376 THE RESPIRATION 



quickly oxidize the lactic acid, so that the still slightly subnormal C H 

 of the blood is unable to excite the center. Apnea therefore supervenes 

 and lasts until lactic acid has again accumulated in the center. To ex- 

 plain why local accumulation of lactic acid in the center should produce 

 a periodic type of breathing, we must further assume that there is con- 

 siderable delay between the moment at which equilibrium of the gases 

 in the blood and alveolar air becomes established and that at which 

 the blood arrives at the respiratory center. This delay is caused by 

 the slowing of the bloodflow on account of the absence of respiratory 

 movements. 



Emphasis is placed on the fact that it is in the center itself and not 

 in the blood that the lactic acid becomes oxidized by the excess of 2 , 

 because lactic acid is known to disappear slowly under these conditions 

 from isolated blood, but to do so very quickly from tissues such as muscle, 

 and presumably therefore also from nervous tissue. 



In support of the above explanation it has been found that, if toward 

 the end of the forced breathing the lungs are filled with sufficient (X 

 so that the tension of this gas in the alveoli is not loAver than 120 mm. 

 Hg, breathing is regular in type when it returns, and the C0 2 tension 

 of the alveolar air is several millimeters above instead of below the nor- 

 mal stimulating level. 



To sum up, the periodic character of the breathing supervening on 

 a period of apnea may be explained as follows: Under ordinary condi- 

 tions of breathing and barometric pressure the. 2 tension of the blood 

 is sufficient between normal respirations to prevent any accumulation of 

 Tactic acid in the respiratory center, so that the stimulus afforded by the 

 C H of the blood produces a constant effect. During the apnea which 

 supervenes upon forced breathing, lactic acid accumulates in the center, 

 causing this to respond to the gradually rising C H of the blood before the 

 latter has reached its physiological level. The hyperpnea thus excited 

 does not, however, bring about a prompt oxidation of the lactic acid 

 in the center or a lowering of the C H of the blood circulating through it, 

 because more time than usual is taken for the blood to get from the 

 lungs to the brain on account of the absence of respiratory movements. 

 When the aerated blood does reach the respiratory center, the excess of 

 Oo which it contains oxidizes the lactic acid so that apnea supervenes, 

 and the lactic acid again accumulates, although not now so much as 

 before because of the gradually rising C H of the blood itself. The essen- 

 tial factor in the causation of periodic breathing is therefore a delayed 

 mass movement of the blood from Ihe pulmonary capillaries to the re- 

 spiratory center. The delay may be caused by cessation of the respira- 



