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Background & aim: Alternative training is a way to improve athletic performance. Oxidative stress caused by periodic exercise programs and pressure on the immune system may cause apoptosis and changes in Bax and Bcl-2 characteristics. Resveratrol may be effective in reducing apoptosis resulting from intermittent exercise. The aim of the present study was to determine the effect of a periodic and complementary reservoir supplementation training on the characteristics of Bax and Bcl-2 in female rats.
 
Methods: In the present experimental study conducted in 2018, 48 Wistar rats with an average weight of 280 g entered the study and were randomly divided into 4 groups: control, periodic exercise, resveratrol supplementation + periodic training and resveratrol. The resveratrol and resveratrol + exercise group was fed 24 mg of the solution daily for 8 weeks. The intermittent training program on treadmills was also scheduled for 8 weeks. At the end of the course, 2 ml of blood was taken to measure the apoptosis characteristics of Bax and Bcl-2. Data were analyzed using Shapiro-Wilk statistical tests, one-way analysis of variance and post-Bonfroni follow-up test.
 
Results: The results indicated a lower average percentage of Bax in the resveratrol group + alternate training and resveratrol than the control group and the alternate training group. The results also indicated a higher percentage of Bcl-2 in the resveratrol group + intermittent exercise and resveratrol than the control group and the alternate training group. Reservoir + alternate exercise (p=.0001 (relative to the periodic and controlled exercise group (p≤ 05).
 
Conclusion: The results of the present study revealed that resveratrol and intermittent exercises improved mitochondrial function and control apoptotic characteristics. Correspondingly, compatibility resulting from interval training and antipyretic effects of resveratrol increased the production of antiseptic proteins and cascade inhibition. Therefore, the balance between Bax and Bcl-2 prevented the death of cellular planning and apoptosis.