Effect of Acute Ketone Monoester Ingestion on Cardiorespiratory Responses to Exercise and the Influence of Blood Acidosis.

PURPOSE: To examine the effect of KE ingestion on exercise cardiac output (Q̇) and the influence of blood acidosis. We hypothesized that KE vs placebo ingestion would increase Q̇ and co-ingestion of the pH buffer bicarbonate would mitigate this effect.

METHODS: In a randomized, double-blind, crossover manner, 15 endurance-trained adults [peak oxygen uptake (V̇O2peak), 60 ± 9 mL/kg/min] ingested either 0.2 g/kg sodium bicarbonate or a salt placebo 60-min pre-exercise, and 0.6 g/kg KE or a ketone-free placebo 30-min before exercise. Supplementation yielded three experimental conditions: basal ketone bodies and neutral pH (CON), hyperketonemia and blood acidosis (KE), and hyperketonemia and neutral pH (KE + BIC). Exercise involved 30 min of cycling at ventilatory threshold intensity, followed by determinations of V̇O2peak and peak Q̇.

RESULTS: Blood [β-hydroxybutyrate], a ketone body, was higher in KE (3.5 ± 0.1 mM) and KE + BIC (4.4 ± 0.2) vs CON (0.1 ± 0.0, p < 0.0001). Blood pH was lower in KE vs CON (7.30 ± 0.01 vs 7.34 ± 0.01, p < 0.001) and KE + BIC (7.35 ± 0.01, p < 0.001). Q̇ during submaximal exercise was not different between conditions (CON: 18.2 ± 3.6, KE: 17.7 ± 3.7, KE + BIC: 18.1 ± 3.5 L/min, p = 0.4). HR was higher in KE (153 ± 9 beats/min) and KE + BIC (154 ± 9) vs CON (150 ± 9, p < 0.02). V̇O2peak (p = 0.2) and peak Q̇ (p = 0.3) were not different between conditions but peak workload was lower in KE (359 ± 61 W) and KE + BIC (363 ± 63) vs CON (375 ± 64, p < 0.02).

CONCLUSIONS: KE ingestion did not increase Q̇ during submaximal exercise despite a modest elevation of HR. This response occurred independent of blood acidosis and was associated with a lower workload at V̇O2peak.