Exercise-induced Cardioprotection Against Myocardial Ischemia-Reperfusion Injury

Free Radic Biol Med. 2008 Jan 15;44(2):193-201. doi: 10.1016/j.freeradbiomed.2007.02.006. Epub 2007 Feb 21.

Abstract

Myocardial ischemia-reperfusion (IR) injury is a major contributor to the morbidity and mortality associated with coronary artery disease. Muscular exercise is a countermeasure to protect against IR-induced cardiac injury in both young and old animals. Specifically, regular bouts of endurance exercise protect the heart against all levels of IR-induced injury. Proposed mechanisms to explain the cardioprotective effects of exercise include alterations in coronary circulation, expression of endoplasmic reticulum stress proteins, increased cyclooxygenase-2 activity, induction of myocardial heat shock proteins, improved cardiac antioxidant capacity, and/or elevation of ATP-sensitive potassium channels on both the sarcolemmal and the mitochondrial inner membranes. Moreover, it seems possible that other, yet to be defined, mechanisms of exercise-induced cardioprotection may also exist. Of the known putative cardioprotective mechanisms, current evidence suggests that elevated myocardial levels of antioxidants and increased expression of sarcolemmal ATP-sensitive potassium channels are both contributors to exercise-induced cardioprotection against IR injury. At present, it is unclear if these two protective mediators act independently or interact to contribute to exercise-induced cardioprotection. Understanding the molecular basis for exercise-induced cardioprotection will provide the required knowledge base to develop therapeutic approaches to protect the heart during an IR insult.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Antioxidants / metabolism
  • Antioxidants / physiology
  • Coronary Circulation / physiology
  • Cyclooxygenase 2 / metabolism
  • Cyclooxygenase 2 / physiology
  • Cytoprotection / physiology*
  • Endoplasmic Reticulum / metabolism
  • Exercise / physiology*
  • Heart / physiology*
  • Heat-Shock Proteins / metabolism
  • Heat-Shock Proteins / physiology
  • Humans
  • KATP Channels / metabolism
  • KATP Channels / physiology
  • Mitochondria, Heart / metabolism
  • Mitochondria, Heart / physiology
  • Models, Biological
  • Myocardial Reperfusion Injury / etiology
  • Myocardial Reperfusion Injury / prevention & control*
  • Myocardium / enzymology
  • Myocardium / metabolism
  • Physical Conditioning, Animal / physiology
  • Sarcolemma / metabolism

Substances

  • Antioxidants
  • Heat-Shock Proteins
  • KATP Channels
  • Cyclooxygenase 2