Current theories about the mechanism of muscular contraction suppose that the level of enzymic and contractile activity is controlled by the intracellular concentration of calcium ions, the degree of overlap between the myosin and actin filaments and the rate of relative sliding of the filaments. It is now known that in most or all muscles there is a further direct influence of mechanical conditions, usually called stretch activation; changes of length lead to a delayed change of active tension. The effect is large and functionally significant in insect fibrillar flight muscle and in mammalian heart muscle; it is present, but small, in vertebrate skeletal muscle, which probably accounts for its late discovery. In insect fibrillar flight muscle, the delayed tension is responsible for the rhythmic mechanical activity during flight. In mammalian heart muscle it may play a rôle in Starling’s Law. In insect fibrillar muscle, extension produces a maintained increase in actomyosin ATPase and active tension; in vertebrate skeletal muscle, stretch activation is a transient phenomenon. Mammalian heart muscle shows greater maintenance of stretch activation than skeletal muscle; the duration of higher ATPase activity has not yet been determined. The effective mechanical parameter is not overall strain but is probably the strain on an internal structure related to overall stress. Various lines of evidence point to the myosin filament as the location of the sensor. A considerable degree of molecular synchronization occurs during natural insect flight.
THE METABOLISM OF n-BUTYRATE-C14 BY MAMMALIAN HEART MUSCLE
