Department of Kinesiology, McMaster University, Hamilton, ON, CANADA.
Department of Medicine, McMaster University, Hamilton, ON, CANADA.
Med Sci Sports Exerc. 2023 Jul 1;55(7):1286-1295. doi: 10.1249/MSS.0000000000003141. Epub 2023 Feb 21.
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.
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 ˙.
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). 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).
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 .
本研究旨在检验酮酯（KE）摄入对运动心输出量（Q˙）的影响以及血液酸中毒的影响。我们假设 KE 摄入相对于安慰剂摄入会增加 Q˙，而同时摄入 pH 缓冲碳酸氢盐会减轻这种影响。
采用随机、双盲、交叉设计，15 名耐力训练的成年人（峰值摄氧量（V̇O2peak），60 ± 9 mL·kg-1·min-1）在运动前 60 分钟分别摄入 0.2 g·kg-1 碳酸氢钠或盐安慰剂，在运动前 30 分钟摄入 0.6 g·kg-1 KE 或无酮安慰剂。补充剂产生了三种实验条件：基础酮体和中性 pH（CON）、高酮血症和血液酸中毒（KE）以及高酮血症和中性 pH（KE+BIC）。运动包括 30 分钟的自行车运动，达到通气阈值强度，然后测定 V̇O2peak 和峰值 Q˙。
血液[β-羟基丁酸]，一种酮体，在 KE（3.5 ± 0.1 mM）和 KE + BIC（4.4 ± 0.2）中高于 CON（0.1 ± 0.0，P < 0.0001）。与 CON（7.30 ± 0.01 比 7.34 ± 0.01，P < 0.001）和 KE + BIC（7.35 ± 0.01，P < 0.001）相比，KE 组的血液 pH 值较低。在亚最大运动期间，Q˙在条件之间没有差异（CON：18.2 ± 3.6，KE：17.7 ± 3.7，KE + BIC：18.1 ± 3.5 L·min-1；P = 0.4）。与 CON（150 ± 9 bpm）相比，KE（153 ± 9 bpm）和 KE + BIC（154 ± 9 bpm）的 HR 更高（P < 0.02）。V̇O2peak（P = 0.2）和峰值 Q˙（P = 0.3）在条件之间没有差异，但 KE（359 ± 61 W）和 KE + BIC（363 ± 63 W）的峰值工作负荷低于 CON（375 ± 64 W，P < 0.02）。
尽管 HR 略有升高，但 KE 摄入并未在亚最大运动期间增加 Q˙。这种反应发生在血液酸中毒之外，与 V̇O2peak 时的较低工作量有关。
