title: Exercise-induced cardioprotection against myocardial ischemia-reperfusion injury.
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.
authors.affiliation: Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL 32611, USA. spowers@hhp.ufl.edu
authors.forename: Scott K
authors.initials: SK
authors.lastname: Powers
authors.forename: John C
authors.initials: JC
authors.lastname: Quindry
authors.forename: Andreas N
authors.initials: AN
authors.lastname: Kavazis
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000502:physiology; D003326:Coronary Circulation / Q000502:physiology; D051546:Cyclooxygenase 2 / Q000378:metabolism / Q000502:physiology; D019610:Cytoprotection / Q000502:physiology*; D004721:Endoplasmic Reticulum / Q000378:metabolism; D015444:Exercise / Q000502:physiology*; D006321:Heart / Q000502:physiology*; D006360:Heat-Shock Proteins / Q000378:metabolism / Q000502:physiology; D006801:Humans; D054086:KATP Channels / Q000378:metabolism / Q000502:physiology; D008929:Mitochondria, Heart / Q000378:metabolism / Q000502:physiology; D008954:Models, Biological; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000517:prevention & control*; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism; D010805:Physical Conditioning, Animal / Q000502:physiology; D012508:Sarcolemma / Q000378:metabolism
chemical_list: D000975:Antioxidants; D006360:Heat-Shock Proteins; D054086:KATP Channels; D051546:Cyclooxygenase 2