Poffé Chiel, Wyns Felix, Ramaekers Monique, Hespel Peter
Exercise Physiology Research Group, Department of Movement Sciences, KU Leuven, Leuven, BELGIUM.
Bakala Academy-Athletic Performance Center, KU Leuven, Leuven, BELGIUM.
Med Sci Sports Exerc. 2021 May 1;53(5):1068-1078. doi: 10.1249/MSS.0000000000002552.
We recently demonstrated that coingestion of NaHCO3 to counteract ketoacidosis resulting from oral ketone ester (KE) intake improves mean power output during a 15-min time trial (TT) at the end of a 3-h cycling race by ~5%. This ergogenic effect occurred at a time when blood ketone levels were low, as ketosis was only induced during the initial ~2 h of the race. Therefore, in the current study, we investigated whether performance also increases if blood ketone levels are increased in the absence of ketoacidosis during high-intensity exercise.
In a double-blind crossover design, 14 well-trained male cyclists completed a 30-min TT (TT30') followed by an all-out sprint at 175% of lactate threshold (SPRINT). Subjects were randomized to receive (i) 50 g KE, (ii) 180 mg·kg-1 body weight NaHCO3 (BIC), (iii) KE + BIC, or (iv) a control drink (CON).
KE ingestion increased blood d-ß-hydroxybutyrate to ~3-4 mM during the TT30' and SPRINT (P < 0.001 vs CON). In KE, blood pH and bicarbonate concomitantly dropped, causing 0.05 units lower pH and 2.6 mM lower bicarbonate in KE compared with CON during the TT30' and SPRINT (P < 0.001 vs CON). BIC coingestion resulted in 0.9 mM higher blood d-ß-hydroxybutyrate (P < 0.001 vs KE) and completely counteracted ketoacidosis during exercise (P > 0.05 vs CON). Mean power output during TT30' was similar between CON and BIC at 281 W, but was 1.5% lower in the KE conditions (main effect of KE: P = 0.03). Time to exhaustion in the SPRINT was ~64 s in CON and KE and increased by ~8% in the BIC conditions (main effect of BIC: P < 0.01).
Neutralization of acid-base disturbance by BIC coingestion is insufficient to counteract the slightly negative effect of KE intake during high-intensity exercise.
我们最近证明,在3小时自行车比赛结束时进行的15分钟计时赛(TT)中,同时摄入碳酸氢钠(NaHCO₃)以抵消口服酮酯(KE)摄入引起的酮症酸中毒,可使平均功率输出提高约5%。这种促力效应发生在血酮水平较低的时候,因为酮症仅在比赛最初约2小时内诱发。因此,在本研究中,我们调查了在高强度运动期间,在无酮症酸中毒的情况下提高血酮水平是否也能提高运动表现。
采用双盲交叉设计,14名训练有素的男性自行车运动员完成了30分钟的计时赛(TT30'),随后以乳酸阈值的175%进行全力冲刺(SPRINT)。受试者被随机分为接受(i)50克KE,(ii)180毫克·千克体重的NaHCO₃(BIC),(iii)KE + BIC,或(iv)对照饮料(CON)。
在TT30'和SPRINT期间,摄入KE使血d-β-羟基丁酸升高至约3 - 4毫摩尔(与CON相比,P < 0.001)。在KE组中,血pH值和碳酸氢盐同时下降,导致在TT30'和SPRINT期间,KE组的血pH值比CON组低0.05个单位,碳酸氢盐低2.6毫摩尔(与CON相比,P < 0.001)。同时摄入BIC使血d-β-羟基丁酸升高0.9毫摩尔(与KE相比,P < 0.001),并完全抵消了运动期间的酮症酸中毒(与CON相比,P > 0.05)。TT30'期间CON组和BIC组的平均功率输出相似,均为281瓦,但在KE组条件下低1.5%(KE的主效应:P = 0.03)。在SPRINT中,CON组和KE组的疲劳时间约为64秒,在BIC组条件下增加了约8%(BIC的主效应:P < 0.01)。
同时摄入BIC对酸碱紊乱的中和不足以抵消高强度运动期间KE摄入的轻微负面影响。