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: issue_documents_importer
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.

References

  • 1.

    Jorge L, Rodrigues B, Teodoro Rosa K, Malfitano Ch, Alba Loureiro TC, Medeiros A, et al. Cardiac and peripheral adjustments induced by early exercise training intervention were associated with autonomic improvement in infarcted rats: role in functional capacity and mortality. Eur Heart J 2010; 32: 904-912.

  • 2.

    Okada H, Takemura G, Kosai KI, Li Y, Takahashi T, Esaki M, Yuge K, et al. Postinfarction gene therapy against transforming growth factor-beta signal modulates infarct tissue dynamics and attenuates left ventricular remode- ling and heart failure. Circulation 2005; 111: 2430-2437.

  • 3.

    Xu X, et al. remodelling in rats. Cardiovascular Research 2008; 78: 523-37.

  • 4.

    Heinemeier KM, Bjerrum SS, Schjerling P, Kjaer M. Expression of extracellular matrix components and related growth factors in human tendon and muscle after acute exercise. Scand J Med Sci Sports 2013; 23: 150-161.

  • 5.

    Morris JN, Crawford MD. Coronary heart disease and physical activity of work. Br Med J 1958; 2: 1485-1490.

  • 6.

    Garza MA, Wason EA, Zhang JQ. Cardiac remodeling and physical training post myocardial infarction. World J Cardiol 2015; 26: 52-64.

  • 7.

    Golbashi R, Gaeini A, Kordi MR, Aboutaleb N, Ghardashi Afousi A. Effect of one period of high-intensity intervaltraining on myocardial collagen-1 and TGF-1and cardiac function in post ischemiareperfusion rats. Daneshvar 2018; 25. (Persian).##.

  • 8.

    Holloway TM, Bloemberg D, da Silva ML, Simpson JA, Quadrilatero J, Spriet LL. High intensity interval and endurance training have opposing effects on markers of heart failure and cardiac remodeling in hypertensive rats. PloS One 2015; 10: e0121138.

  • 9.

    Yengo CM, Zimmerman SD, McCormick RJ, Thomas DP. Exercise training post-MI favorably modifies heart extracellular matrix in the rat. Med Sci Sports Exerc 2012; 44: 1005-1012.

  • 10.

    Kraljevic J, Marinovic J, Pravdic D, Zubin P, Dujic Z, Wisloff U, Ljubkovic M. Aerobic interval training attenuates remodelling and mitochondrial dysfunction in the post-infarction failing rat heart. Cardiovasc Res 2013; 99: 55-64.

  • 11.

    Van Laake LW, Hassink R, Doevendans PA, Mummery C. Heart repair and stem cells. J Physiol 2006; 577: 467-478.

  • 12.

    Lu K. Effects of high-intensity interval versus continuous moderate-intensity aerobic exercise on apoptosis, oxidative stress and metabolism of the infarcted myocardium in a rat model. Mol Med Rep 2015; 12: 2374-2382.

  • 13.

    Yadegari M, Riahy S, Mirdar S, Hamidian G. Effect of the adiantum capillus veneris extract on bax and Bcl2 apoptotic markers of lung modulation in trained rats and exposed to hypoxic stress. J Med Plants 2018; 2: 162-171.

  • 14.

    Di Cataldo S, Ficarra E, Acquaviva A, Macii E. Automated segmentation of tissue images forcomputerized IHC analysis. Comp Methods Prog Biomed 2010; 100: 1-15.

  • 15.

    Fan D, Takawale A, Lee J, Kassiri Z. Cardiac fibroblasts, fibrosis and extracellular matrix remodeling in heart disease. Fibrogenesis Tissue Repair 2012; 5: 15.

  • 16.

    Gourdie RG, Dimmeler S, Kohl P. Novel therapeutic strategies targeting fibroblasts and fibrosis in heart disease. Nat Rev Drug Discov 2016; 5: 620-638.

  • 17.

    Puhl SL, Mller A, Wagner M, Devaux Y, Bhm M, Wagner DR, Maack Ch. Exercise limits scar thinning after myocardial infarction in mice. Am J Physiol Heart Circ Physiol 2015; 309: 345-359.

  • 18.

    Liao Z, Dan Y. Early moderate exercise benefits myocardial infarction healing via improvement of inflammation and ventricular remodeling in rats. Cell Mol Med 2010; 23: 28-42.

  • 19.

    Ramez M, Rajabi H, Ramezani F, Naderi N, Darbandi-Azar A, Nasirinezhad F. The greater effect of high-intensity interval training versus moderate-intensity continuous training on cardioprotection against ischemia-reperfusion injury through Klotho levels and attenuate of myocardial TRPC6 expression. BMC Cardiovasc Disord 2019; 19: 118.

  • 20.

    Orenstein TL, Parker TG, Butany JW, Goodman JM, Dawood F, Wen WH, et al. Favorable left ventricular remodeling following large myocardial infarction by exercise training. Effect on ventricular morphology and gene expression. J Clin Invest 1955; 96: 858-866.

  • 21.

    Azamianjazi A, Hafezi M, Cheraghi J, Abdi H. The combined effect of endurance trainin and atorvastatin on the extent of necrosis damageand fibrosis tissue in male wistar rats heart after experimental myocardial infarction. Sci J Ilam Univ Med Sci 2015; 28. (Persian).

  • 22.

    Jain M, Liao R, Ngoy S, Whittaker P, Apstein CS, Eberli FR. Angiotensin II receptor blockade attenuates the deleterious effects of exercise training on post-MI ventricular remodelling in rats. Cardiovasc Res 2000; 46: 66-72.##https://doi.org/10.1016/S0008-6363(99)00429-0.

  • 23.

    Batista DF, Gonalves AF, Rafacho BP, Santos PP, Minicucci MF, Azevedo PS, et al. Delayed rather than early exercise training attenuates ventricular remodeling after myocardial infarction. Int J Cardiol 2013; 170: e3-e4.

  • 24.

    Holloway TM, Bloemberg D, da Silva ML, Simpson JA, Quadrilatero J, Spriet LL. High intensity interval and endurance training have opposing effects on markers of heart failure and cardiac remodeling in hypertensive rats. PloS One 2015; 10: 121138.

  • 25.

    Hu J, Van den Steen PE, Sang QA, Opdenakker G. Matrix metalloproteinase inhibitors as therapy for inflammatory and vascular diseases. Nat Rev Drug Discov 2007; 6: 480-498.