{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T22:39:03Z","timestamp":1793140743112,"version":"4.5.0"},"reference-count":39,"publisher":"SAGE Publications","issue":"9","license":[{"start":{"date-parts":[[2017,1,10]],"date-time":"2017-01-10T00:00:00Z","timestamp":1484006400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[2017,9]]},"abstract":"<jats:p>\n                    The cerebral metabolic rate of oxygen (CMRO\n                    <jats:sub>2<\/jats:sub>\n                    ) is reduced during apnea that yields profound hypoxia and hypercapnia. In this study, to dissociate the impact of hypoxia and hypercapnia on the reduction in CMRO\n                    <jats:sub>2<\/jats:sub>\n                    , 11 breath-hold competitors completed three apneas under: (a) normal conditions (NM), yielding severe hypercapnia and hypoxemia, (b) with prior hyperventilation (HV), yielding severe hypoxemia only, and (c) with prior 100% oxygen breathing (HX), yielding the greatest level of hypercapnia, but in the absence of hypoxemia. The CMRO\n                    <jats:sub>2<\/jats:sub>\n                    was calculated from the product of cerebral blood flow (ultrasound) and the radial artery-jugular venous oxygen content difference (cannulation). Secondary measures included net-cerebral glucose\/lactate exchange and nonoxidative metabolism. Reductions in CMRO\n                    <jats:sub>2<\/jats:sub>\n                    were largest in the HX condition (\u221244\u2009\u00b1\u200915%, p\u2009&lt;\u20090.05), with the most severe hypercapnia (PaCO\n                    <jats:sub>2<\/jats:sub>\n                    \u2009=\u200958\u2009\u00b1\u20095\u2009mmHg) but maintained oxygen saturation. The CMRO\n                    <jats:sub>2<\/jats:sub>\n                    was reduced by 24\u2009\u00b1\u200927% in NM ( p\u2009=\u20090.05), but unchanged in the HV apnea where hypercapnia was absent. A net-cerebral lactate release was observed at the end of apnea in the HV and NM condition, but not in the HX apnea (main effect p\u2009&lt;\u20090.05). These novel data support hypercapnia\/pH as a key mechanism mediating reductions in CMRO\n                    <jats:sub>2<\/jats:sub>\n                    during apnea, and show that severe hypoxemia stimulates lactate release from the brain.\n                  <\/jats:p>","DOI":"10.1177\/0271678x16686093","type":"journal-article","created":{"date-parts":[[2017,1,10]],"date-time":"2017-01-10T22:17:01Z","timestamp":1484086621000},"page":"3231-3242","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":47,"title":["Hypercapnia is essential to reduce the cerebral oxidative metabolism during extreme apnea in humans"],"prefix":"10.1177","volume":"37","author":[{"given":"Anthony R","family":"Bain","sequence":"first","affiliation":[{"name":"Centre for Heart Lung and Vascular Health, University of British Columbia, Kelowna, BC, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philip 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