Abstract
Thin sartorius muscles (frog) were subjected to prolonged O want at rest in Ringer''s solution, so that the lactic acid formed might escape by diffusion. They were often still in good condition at a time when rigor would have set in if they had been suspended in N. The only obvious effect of prolonged anaerobic survival, when lactic acid accumulation is thus prevented, is a great slowing of the contraction. This slowing is presumably not due to increased H-ion concentration, since the Ringer''s solution was usually buffered. It may perhaps be due to a diminution in the phosphagen. The slowing persists after "recovery" in O. On replacing the Ringer''s solution by O a recovery process sets in, as in the case of a stimulated muscle. The recovery heat is not large: it corresponds to the oxidative removal of the small amount of lactic acid present during a "steady state" in which formation is balanced by outward diffusion. There is no evidence, so long as a muscle remains in good condition, of any process, other than lactic acid formation and phosphagen breakdown, occurring during anaerobic survival. In muscles in "good" condition, after prolonged anaerobic survival in Ringer''s solution, the rate of heat production at rest, in 0 or in N, is the same as for a fresh muscle. In muscles in "poor" condition, after the same treatment, the resting heat rate is higher. The increment in anaerobic resting heat rate produced by survival, or by stimulation, in N, previously described, has been further investigated and confirmed. It is shown to be due, however, to a fall in vapor pressure of the stimulated muscle, allowing water vapor to pass over and to condense on the latter.

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