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1 Myocardial Biology Unit, Boston University Medical Center, Boston, MA, USA
2 Department of Exercise and Sport Sciences, Pharmaceutics, and Physiology, University of Florida, Gainesville, FL, USA
3 Department of Medicine, Division of Cardiology, University of Arkansas Health Science Center, Little Rock, AR, USA
* To whom correspondence should be addressed. E-mail: spowers{at}hhp.ufl.edu.
Endurance exercise provides cardioprotection against ischemia-reperfusion (I-R)-induced myocardial stunning and infarction. A recent study demonstrates that an exercise-induced increase in myocardial manganese superoxide dismutase (MnSOD) activity is essential to protect the heart against infarction. It is unknown if an elevation in cardiac MnSOD is also a prerequisite to achieve exercise-induced protection against myocardial stunning. Therefore, this study determined if an exercise-induced increase in myocardial MnSOD activity is a requirement to achieve protection against myocardial stunning. Adult male rats remained sedentary or performed successive bouts of endurance exercise. Hearts were exposed to 25 min of global ischemia followed by reperfusion in an isolated working heart preparation. Post-ischemic recovery of cardiac external work during reperfusion was significantly higher (84±3% vs. 67±4%) in exercised animals compared to sedentary controls. Further, prevention of exercise-induced expression of myocardial MnSOD via antisense oligonucleotides did not retard this exercise-induced protection against myocardial stunning. These data demonstrate that exercise-induced increases in cardiac MnSOD activity are not essential to achieve exercise-mediated protection against myocardial stunning. Therefore, we conclude that different mediators are responsible for exercise-induced cardioprotection against myocardial stunning and infarction.
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