1- Department of Physical Education, Farhangian University, Tehran, Iran
2- Department of Sport Sciences, School of Education and Psychology, Shiraz university, Shiraz, Iran
3- Department of Sports Physiology, Faculty of physical and Sports Sciences, University of Tehran, Tehran, Iran , arman.rastegari@ut.ac.ir
4- Department of Sport Sciences, Apadana Institute of Higher Education, Shiraz, Iran
Abstract: (506 Views)
Background: Muscle atrophy is one of the serious complications of type 1 diabetes. Important cellular mechanisms including pathways related to mTOR protein are very important in regulating muscle mass; Therefore, this research was conducted to investigate the effect of high-intensity interval training (HIIT) on the intracellular content of the central protein of mechanical target of rapamycin 1/2 complexes in EDL skeletal muscle of rats with type 1 diabetes.
Methods: In this experimental study, 12 three-month-old male Sprague-Dawley rats with an average weight of 300±20 grams were selected. Type 1 diabetes was induced through intraperitoneal injection of streptozotocin solution (50 mg/kg of body weight). These rats were randomly divided into two groups, diabetic exercise, and diabetic control; The training group performed HIIT for six weeks at an intensity of 85-95% of maximum speed. Data analysis was done through an independent t-test in SPSS software version 28. A significance level of 0.05 was considered.
Results: The intracellular content of total and phosphorylated forms of mTOR protein showed a significant increase after six weeks of HIIT (P=0.0001). Also, the ratio of total to phosphorylated intracellular content of mTOR protein showed a significant increase in the training group compared to the control group (P=0.0001).
Conclusion: HIIT increased the intracellular content of total and phosphorylated forms of mTOR protein, which could possibly lead to protein synthesis and increased muscle hypertrophy.
Type of Study:
Research |
Subject:
Special Received: 2023/06/13 | Accepted: 2023/08/22 | Published: 2023/12/31