Hypercapnia suppresses oxidative metabolism in humans, as modelling showed a decrease in metabolic substrate supply explains both cytochrome oxidation and reduced brain oxygen consumption.
Does hypercapnia alter cerebral metabolism and oxygen consumption in awake human volunteers?
Hypercapnia may suppress oxidative metabolism in humans by decreasing metabolic substrate supply, perturbing mitochondrial signalling pathways.
Hypercapnia increases cerebral blood flow. The effects on cerebral metabolism remain incompletely understood although studies show an oxidation of cytochrome c oxidase, Complex IV of the mitochondrial respiratory chain. Systems modelling was combined with previously published non-invasive measurements of cerebral tissue oxygenation, cerebral blood flow, and cytochrome c oxidase redox state to evaluate any metabolic effects of hypercapnia. Cerebral tissue oxygen saturation and cytochrome oxidase redox state were measured with broadband near infrared spectroscopy and cerebral blood flow velocity with transcranial Doppler ultrasound. Data collected during 5-min hypercapnia in awake human volunteers were analysed using a Fick model to determine changes in brain oxygen consumption and a mathematical model of cerebral hemodynamics and metabolism (BrainSignals) to inform on mechanisms. Either a decrease in metabolic substrate supply or an increase in metabolic demand modelled the cytochrome oxidation in hypercapnia. However, only the decrease in substrate supply explained both the enzyme redox state changes and the Fick-calculated drop in brain oxygen consumption. These modelled outputs are consistent with previous reports of CO2 inhibition of mitochondrial succinate dehydrogenase and isocitrate dehydrogenase. Hypercapnia may have physiologically significant effects suppressing oxidative metabolism in humans and perturbing mitochondrial signalling pathways in health and disease.
Highton et al. (Fri,) conducted a other in Healthy volunteers. Hypercapnia was evaluated on Changes in brain oxygen consumption and mechanisms of cytochrome oxidation. Hypercapnia suppresses oxidative metabolism in humans, as modelling showed a decrease in metabolic substrate supply explains both cytochrome oxidation and reduced brain oxygen consumption.