Abstract
BackgroundThe mechanisms whereby aerobic training reduces the occurrence of sudden cardiac death in humans are not clear. We test the hypothesis that exercise-induced increased resistance to ventricular tachycardia and fibrillation (VT/VF) involve an intrinsic remodeling in healthy hearts.Methods and ResultsThirty rats were divided into a sedentary (CTRL, n = 16) and two exercise groups: short- (4 weeks, ST, n = 7) and long-term (8 weeks, LT, n = 7) trained groups. Following the exercise program hearts were isolated and studied in a Langendorff perfusion system. An S1–S2 pacing protocol was applied at the right ventricle to determine inducibility of VT/VF. Fast Fourier transforms were applied on ECG time-series. In-vivo measurements showed training-induced increase in aerobic capacity, heart-to-body weight ratio and a 50% low-to-high frequency ratio reduction in the heart rate variability (p<0.05). In isolated hearts the probability for VF decreased from 26.1±14.4 in CTRL to 13.9±14.1 and 6.7±8.5% in the ST and LT, respectively (p<0.05). Duration of VF also decreased from 19.0±5.7 in CTRL to 8.8±7.1 and 6.0±5.8 sec in ST and LT respectively (p<0.05). Moreover, the pacing current required for VF induction increased following exercise (2.9±1.7 vs. 5.4±2.1 and 8.5±0.9 mA, respectively; p<0.05). Frequency analysis of ECG revealed an exercise-induced VF transition from a narrow single peak spectrum at 17 Hz in CTRL to a broader range of peaks ranging between 8.8 and 22.5 Hz in the LT group (p<0.05).ConclusionExercise in rats leads to reduced VF propensity associated with an intrinsic cardiac remodeling related to a broader spectral range and faster frequency components in the ECG.
Highlights
Many epidemiological studies support the concept that regular exercise correlates with reduced cardiovascular and overall mortality in apparently healthy individuals [1,2,3,4] and in patients with cardiovascular disease [5]
The rats were randomly divided into three groups: A control group (CTRL, n = 16) which remained sedentary for 8 weeks; a short term (ST, n = 7) trained group which remained sedentary for 4 weeks and exercised for 4 weeks; a long term (LT, n = 7) trained group which exercised for 8 weeks
The major finding of this study is that a continuous exercise program in normal rats is characterized by alterations in the properties of VF that are associated with alterations that are exclusively intrinsic to the heart
Summary
Many epidemiological studies support the concept that regular exercise correlates with reduced cardiovascular and overall mortality in apparently healthy individuals [1,2,3,4] and in patients with cardiovascular disease [5]. Billman et al [12] show that daily exercise prevented VF induced by acute myocardial ischemia in a subpopulation of dogs that were identified as susceptible to SCD. They demonstrate that exercise altered the autonomic tone toward the parasympathetic arm. Posel et al [13] revealed that exercise training increases the ventricular threshold of the previously infracted isolated rat heart before and after the onset of re-infarction. This effect was attributed again to altered autonomic tone toward the parasympathetic arm. We test the hypothesis that exercise-induced increased resistance to ventricular tachycardia and fibrillation (VT/VF) involve an intrinsic remodeling in healthy hearts
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