Cerebral oxidative metabolism is decreased with extreme apnea in humans; impact of acidosis

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Author
Bain, Anthony
Ainslie, Philip
Hoiland, Ryan
Barak, Otto
Cavar, Marija
Drvis, Ivan
Stembridge, Mike
MacLeod, Douglas
Bailey, Damien
Dujic, Zeljko
MacLeod, David
Date
2016-06-03Acceptance date
2016-05-18
Date Deposited
2016-06-03
Type
Article
acceptedVersion
Publisher
Wiley
ISSN
0022-3751
1469-7793 (ESSN)
Metadata
Show full item recordAbstract
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 hypercapnicinduced 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.
Journal/conference proceeding
Journal of Physiology
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
Description
This article was published in Journal of Physiology on 3 June 2016 (online). The definitive version of record is available at
http://dx.doi.org/10.1113/JP272404
Rights
Non-Commercialhttp://www.rioxx.net/licenses/all-rights-reservedSponsorship
This study was funded through a Canadian Research Chair and
NSERC Discovery grant held by Prof Ainslie. Drs. Dujic, Barak, and Ainslie were also
funded through the Croatian Science Foundation (IP-2014-09-1937). Mr. Bain was
funded through a postgraduate NSERC scholarship. We thank Dr Hitesh Gokani (Epsom
and St Helier University Hospitals NHS Trust, UK) for his technical input. Lastly we
would like to specially acknowledge the apnea divers from the Croatia National Apnea
team for their participation.
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