Intrinsic regulatory properties of contractility in the myocardium.

We studied tension changes in vertebrate cardiac muscles resulting from quick stretches and releases and sinusoidal length changes during sustained contractures at various amplitudes of length change and at various temperatures. Muscles in contracture respond to lengthening with activation and to release with deactivation in tension, both of which are delayed. The amplitude of the delayed tension reached as much as 100 g/cm 1 % AL but was dependent on the musde length and level of activation. Delayed tension amplitude averaged about 15 to 25 g/ cm 1% AL. The delayed tension rise is an active process, a reaction of the rayofibrillar system to the length change. Muscle stiffness increases during the delayed tension rise while muscle length is kept constant. With sinusoidal length changes, characteristic frequency responses appear in tension and in stiffness. At room temperature, in papillary muscle, tension change is delayed in respect to the length changed in the frequency range 0.05-1.2 cycles/sec, giving rise to work output. The power output increases with the square of the amplitude and can exceed 0.6 mNm/cyde • g. At the frequency of m^rimal work output, the phase shift may be more than 50°, leading to the paradox that muscle force decreases for a period of time while the muscle U undergoing stretch. At higher frequencies (>1.2 cycles/sec), the tension change precedes the length change, Indicating that the muscle now absorbs work. In the latter same frequency range, the dynamic stiffness may drop by as much as a factor of 6. The time constant of delayed tension onset, the frequency range of power output, and stiffness changes suggest that the kinetics and turnover frequency of the crossbridges are specific for each animal and that an optimal timing exists between the biochemical and mechanical cycle such that the optimal frequency of mechanical performance correlates with the frequency of the natural heart beat.