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.
