Twitches are the unitary contractile events in both heart and skeletal muscles, but twitch plasticity in terms of force and the kinetics of force development differs considerably in the two muscle types. In skeletal muscle, twitch contractions are relatively invariant as long as temperature is constant and the muscle is well rested. In contrast, twitches in heart muscle exhibit much greater dynamic range, such that both force and the kinetics of force development can vary tremendously on a beat-to-beat basis. These differences are in part due to muscle-specific differences in the delivery of Ca²⁺ to the myoplasm during excitation-contraction coupling. In skeletal muscle, a single action potential elicits a transient increase in intracellular Ca²⁺ sufficient to saturate thin filament regulatory sites on troponin-C. Because of this, force development and the ability to do work depend upon the duration of the Ca²⁺ transient and therefore the time available for cross-bridge binding to actin, which in skeletal muscles can be prolonged by tetanic stimulation. In heart muscle, the increase in intracellular Ca²⁺ during a twitch is typically insufficient to saturate thin filament sites, so that twitch force and work production are sub-maximal. In contrast to skeletal muscle, cardiac muscle cannot be tetanized under physiological conditions, but twitch force and power can be varied by regulating the delivery of Ca²⁺ to the myoplasm and also by agonist-induced regulation of cross-bridge cycling kinetics.