The time course of XXXX contractures of single muscle fibres.

@entity3406 @entity6513 @entity460 @entity972 @entity2701
1. At 3 degrees C the long duration of @entity972 contractures and the delay in the repriming process allow one to carry out solution changes while the responses are still in progress, making it possible to study the processes that determine the contracture time course.2. The contractures can be cut short by suddenly lowering the external @entity972 concentration to normal values. Re-exposure to the high @entity972 medium causes the fibres to redevelop @entity2701 , in a way that depends on the time at which the original response was interrupted.3. The period of interruption can be prolonged beyond the duration of the original contracture without affecting the second response. This redevelopment of @entity2701 is not associated with repriming since this process is much delayed. For thirty-five interrupted contractures the mean of the sum of the time integrals of @entity2701 in the two responses amounts to 98% of the mean of the time integral of @entity2701 in the uninterrupted contractures.4. Addition of @entity6513 or removal of @entity460 also causes the fibre to relax from a @entity972 contracture, although at a slower rate than that obtained by lowering the external @entity972 concentration. In these cases, however, no @entity2701 is redeveloped when the standard contracture medium is reapplied. When @entity460 in the contracture medium is replaced by @entity3406 , the contracture time course is not diminished.5. The results obtained with @entity972 contractures clearly show that the contractile activator is released continuously during a contracture. The prolonged time course of contractile responses in the cold can be explained at least in part by a prolonged release of @entity460 . There are no reasons to believe that at low temperature there is more activator available for release, and therefore it can be concluded that in the cold release of @entity460 proceeds at a slower rate.6. Release of @entity460 is under control of the membrane potential, and its time course can be determined either by a fixed store of available @entity460 that is depleted or by a membrane mechanism which is activated upon depolarization and later inactivates with time. The evidence obtained in the present work does not allow one to decide in favour of one of these two possibilities. However, the fact that contractures are prolonged in the cold, and the finding that repriming is delayed, can be utilized in further studies to clarify the mechanism that controls the release of @entity460 .
