Acute Ketone Monoester Supplementation Does Not Change Exercise Efficiency during Incremental Cycling in Trained Individuals.

METHODS: 28 adults (16 males and 12 females) aged 30 ± 10 y [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 flavour-matched placebo (PLAC) ~30 min prior to exercise. Exercise involved a 3-minute warm-up, three 5-minute 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 to 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 to 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 to 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.

Biological sex does not influence the peak cardiac output response to twelve weeks of sprint interval training.

Sprint interval training (SIT) increases peak oxygen uptake (V̇O2peak) but the mechanistic basis is unclear. We have reported that 12 wk of SIT increased V̇O2peak and peak cardiac output (Q̇peak) and the changes in these variables were correlated. An exploratory analysis suggested that Q̇peak increased in males but not females. The present study incorporated best practices to examine the potential influence of biological sex on the Q̇peak response to SIT. Male and female participants (n = 10 each; 21 ± 4 y) performed 33 ± 2 sessions of SIT over 12 wk. Each 10-min session involved 3 × 20-s 'all-out' sprints on an ergometer. V̇O2peak increased after SIT (3.16 ± 1.0 vs. 2.89 ± 1.0 L/min, η2p = 0.53, p < 0.001) with no sex × time interaction (p = 0.61). Q̇peak was unchanged after training (15.2 ± 3.3 vs. 15.1 ± 3.0 L/min, p = 0.85), in contrast to our previous study. The peak estimated arteriovenous oxygen difference increased after training (204 ± 30 vs. 187 ± 36 ml/L, p = 0.006). There was no effect of training or sex on measures of endothelial function. We conclude that 12 wk of SIT increases V̇O2peak but the mechanistic basis remains unclear. The capacity of inert gas rebreathing to assess changes in Q̇peak may be limited and invasive studies that use more direct measures are needed.

The effect of bodyweight exercise on 24-h glycemic responses determined by continuous glucose monitoring in healthy inactive adults: a randomized crossover study.

Vigorous intermittent exercise can improve indices of glycemia in the 24 h postexercise period in apparently healthy individuals. We examined the effect of a single session of bodyweight exercise (BWE) on glycemic responses using continuous glucose monitoring (CGM) under controlled dietary conditions. Healthy inactive adults (n = 27; 8 males, 19 females; age: 23 ± 3 years) completed 2 virtually supervised trials spaced ~ 1 week apart in a randomized, crossover manner. The trials involved an 11-min BWE protocol that consisted of 5 × 1-min bouts performed at a self-selected pace interspersed with 1-min active recovery periods or a non-exercise sitting control period (CON). Mean heart rate during the BWE protocol was 147 ± 14 beats per min (75% of age-predicted maximum). Mean 24 h glucose after BWE and CON was not different (5.0 ± 0.4 vs 5.0 ± 0.5 mM respectively; p = 0.39). There were also no differences between conditions for measures of glycemic variability or the postprandial glucose responses after ingestion of a 75 g glucose drink or lunch, dinner, and breakfast meals. This study demonstrates the feasibility of conducting a remotely supervised BWE intervention using CGM under free-living conditions. Future studies should investigate the effect of repeated sessions of BWE training or responses in people with impaired glycemic control.

Acute Ketone Monoester Supplementation Impairs 20-min Time-Trial Performance in Trained Cyclists: A Randomized, Crossover Trial.

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 [ß-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.

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

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 (V̇O 2peak ), 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 V̇O 2peak and peak Q ˙. RESULTS: Blood [ß-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). V̇O 2peak ( 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 V̇O 2peak .

Peak Cardiac Output Determined Using Inert Gas Rebreathing: A Comparison of Two Exercise Protocols.

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 V̇O 2peak tests to determine peak heart rate (HR peak ) and peak work rate ( Wpeak ). 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 V̇O 2peak test followed 10 min later by cycling at 90% Wpeak , 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 HR peak . 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 V̇O 2peak (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.

Twelve weeks of sprint interval training increases peak cardiac output in previously untrained individuals.

INTRODUCTION: Sprint interval training (SIT), characterized by brief bouts of 'supramaximal' exercise interspersed with recovery periods, increases peak oxygen uptake ([Formula: see text]) despite a low total exercise volume. Per the Fick principle, increased [Formula: see text] is attributable to increased peak cardiac output ([Formula: see text]) and/or peak arterio-venous oxygen difference (a-vO2diff). There are limited and equivocal data regarding the physiological basis for SIT-induced increases in [Formula: see text], with most studies lasting ≤ 6 weeks. PURPOSE: To determine the effect of 12 weeks of SIT on [Formula: see text], measured using inert gas rebreathing, and the relationship between changes in [Formula: see text] and [Formula: see text]. METHODS: 15 healthy untrained adults [6 males, 9 females; 21 ± 2 y (mean ± SD)] performed 28 ± 3 training sessions. Each session involved a 2-min warm-up at 50 W, 3 × 20-s 'all-out' cycling bouts (581 ± 221 W) interspersed with 2-min of recovery, and a 3-min cool-down at 50 W. RESULTS: Measurements performed before and after training showed that 12 weeks of SIT increased [Formula: see text] (17.0 ± 3.7 vs 18.1 ± 4.6 L/min, p = 0.01, partial η2 = 0.28) and [Formula: see text] (2.63 ± 0.78 vs 3.18 ± 1.1 L/min, p < 0.01, partial η2 = 0.58). The changes in these two variables were correlated (r2 = 0.46, p < 0.01). Calculated peak a-vO2diff also increased after training (154 ± 22 vs 174 ± 23 ml O2/L; p < 0.01) and was correlated with the change in [Formula: see text] (r2 = 0.33, p = 0.03). Exploratory analyses revealed an interaction (p < 0.01) such that [Formula: see text] increased in male (+ 10%, p < 0.01) but not female participants (+ 0.6%, p = 0.96), suggesting potential sex-specific differences. CONCLUSION: Twelve weeks of SIT increased [Formula: see text] by 6% in previously untrained participants and the change was correlated with the larger 21% increase in [Formula: see text].

Increased cardiorespiratory stress during submaximal cycling after ketone monoester ingestion in endurance-trained adults.

There is growing interest in the effect of exogenous ketone body supplementation on exercise responses and performance. The limited studies to date have yielded equivocal data, likely due in part to differences in dosing strategy, increase in blood ketones, and participant training status. Using a randomized, double-blind, counterbalanced design, we examined the effect of ingesting a ketone monoester (KE) supplement (600 mg/kg body mass) or flavour-matched placebo in endurance-trained adults (n = 10 males, n = 9 females; V̇O2peak = 57 ± 8 mL/kg/min). Participants performed a 30-min cycling bout at ventilatory threshold intensity (71 ± 3% V̇O2peak), followed 15 min later by a 3 kJ/kg body mass time-trial. KE versus placebo ingestion increased plasma ß-hydroxybutyrate concentration before exercise (3.9 ± 1.0 vs 0.2 ± 0.3 mM, p < 0.0001, dz = 3.4), ventilation (77 ± 17 vs 71 ± 15 L/min, p < 0.0001, dz = 1.3) and heart rate (155 ± 11 vs 150 ± 11 beats/min, p < 0.001, dz = 1.2) during exercise, and rating of perceived exertion at the end of exercise (15.4 ± 1.6 vs 14.5 ± 1.2, p < 0.01, dz = 0.85). Plasma ß-hydroxybutyrate concentration remained higher after KE vs placebo ingestion before the time-trial (3.5 ± 1.0 vs 0.3 ± 0.2 mM, p < 0.0001, dz = 3.1), but performance was not different (KE: 16:25 ± 2:50 vs placebo: 16:06 ± 2:40 min:s, p = 0.20; dz = 0.31). We conclude that acute ingestion of a relatively large KE bolus dose increased markers of cardiorespiratory stress during submaximal exercise in endurance-trained participants. Novelty: Limited studies have yielded equivocal data regarding exercise responses after acute ketone body supplementation. Using a randomized, double-blind, placebo-controlled, counterbalanced design, we found that ingestion of a large bolus dose of a commercial ketone monoester supplement increased markers of cardiorespiratory stress during cycling at ventilatory threshold intensity in endurance-trained adults.