Abstract
Exogenous ketone esters have demonstrated the capacity to increase oxygen availability during acute hypoxic exposure leading to the potential application of their use to mitigate performance declines at high altitudes. Voluntary hypoventilation (VH) with exercise reliably reduces oxygen availability and increases carbon dioxide retention without alterations to ambient pressure or gas content. Utilizing a double-blind randomized crossover design, fifteen recreational male distance runners performed submaximal exercise (4 × 5 min; 70% VO2 Max) with VH. An exogenous ketone ester (KME; 573 mg⋅kg–1) or iso-caloric flavor matched placebo (PLA) was consumed prior to exercise. Metabolites, blood gases, expired air, heart rate, oxygen saturation, cognition, and perception metrics were collected throughout. KME rapidly elevated R-β-hydroxybutyrate and reduced blood glucose without altering lactate production. KME lowered pH, bicarbonate, and total carbon dioxide. VH with exercise significantly reduced blood (SpO2) and muscle (SmO2) oxygenation and increased cognitive mean reaction time and respiratory rate regardless of condition. KME administration significantly elevated respiratory exchange ratio (RER) at rest and throughout recovery from VH, compared to PLA. Blood carbon dioxide (PCO2) retention increased in the PLA condition while decreasing in the KME condition, leading to a significantly lower PCO2 value immediately post VH exercise (IPE; p = 0.031) and at recovery (p = 0.001), independent of respiratory rate. The KME’s ability to rapidly alter metabolism, acid/base balance, CO2 retention, and respiratory exchange rate independent of respiratory rate changes at rest, during, and/or following VH exercise protocol illustrates a rapid countermeasure to CO2 retention in concert with systemic metabolic changes.
Highlights
Acute and chronic hypoxia exposure has been demonstrated to induce alterations in cognitive function (McMorris et al, 2017; Jung et al, 2020)
Blood R-βHB increased significantly from baseline to 30 min post in ketone monoester supplement (KME) condition and remained significantly elevated throughout the trial compared to PLA (P < 0.001)
Blood glucose was significantly lower in KME condition at 30min post exercise, Voluntary hypoventilation (VH) Set 1, VH Set 2, and during recovery compared to PLA
Summary
Acute and chronic hypoxia exposure has been demonstrated to induce alterations in cognitive function (McMorris et al, 2017; Jung et al, 2020). Cognition deficits are observed during moderate declines in systemic O2 as circulating O2 levels function as a strong predictor of cognitive performance during hypoxia exposure (McMorris et al, 2017). These effects appear dose dependent as performance is weaker at lower circulating O2 levels. Endogenous compensatory mechanisms which mitigate cognitive decline in hypoxia include vasoconstriction and increased cerebral blood flow (CBF; Feldman et al, 2013). These effects are typically only observed with severe drops in O2 partial pressure (60 mmHg) and cognitive decline is observed well before these levels are achieved. Any intervention or treatment that increases CBF while maintaining a higher circulating O2 may mitigate the cognitive decline observed during moderate to low systemic O2 concentrations
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