JEAN BOTTS 93 



some anion, such as chloride, partici[)ales in a process takinj^ place at the fiber 

 membrane during the very early phases of contraction, and that this process is 

 closely concerned with activation of the contractile component in muscle. What 

 this process may be is not known, though several possibilities have been dis- 

 cussed (45, 57). Etzensperger (29) suggests that the action of abnormal anions 

 in prolonging the negative after-potential is in accord with the hypothesis that 

 the active state persists as long as the membrane potential remains below some 

 critical value. If one attempts to interpret the negative after-potential effect in 

 terms of ion fluxes, it can be speculated that this after-potential reflects, in part, 

 an influx of chloride. It is known that in muscle, in the presence of excess 

 potassium, the anion penetration rate decreases when abnormal anions are 

 substituted for chloride, the rate efifect being in the order CI > Br > NO3 (15). 

 A prolongation of the negative after-potential might therefore be interpreted in 

 terms of a slower penetration rate of abnormal anions. One might also look for 

 alterations in the recovery processes taking place at the membrane in the wake 

 of the action potential, and speculate that a delay in the initiation of some such 

 process prolongs an inwardly directed activation step. There is indirect evi- 

 dence, for example, that in nerve sodium can be extruded in company with some 

 unidentified anion (52). Although phosphate, formed as an intracellular break- 

 down product, would seem a likely candidate, Harris finds only a small loss of 

 phosphate from muscle and essentially no reincorporation (41). It may be that 

 chloride normally participates in a sodium extrusion process already initiated in 

 the early stages of contraction. 



Since the immediate sequence of events taking place in the muscle fiber 

 following stimulation is not known, it is difficult to speculate on the role which 

 triggering may {)lay at this level. It is generally agreed that the propagation of 

 the wave of excitation is a triggered process in that the 'output' is independent 

 of the 'input' beyond some critical level of the latter. If one adopts the view that 

 contraction depends directly on the depolarization of the fiber membrane i.e., 

 if there are no intermediate steps between depolarization and contraction — then 

 no further triggered processes can be postulated. Although such a seemingly 

 direct relationship has been described in some muscle fibers, other evidence 

 suggests that the situation is more complex. For example, it can be supposed 

 instead that ion shifts associated with membrane depolarization or repolariza- 

 tion are directly responsible for initiating further changes within the fiber. In 

 this case, the final unleashing of contractile energy can occur at a later stage and 

 the possibility of additional triggered processes can be considered. 



Prior to the development of positive tension in stimulated muscle, various 

 manifestations of changes taking place within the fiber have been observed. 

 Sandow has made an extensive study of 'latency relaxation', a term applied to 

 the very small drop in tension immediately preceding the onset of contraction 

 in stimulated muscle fibers. Analysis of the magnitude and time course of this 



