Response to Letters Regarding Article, "Cardiac Arrhythmogenic Remodeling in a Rat Model of Long-Term Intensive Exercise Training"

B. Benito, G. Gay-Jordi, A. Serrano-Mollar, E. Guasch, Y. Shi, J.-C. Tardif, J. Brugada, S. Nattel, L. Mont
2011 Circulation  
We would like to thank Maass and Maier and Ruiz et al for their interesting comments on our study. 1 Maass et al stress the potential benefit of exercise in improving the evolution of certain cardiac diseases, and also the need to analyze the benefits of exercise in animal models. In particular, they comment on the beneficial effects of voluntary exercise through diverse pathological conditions. We fully agree with their cautionary comments, and certainly our results cannot be directly
more » ... e directly extrapolated to models of voluntary exercise training. Our model attempted to replicate extreme endurance training conditions, often present in endurance sports training. The authors also pointed out the potential damage caused by stress due to the use of electric discharges to stimulate running. Although we recognize this potential limitation (as discussed in the Potential Limitations section of our article), we do not believe that the animals were under great stress because of the major efforts taken in our protocol to minimize stress responses. Animals were trained before becoming adults, and those animals that did not adapt efficiently to the program, or that received Ͼ15 s electric shock per hour, were excluded from the study. Ruiz et al state an opinion that the training performed in our rats was not comparable to that experienced by an endurance athlete. The authors argue that rats were submitted to a much stronger regime of training than a professional athlete, who receives a careful training under supervision. In response to this observation, we believe that it is certainly difficult to directly relate the intensity of exercise in an animal model to the exercise of a human involved in endurance training. However, the rough calculations provided in our article suggest that 1 hour of daily training during 16 weeks in our rats may be equivalent to 10 years of daily training in athletes. On the other hand, the experiment was designed as a test of concept study, trying to determine whether excessive endurance training may produce deleterious effects in the heart. As Ruiz et al point out, there is good evidence suggesting that long-term endurance training is a risk factor for the development of atrial fibrillation. 2 On the other hand, there are also studies showing that exercise may increase ventricular premature beats, 3 and that detraining may dramatically reduce the degree of arrhythmia. 4 Other authors have also suggested that endurance training may create pathological structural changes in the right ventricle, although the probability of creating fatal arrhythmias is low. 5 Therefore, long-term endurance training appears to have the potential to create a substrate that in certain patients may facilitate arrhythmia. Consistent with this notion, a recently published study demonstrated an increase in myocardial fibrosis in veteran athletes related to the number of years spent training and the number of marathons and ultraendurance marathons completed. 6 Therefore, whether there is a safety limit between the positive effects of exercise and the pathological changes induced by intensive long-lasting exercise training, and, if so, how the limit can be defined, remains to be elucidated in future studies. Disclosures None.
doi:10.1161/circulationaha.111.032987 fatcat:pshha7hfyvhgndy7ut5tpojh7y