Thus, these results suggested that LTE prevented age-related accelerated decline of cardiac contractility and age-related accelerated increase of arrhythmias induced by a HSI, and the mechanism of that may be related to dow-regulation of heart salt gene expression and oxidative stress/dTOR pathway, and up-regulation of heart dFOXO/PGC-1α pathway. Here, PPARGC1A is linked to cardiac arrhythmia.