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* To whom correspondence should be addressed. E-mail: hcollins{at}med.wayne.edu.
Epidemiological data document that regular exercise protects against the morbidity and mortality associated with ischemic heart disease. Therefore, we tested the hypothesis that daily exercise (DE) increases the ventricular arrhythmia threshold (VAT), induced by coronary artery occlusion, and alters the expression of calcium regulatory proteins. The VAT was defined as the time from coronary occlusion to sustained ventricular tachycardia resulting in a reduction in arterial pressure. To test this hypothesis, we recorded the VAT in conscious sedentary normotensive, sedentary hypertensive and DE hypertensive rats and associated these thresholds with the protein expression of the L-type calcium channel, Na+/Ca2+ exchanger, phospholamban, and SERCA2a. Results document a significantly reduced time to ventricular arrhythmias (sedentary hypertensive; 3.7 ± 0.3 min vs. sedentary normotensive; 4.8 ± 0.3 min), an increased Na+/Ca2+ exchanger protein expression (47%), and a decreased phospholamban protein expression (-34%) in conscious hypertensive rats. DE increased the VAT (5.9 ± 0.2 min), decreased the protein expression of the Na+/Ca2+ exchanger and normalized the protein expression of phospholamban in the hypertensive rats. Thus, DE may be a primary prevention approach for reducing the incidence of arrhythmias by altering calcium regulatory proteins in hypertensive rats.
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