Document Type : Original Article

Authors

1 Ph. D Student in Exercise Physiology, Faculty of Sport Sciences, Razi University, Kermanshah, Iran.

2 Associate Professor, Exercise Physiology Department, Faculty of Sport Sciences, Razi University, Kermanshah, Iran.

Abstract

Background and Aim: The term of diabetic heart disease has veen defined as the term of diabetic heart disease in the presence of a heart problem by the institute of National Health, particularly in some diabetic patient which pathologic left ventricular hypertrophy. However, physical activity can be affect structurally and functionally the myocardium in diabetic patients. Nevertheless; the molecular regulation of physiological heart growth has not been studied well as a supplement therapy protocol against pathologic hypertrophy. Therefore, the present study investigated the effect of 8 weeks of high intensity interval training (HIIT) on phosphatidylinositol kinase 3 (PI3K) gene expression, insulin resistance, heart weight, glucose and serum insulin in male Wistar rats with type 2 diabetes. Materials and Methods: Twenty male Wistar rats, 10 weeks old, weight 120±20gr were randomly divided into two groups including HIIT and control groups. After familiarization, the training group was participated in an 8-week of training protocol, 5 sessions per week, for 30 minutes per session. The gene expression of PI3K, insulin resistance, serum glucose and insulin levels were measured by the RT-PCR, HOMA -IR hemostasis, and ELISA methods respectively. The data were analyzed by the t-test for independent groups at pResults: The result indicated that in the HIIT group, PI3K expression was significantly higher than control group (p < 0.003). The insulin resistance (p < 0.0001) and serum glucose index (p < 0.0001) were significantly decreased, while serum insulin increased significantly (p < 0.04). In addition, heart weight significantly increased in the exercise group (p < 0.0001). Conclusion: HIIT exercise increases the expression of PI3K gene, stimulates the physiological molecular pathway of hypertrophy and could plays a role in preventing left ventricular hypertrophy as a complementary treatment.

Keywords

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