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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; VO2peak=57±8 ml/kg/min). Participants performed a 30-min cycling bout at ventilatory threshold intensity (71±3% VO2peak), followed 15 min later by a 3 kJ/kg body mass time-trial. KE versus placebo ingestion increased plasma [β-hydroxybutyrate] 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 [β-hydroxybutyrate] 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 bullets: •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.

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.

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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.PurposeThis 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.MethodsIn 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˙.ResultsBlood [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).ConclusionsKE 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.

There is renewed interest in the potential for interval (INT) training to increase skeletal muscle mitochondrial content including whether the response differs from continuous (CONT) training. Comparisons of INT and CONT exercise are impacted by the manner in which protocols are “matched”, particularly with respect to exercise intensity, as well as inter‐individual differences in training responses. We employed single‐leg cycling to facilitate a within‐participant design and test the hypothesis that short‐term INT training would elicit a greater increase in mitochondrial content than work‐ and intensity‐matched CONT training. Ten young healthy adults (five males and five females) completed 12 training sessions over 4 weeks with each leg. Legs were randomly assigned to complete either 30 min of CONT exercise at a challenging sustainable workload (~50% single‐leg peak power output; Wpeak) or INT exercise that involved 10 × 3‐min bouts at the same absolute workload. INT bouts were interspersed with 1 min of recovery at 10% Wpeak and each CONT session ended with 10 min at 10% Wpeak. Absolute and mean intensity, total training time, and volume were thus matched between legs but the pattern of exercise differed. Contrary to our hypothesis, biomarkers of mitochondrial content including citrate synthase maximal activity, mitochondrial protein content and subsarcolemmal mitochondrial volume increased after CONT (p < 0.05) but not INT training. Both training modes increased single‐leg Wpeak (p < 0.01) and time to exhaustion at 70% of single‐leg Wpeak (p < 0.01). In a work‐ and intensity‐matched comparison, short‐term CONT training increased skeletal muscle mitochondrial content whereas INT training did not.

TO THE EDITOR: Podlogar et al. ( 1) have nicely discussed current methods for classifying athletes in applied physiology studies attending to their training or performance level. We agree with them that relying on a single physiological marker such as maximum oxygen uptake is not without limitations and endorse the use of more performance-based indicators. However, before proposing critical power/speed (CP/ CS) as the primary indicator of an athlete's training status, the robustness of these variables and the best method for their determination remains to be confirmed. Differences in mathematical models or test durations can indeed have a remarkable impact on an individual's CP/CS (e.g., up to $1 km/ h for CS in top-level runners) (2).More research is needed to provide reference or "normative" values of CP/CS allowing classification of athletes into different performance/fitness categories. An alternative, at least in cycling, might be classifying athletes attending to the highest power output that they can achieve for a given duration-the so-called "mean maximum power" (MMP) (3). This approach does not require the use of mathematical calculations or additional laboratory testing and is sensitive enough to allow discerning actual performance even between the two highest category levels-Union Cycliste Internationale [UCI] ProTeam versus UCI WorldTour-in professional cyclists (4). We have recently reported normative MMP values for male (n = 144) (4) and female professional cyclists (n = 44) (5). If a similar approach was used in cyclists of a lower training/competition level, scientists and coaches could accurately classify participants in cycling physiology studies.