THE PHYSIOLOGY OF MUSCULAR WORK 241 



the hyperpncea was produced by some product of muscular activity 

 which was absorbed by the blood, and thus carried to the medulla 

 oblongata, where it stimulated the respiratory centre. Loewy ( 37 ) 

 also maintained that carbon dioxide was not the factor, for he 

 found that, whereas the rate of respiration was doubled by muscular 

 work when the increase above the normal amount of carbon dioxide 

 in the expired air was only O5 per cent., the same amount of 

 dyspnoea could be produced during rest only by artificially raising 

 the percentage of carbon dioxide to a much higher point, about 

 5 per cent. 



The alkalinity of the blood is diminished during muscular 

 activity, and this observation revived the question whether pro- 

 ducts of activity stimulated the respiratory centre. Forty years 

 ago Pfliiger ( M ) suggested that lack of oxygen might act indirectly 

 as a stimulus to respiration ; products such as lactic acid un- 

 oxidised owing to the deficiency of oxygen in the tissues might 

 be the exciting agents. 



The work of Haldane and Priestley effected a return to the 

 view that carbon dioxide was the chief factor which increased the 

 respiration during muscular work. But quite recently the whole 

 question of muscular hyperpnoea and dyspnoea has been reopened, 

 and it is necessary to consider the possible action of such factors 

 as lack of oxygen, metabolites such as lactic acid, increased tem- 

 perature of the body and nervous impulses from various parts. 

 The muscular work performed by Haldane and Priestley was 

 slight, and their analyses of the alveolar air do not include the 

 amount of oxygen. After vigorous exercise the alveolar air some- 

 times shows a considerable rise in the percentage of carbon dioxide, 

 and at other times a fall below the normal ( 39 ). It becomes im- 

 portant, therefore, to determine the respiratory quotient, the ratio 

 of the carbon dioxide discharged to the oxygen absorbed. Such 

 analyses show quotients as high as 1*2 during muscular dyspnoea. 



It is necessary to consider whether the lack of oxygen produces 

 dyspnoea directly or indirectly through metabolites which remain 

 unoxidised owing to the lack of that gas. A man at rest breathes 

 with practically the same frequency and depth whether he be 

 breathing air or pure oxygen ( 40 ), and his response to an increase of 

 carbon dioxide in his lungs appears to be unaffected by breathing 

 oxygen ( 41 ). Directly after exercise, however, breathing oxygen 

 diminishes the dyspnoea, and enables the man to tolerate a higher 



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