Ball D, Greenhaff P L, Maughan R J
Department of Enviromental and Occupational Medicine, University Medical School, Foresterhill, Aberdeen, UK.
Eur J Appl Physiol Occup Physiol. 1996;73(1-2):105-12. doi: 10.1007/BF00262817.
The present experiment was designed to investigate whether a diet-induced metabolic acidosis was a major factor in the earlier onset of fatigue during high-intensity exercise. Six healthy males cycled to exhaustion at a workload equivalent to 95 percent of maximum oxygen uptake on four separate occasions. Exercise tests were performed after an overnight fast and each test was preceded by one of four experimental conditions. Two experimental diets were designed, either to replicate each subject's own normal diet [N diet, mean (SD) daily energy intake (E) = 13 (0.7) MJ, 14.5 (0.8) percent protein (Pro), 37.5 (2.2) percent fat (Fat) and 47.5 (2.1) percent carbohydrate (CHO)], or a low-carbohydrate diet [E = 12.6 (0.8) MJ, 33.6 (1.3) percent Pro, 64.4 (1.5) percent Fat and 2.2 (0.4) percent CHO]. These diets were prepared and consumed within the department over a 3-day period. Over a 3-period prior to the exercise trial subjects ingested either NaHCO(3) or CaCO(3) (3.6 and 3.0 mmol*kg body mass), thus giving four experimental conditions: N diet and treatment, N diet and placebo, low-CHO diet and treatment and low-CHO diet and placebo. Treatments were assigned using a randomised protocol. Arterialised venous blood samples were taken for the determination of acid-base status and metabolite concentrations at rest prior to exercise and at intervals for 30 min following exhaustion. Consumption of the low-CHO diet induced a mild metabolic acidosis which was reversed by the ingestion of NaHCO(3). Blood pH, bicarbonate (HCO-(3)) and base excess (BE) were higher following NaHCO(3) ingestion after the normal diet than all of the other experimental conditions (P <0.01). Exercise time following the low-CHO diet was less than on the normal diet conditions (P <0.05): bicarbonate ingestion had no effect on exercise time on either of the diet conditions. Post-exercise blood pH, HCO-(3); and BE were higher following the ingestion of NaHCO(3) irrespective of the pre-exercise diet (P <0.05). Blood lactate concentration was higher 2 min after exercise following the N diet with NaHCO(3) when compared to the low-CHO diets with either NaHCO(3) or placebo (P <0.05). Plasma ammonia accumulation was not significantly different between experimental conditions. These data confirm previous data showing that the ingestion of a low-CHO diet reduces the capacity to perform high-intensity exercise, but it appears that the metabolic acidosis induced by the low-CHO diet is not the cause of the reduced exercise capacity observed during high-intensity exercise under these conditions.
本实验旨在研究饮食诱导的代谢性酸中毒是否是高强度运动期间疲劳提前出现的主要因素。六名健康男性在四个不同场合，以相当于最大摄氧量95%的工作量骑车至力竭。在空腹过夜后进行运动测试，每次测试前有四种实验条件之一。设计了两种实验饮食，一种是复制每个受试者自己的正常饮食（N饮食，平均（标准差）每日能量摄入量（E）=13（0.7）兆焦耳，蛋白质（Pro）14.5（0.8）%，脂肪（Fat）37.5（2.2）%，碳水化合物（CHO）47.5（2.1）%），另一种是低碳水化合物饮食（E = 12.6（0.8）兆焦耳，Pro 33.6（1.3）%，Fat 64.4（1.5）%，CHO 2.2（0.4）%）。这些饮食在部门内制备并在3天内食用。在运动试验前的3天期间，受试者摄入NaHCO₃或CaCO₃（3.6和3.0毫摩尔/千克体重），从而产生四种实验条件：N饮食和治疗、N饮食和安慰剂、低碳水化合物饮食和治疗以及低碳水化合物饮食和安慰剂。使用随机方案分配治疗。在运动前休息时以及力竭后每隔30分钟采集动脉化静脉血样，用于测定酸碱状态和代谢物浓度。食用低碳水化合物饮食会诱发轻度代谢性酸中毒，而摄入NaHCO₃可使其逆转。正常饮食后摄入NaHCO₃后的血液pH值、碳酸氢盐（HCO₃⁻）和碱剩余（BE）高于所有其他实验条件（P <0.01）。低碳水化合物饮食后的运动时间比正常饮食条件下短（P <0.05）：摄入碳酸氢盐对两种饮食条件下的运动时间均无影响。无论运动前饮食如何，摄入NaHCO₃后运动后的血液pH值、HCO₃⁻和BE均较高（P <0.05）。与摄入NaHCO₃或安慰剂的低碳水化合物饮食相比，N饮食加NaHCO₃后运动2分钟时的血乳酸浓度更高（P <0.05）。各实验条件下血浆氨的积累无显著差异。这些数据证实了先前的数据，即摄入低碳水化合物饮食会降低进行高强度运动的能力，但在这些条件下，低碳水化合物饮食诱发的代谢性酸中毒似乎不是高强度运动期间观察到的运动能力下降的原因。
