Hypercapnia is essential to reduce the cerebral oxidative metabolism during extreme apnea in humans

Anthony R Bain, Philip Ainslie, Otto F Barak, Ryan L Hoiland, Ivan Drvis, Tanja Mijacika, Damian M Bailey, Antoinette Santoro, Daniel K DeMasi, Zeljko Dujic, David B MacLeod

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Abstract

The cerebral metabolic rate of oxygen (CMRO2) 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 CMRO2, 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 CMRO2 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 CMRO2 were largest in the HX condition (-44 ± 15%, p < 0.05), with the most severe hypercapnia (PaCO2 = 58 ± 5 mmHg) but maintained oxygen saturation. The CMRO2 was reduced by 24 ± 27% in NM ( p = 0.05), 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 < 0.05). These novel data support hypercapnia/pH as a key mechanism mediating reductions in CMRO2 during apnea, and show that severe hypoxemia stimulates lactate release from the brain.

Original languageEnglish
Pages (from-to)3231-3242
JournalJournal of Cerebral Blood Flow and Metabolism
Volume37
Issue number9
DOIs
Publication statusPublished - 10 Jan 2017

Keywords

  • Hypoxia
  • breath-holding
  • cerebral lactate release
  • cerebral nonoxidative metabolism
  • brain metabolism

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