JEAN BOTTS 89 



lion which depends only on the geometry and ionic environment of the Hving 

 fiber. Various calculations have been made for nerve and muscle fibers to 

 estimate the energy released during a single impulse (36, 50, 81). If the mem- 

 brane capacity C (56 microfarads cm^-) and the maximum amplitude of the 

 action potential V (.120 v.) are substituted in the equation: energy = CV"', 

 then for a fiber i cm long and 100 n in diameter the value obtained is about .02 

 ergs impulse '. Although this value may be considerably larger than the cor- 

 responding energy change induced at the end-plate, it is still only about io~^ 

 times the work output available from a single twitch of such a muscle fiber. 



The amount of sodium transferred from the outside to the inside of the 

 muscle fiber during one impulse can be similarly calculated (quantity of charge 

 — Q = CV; ref. 50). A value of about 4 X io~''- moles impulse^' cm~'- is found. 

 As Hodgkin (50) has pointed out, calculations based on electrical measurements 

 on the fiber membrane give only a minimum estimate of the energy released or 

 the number of moles of electrolyte transferred, since these measurements do not 

 take into account any inflow of sodium which is partially balanced by a simul- 

 taneous inflow of chloride or outflow of potassium. 



Some recent measurements of the fluxes of Na'^ and K^' have been made on 

 resting muscle (16, 18, 59) and on contracting smooth muscle (6). However, 

 problems of diffusion (42, 58) and the possibility of rapid, undetected reabsorp- 

 tion of potassium and re-extrusion of sodium from incompletely mixed pools in 

 the immediate vicinity of individual fiber boundaries complicate the interpreta- 

 tion of these results. The probable interlinking of the cation fluxes in nerve has 

 been discussed by Hodgkin and Keynes (52). Steinbach (84) has given evidence 

 that in frog sartorius muscle the uptake of potassium is dependent on sodium 

 extrusion, and Keynes has found that the rate of sodium loss from frog sartorius 

 or toe muscle is jncreased when the muscle is transferred to a potassium-rich 

 medium. Weidman (90) has suggested that the effect of potassium on turtle 

 heart action potentials may be explainable on such a basis. In the turtle heart, 

 which has a protracted action potential lasting several seconds at io°C, an in- 

 crease in the extracellular potassium concentration during the action potential 

 (by injection into the coronary artery) brings about an abrupt, early fall in the 

 action potential to about half the resting level (90). The Hodgkin and Huxley 

 scheme (51) would seem to require a slower fall in action potential under these 

 conditions. However, if superimposed on this slowed response there is an in- 

 creased rate of sodium efflux induced by the increased potassium concentration, 

 observations on the turtle heart are not inconsistent with that scheme. It is also 

 noted that increasing the extracellular potassium concentration prior to initia- 

 tion of the action potential causes a slower rate of rise of the action potential. 

 This suggests that even during the rising phase of this slow-motion action 

 potential, some of the sodium inflow is already being countered-balanced by an 

 increased rate of sodium extrusion. 



