85 - Cerebral oxidative metabolism is decreased with extreme apnea in humans-Stembridge M.pdf (816.75 kB)
Download file

Cerebral oxidative metabolism is decreased with extreme apnoea in humans; impact of hypercapnia

Download (816.75 kB)
journal contribution
posted on 2023-01-24, 12:09 authored by Anthony Bain, Philip Ainslie, Ryan Hoiland, Otto Barak, Marija Cavar, Ivan Drvis, Michael StembridgeMichael Stembridge, Douglas MacLeod, Damian Bailey, Zeljko Dujic, David Macleod

 Prolonged apnea in humans is reflected in progressive hypoxemia and acidosis. Here, we explore the cerebral metabolic responses under extreme hypoxia and acidosis associated with  prolonged  apnea.  We  hypothesized  that  the  cerebral  metabolic  rate  for  oxygen (CMRO2) will be reduced near the termination of apnea, attributed in part to the acidosis. Fourteen elite apnea-divers performed a maximal apnea (range: 3:36 to 7:26 minutes) under dry laboratory-conditions. In a subset study with the same divers, the impact of acidosis  on  cerebral  metabolism in  the  background  of  hypoxia  was  determined  using varying levels of hypercapnic breathing. In both studies the CMRO2 was calculated from the  product  of  cerebral  blood  flow  (ultrasound)  and  the  radial artery-jugular  venous oxygen content difference. Non-oxidative cerebral metabolism was calculated from the ratio  of  oxygen  and  carbohydrate  (lactate  and  glucose)  metabolism.  The  CMRO2 was reduced  by  ~29%  (P<0.01,  Cohen’s  d  =  1.18)  near  the  termination  of  apnea  when compared to baseline, but non-oxidative metabolism remained unaltered. In the subset study,  in  the  background  of  hypoxia  (arterial  oxygen  tension:  ~38.4  mmHg),  severe acidosis  (arterial  pH:  ~7.30),  but  not  mild-acidosis  (arterial pH:  7.38),  significantly depressed the CMRO2 (~17%, P=0.04, Cohen’s d = 0.87). Similarly to the apnea, there was no change in the non-oxidative metabolism. These data indicate that hypercapnic-induced acidosis can in part explain the reduction in CMRO2 near apnea breakpoint. This acidosis-induced oxygen conservation may protect the brain against severe hypoxemia associated with prolonged apnea.  

Funding

Hrvatska Zaklada za Znanost (Croatian Science Foundation): Philip NAinslie, Otto F Barak, Zeljko Dujic, IP-2014-09-1937; Canadian research chair: PhilipN Ainslie

History

Published in

The Journal of Physiology

Publisher

Wiley

Version

AM (Accepted Manuscript)

Citation

Bain, A.R., Ainslie, P.N., Hoiland, R.L., Barak, O.F., Cavar, M., Drvis, I., Stembridge, M., MacLeod, D.M., Bailey, D.M., Dujic, Z. and MacLeod, D.B. (2016) 'Cerebral oxidative metabolism is decreased with extreme apnea in humans; impact of hypercapnia', The Journal of Physiology, 594 (18), pp.5317-5328

Print ISSN

0022-3751

Electronic ISSN

1469-7793

Cardiff Met Affiliation

  • Cardiff School of Sport and Health Sciences

Cardiff Met Authors

Mike Stembridge

Cardiff Met Research Centre/Group

  • Cardiovascular Physiology

Copyright Holder

© The Publisher

Language

en

Usage metrics

Read the peer-reviewed publication

Exports