In present study we demonstrate that in healthy humans the cerebral lactate concentration increases during inhalation of hypoxic air but not after exposure to carbon monoxide. This suggests a regulatory mechanism of cerebral glycolytic activity possibly mediated by sensing of arterial oxygen pressure and that the lactate production is not solely a result of hindered oxidative metabolism, at least during non-threatening hypoxic exposure. Phase-contrast mapping and susceptibility-based oximetry were used to acquire global cerebral blood flow and oxygen consumption and MR-spectroscopy was used to measure the lactate concentration in the occipital lope in a total of 51 healthy humans.
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