MnSOD antisense treatment and exercise-induced protection against arrhythmias

Karyn L. Hamilton, John C. Quindry, Joel P. French, Jess Staib, Jeffrey Hughes, Jawahar L. Mehta, Scott K. Powers

Research output: Contribution to journalArticlepeer-review

69 Scopus citations


Exercise provides protection against ischemia-reperfusion (I-R)-induced arrhythmias, myocardial stunning, and infarction. An exercise-induced increase in myocardial manganese superoxide dismutase (MnSOD) activity has been reported to be vital for protection against infarction. However, whether MnSOD is essential for exercise-induced protection against ventricular arrhythmias is unknown. We determined the effects of preventing the exercise-induced increase in MnSOD activity on arrhythmias during I-R resulting in myocardial stunning. Male rats remained sedentary or were subjected to successive bouts of endurance exercise. During in vivo myocardial I-R, the incidence of arrhythmias was significantly lower in the exercise-trained rats than in the sedentary rats as evidenced by the arrhythmia. When exercised rats were pretreated with antisense oligonucleotides directed against MnSOD, protection from arrhythmias was attenuated. Moreover, I-R resulted in significant increases in nitro-tyrosine (NT) in the sedentary group. Exercise abolished this I-R-induced NT formation but this protection was unchanged by antisense treatment. Protein carbonyls were increased by I-R, but neither exercise nor antisense treatment impacted carbonyl formation. These data demonstrate that an exercise-induced increase in MnSOD activity is important for protection against arrhythmias. The mechanism by which MnSOD provides protection does not appear to be linked to protein nitrosylation or oxidation.

Original languageEnglish
Pages (from-to)1360-1368
Number of pages9
JournalFree Radical Biology and Medicine
Issue number9
StatePublished - Nov 1 2004


  • Antioxidants
  • Arrhythmia
  • Carbonyls
  • Exercise
  • Free radicals
  • Ischemia
  • Nitro-tyrosine


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