Endurance exercise training prevented ischemia-induced ventricular fibrillation in 94% (16 of 17) of susceptible post-myocardial infarction dogs compared to 0% (0 of 10) in the sedentary group.
Does endurance exercise training prevent ventricular fibrillation and normalize cellular electrophysiology and calcium handling in a canine model of sudden cardiac death?
In a canine model of sudden cardiac death, 10 weeks of endurance exercise training prevented ischemia-induced ventricular fibrillation and normalized cellular electrophysiology and calcium handling.
Absolute Event Rate: 5.9% vs 100%
p-value: p=<0.00001
The risk of sudden cardiac death is increased following myocardial infarction. Exercise training reduces arrhythmia susceptibility, but the mechanism is unknown. We used a canine model of sudden cardiac death (healed infarction, with ventricular tachyarrhythmias induced by an exercise plus ischemia test, VF+); we previously reported that endurance exercise training was antiarrhythmic in this model (Billman GE. Am J Physiol Heart Circ Physiol 297: H1171-H1193, 2009). A total of 41 VF+ animals were studied, after random assignment to 10 wk of endurance exercise training (EET; n = 21) or a matched sedentary period (n = 20). Following (>1 wk) the final attempted arrhythmia induction, isolated myocytes were used to test the hypotheses that the endurance exercise-induced antiarrhythmic effects resulted from normalization of cellular electrophysiology and/or normalization of calcium handling. EET prevented VF and shortened in vivo repolarization (P < 0.05). EET normalized action potential duration and variability compared with the sedentary group. EET resulted in a further decrement in transient outward current compared with the sedentary VF+ group (P < 0.05). Sedentary VF+ dogs had a significant reduction in repolarizing K(+) current, which was restored by exercise training (P < 0.05). Compared with controls, myocytes from the sedentary VF+ group displayed calcium alternans, increased calcium spark frequency, and increased phosphorylation of S2814 on ryanodine receptor 2. These abnormalities in intracellular calcium handling were attenuated by exercise training (P < 0.05). Exercise training prevented ischemically induced VF, in association with a combination of beneficial effects on cellular electrophysiology and calcium handling.
Bonilla et al. (2012) studied Myocardial infarction with susceptibility to ventricular fibrillation (canine model) (n=41). Endurance exercise training vs. Matched sedentary period in a transport cage was evaluated on Incidence of ventricular fibrillation during exercise plus ischemia test (p=<0.00001). Endurance exercise training prevented ischemia-induced ventricular fibrillation in 94% (16 of 17) of susceptible post-myocardial infarction dogs compared to 0% (0 of 10) in the sedentary group.