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Acute ketone monoester (KE) supplementation can alter exercise responses, but the performance effect is unclear. The limited and equivocal data to date are likely related to factors including the KE dose, test conditions, and caliber of athletes studied. We tested the hypothesis that mean power output during a 20-min cycling time trial (TT) would be different after KE ingestion compared to a placebo (PL). A sample size of 22 was estimated to provide 80% power to detect an effect size dz of 0.63 at an alpha level of.05 with a two-tailed paired t test. This determination considered 2.0% as the minimal important difference in performance. Twenty-three trained cyclists (N = 23; peak oxygen uptake: 65 ± 12 ml·kg−1 min−1; M ± SD), who were regularly cycling >5 hr/week, completed a familiarization trial followed by two experimental trials. Participants self-selected and replicated their diet and exercise for ∼24 hr before each trial. Participants ingested either 0.35 g/kg body mass of (R)-3-hydroxybutyl (R)-3-hydroxybutyrate KE or a flavor-matched PL 30 min before exercise in a randomized, triple-blind, crossover manner. Exercise involved a 15-min warm-up followed by the 20-min TT on a cycle ergometer. The only feedback provided was time elapsed. Preexercise venous [β-hydroxybutyrate] was higher after KE versus PL (2.0 ± 0.6 vs. 0.2 ± 0.1 mM, p <.0001). Mean TT power output was 2.4% (0.6% to 4.1%; mean [95% confidence interval]) lower after KE versus PL (255 ± 54 vs. 261 ± 54 W, p <.01; dz = 0.60). The mechanistic basis for the impaired TT performance after KE ingestion under the present study conditions remains to be determined. [ABSTRACT FROM AUTHOR]

The article analyzes the impact of acute ingestion of a commercial (R)-3-hydroxybutyl (R)-3-hydroxybutyrate ketone monoester (KE) supplement on exercise responses and performance in endurance-trained participants. It has been hypothesized that nutritional ketosis induced by actue KE ingestion would decrease indices of cardiorespiratory and perceived stress and improves time-trial performance.

Peak cardiac output (Q˙ peak) can be measured noninvasively using inert gas rebreathing (IGR). There is no consensus on the optimal protocol to measure Q˙ peak using IGR, which requires a rebreathing period of ~10 s as close to "maximal" exercise as possible. Purpose: This study aimed to compare Q˙ peak elicited by a constant load protocol (Q˙ CL) and an incremental step protocol (Q˙ step). Methods: A noninferiority randomized crossover trial was used to compare Q˙ peak between protocols using a noninferiority margin of 0.5 L·min−1. Participants (n = 34 (19 female, 15 male); 25 ± 5 yr) performed two baseline V̇O2peak tests to determine peak heart rate (HRpeak) and peak work rate (W peak). Participants then performed the Q˙ CL and Q˙ step protocols each on two separate occasions with the order of the four visits randomized. Q˙ peak was measured using IGR (Innocor; COSMED, Rome, Italy). The Q˙ CL protocol involved a V̇O2peak test followed 10 min later by cycling at 90% W peak, with IGR initiated after 2 min. Q˙ step involved an incremental step test with IGR initiated when the participant's HR reached 5 bpm below their HRpeak. The first Q˙ CL and Q˙ step tests were compared for noninferiority, and the second series of tests was used to measure repeatability (typical error (TE)). Results: The Q˙ CL protocol was noninferior to Q˙ step (Q˙ CL = 17.1 ± 3.2, Q˙ step = 16.8 ± 3.1 L·min−1; 95% confidence intervals, −0.16 to 0.72 L·min−1). The baseline V̇O2peak (3.13 ± 0.83 L·min−1) was achieved during Q˙ CL (3.12 ± 0.72, P = 0.87) and Q˙ step (3.12 ± 0.80, P = 0.82). The TE values for Q˙ peak were 6.6% and 8.3% for Q˙ CL and Q˙ step, respectively. Conclusions: The Q˙ CL protocol was noninferior to Q˙ step and may be more convenient because of the reduced time commitment to perform the measurement. [ABSTRACT FROM AUTHOR]

Acute ketone monoester (KE) supplementation can alter exercise responses related to endurance performance. There are limited and equivocal data regarding the effect on exercise efficiency including the influence of supplement dose. We therefore examined the effect of KE ingestion on indices of exercise efficiency during submaximal incremental cycling in trained participants. Methods: Twenty-eight adults (16 males and 12 females) aged 30 ± 10 yr (peak oxygen uptake (V̇O2peak): 59 ± 11 mL·kg−1·min−1) completed three experimental trials in a randomized, crossover, and double-blinded manner. Participants ingested either 0.3 (KE-LO) or 0.6 (KE-HI) g·kg−1 body mass of KE or a flavor-matched placebo (PLAC) ~30 min before exercise. Exercise involved a 3-min warm-up, three 5-min stages at fixed incremental workloads corresponding to 75%, 100%, and 125% of individual ventilatory threshold, followed by a ramp protocol to volitional exhaustion to determine peak power output (PPO). Results: Venous blood [ß-hydroxybutyrate], the major circulating ketone body, was higher after KE ingestion compared with PLAC (KE-HI: 3.0 ± 1.1 ≥ KE-LO: 2.3 ± 0.6 ≥ PLAC: 0.2 ± 0.1 mM; all P ≤ 0.001. There were no differences between conditions in the primary outcome exercise economy, nor gross efficiency or delta efficiency, when analyzed over the entire submaximal exercise period or by stage. Heart rate and ventilation were higher in KE-HI and KE-LO compared with PLAC when assessed over the entire submaximal exercise period and by stage (all P ≤ 0.05). PPO after the ramp was lower in KE-HI compared with both KE-LO and PLAC (329 ± 60 vs 339 ± 62 and 341 ± 61 W, respectively; both P < 0.05) despite no difference in V̇O2peak. Conclusions: KE ingestion did not change indices of exercise efficiency but increased markers of cardiorespiratory stress during submaximal incremental cycling and reduced PPO. [ABSTRACT FROM AUTHOR]

Ketone monoester (KE) ingestion can induce hyperketonemia and blood acidosis. We previously found that acute ingestion of 0.6 g·kg−1 body mass KE increased exercise heart rate (HR) compared with placebo. Purpose: This study aimed to examine the effect of KE ingestion on exercise cardiac output (Q˙) and the influence of blood acidosis. We hypothesized that KE versus placebo ingestion would increase Q ˙, and coingestion 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−1·min−1) ingested either 0.2 g·kg−1 sodium bicarbonate or a salt placebo 60 min before exercise, and 0.6 g·kg−1 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 Q ˙. Results: Blood [β-hydroxybutyrate], a ketone body, was higher in KE (3.5 ± 0.1 mM) and KE + BIC (4.4 ± 0.2) versus CON (0.1 ± 0.0, P < 0.0001). Blood pH was lower in KE versus CON (7.30 ± 0.01 vs 7.34 ± 0.01, P < 0.001) and KE + BIC (7.35 ± 0.01, P < 0.001). Q ˙ 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−1; P = 0.4). HR was higher in KE (153 ± 9 bpm) and KE + BIC (154 ± 9) versus CON (150 ± 9, P < 0.02). V̇O2peak (P = 0.2) and peak Q ˙ (P = 0.3) were not different between conditions, but peak workload was lower in KE (359 ± 61 W) and KE + BIC (363 ± 63) versus CON (375 ± 64, P < 0.02). Conclusions: KE ingestion did not increase Q ˙ 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. [ABSTRACT FROM AUTHOR]