Cardiac electrophysiological remodeling associated with enhanced arrhythmia susceptibility in a canine model of elite exercise

The health benefits of regular physical exercise are well known. Even so, there is increasing evidence that the exercise regimes of elite athletes can evoke cardiac arrhythmias including ventricular fibrillation and even sudden cardiac death (SCD). The mechanism of exercise-induced arrhythmia and SC...

Teljes leírás

Elmentve itt :
Bibliográfiai részletek
Szerzők: Polyák Alexandra Júlia
Topal Leila
Zombori-Tóth Noémi
Tóth Noémi
Prorok János
Kohajda Zsófia
Déri Szilvia
Demeter-Haludka Vivien
Hegyi Péter
Venglovecz Viktória
Ágoston Gergely
Husti Zoltán
Gazdag Péter
Szlovák Jozefina
Árpádffy-Lovas Tamás
Naveed Muhammad
Sarusi Annamária
Jost Norbert László
Virág László
Nagy Norbert
Baczkó István
Farkas Attila
Varró András
Dokumentumtípus: Cikk
Megjelent: 2023
Sorozat:ELIFE 12
Tárgyszavak:
doi:10.7554/eLife.80710

mtmt:33685694
Online Access:http://publicatio.bibl.u-szeged.hu/26697
Leíró adatok
Tartalmi kivonat:The health benefits of regular physical exercise are well known. Even so, there is increasing evidence that the exercise regimes of elite athletes can evoke cardiac arrhythmias including ventricular fibrillation and even sudden cardiac death (SCD). The mechanism of exercise-induced arrhythmia and SCD is poorly understood. Here, we show that chronic training in a canine model (12 sedentary and 12 trained dogs) that mimics the regime of elite athletes induces electrophysiological remodeling (measured by ECG, patch-clamp and immunocytochemical techniques) resulting in increases of both the trigger and the substrate for ventricular arrhythmias. Thus, 4 months sustained training lengthened ventricular repolarization (QTc: 237.1±3.4 ms vs. 213.6±2.8 ms, n=12; APD90: 472.8±29.6 ms vs. 370.1±32.7 ms, n=29 vs. 25), decreased transient outward potassium current (6.4±0.5 pA/pF vs. 8.8±0.9 pA/pF at 50 mV, n=54 vs. 42) and increased the short term variability of repolarization (29.5±3.8 ms vs. 17.5±4.0 ms, n=27 vs. 18). Left ventricular fibrosis and HCN4 protein expression were also enhanced. These changes were associated with enhanced ectopic activity (number of escape beats from 0/hour to 29.7±20.3/hour) in vivo and arrhythmia susceptibility (elicited ventricular fibrillation: 3 of 10 sedentary dogs vs. 6 of 10 trained dogs). Our findings provide in vivo, cellular electrophysiological and molecular biological evidence for the enhanced susceptibility to ventricular arrhythmia in an experimental large animal model of endurance training.
Terjedelem/Fizikai jellemzők:27
ISSN:2050-084X