The control of tension and shortening in cardiac and skeletal muscle

Abstract: The development of tension and shortening in cardiac and skeletal muscle exhibits phenomena suggestive of control by feedback mechanisms at the molecular level. Two of these, presented here, may have surprising implications for the cross-bridge theory of muscular contraction. It can be argued, from the basis of the cross-bridge theory, that the extended muscle is unstable against further imposed stretch by reason of a corresponding decrease of generated tension. Certain measurements of static tension versus muscle length appear to corroborate this conclusion. On the other hand, there is direct evidence for the dynamic stability of muscle at longer lengths. The cross-bridge theory may be incorrect in this regard, and cross-bridges may contain a negative feedback mechanism; but it may be the case that the contradiction arises out of inappropriately extrapolating the static length-tension data to a dynamic situation. By monitoring the sarcomere length of a contracting muscle, it can be seen that shortening does not proceed smoothly, but in more or less discontinuous jumps. This “stepwise” shortening shows evidence of synchronization across a region of a muscle, and suggests some positive feedback process at work. Some speculations are offered as to possible mechanisms, including load-dependent signalling, diffusion, cooperative effects, and repeated cycles of substrate consumption, concomitant with shortening, alternating with a “catch-up” period of substrate production.