Key result
Endurance exercise prevents ischemia-induced VF in susceptible dogs, driven by ~60% lower cardiac NCX1 expression.
Why the study?
Increased Na+/Ca2+ exchanger activity may provoke arrhythmias, and exercise training may reduce NCX1 expression and risk for ventricular fibrillation in susceptible animals.
Does 10-week exercise training reduce cardiac NCX1 expression and prevent ventricular fibrillation in dogs with healed myocardial infarctions?
RCT (n=36)
randomly assigned
Does 10-week exercise training reduce cardiac NCX1 expression and prevent ventricular fibrillation in dogs with healed myocardial infarctions?
Endurance exercise training reduces cardiac NCX1 expression and prevents ventricular fibrillation in a canine model of healed myocardial infarction.
Exercise training normalizes NCX1 in VF-susceptible post-MI dogs; leaves open antiarrhythmic translation to patients.
Increased Na + /Ca 2+ exchanger activity (NCX1, an important regulator of cardiomyocyte cystolic Ca 2+ ) may provoke arrhythmias. Exercise training can decrease NCX1 expression in animals with heart failure, improve cytosolic Ca 2+ regulation, and could thereby reduce the risk for ventricular fibrillation (VF). To test this hypothesis, a 2‐min coronary occlusion was made during the last min. of exercise in dogs with healed myocardial infarctions; 23 had VF (S, susceptible) and 13 did not (R, resistant). The animals were randomly assigned to either 10‐wk exercise training (progressively increasing treadmill running) (S n = 9; R n = 8) or 10‐wk sedentary (S n = 14; R n = 5) groups. At the end of the 10‐wk period, the exercise + ischemia test provoked VF in sedentary but not trained susceptible dogs. After euthanasia, cardiac tissue was harvested and NCX1 protein expression was determined by Western blot. In the sedentary group, NCX1 expression was 4 fold higher in susceptible (4.2 ± 1.3 AU) compared to resistant (1.0 ± 0.1 AU) dogs. In contrast, post‐training NCX1 levels were similar in the resistant and susceptible animals (S = 1.7 ± 0.3 AU). Thus, exercise training can restore a more normal NCX1 level in VF susceptible dogs and could improve cystolic Ca 2+ regulation reducing the risk for sudden death. (supported by NIH grant HL‐68609)
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Kukielka et al. (2007) conducted an RCT in Healed myocardial infarction with or without susceptibility to ventricular fibrillation (n=36). Endurance exercise training vs. Sedentary was evaluated on Cardiac NCX1 protein expression in susceptible dogs (AU). 10-week endurance exercise training reduced cardiac NCX1 expression in VF-susceptible dogs (1.7 vs 4.2 AU in sedentary dogs) and prevented ischemia-induced ventricular fibrillation.
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