THE CHEMISTRY OF MUSCLE 89 



absorbed and distributed to the different tissues through the circulation, but as the 

 different media of the body are normally neutral or faintly alkaline, no change in 

 color will result. If one of the posterior extremities is now tetanized by stimulating 

 its sciatic nerve, the muscles so activated gradually assume a reddish hue. This 

 change appears more quickly, if the corresponding femoral artery is ligated after 

 the injection of the fuchsin, because lessening the oxygen supply greatly favors 

 the accumulation of lactic acid. 



The origin of the lactic acid in muscle has been the subject of much contro- 

 versical discussion. Some investigators, indeed, have sought to displace the old 

 view of Liebig which holds that the acidity of muscle is due to the formation of 

 lactic acid, by the theory that it is caused by the mono-phosphate of potassium. ^ 

 Again, it has been assumed that the free lactic acid acts on the potassium biphos- 

 phate normally present in muscle and forms potassium lactate by the reduction of 

 the neutral into acid phosphate. It is also believed that lactic acid arises in the 

 course of the disintegration of glycogen, but this view seems untenable because it 

 has been shown that the glycogen content of muscle in death-rigor remains prac- 

 tically the same, in spite of the fact that its content in lactic acid is very high, 

 namely 0.5 per cent. In addition, it has been proved that muscles which have been 

 deprived of their glycogen by fasting, yield as much lactic acid as normal muscles. 

 Hill, 2 moreover, claims that the precursor of lactic acid is a substance which 

 possesses a heat value at least 70 per cent, greater than that of this acid. But 

 the heat liberated by dextrose, is only slightly greater (3 per cent.) than that of 

 lactic acid, and furthermore, an excised muscle frequently yields a quantity of acid 

 which is considerably above that actually to be derived from the glycogen normally 

 present in muscle. These results clearly demonstrate that glycogen cannot be the 

 mother-substance of this acid. The only alternative, therefore, is that it is a de- 

 rivative of the proteins. More recently, it has been asserted that muscle tissue 

 contains a carbohydrate-phosphoric acid group which yields lactic and phosphoric 

 acids in about equimolecular amounts. It is believed that the sugar of muscle is 

 synthetized with phosphoric acid and other constituents into the aforesaid complex 

 compound. On breaking down, the carbohydrate group of this body gives rise 

 to lactic acid. « 



The Disappearance of Glycogen. — Weiss^ has shown that frog's muscle loses 

 from 24 to 50 per cent, of its glycogen on tetanization. This observation has been 

 confirmed repeatedly by other investigators so that it may now be considered as 

 definitely proven that this constituent of muscle diminishes during activity. A 

 normal resting muscle, on the other hand, increases its store in glycogen and much 

 more rapidly, if its motor nerve is cut to prevent contraction. In a similar way, 

 it may be proved that general muscular exercise reduces not only the glycogen store 

 of the muscles, but also that of the liver. This consumption of glycogen may be 

 rendered even more striking by temporarily discontinuing the intake of food. 

 Cardiac muscle, in particular, possesses very marked storing qualities, and retains 

 its glycogen even more tenaciously than skeletal muscle.'* 



The liberation of heat and electrical changes concomitant with muscular con- 

 traction, will be discussed in a later chapter. Suffice it to say at this time that the 

 muscles constitute the chief heat producing tissue of our body and that their 

 activity is associated with clearly recognizable electrical variations. 



The Chemistry of the Fatigue of Muscle. — We have previously 

 seen that the continued or excessive stimulation of muscle eventually 

 causes it to become functionally useless. It loses its irritability and 

 contractility so that even the strongest stimulus is no longer able to 



1 Dreser, Zentralbl. fiir Physiol., i, 1887, 195. 



2 Jour, of Physiol., xlvi, 1913, 28. 

 sgitzungsb. der Wiener Akad., Ixiv, 1871. 



* Aldehoff, Zeitschr. fiir Biol., xxv, 1889, 137. 



