Deletion of Kvβ2 abolished differences in myocardial perfusion following exercise training; (4) whereas wt mice subjected to a moderate-intensity running protocol demonstrated cardiac hypertrophy, this effect was absent in mice lacking Kvβ2; and, (5) the impacts of global deletion of Kvβ2 on exercise-induced enhancement in exercise capacity, augmentation of myocardial perfusion, and cardiac growth were recapitulated via selective increases in Kvβ1:β2 ratio in smooth muscle (i.e., rtTA-Kcnab1 mice). This evidence concerns the gene KCNAB1 and cardiac hypertrophy.