Vertebrate skeletal muscle has a negative, -90 mV, resting potential arising from Na+-K+-ATPase-generated transmembrane ionic gradients and inwardly rectifying K+, and Cl- membrane conductances. Three-electrode and loose-patch voltage-clamp experiments demonstrated that, as in nerve, muscle action potentials involve voltage-dependent Na+ followed by K+ channel activation. An additional transverse tubular action potential contributes a discrete and separable delayed component to the recorded voltage change. It is triggered by low-frequency components of the surface-membrane action-potential leaving high-frequency components to ensure rapid propagation of the surface wave. Tubular Cl- conductances decrease in both fast and slow twitch muscle and ATP-dependent K+ channel conductances increase in fast twitch muscle, in early and prolonged exercise. Mathematical modelling demonstrates that these respectively enhance and reduce tubular excitability and its triggering of contractile activity. They potentially furnish enhancing and fatiguing mechanisms for muscle activation and for clinical myotonia congenita.