No abstract

Background and Objective. Studies have shown that physical activity not only reduces cardiovascular risk factors but also improves cardiac protection against ischemia-reperfusion. One of the protective pathways of the heart against ischemia is mitochondrial function protection, and the role of exercise preconditioning in this mechanism is important. We investigated the exercise pretraining on mitochondrial biogenesis effect, angiogenesis, and cardiac tissue injury in male rats following stroke. Materials and Methods. Twenty-four male rats were divided into 4 groups including MI, Sham, HIIT, and HIIT+MI ( N = 6 ). HIIT and HIIT+MI which underwent high-intensity interval training (HIIT) for 4 weeks (5 days a week). The training protocol included 10 intervals of 1-minute running, with 2 minutes rest between each interval. The training intensity was different every week according to the peak treadmill running speed (v peak) percentage of each rat. Isoproterenol injection was used to induce myocardial infarction (MI). Expressions of creatine kinase-MB (CK-MB), PGC-1α troponin-I, mitochondrial transcription factor A (TFAM), vascular endothelial growth factor (VEGF), and microRNA 126 (miR-126) genes were measured. The variables were measured using biochemical and RT-PCR methods. The significance level ( P value≤0.05) was analyzed using ANOVA test. Results. The results showed that 4 weeks of HIIT training led to a significant increase in PGC-1α, TFAm, and VEGF levels in the MI, HIIT, and HIIT+MI groups compared to the sham group ( P = 0.001 ). HIIT exercises increased miR-126 in the different groups compared to the sham group; however, it was not significant. Conclusion. The results obtained showed that HIIT exercise exerts cardio-protective effects to reduce cardiac tissue injury and necrosis against MI. These effects increase mitochondrial biogenesis and angiogenesis by inducing the increased expression of VEGF, TFAM, PGC-1α, and miR-126 genes in the heart tissue. Therefore, HIIT training, as a preconditioning program, was able to protect the cardiac tissue against MI.