REGULATION OF THE RESPIRATORY MOVEMENTS 1135 



ing the alkalinity of this fluid and therefore lowering its carrying power for 

 carbon dioxide. As a matter of fact, one can produce dyspnoea by diminish- 

 ing the alkalinity of the blood by the injection of acids; and attacks of 

 dyspnoea are observed in the later stages of diabetes, when the alkalinity 

 of the blood is decreased in consequence of the production of such bodies 

 as oxy butyric acid. This dyspnoea has been ascribed to the fact that a 

 diminished carrying power of the blood for carbon dioxide will raise the 

 tension of this gas in the tissues where it is formed, so that a diminished 

 alkalinity of the blood may cause a higher tension of carbon dioxide around 

 the respiratory centre. It has been shown by Ryffel that even a short 

 period of sufficiently violent muscular exercise, i. e. one giving rise to 

 dyspnoea, causes a subsequent increase of lactic acid in the urine, and that 

 the blood itself at the close of the period of exercise contains a demonstrable 

 amount of this acid. Thus in one case the urine, passed thirty minutes 

 after running one-third of a mile in two minutes, contained 454 mg. lactic 

 acid as against a normal excretion of between 3 and 4 mg. lactic acid 

 per hour. In another experiment blood was obtained from the fore-arm 

 before exercise, immediately after exercise, and three-quarters of an hour 

 later. The exercise, which consisted of running rapidly, lasted two minutes 

 forty-five seconds. The following Table represents the results obtained : 



Lactic acid per 100 c.c. 



Blood before starting . ... 12-5 mg. 



Blood immediately after stopping . . . 70'8 

 Blood 45 minutes later . . . . . 15*9 



The production of lactic acid during muscular exercise may thus be 

 regarded as a second line of defence for the organism, tending to maintain 

 the increased ventilation of the lungs even when the supply of oxygen is 

 insufficient to oxidise completely the materials consumed in the production 

 of tHe muscular energy. This acid mechanism is however employed only 

 when the supply of oxygen lags behind the respiratory needs of the body 

 (cp. Fig. 521). Ordinary exercise, even when considerable (e.g. a twenty- 

 four hours' track walking race), does not cause, as Ryffel has shown, any 

 appreciable increase in the ehmination of lactic acid by the urine. Under 

 normal circumstances the depth and rhythm of respiration depend on the 

 carbon dioxide pressure in the respiratory centre, a rise of 0-2 per cent, of 

 an atmosphere in the tension of this gas in the alveoli being sufficient to 

 double the amount of alveolar ventilation during rest. 



The first phase in the phenomena of asphyxia is thus conditioned simply 

 by the changes in the carbon dioxide tension. A little later the gradual 

 exhaustion of oxygen in the blood round the centre begins to make itself 

 felt. The respiratory centre shares with the rest of the central .nervous 

 system a sensitiveness to the absence of oxygen, deprivation of oxygen 

 having first an excitatory and later a paralytic effect. In asphyxia the 

 first centres to feel this effect are those of the cortex, and during the first 

 stage there is mental excitation terminating rapidly in abolition of con- 

 sciousness. During the second stage there is a discharge of -energy, which 



