450 



Dr. W. M. Fletcher and Prof. F. G. Hopkins. 



acid is continuously produced (5) and rjroportionate volumes of preformed 

 carbon dioxide are expelled ; as we saw earlier, the slow yield of carbon 

 dioxide is steadily maintained for many hours from an isolated muscle (1). 

 On contraction, and especially in nitrogen, acid production is faster, and the 

 carbon dioxide is expelled faster (3). So we return to the ancient observa- 

 tion of Spallanzani that carbon dioxide is yielded (as he thought, freshly 

 produced) without the immediate presence of oxygen, and, as we have seen, 

 it was largely upon this supposed evidence of a previously oxygenated 

 precursor of carbon dioxide in the muscle that the inogen theory was later to 

 be erected. 



The Effects of Oxygen upon Muscle. 



According to the ancient view that the irritability and activity of a muscle 

 depended upon its combustibility, oxygen would be expected to hasten the 

 energy discbarge by muscle, and so to act as a stimulant or irritant, very much 

 as oxygen kindles glowing tinder to a flame. But on the inogen hypothesis 

 as developed by Hermann, while oxygen should restore and maintain the 

 capacity for energy discharge by completion of the oxygenation of the inogen 

 molecule, it would not be expected to cause or to favour the explosive 

 splitting of the molecule. 



Humboldt in 1795, and many others after, had shown that isolated muscle 

 maintained its irritability longer with an abundant oxygen supply than 

 without, and was longer preserved from fatigue after stimulation. Hermann 

 spoke with uncertain voice on this fundamental point. He claimed that 

 oxygen was irritant and destructive at the surface of a muscle, hastening 

 death, but that in bulky muscles exposed to it, it had a preservative action, 

 maintaining irritability below the surface layers. But he used faulty 

 methods, gave few actual data, and obtained obscure results. 



With more appropriate methods it was found at Cambridge (2), as we have 

 seen already, that in oxygen the carbon dioxide yield of the muscle was 

 increased threefold or more (see fig. 1) and that, nevertheless, in spite of this 

 increased combustion the irritability, as many from Humboldt to Joteyko had 

 previously found, was not more quickly exhausted but longer maintained. 

 All irritant gases increase the yield of carbon dioxide by quickening the 

 production of the lactic acid, which expels preformed carbon dioxide held in 

 the muscle. But oxygen, while it would set a combustion flaring, not only 

 delays the stiffening of the muscle, but may altogether inhibit its onset. A 

 muscle forced by stimulation to stiffening may be recalled again by oxygen 

 to its previous flaccidity (3). 



This seems to us to be a crucial experiment manifesting an immediate 



