To better understand the mechanisms underlying apoptosis and exercise-induced cardioprotection against apoptosis, we tested the following hypotheses based on the available literature (6, 16): (1) High glucose concentrations in vitro up-regulate the expression of miR-206, leading to decreased HSP60 and increased apoptosis-related markers, (2) Both HIIT and MICT down-regulate the expression of miR-206 and apoptotic markers and up-regulate HSP60 levels, and (3) HIIT produces greater benefits in the molecular and functional markers of DCM. This evidence concerns the gene HSPD1 and familial dilated cardiomyopathy.