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This Article Full Text Full Text (PDF) All Versions of this Article: 290/6/H2590    most recent 01220.2005v2 01220.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Billman, G. E. Articles by Altschuld, R. A. Search for Related Content PubMed PubMed Citation Articles by Billman, G. E. Articles by Altschuld, R. A.

Endurance exercise training attenuates cardiac ₂-adrenoceptor responsiveness and prevents ventricular fibrillation in animals susceptible to sudden death

¹Department of Physiology and Cell Biology and ²Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio

Submitted 18 November 2005 ; accepted in final form 13 December 2005

Enhanced cardiac ₂-adrenoceptor (₂-AR) responsiveness can increase susceptibility to ventricular fibrillation (VF). Exercise training can decrease cardiac sympathetic activity and could, thereby, reduce ₂-AR responsiveness and decrease the risk for VF. Therefore, dogs with healed myocardial infarctions were subjected to 2 min of coronary occlusion during the last minute of a submaximal exercise test; VF was observed in 20 susceptible, but not in 13 resistant, dogs. The dogs were then subjected to a 10-wk exercise-training program (n = 9 susceptible and 8 resistant) or an equivalent sedentary period (n = 11 susceptible and 5 resistant). Before training, the ₂-AR antagonist ICI-118551 (0.2 mg/kg) significantly reduced the peak contractile (by echocardiography) response to isoproterenol more in the susceptible than in the resistant dogs: –45.5 ± 6.5 vs. –19.2 ± 6.3%. After training, the susceptible and resistant dogs exhibited similar responses to the ₂-AR antagonist: –12.1 ± 5.7 and –16.2 ± 6.4%, respectively. In contrast, ICI-118551 provoked even greater reductions in the isoproterenol response in the sedentary susceptible dogs: –62.3 ± 4.6%. The ₂-AR agonist zinterol (1 µM) elicited significantly smaller increases in isotonic shortening in ventricular myocytes from susceptible dogs after training (n = 8, +7.2 ± 4.8%) than in those from sedentary dogs (n = 7, +42.8 ± 5.8%), a response similar to that of the resistant dogs: +3.0 ± 1.4% (n = 6) and +3.2 ± 1.8% (n = 5) for trained and sedentary, respectively. After training, VF could no longer be induced in the susceptible dogs, whereas four sedentary susceptible dogs died during the 10-wk control period and VF could still be induced in the remaining seven animals. Thus exercise training can restore cardiac -AR balance (by reducing ₂-AR responsiveness) and could, thereby, prevent VF.

-adrenergic receptor; myocardial infarction; myocardial ischemia

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