Document Type : Original Article
Authors
1 Cardiovascular Department of Sport Sciences faculty, Guilan University of Iran
2 Rajaie Cardiovascular, Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran.
3 Veterinary Surgeon, Rajaie Cardiovascular, Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran.
4 Professor, Dept. of Cardiovascular Exercise Physiology, facultyof Exercise Sciences, Guilan University, Rasht, Iran
Abstract
Background & Objectives: Myocardial infarction (MI) is a common heart disease in humans, and mitochondrial dysfunction has been implicated in its development. Exercising plays a protective role against the disease; however, the role of certain proteins and mitophagy is not well understood. The aim of this study was to investigate the effects of exercise intensity on the levels of mitochondrial proteins and reactive oxygen species (ROS) in the heart tissue of male rats post MI.
Materials & Methods: We induced MI in 40 male Wistar rats by ligating left anterior descending artery. Animals were divided into five groups as follows: three exercise groups (high, moderate & low) post MI, one sedentary group post MI, and one control group without MI or exercising. The levels of P62 and Parkin proteins, and ROS were determined in the heart tissue by ELISA and DCFDA methods.
Results: Data analysis showed the levels of free P62 and Parkin proteins decreased significantly in the sedentary group compared to those in the controls (P≤0.05). The cardiac tissue ROS level decreased significantly in the moderate intensity group compared to that in the sedentary group, but it increased compared to that of the control group (P≤0.05).
Conclusions: Moderate-intensity exercise significantly increased the levels of free P62 and Parkin proteins and reduced the ROS in the heart tissue post MI. The findings support the hypothesis that improvements in the levels of ROS and proteins involved in the mitophagy are stimulated by performing moderate intensity exercises
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