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Animal findings raise possibility of exercise-induced arrhythmogenic remodeling; leaves open human relevance pending prospective studies.
In this animal model, we documented cardiac fibrosis after long-term intensive exercise training, together with changes in ventricular function and increased arrhythmia inducibility. If our findings are confirmed in humans, the results would support the notion that long-term vigorous endurance exercise training may in some cases promote adverse remodeling and produce a substrate for cardiac arrhythmias.
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Benito et al. (2010) studied this question.
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