Aerobic training: an approach to regulate oxidative stress in heart tissue of diabetic rats

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

Authors

1 Assistant Professor, Department of Exercise Physiology, Faculty of Physical Education and Sports Sciences, Tabriz University, Tabriz, Iran; epiralaiy@yahoo.com

2 Ph.D student, Exercise physiology, Department of Exercise Physiology, Faculty of Physical Education and Sports Sciences, University of Tabriz, Tabriz, Iran.

Abstract

Aim:  Diabetes increases the production of free radicals and inflammatory agents in the heart tissue. Training plays a role in improving cardiovascular disease, antioxidant activity, and oxidative stress levels. Therefore, this study aimed to investigate the effect of aerobic training on SOD, GPX, TAC, and MDA in the heart tissue of rats with type 2 diabetes. Methods: 24 male rats (weighing 200±20 gr) and (age eight weeks) were randomly divided into four groups: 1) healthy control, 2) diabetic control, 3) healthy training, and 4) diabetic training.   The training protocol was obtained on the treadmill five days per week with the principle of overload in the first week at a speed of 5-10 m/min for 10-15 minutes and in the eighth week at a speed of 18-24 m/min for 60 minutes. The levels of SOD, GPX, TAC, and MDA were measured in heart tissue. One-way ANOVA and Tukey post hoc tests were used at the significance level of P<0.05. Results:  The findings showed that eight weeks of diabetes caused a significant decrease in SOD, GPX, and TAC levels and an increase in glucose and MDA levels (P=0.001). Also, in both healthy training groups (P=0.001) and diabetic training groups (P<0.05) compared to diabetes control, a significant increase in SOD, GPX, and TAC levels and a decrease in glucose and MDA levels were observed. Conclusions:   Aerobic training can reduce the level of glucose and MDA in the heart tissue of diabetic rats and increase SOD, GPX, and TAC activities. In addition, aerobic training may be considered a useful tool for reducing oxidative stress in diabetes.

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References

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History

  • Receive Date: 15 March 2024
  • Revise Date: 12 May 2024
  • Accept Date: 29 May 2024

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