To meet the energetic demands of exercise, the autonomic system alters heart frequency at the level of the sinoatrial node and concomitantly modifies the cell machinery of ventricular cells by altering ionic channels, pumps, and myofilament sensitivity to produce a stronger contraction with faster relaxation. Shown is a simulation of rabbit action potentials, Ca2+ transients, and force obtained with LabHEART 5.3. IKr, delayed rectifier K+ current; ICaL, L-type Ca2+ current; SERCA, sarco(endo)plasmic reticulum Ca2+-ATPase.