88 PHYSIOLOGICAL TRIGGERS 



potential of about 99 millivolts. Since muscle fibers have been shown to be 

 permeable to sodium, an energy-consuming 'pump' mechanism located in the 

 cell membrane has been postulated (50) to extrude sodium and thereby main- 

 tain a low concentration of intracellular sodium. Ling (64) has proposed an 

 alternative 'fixed charge hypothesis' for maintaining electrolyte distributions 

 in muscle. This depends on the existence within the cell of a network of protein 

 chains bearing a large number of negative charges. Since the effective (hydrated) 

 diameter of K+ is believed to be smaller than that of Na+, the potassium could, 

 on the average, be more closely associated with the fixed negative charges of the 

 proteins than could the larger sodium ions. By this mechanism, it is postulated 

 that potassium might be selectively accumulated within the cell — and sodium 

 essentially excluded — without appeal to a sodium pump. A similar mechanism 

 is proposed at the cell surface to account for the relatively low permeability to 

 sodium. Although the pump theory has won more general acceptance, the 

 arguments presented by Ling must be carefully considered. 



In the normal excitation of muscle twitch fibers, the action potential arising 

 from the end-plate region travels in a wave of depolarization down the surface 

 of the muscle fiber. The effects of this disturbance are transmitted inward, in- 

 ducing the 'active state' which gives rise to the actual contraction. 



According to the theory set forth by Hodgkin (50) and Hodgkin and Huxley 

 (51), the depolarization initiated in the region ahead of the travelling action 

 potential induces a marked increase in the fiber membrane permeability, the 

 action potential reflecting a rapid entry of sodium into the fiber (rising phase of 

 the action potential) followed by an outflow of potassium (declining phase of 

 the action potential). There is considerable circumstantial evidence in support 

 of this theory for the basis of the action potential in muscle as well as nerve (50). 

 With sartorius muscle fibers, the height of the action potential iTicreases linearly 

 with the logarithm of the extracellular sodium ion concentration (74) and de- 

 creases correspondingly as the intracellular sodium concentration is raised (24). 

 Similarly, the maximum rate of rise of the action potential is proportional to 

 the external sodium concentration and is essentially unaffected by the internal 

 sodium concentration; whereas the maximum rate of fall of the action potential 

 is proportional to the internal concentration of potassium and is little aff'ected 

 by the external potassium concentration (24). 



It was long ago demonstrated that the propagation of the action potential 

 depends on the local state of the fiber. If the local flow of ions from higher to 

 lower concentrations can be viewed as a down-hill (energy-yielding) process (or, 

 more precisely, if this process results in a decrease in free energy for the system 

 composed of the fiber and the medium in which it is immersed), the cost in- 

 volved in the propagation of the action potential may be readily taken care of. 

 Here again are the essentials of a triggered process: a presumably small but ade- 

 quate energy input at the end-plate region rapidly causing an energy amplifica- 



