1 68 SCIENCE PROGRESS 



As to the intermediate products of muscle activity, there is 

 not much definite information, but undoubtedly sarcolactic acid 

 is one of them. The recent results of Fletcher and Hopkins 

 show that absolutely fresh muscle (of the frog) contains only 

 traces of lactic acid ('015 per cent, or possibly less). Fatigued 

 muscle, on the other hand, may contain a considerable amount 

 of lactic acid ("ii to - 2i per cent), and rigored muscle still more 

 (•24 to '40 per cent.). The amount of lactic acid any given muscle 

 can develop seems practically constant, whether it be formed 

 suddenly by exposing the muscle to a temperature of 45 , or 

 more slowly by tetanising the muscle when placed in an atmo- 

 sphere of hydrogen or oxygen, and finally inducing heat rigor. 

 It is formed gradually in resting excised muscle, if this muscle 

 be kept in an atmosphere of hydrogen or nitrogen, i.e. under 

 anaerobic conditions, but if kept in air it is formed only very 

 slowly, and if kept in oxygen it is not formed at all. On the 

 contrary, as might be expected from Fletcher's results on the 

 restorative power of oxygen on irritability, if muscles in which 

 a considerable lactic acid formation has been induced by 

 tetanistion are placed in oxygen, a good deal of this lactic acid 

 disappears. Such disappearance of lactic acid was found to be 

 dependent on the integrity of the muscle, no diminution showing 

 itself in chopped-up muscle. 



Other evidence of lactic acid formation was obtained by 

 Spiro, who found that blood collected from the carotid of a 

 dog in which the muscles of the hind limbs had been tetanised 

 for an hour and a quarter showed quite an appreciable increase 

 of sarcolactic acid. Again, Max von Frey and Gruber found that 

 if an isolated muscle of the dog were perfused with an artificial 

 circulation of blood, and were made to contract, there was a 

 considerable increase in the absorption of oxygen, but a by no 

 means corresponding increase in the output of C0 2 . There was 

 a striking rise in the sarcolactic acid in the blood, however, which 

 more than accounted for the deficiency of C0 2 . Presumably this 

 acid was not oxidised further in the tissues owing to the abnormal 

 conditions of experiment, but it is possible, as suggested by 

 Von Frey, that even in the intact living animal the lactic acid 

 formed in the muscles may be to some extent oxidised else- 

 where. In support of this view may be quoted the observations 

 of Meyer, who found that the diminution of C0 2 production 

 induced by arsenic and phosphorus poisoning was accompanied 



