Early moderate exercise benefits myocardial infarction healing via improvement of inflammation and ventricular remodelling in rats

J Cell Mol Med. 2019 Dec;23(12):8328-8342. doi: 10.1111/jcmm.14710. Epub 2019 Oct 15.

Abstract

Thus far, the cellular and molecular mechanisms related to early (especially within 24 hours after acute myocardial infarct (MI)) exercise-mediated beneficial effects on MI have not yet been thoroughly established. In the present study, we demonstrated that acute MI rats that underwent early moderate exercise training beginning one day after MI showed no increase in mortality and displayed significant improvements in MI healing and ventricular remodelling, including an improvement in cardiac function, a decrease in infarct size, cardiomyocyte apoptosis, cardiac fibrosis and cardiomyocyte hypertrophy, and an increase in myocardial angiogenesis, left ventricular wall thickness and the number of cardiac telocytes in the border zone. Integrated miRNA-mRNA profiling analysis performed by the ingenuity pathway analysis system revealed that the inhibition of the TGFB1 regulatory network, activation of leucocytes and migration of leucocytes into the infarct zone comprise the molecular mechanism underlying early moderate exercise-mediated improvements in cardiac fibrosis and the pathological inflammatory response. The findings of the present study demonstrate that early moderate exercise training beginning one day after MI is safe and leads to significantly enhanced MI healing and ventricular remodelling. Understanding the mechanism behind the positive effects of this early training protocol will help us to further tailor suitable cardiac rehabilitation programmes for humans.

Keywords: cardiac telocytes; early post-MI moderate exercise; inflammation; myocardial infarction; remodelling.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Disease Models, Animal
  • Echocardiography
  • Female
  • Gene Expression Profiling / methods
  • Gene Regulatory Networks
  • Heart / physiopathology
  • Humans
  • Inflammation / genetics
  • Inflammation / pathology
  • Inflammation / physiopathology*
  • MicroRNAs / genetics
  • Myocardial Infarction / genetics
  • Myocardial Infarction / pathology
  • Myocardial Infarction / physiopathology*
  • Myocardium / metabolism
  • Myocardium / pathology
  • Myocytes, Cardiac / metabolism
  • Myocytes, Cardiac / pathology
  • Physical Conditioning, Animal / physiology*
  • RNA, Messenger / genetics
  • Rats, Sprague-Dawley
  • Ventricular Remodeling / genetics
  • Ventricular Remodeling / physiology*

Substances

  • MicroRNAs
  • RNA, Messenger