Volume 32, Issue 8 (11-2024)
JSSU 2024, 32(8): 8173-8186 |
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Rostami N, Afroundeh R, Seifi-skishahr F, Pourrahim houroghchi A. Effect of Moderate Intensity Interval Training on the Expression of Genes Related to Necroptosis of Heart Tissue in Male Heart Attack Model Rats. JSSU 2024; 32 (8) :8173-8186
URL: http://jssu.ssu.ac.ir/article-1-6230-en.html
URL: http://jssu.ssu.ac.ir/article-1-6230-en.html
Abstract: (84 Views)
Introduction: Myocardial ischemia-reperfusion injury is a set of cellular and molecular patho-mechanisms that lead to the death of living cardiomyocytes and compromised cardiac function. The aim of this study was to determine the effect of moderate intensity interval training on the expression of RIPK-1, RIPK-3 and MLKL genes in the heart of male heart attack model rats.
Methods: In this experimental study, thirty 16-week-old male Wistar rats weighing 220 to 280 gr were randomly divided into three groups: control (healthy), myocardial infarction (MI), and moderate intensity interval training. Myocardial infarction was performed by direct intervention with occlusion in the left anterior descending artery (LAD) for 30 minutes. Interval training protocol was performed three days a week, for 8 weeks, with moderate intensity of 60 minutes of interval running on a treadmill, each interval including 4 minutes of running with an intensity of 65-70% of VO2max and 2 minutes of active recovery with an intensity of 50-60% of VO2max. qRT-PCR method was used to check the gene expression of research variables. Data were compared using SPSS software version 16, one-way analysis of variance and Tukey's post hoc test at a significance level of p<0.05.
Results: The expression of cardiac RIPK-1, RIPK-3 and MLKL genes were higher in the MI group compared to the control group; however, moderate intensity interval training decreased the expression of RIPK-1, RIPK-3 and MLKL genes compared to the MI group (p=0.001 and p=0.006, respectively).
Conclusion: The results of the research showed that myocardial infarction is associated with the activation of the necroptosis cell death pathway, likewise, interval training with moderate intensity has an effect on reducing the expression of necroptosis genes (RIPK1, RIPK3, and MLKL). However, due to the lack of evidences and limitations of research, it still needs more investigations.
Methods: In this experimental study, thirty 16-week-old male Wistar rats weighing 220 to 280 gr were randomly divided into three groups: control (healthy), myocardial infarction (MI), and moderate intensity interval training. Myocardial infarction was performed by direct intervention with occlusion in the left anterior descending artery (LAD) for 30 minutes. Interval training protocol was performed three days a week, for 8 weeks, with moderate intensity of 60 minutes of interval running on a treadmill, each interval including 4 minutes of running with an intensity of 65-70% of VO2max and 2 minutes of active recovery with an intensity of 50-60% of VO2max. qRT-PCR method was used to check the gene expression of research variables. Data were compared using SPSS software version 16, one-way analysis of variance and Tukey's post hoc test at a significance level of p<0.05.
Results: The expression of cardiac RIPK-1, RIPK-3 and MLKL genes were higher in the MI group compared to the control group; however, moderate intensity interval training decreased the expression of RIPK-1, RIPK-3 and MLKL genes compared to the MI group (p=0.001 and p=0.006, respectively).
Conclusion: The results of the research showed that myocardial infarction is associated with the activation of the necroptosis cell death pathway, likewise, interval training with moderate intensity has an effect on reducing the expression of necroptosis genes (RIPK1, RIPK3, and MLKL). However, due to the lack of evidences and limitations of research, it still needs more investigations.
Type of Study: Original article |
Subject:
Exercise Physiology
Received: 2024/06/24 | Accepted: 2024/09/8 | Published: 2024/11/5
Received: 2024/06/24 | Accepted: 2024/09/8 | Published: 2024/11/5
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