The reduced power of the failing heart can be ascribed to a combination of reduced force and slower contraction. We investigated the role of electrical remodeling in cardiomyocytes i rat model of post infarction congestive heart failure (CHF). Shortening and shortening velocity (SV) in isolated cardiomyocytes were measured during different stimulation protocols. Electrical remodelling occurred in CHF cells, which were depolarized and had prolonged action potentials (AP) compared to sham cells. The role of electrical remodeling was examined by stimulating sham and CHF cells with CHF and Sham APs, respectively. Fractional shortening (FS) was increased in CHF compared to sham independent of stimulation protocol. Larger FS was accompanied by increased sarcoplasmic reticulum (SR) Ca2+ load and depended on the electrical remodelling. Time to peak contraction (TTP) was increased in CHF compared to sham cells, but in contrast to FS, TTP was only slightly affected when the cells were stimulated with sham APs and sham diastolic membrane potential (DMP). We conclude that electrical remodeling affecting DMP and AP duration (APD) significantly affects the size of contraction in failing cardiomyocytes, whereas the mechanism for slowing of contraction in CHF is different.