Author(s): MINERS, N., THIESSEN, J., STAPLETON, R., BOMMARITO, J., TSIOROS, S., TYMKO, M., BURR, J., MILLAR, P., MCCARTHY, D., Institution: UNIVERSITY OF GUELPH, Country: CANADA, Abstract-ID: 2664

INTRODUCTION:
Athletes report using exogenous ketone supplements, but the scientific basis of this practice remains unproven. Ketone monoester (KME) ingestion increases submaximal exercise heart rate and minute ventilation and attenuates arterial oxygen desaturation at high altitude, suggesting a potential increase in systemic oxygen delivery and maximal oxygen uptake (V̇O2max) under hypoxic conditions. However, peak power output, assessed after two hours of high-altitude exposure (4000m), was impaired by KME ingestion. Since athletes typically race at moderate altitudes (~2000-3000m) and physiological responses to moderate vs. high altitude may differ, more research is required to understand how KME affects exercise responses. We hypothesized that KME ingestion would increase peak power output and V̇O2max under normobaric hypoxia (~2800m) compared to a placebo (PL).
METHODS:
Twenty-four recreationally active to endurance trained adults (23±3 years, 11 females, V̇O2max 46.5±11.2 mL/kg/min) ingested either 0.6 g/kg body mass KME or a flavour-matched PL in a randomized, double-blind, crossover design. Two hrs post-supplementation, participants entered a normobaric hypoxia chamber (14.73±0.37% O2) for a 15-min acclimation period. Participants completed 10-min of moderate-intensity cycling, below lactate threshold, then a ramp-incremental test (30 W/min) until cadence <60 rpm. V̇O2max was verified by a V̇O2 plateau (<150 mL/min increase in final 30s) and respiratory exchange ratio >1.1. Cardiac measures were collected using impedance cardiography (Physioflow Enduro) and cardiorespiratory via indirect calorimetry (Quark CPET).
RESULTS:
KME resulted in higher pre-exercise venous β-hydroxybutyrate (3.3±0.7 vs. 0.3±0.2 mM, p<0.0001) and lower pH throughout exercise (p<0.01). At moderate-intensity, heart rate (132±7 vs. 127±8 beats/min, p=0.02), ventilation (42±8 L/min vs. 39±7, p=0.01) and end-tidal O2 (67±5 vs. 64±5 mmHg, p=0.2) were higher with KME, whereas cardiac output (10.3±1.2 vs. 11.0±1.5 L/min, p=0.01) and stroke volume (77±9 vs. 85±10 mL, p=0.0003) were lower, but V̇O2 was not altered (1.34±0.28 vs. 1.34±0.29 L/min, p=0.9). At maximal exercise, V̇O2max (2612±561 vs. 2740±684 mL/min, p=0.01), cardiac output (15.1±1.7 vs. 16.9±2.2 L/min, p = 0.002), stroke volume (84±9 vs. 93±12 mL, p=0.003), and blood lactate (6.1±2.0 vs 7.1±1.9 mM, p=0.04) were lower with KME. However, power output (269±56 vs. 268±59 W, p=0.6), heart rate (185±8 vs. 184±7 beats/min, p=0.4), minute ventilation (133±30 vs. 132±34 L/min, p=0.7), and end-tidal O2 (77±5 vs. 77±4 mmHg, p=0.7) were not different with KME. Baseline V̇O2max was unrelated to the change in V̇O2max between conditions (r=-0.05, p=0.8).
CONCLUSION:
In contrast to our hypothesis, KME decreased V̇O2max without altering peak power output at simulated ~2800m altitude, accompanied by attenuated cardiac output and blood acidosis. These findings suggest acute KME ingestion is not ergogenic for endurance sport during acute exposure to moderate altitude.