was used to determine the gene expression of RyR2, SERCA2a and PLB. To compare the two groups, independent t test was used at alpha level of 0.05. The results revealed that 4 weeks of HIIT significantly increased gene expression of RyR2 in the left ventricle of the heart of HIIT group (P=0.03). Although gene expression of SERCA2a and phospholamban increased, they were not significantly different. Based on these findings, it can be concluded that 4 weeks of HIIT could prevent and  minimize the maladjustments in these 2 proteins affecting cycle of cardiac contraction and reduce the risk of diabetic cardiomyopathy through increased RyR2 gene expression in the heart of diabetic rats.

Keywords

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