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1 Department of Exercise and Sport Sciences, University of Florida, Gainesville, FL, USA
2 Division of Cardiovascular Medicine, University of Arkansas for Medical Sciences and Central Arkansas Veterans Healthcare System, Little Rock, AR, USA
* To whom correspondence should be addressed. E-mail: jquindry{at}ufl.edu.
Endurance exercise provides cardioprotection against ischemia-reperfusion (I-R) injury. Exercise-induced cardioprotection is associated with increases in cytoprotective proteins including heat shock protein 72 (HSP72) and increases in antioxidant enzyme activity. Based upon the reported half-life of these putative cardioprotective proteins, we hypothesized that exercise-induced cardioprotection against I-R injury would be lost within days after cessation of exercise. To test this, male rats (4 months) were randomly assigned to one of five experimental groups: 1) sedentary control; 2) exercise followed by 1 day rest; 3) exercise followed by 3 days rest; 4) exercise followed by 9 days rest; 5) exercise followed by 18 days rest. Exercise-induced increases (p<0.05) in left ventricular catalase activity and HSP72 were evident at 1 and 3 days post-exercise. However, at 9 days post-exercise, myocardial HSP72 and catalase levels declined to sedentary control values. To evaluate cardioprotection during recovery from I-R, hearts were isolated, placed in working heart mode, and subjected to 20.5 min global ischemia followed by 30 min reperfusion. Compared to sedentary controls, exercised animals sustained less I-R injury as evidenced by maintenance of a higher (p<0.05) percentage of pre-ischemia cardiac work during reperfusion at 1, 3, and 9 days post-exercise. The exercise-induced cardioprotection vanished by 18 days following exercise cessation. Based upon the time-course of the loss of cardioprotection and the return of HSP72 and catalase to pre-exercise levels, we conclude that HSP72 and catalase are not essential for exercise-induced protection during myocardial stunning. Therefore, other cytoprotective molecules are responsible for providing protection during I-R.
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