Key result
Four weeks of exercise preconditioning with high-intensity interval training significantly reduced cardiac injury and necrosis markers (CK and LDH) following induced myocardial infarction in male rats.
Why the study?
Exercise training prevents adverse effects of myocardial infarction and ischemia/reperfusion with mitochondria appearing to play a role, prompting investigation into whether HIIT preconditioning affects cardiac damage and mitochondrial dynamic proteins following MI.
Does exercise preconditioning with high-intensity interval training reduce cardiac damage and alter mitochondrial dynamic proteins following induced myocardial infarction in male rats?
Does exercise preconditioning with high-intensity interval training reduce cardiac damage and alter mitochondrial dynamic proteins following induced myocardial infarction in male rats?
Four weeks of high-intensity interval training preconditioning reduces markers of cardiac injury and necrosis following induced myocardial infarction in a rat model, though it does not significantly alter mitochondrial dynamic protein expression.
Answers are grounded in this paper and cite their sources.
HIIT preconditioning may attenuate MI damage via mitochondrial dynamics in rats; leaves open human translation and clinical adoption.
Exercise training prevents the adverse effects of Myocardial Infarction (MI) and Ischemia/Reperfusion (I / R) and it seems that mitochondria have an important role in exercise-induced cardioprotection. So, the purpose of this study was to investigate the effects of exercise preconditioning with 4 weeks of High-Intensity Exercise Training (HIIT) on cardiac damage and mitochondrial dynamic proteins as effective factors in cardiac protection following MI. Twenty Male Wistar rats were randomly divided into 4 groups HIIT + MI, MI, HIIT, and Control. Training groups performed 4 weeks (5 days per week) of high-intensity interval training. HIIT protocol consisted of 10*1min running intervals that were separated by 2 min rest. Training intensity varied every week. For induction of myocardial infarction, a subcutaneous injection of isoproterenol was used. Creatine Kinase (CK) and lactate Dehydrogenase (LDH) were measured in serum and Drp1, and Mfn2 gene expression were measured by the real-time PCR method in the heart tissue. The results of the present study showed that CK and LDH in MI were significantly higher in HIIT + MI (p < 0.05). myocardial infarction results in a significant increase in Drp1 gene expression in the MI and HIIT + MI groups relative to the Control group. The expression of the Drp1 gene was lower in the HIIT + MI group than in the MI group, but it was not statistically significant. Also, the results demonstrated that Mfn2 was no significant difference between the groups (p > 0.05). It seems that four weeks of exercise preconditioning with HIIT training reduced injury and necrosis in cardiac tissue and can increase cardio-protection. Also, no significant effect was observed in reducing Drp1 expression due to HIIT which may indicate the need for a longer training period.
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Ahmadi et al. (2023) studied Myocardial Infarction (n=24). High-Intensity Interval Training (HIIT) vs. No exercise (MI only or Control) was evaluated on Cardiac injury markers (CK and LDH) and mitochondrial dynamic proteins (Drp1, Mfn2 gene expression) (p=<0.05). Four weeks of exercise preconditioning with high-intensity interval training significantly reduced cardiac injury and necrosis markers (CK and LDH) following induced myocardial infarction in male rats.
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