Zoładź J, Duda K, Majerczak J, Emmerich J, Domański J
Department of Physiology and Biochemistry, AWF, Kraków, Poland.
J Physiol Pharmacol. 1998 Sep;49(3):443-55.
Five healthy non-smoking men, aged 22.2 +/- 0.8 years (mean SD), VO2 max 50.2 +/- 6.2 ml.min-1.kg-1) performed two 6 minutes constant power output (PO) bouts of cycling at 70 rev.min-1, separated by a 20 minutes of rest. The power output during the first bout of exercise corresponded to 40% VO2max, while the second exercise corresponded to 75% VO2max. The first bout of exercise was performed at a power output below the lactate threshold (LT)--determined during an incremental exercise test. In the second bout of exercise the subjects exercised above the LT. This experimental protocol was performed twice. Once as a control test (test C) and on a separate day, at about 90 minutes after ingestion of 3 mmol.kg-1 BW of NH4Cl (test A). Ingestion of ammonium chloride developed a state of metabolic acidosis. Antecubital venous blood samples taken every one minute of cycling were analysed for pH, HCO-3, BE, pO2, pCO2 and plasma lactate concentration [La]pl. Oxygen uptake was measured continuously using breath by breath system. The obtained acidotic shift of blood acid-base balance was also present throughout the 6 minutes bouts of exercise. No significant difference in VO2 during the exercise corresponding to 40% VO2 max in the test C and the test A was observed. The total oxygen consumed throughout the 6 min cycling at the PO corresponding to 75% of VO2 max was not significantly different in test C and test A (13.532 vs. 13.422 l O2, respectively). The slow component of VO2 kinetics as expressed by the delta VO2(6-3 min) of exercise was significantly higher (p = 0.03) in test A than in test C (183 +/- 97 vs. 106 +/- 53 ml.min-1 O2, respectively). It should be noted that in each subject, the magnitude of the slow component of VO2 kinetics after pre-exercise acidification was consistently higher than in control experiment.
The original finding of our study is that pre-exercise acidification induced by ingestion of 3 mmol.kg-1 B.W. of NH4Cl was accompanied by a significant increase in the magnitude of the slow component of VO2 kinetics. This is why we postulate that acidosis may play a significant role in the physiological mechanism responsible for the slow component of VO2 kinetics in humans.
五名健康的非吸烟男性，年龄为22.2±0.8岁（平均值±标准差），最大摄氧量（VO2 max）为50.2±6.2 ml·min⁻¹·kg⁻¹，以70转/分钟的速度进行了两次6分钟的恒定功率输出（PO）骑行试验，中间休息20分钟。第一次运动试验的功率输出相当于40%的VO2 max，而第二次运动试验的功率输出相当于75%的VO2 max。第一次运动试验在乳酸阈值（LT）以下的功率输出下进行（在递增运动试验中确定）。在第二次运动试验中，受试者在高于LT的强度下运动。该实验方案进行了两次。一次作为对照试验（试验C），在另一天，在摄入3 mmol·kg⁻¹体重的氯化铵后约90分钟进行（试验A）。摄入氯化铵会导致代谢性酸中毒状态。在骑行过程中每分钟采集的肘前静脉血样用于分析pH值、HCO₃⁻、碱剩余（BE）、pO₂、pCO₂和血浆乳酸浓度[La]pl。使用逐次呼吸系统连续测量摄氧量。在整个6分钟的运动试验中，均出现了酸碱平衡的酸中毒偏移。在试验C和试验A中，对应于40% VO2 max的运动过程中，VO2没有显著差异。在对应于75% VO2 max的功率输出下，整个6分钟骑行消耗的总氧量在试验C和试验A中没有显著差异（分别为13.532升O₂和13.422升O₂）。试验A中运动的VO2动力学慢成分（用运动的δVO2(6 - 3 min)表示）显著高于试验C（分别为183±97和106±53 ml·min⁻¹ O₂，p = 0.03）。需要注意的是，在每个受试者中，运动前酸化后VO2动力学慢成分的幅度始终高于对照实验。
我们研究的最初发现是，摄入3 mmol·kg⁻¹体重的氯化铵引起的运动前酸化伴随着VO2动力学慢成分幅度的显著增加。这就是为什么我们推测酸中毒可能在人类VO2动力学慢成分的生理机制中起重要作用。
