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Aging, Exercise, and Cardioprotection
SCOTT K. POWERS,
JOHN QUINDRY AND
KARYN HAMILTON
Department of Exercise and Sport Sciences and Physiology, Center for Exercise Science, University of Florida, Gainesville, Florida 32611, USA
Address for correspondence: Scott K. Powers, Department of Exercise and Sport Sciences, Center for Exercise Science, University of Florida, Gainesville, FL 32611. Voice: 352-392-9575, ext. 1343; fax: 352-392-0316. spowers{at}hhp.ufl.edu Ann. N.Y. Acad. Sci. 1019: 462-470 (2004).
Myocardial ischemia-reperfusion (I-R) injury is a major contributor to the morbidity and mortality associated with coronary artery disease. The incidence of I-R events is greatest in older persons, and studies also indicate that the magnitude of myocardial I-R injury is greater in senescent individuals compared to younger adults. Regular exercise has been confirmed as a pragmatic countermeasure to protect against I-R-induced cardiac injury. Specifically, endurance exercise has been proven to provide cardioprotection against an I-R insult in both young and old animals. Proposed mechanisms to explain the cardioprotective effect of exercise include the induction of myocardial heat shock proteins (HSPs), improved cardiac antioxidant capacity, and/or elevation of other cardioprotective proteins. Of these potential mechanisms, evidence indicates that elevated myocardial levels of heat shock proteins or antioxidants can provide myocardial protection against I-R injury. At present, which of these protective mechanisms is essential for exercise-induced cardioprotection remains unclear. Understanding the molecular basis for exercise-induced cardioprotection is important in developing exercise paradigms to protect the heart during an I-R insult.
Key Words: heart ischemia-reperfusion antioxidants heat shock proteins
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