The most important findings of the study are: (i) ventricular hypertrophy and increased cardiac output in trained rats is associated with enhanced arrhythmogenic trigger activity; (ii) these arrhythmogenic events are predominantly of ventricular origin, suggesting delayed afterdepolarizations via increased SR Ca2+ content as an underlying mechanism; (iii) the enhanced SR Ca2+ content is maintained by increased expression of the phosphorylated form of phospholamban, and increased level of calsequestrin. The gene discussed is PLN; the disease is Ventricular hypertrophy.