The time course of potassium contracture of single muscle fibres

Abstract

1. At 3 degrees C the long duration of potassium 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 potassium concentration to normal values. Re-exposure to the high potassium medium causes the fibres to redevelop tension, 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 tension 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 tension in the two responses amounts to 98% of the mean of the time integral of tension in the uninterrupted contractures.4. Addition of tetracaine or removal of calcium also causes the fibre to relax from a potassium contracture, although at a slower rate than that obtained by lowering the external potassium concentration. In these cases, however, no tension is redeveloped when the standard contracture medium is reapplied. When calcium in the contracture medium is replaced by nickel, the contracture time course is not diminished.5. The results obtained with potassium 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 calcium. 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 calcium proceeds at a slower rate.6. Release of calcium is under control of the membrane potential, and its time course can be determined either by a fixed store of available calcium 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 calcium.