| Popis: |
The end point of isotonic shortening in isolated heart muscle is independent of initial sarcomere length unless the latter is longer than 2.0 µm at the onset of isotonic motion. An increase in force or a decrease in activation lengthens the sarcomere at peak shortening, but only so in direct proportion to the increment in sarcomere length above 2.0 µms at this time. Thus, a relatively simple relationship characterizes the complex interaction between length, force, and time to modify isotonic shortening in heart muscle. The instantaneous influence of length on the progressive slowing of shortening suggests that the effect of isotonic motion is equivalent to an increase in the internal load on the shortening sarcomere. An inactive region at the ends of the sarcomere, established by the time of the onset of isotonic motion, can explain how activation, nature of loading, and length might interact dynamically to influence variably the contractile performance of the heart. It has a further consequence for an equilibrium between activation and secondary adjustments in end diastolic volume. |
