Effect of high- intensity interval training on tissue changes of collagen type 1 and fibrosis percent in male rats with myocardial infarction

authors:

avatar Rahman Soori ORCID , * , avatar Parisa Pournemati , avatar zahra mosayebi

Koomesh: Vol.23, issue 2; 267-274
published online: June 07, 2021
article type: Research Article
received: January 01, 2020
accepted: September 07, 2020

how to cite: Soori R, Pournemati P, mosayebi Z. Effect of high- intensity interval training on tissue changes of collagen type 1 and fibrosis percent in male rats with myocardial infarction. koomesh. 2021;23(2):e153265. 

Abstract

Introduction: Myocardial infarction (MI) is defined pathologically as cardiac muscle cell death due to abnormal blood flow, prolonged coronary artery ischemia, and replacement of cardiac tissue necrosis as a dense fibrotic lesion. Expression of collagen-1 protein levels and fibrosis increase after myocardial infarction in cardiac tissue. The aim of present study was to investigate the effect of high- intensity interval training in tissue levels of collagen-1 and fibrosis in male rats with MI. Materials and Methods: Thirty male Wistar rats (weight: 270±25gr) were randomly divided into three groups (n =10 each): Healthy control (sham), MI (control), and MI (trained). Correspondingly, in order to induce MI, the rats underwent left-anterior descending-coronary-artery coronary artery bypass grafting and then MI was confirmed by echocardiography. The rats performed the exercise protocols for 8 weeks and 5 sessions per week. At the end of intervention, the rats were sacrificed and the data were analyzed (P≤0.05). Results: The expression of levels of collagen-1 and fibrosis in cardiac tissue of rats with MI was significantly lower than control group (P≤0.001). Conclusion: It seems that high- intensity interval exercises can prevent the negative effects of scar and fibrosis by attenuating the expression of tissue levels of collagen-1 and fibrosis in the cardiac tissue of rats with myocardial infarction, which is an important mechanism for cardiac function and prevention of heart damage.

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