Increased Ca2+ content of the sarcoplasmic reticulum provides arrhythmogenic trigger source in swimming-induced rat athlete’s heart model View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2020-11-11

AUTHORS

Péter Gazdag, Kinga Oravecz, Károly Acsai, Vivien Demeter-Haludka, Balázs Ördög, Jozefina Szlovák, Zsófia Kohajda, Alexandra Polyák, Bálint András Barta, Attila Oláh, Tamás Radovits, Béla Merkely, Julius Gy. Papp, István Baczkó, András Varró, Norbert Nagy, János Prorok

ABSTRACT

Sudden cardiac death among top athletes is very rare, however, it is 2–4 times more frequent than in the age-matched control population. In the present study, the electrophysiological consequences of long-term exercise training were investigated on Ca2+ homeostasis and ventricular repolarization, together with the underlying alterations of ion channel expression, in a rat athlete's heart model. 12-week swimming exercise-trained and control Wistar rats were used. Electrophysiological data were obtained by using ECG, patch clamp and fluorescent optical measurements. Protein and mRNA levels were determined by the Western immunoblot and qRT-PCR techniques. Animals in the trained group exhibited significantly lower resting heart rate, higher incidence of extrasystoles and spontaneous Ca2+ release events. The Ca2+ content of the sarcoplasmic reticulum (SR) and the Ca2+ transient amplitude were significantly larger in the trained group. Intensive physical training is associated with elevated SR Ca2+ content, which could be an important part of physiological cardiac adaptation mechanism to training. However, it may also sensitize the heart for the development of spontaneous Ca2+ release and extrasystoles. Training-associated remodeling may promote elevated incidence of life threatening arrhythmias in top athletes. More... »

PAGES

19596

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41598-020-76496-2

DOI

http://dx.doi.org/10.1038/s41598-020-76496-2

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1132501476

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/33177643


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