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1. The time course of potassium contractures can be significantly prolonged by low concentrations of caffeine. 2. This effect of caffeine is not due to impairment of the fibre relaxing system. 3. Under conditions were contractile repriming is delayed (low temperature) an extra amount of activator can be released by caffeine, in addition to that released by potassium. 4. The source of this extra amount of activator is intracellular since its release can be shown in a O calcium EGTA medium. 5. Local anaesthetics, tetracaine, and to a lesser extent procaine, affect the release of contractile activator, without impairing the contractile machinery itself. 6. The results of the present paper support the view that the time course of potassium contracture is controlled by a membrane mechanism which is activated upon depolarization and later inactivates with time. 7. The effect of caffeine and local anaesthetics can be explained by assuming that the former prolongs the inactivation time course while the latter shortens it.

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