Failure of neuromuscular propagation in rats

Abstract

Many interpretations have been given of the mechanism of muscle fatigue. It is evident that deficient contraction may result from failure at any point in a long chain of events. Various authors disagree as to which link in this chain is the most vulnerable. However, all agree that the nerve trunk is for practical purposes indefatigable, and most authors recognize the occurrence of two main types of peripheral fatigue: fatigue of neuromuscular transmission, and fatigue of the contractile system (del Pozo, 1942; Steiman, 1943; Rosenblueth, 1950; Naess & Storm-Mathisen, 1955). Failure of neuromuscular transmission is commonly ascribed to a deficiency or an excess of transmitter substance (Feng, 1937, 1941; Rosenblueth & Morison, 1937). Other schools of thought may be distinguished. Merton (1954) places all emphasis on fatigue of the contractile mechanism, the occurrence of which, on the other hand, is denied by Ramsey & Street (1941, 1942). Other authors have stressed the importance of fatigue in the central nervous system as the determining factors in fatigue of voluntary contraction (Wailer, 1891; Reid, 1929). In the experiments about to be described, we have studied with intracellular micro-electrodes both in vitro and In situ the mechanism of neuromuscular failure in rats; a number of observations were made which, we believe, may throw some new light on this subject. A preliminary account of some of these experiments has already appeared (Krnjevid & Miledi, 1957).