438 



SCIENCE 



[N. S. Vol. XLIX. No. 1271 



ology that defieiency of oxygen, or ano- 

 xemia, causes an "acidosis." Recent and 

 as yet unpublished work of Dr. Haggard 

 and myself indicates that the process in- 

 volved is almost diametrically the opposite 

 of that which has heretofore heen supposed 

 to occur, and that the result is not a true 

 acidosis. Under low oxygen, instead of the 

 blood becoming at first more acid with a 

 compensatory blowing off of CO2, what 

 actually occurs is that, as the first step, the 

 anoxemia induces excessive breathing. This 

 lowers the C0„ of the blood, rendering it 

 abnormally alkaline ; and alkali passes out 

 of the blood to compensate what would 

 otherwise be a condition of alkalosis. 



"We regard the current explanation, based 

 on the production of lactic acid, as needing 

 reversal. 



The application of this idea to the 

 changes of breathing and of the blood 

 alkali in acclimatization clears up some of 

 the points which heretofore have been ob- 

 scure. Thus on Pike 's Peak we saw that per- 

 sons whose breathing under the stimulant 

 of oxygen deficiency increased quickly to 

 the amount normal for the altitude suffered 

 corresponding'ly little, while those whose 

 respiratory center was relatively insensitive 

 to this influence suffered severely. The one 

 type readily developed the acapnia and in 

 consequence the pseudo-aeidosis which the 

 altitude requires. The other did not. 



Here let me pause a moment to bring 

 these conceptions into some degree of har- 

 mony with fundamental doctrines regard- 

 ing respiration. For more than a century, 

 in fact ever since the days of Lavoisier, the 

 argument has been active whether our 

 breathing is controlled by oxygen need or 

 by the output of COj. For the past thirty 

 years, and especially during the last ten or 

 twelve, the theory of regulation by CO,, or 

 in its later form toy C , has held the field. 

 Indeed it is established now — almost beyond 



the possibility of contradiction, it would 

 seem — that during any brief period of 

 time, and under conditions to which the 

 individual is accustomed, the amount of 

 COo produced in the tissues of the body, 

 through its influence on the Ch of the 

 blood, is the factor controlling the volume 

 of air breathed. Its effects are immediate. 

 But when we view the matter more 

 broadly it is clear that this is by no means 

 the whole story. The oxygen tension of 

 the air is the influence which determines 

 just how sensitive the respiratory center is 

 to excitement by CO,. But the effects of 

 any change of oxygen tension are slow in 

 developing, requiring in some persons, as 

 we saw on Pike 's Peak, hours to begin and 

 several days to become complete. In fact 

 there are many perfectly healthy persons 

 who, if caused to breathe progressively low- 

 ered tensions of oxygen down to 6 or 7 per 

 cent, in the course of half an hour, feel 

 nothing. Their breathing shows- no con- 

 siderable augmentation. They simply lose 

 consciousness, and if left alone they would 

 die, -without any apparent effort on the 

 part of respiration to compensate for the 

 deficiency of oxygen. In such persons the 

 stim^^lant of oxygen deficiency exerts only 

 a slowly developing influence upon the 

 sensitiveness of the respiratory center to 

 the stimulus of COj. They can become ac- 

 climatized to great altitude only at the 

 cost of prolonged mountain sickness. Evi- 

 dently they are not suited to be aviators. 



In very sensitive subjects, on the con- 

 trary, the period of readjustment is much 

 shorter. It is a matter not of days but of 

 hours, and the functional alterations begin 

 to develop almost immediately even under 

 slight oxygen deficiency. The upper air is 

 for those men whose organization readily 

 responds with vigorous compensatory reac- 



