Sudden cardiac death in athletes is rare and most often unexpectable. For a better understanding of cardiac remodeling, this study presents the effects of chronic vigorous exercise on cardiac structure and electrophysiology in new rabbit and dog athlete's heart models. Rabbits and dogs were randomized into sedentary ('Sed'), exercised (subjected to 16 weeks chronic treadmill exercise ('Ex') groups, and a testosterone-treated ('Dop') group in dogs. Echocardiography and electrocardiogram were performed. Proarrhythmic sensitivity and autonomic responses were tested in conscious dogs. 'Ex' animals exhibited left ventricular enlargement with bradycardia (mean RR in 'Ex' vs. 'Sed' rabbits: 335 ± 15 vs. 288 ± 19 ms, p ≤ 0.05, and in 'Dop' vs. 'Ex' vs. 'Sed' dogs: 718 ± 6 vs. 638 ± 38 vs. 599 ± 49 ms) accompanied by an increase of heart rate variability in both species (e.g. SD RR in 'Ex' vs. 'Sed' rabbits: 3.4 ± 0.9 vs. 1.4 ± 0.1 ms, p ≤ 0.05, and in 'Dop' vs. 'Ex' vs. 'Sed' dogs: 156 ± 59 vs. 163 ± 44 vs. 111 ± 49 ms) indicating an increased vagal tone. A lower response to parasympatholytic agent atropine and more pronounced QT c interval lengthening after dofetilide challenge were found in 'Ex' and 'Dop' dogs compared to the 'Sed' group. No morphological and functional changes were found after chronic steroid treatment in dogs. The structural-functional findings share more similarities with human athlete's heart. Slight repolarization sensitivity in the exercised dogs may indicate an increased risk of arrhythmias in athletes under different circumstances. These animal models might be useful for the further investigations of the cardiovascular effects of competitive training.

No abstract

In the present study, the effect of long-term exercise training was investigated on myocardial morphological and functional remodeling and on proarrhythmic sensitivity in a rabbit athlete’s heart model. New-Zealand white rabbits were trained during a 12-week long treadmill running protocol and compared with their sedentary controls. At the end of the training protocol, echocardiography, in vivo and in vitro ECG recordings, proarrhythmic sensitivity with dofetilide (nM) were performed in isolated hearts, and action potential duration (APD) measurements at different potassium concentrations (4.5 and 2 mM) were made in the isolated papillary muscles. Expression levels of the slow component of delayed rectifier potassium current and fibrosis synthesis and degradation biomarkers were quantified. Echocardiography showed a significantly dilated left ventricle in the running rabbits. ECG PQ and RR intervals were significantly longer in the exercised group (79 ± 2 vs. 69 ± 2 ms and 325 ± 11 vs. 265 ± 6 ms, p < 0.05, respectively). The in vivo heart rate variability (HRV) (SD of root mean square: 5.2 ± 1.4 ms vs. 1.4 ± 0.2 ms, p < 0.05) and Tpeak-Tend variability were higher in the running rabbits. Bradycardia disappeared in the exercised group in vitro. Dofetilide tended to increase the QTc interval in a greater extent, and significantly increased the number of arrhythmic beats in the trained animals in vitro. APD was longer in the exercised group at a low potassium level. Real-time quantitative PCR (RT-qPCR) showed significantly greater messenger RNA expression of fibrotic biomarkers in the exercised group. Increased repolarization variability and higher arrhythmia incidences, lengthened APD at a low potassium level, increased fibrotic biomarker gene expressions may indicate higher sensitivity of the rabbit “athlete’s heart” to life-threatening arrhythmias.

In isolated hearts, cycle length irregularity increases the slope of the positive linear correlation between mean ventricular rate and coronary flow via producing beats in which left ventricular pressure remains below perfusion pressure. This means that changes in rhythm have the capacity to influence coronary flow independently of heart rate in isolated hearts perfused at constant pressure, which should be noted in drug studies on arrhythmias performed in Langendorff hearts.

pontosan nem ismert. Munkánkban a tartós intenzív állóképességi tréning szívmorfológiára és a szívizom elektromos tevékenységére kifejtett hatását vizsgáltuk állatmodellekben.