Key result
Voluntary wheel running induces cardiac hypertrophy without altering resting ECG parameters or in vivo arrhythmic susceptibility.
Why the study?
In human studies, it is difficult to relate extrinsic and intrinsic influences on intact hearts to exercise-induced changes seen at the single-cell level and determine their effect on arrhythmic susceptibility.
Does voluntary wheel running alter cardiac electrical activity and arrhythmic susceptibility in female rats?
Does voluntary wheel running alter cardiac electrical activity and arrhythmic susceptibility in female rats?
Answers are grounded in this paper and cite their sources.
Mild voluntary exercise induces intrinsic electrical remodeling in the heart that is not attenuated by electronic loading but may be masked by neuro-hormonal control in vivo.
Regular mild exercise is recommended to the general population as beneficial to health. Regular exercise typically leads to structural and electrical remodelling of the heart but in human studies it is difficult to relate the extrinsic and intrinsic influences on intact hearts to changes seen at the single cell level. In this study we wished to test whether changes in electrical activity in intact hearts, in response to voluntary wheel running exercise training, were consistent with our previous observations in single cardiac myocytes and whether these changes resulted in altered susceptibility to arrhythmic stimuli. Female rats performed 5 weeks of voluntary wheel running. Implanted telemetry transmitters were used to measure electrocardiograms (ECGs) and determine heart rate variability (HRV) in conscious, unrestrained, trained (TRN) and sedentary (SED) animals. In isolated hearts, left ventricular epicardial monophasic action potentials (MAPs) were recorded and the responses to potentially arrhythmic interventions were assessed. Exercise training caused cardiac hypertrophy, as indexed by a significantly greater heart weight to body weight ratio. Consistent with previous measurements of action potential duration in single myocytes, MAPs were significantly longer at 50%, 75% and 90% repolarization. Arrhythmic susceptibility was not different between SED and TRN hearts. Trained animals displayed significantly altered HRV by week 5, in a manner consistent with reduced sympathetic tone, however resting ECG parameters, including those most associated with repolarisation duration, were unaltered. We conclude that intrinsic changes to cellular cardiac electrophysiology, induced by mild voluntary exercise, are not attenuated by the electronic loading that occurs in intact hearts. However, in vivo, extrinsic neuro-hormonal control of the heart may minimize the effects of intrinsic alterations in electrical activity.
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Stones et al. (2020) studied Healthy (n=60). Voluntary wheel running vs. Sedentary control was evaluated on Changes in electrical activity (ECG, HRV, and monophasic action potentials). Voluntary wheel running induced cardiac hypertrophy and prolonged monophasic action potentials in isolated hearts, but did not alter resting ECG parameters or arrhythmic susceptibility in vivo.
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