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dc.contributor.authorBain, Anthony
dc.contributor.authorAinslie, Philip
dc.contributor.authorHoiland, Ryan
dc.contributor.authorBarak, Otto
dc.contributor.authorCavar, Marija
dc.contributor.authorDrvis, Ivan
dc.contributor.authorStembridge, Mike
dc.contributor.authorMacLeod, Douglas
dc.contributor.authorBailey, Damien
dc.contributor.authorDujic, Zeljko
dc.contributor.authorMacLeod, David
dc.date.accessioned2016-06-03T09:01:17Z
dc.date.available2016-06-03T09:01:17Z
dc.date.issued2016-06-03
dc.identifierhttps://repository.cardiffmet.ac.uk/bitstream/id/22090/Cerebral%20oxidative%20metabolism%20is%20decreased%20with%20extreme%20apnea%20in%20humans-Stembridge%20M.pdf
dc.identifier.citationBain, 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
dc.identifier.issn0022-3751
dc.identifier.issn1469-7793 (ESSN)
dc.identifier.urihttp://hdl.handle.net/10369/7899
dc.descriptionThis 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/JP272404en_US
dc.description.abstractProlonged 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.en_US
dc.description.sponsorshipThis 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.en_US
dc.language.isoenen_US
dc.publisherWiley
dc.relation.ispartofseriesJournal of Physiology
dc.rightsNon-Commercial
dc.subjectcerebral blood flowen_US
dc.subjectApnoeaen_US
dc.subjectdivingen_US
dc.titleCerebral oxidative metabolism is decreased with extreme apnea in humans; impact of acidosisen_US
dc.typeArticleen_US
dc.typeacceptedVersion
dc.date.dateAccepted2016-05-18
dc.rights.embargodate2017-06-03
dc.rights.embargoreason12 month embargo requested by publisher
dcterms.dateAccepted2016-05-18
rioxxterms.versionAM
rioxxterms.versionofrecordhttp://dx.doi.org/10.1113/JP272404
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.publicationdate2016-06-03
dc.date.refFCD2016-06-03
rioxxterms.freetoread.startdate2017-06-03


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