Hypoxia and exercise provoke both lactate release and lactate oxidation by the human brain

Morten Overgaard, Peter Rasmussen, Aske M Bohm, Thomas Seifert, Patrice Brassard, Morten Zaar, Pernille Halberg Homann, Kevin A Evans, Henning B Nielsen, Niels H Secher, Henning M Bay Nielsen

    47 Citations (Scopus)

    Abstract

    Lactate is shuttled between organs, as demonstrated in the Cori cycle. Although the brain releases lactate at rest, during physical exercise there is a cerebral uptake of lactate. Here, we evaluated the cerebral lactate uptake and release in hypoxia, during exercise and when the two interventions were combined. We measured cerebral lactate turnover via a tracer dilution method ([1-13C]lactate), using arterial to right internal jugular venous differences in 9 healthy individuals (5 males and 4 females), at rest and during 30 min of submaximal exercise in normoxia and hypoxia (FiO 2 10%, arterial oxygen saturation 72±10%, mean±SD). Whole-body lactate turnover increased 3.5- fold and 9-fold at two workloads in normoxia and 18-fold during exercise in hypoxia. Although middle cerebral artery mean flow velocity increased during exercise in hypoxia, calculated cerebral mitochondrial oxygen tension decreased by 13 mmHg (P<0.001). At the same time, cerebral lactate release increased from 0.15 ± 0.1 to 0.8 ± 0.6 mmol min-1 (P<0.05), corresponding to ~10% of cerebral energy consumption. Concurrently, cerebral lactate uptake was 1.0 ± 0.9 mmol min-1 (P<0.05), of which 57 ± 9% was oxidized, demonstrating that lactate oxidation may account for up to ~33% of the energy substrate used by the brain. These results support the existence of a cell-cell lactate shuttle that may involve neurons and astrocytes.

    Original languageEnglish
    JournalF A S E B Journal
    Pages (from-to)3012-20
    ISSN0892-6638
    DOIs
    Publication statusPublished - Jul 2012

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