Computational models of cardiac myocytes are important tools for understanding ionic mechanisms of arrhythmia. This work presents a new model of the canine epicardial myocyte that reproduces a wide range of experimentally observed rate dependent behaviors in cardiac cell and tissue, including action potential duration (APD) adaptation, restitution and accommodation. Model behavior depends on updated formulations for the 4-AP sensitive transient outward current (I_to1), the slow component of the delayed rectifier potassium current (_IKs), the L-type Ca²⁺ channel (I_Ca,L) and the sodium-potassium pump (INaK) fit to data from canine ventricular myocytes. We find that Ito1 plays a limited role in potentiating peak I_Ca,L and sarcoplasmic reticulum Ca²⁺ release for propagated APs, but modulates the time course of APD restitution. I_Ks plays an important role in APD shortening at short diastolic intervals, despite a limited role in AP repolarization at longer cycle lengths. In addition, we find that I_Ca,L plays a critical role in APD accommodation and rate dependence of APD restitution through its indirect role in intracellular Na+ accumulation and increased outward I_NaK at rapid heart rates. Our simulation results provide valuable insight into the mechanistic basis of rate-dependent phenomena important for determining the heart's response to rapid and irregular pacing rates (e.g. arrhythmia). Accurate simulation of rate dependent phenomena and increased understanding of their mechanistic basis will lead to more realistic multicellular simulations of arrhythmia and identification of molecular therapeutic targets.