ABSTRACT
Nerve action potentials propagated along the axons of motoneurons are transmitted to the postsynaptic membrane (sarcolemma) by an electrochemical process. A muscle action potential is propagated along the sarco lemma at velocities ranging from 1 to ~4 m·s-1. This conduction velocity can be measured with surface electromyography (see, for example, Farina and Merletti, 2004). It depends on a number of anatomical, physio logical and recruitment factors, and it has also been reported that it can be increased to approximately 6 m·s-1 with resistance training (Kereshi et al. 1983). The muscle action potential causes Ca2+ release that disinhibits the regulatory proteins of the thin fi laments. This allows the myosin globular heads to attach to binding sites on the actin fi laments and form cross-bridges. The interaction of the actin and myosin filaments causes them to slide past one another and generate force, which is transmitted to the Z discs of the sarcomere. This is known as the sliding filament theory. The details of the exact mechanism responsible for the transformation of adenosine triphosphate energy from a chemical to a mechanical form in the crossbridge cycle are not completely known (e.g. Pollack 1983), despite recent advances in the understanding of cross-bridge kinetics (Horiuti 1997; Spudich 2001) and the effects of previous stretch history (Herzog et al. 2006; Herzog 2004, 2005). For a detailed discussion of the electrochemical events associated with muscular contraction the reader is referred to the text by MacIntosh et al. (2005).
