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 (AP) duration (APD) adaptation, restitution, and accommodation. Model behavior depends on updated formulations for the 4-aminopyridine-sensitive transient outward current ( I_to1), the slow component of the delayed rectifier K⁺ current ( I_Ks), the L-type Ca²⁺ channel current ( I_Ca,L), and the Na⁺-K⁺ pump current ( I_NaK) fit to data from canine ventricular myocytes. We found that I_to1 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 found that I_Ca,L plays a critical role in APD accommodation and rate dependence of APD restitution. Ca²⁺ entry via I_Ca,L at fast rate drives increased Na⁺-Ca²⁺ exchanger Ca²⁺ extrusion and Na⁺ entry, which in turn increases Na⁺ extrusion via outward I_NaK. APD accommodation results from this increased outward I_NaK. 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.