Wasserman K
Department of Medicine, Harbor-University of California Los Angeles Medical Center.
Am J Physiol. 1994 Apr;266(4 Pt 1):E519-39. doi: 10.1152/ajpendo.1994.266.4.E519.
The changes in cellular respiration needed to increase energy output during exercise are intimately and predictably linked to external respiration through the circulation. This review addresses the mechanisms by which lactate accumulation might influence O2 uptake (VO2) and CO2 output (VCO2) kinetics. Respiratory homeostasis (a steady state with respect to VO2 and VCO2) is achieved by 3-4 min for work rates not associated with an increase in arterial lactate. When blood lactate increases significantly above rest for constant work rate exercise, VO2 characteristically increases past 3 min (slow component) at a rate proportional to the lactate concentration increase. The development of a similar slow component in VCO2 is not evident. The divergence of VCO2 from VO2 increase can be accounted for by extra CO2 release from the cell as HCO3- buffers lactic acid. Thus the slow component of aerobic CO2 production (parallel to VO2) is masked by the increase in buffer VCO2. This CO2, and the consumption of extracellular HCO3- by the lactate-producing cells, shifts the oxyhemoglobin dissociation curve rightward (Bohr effect). The exercise lactic acidosis has been observed to occur after the minimal capillary PO2 is reached. Thus the lactic acidosis serves to facilitate oxyhemoglobin dissociation and O2 transport to the muscle cells without a further decrease in end-capillary PO2. From these observations, it is hypothesized that simultaneously measured dynamic changes in VO2 and VCO2 might be useful to infer the aerobic and anaerobic contributions to exercise bioenergetics for a specific work task.
运动期间为增加能量输出所需的细胞呼吸变化，通过循环系统与外呼吸密切且可预测地联系在一起。本综述探讨了乳酸积累可能影响氧气摄取（VO₂）和二氧化碳排出（VCO₂）动力学的机制。对于与动脉血乳酸增加无关的工作强度，呼吸稳态（关于VO₂和VCO₂的稳定状态）在3 - 4分钟内即可实现。当以恒定工作强度进行运动，且血乳酸显著高于静息水平时，VO₂通常在3分钟后（慢成分）开始增加，其增加速率与乳酸浓度的增加成正比。而VCO₂中类似慢成分的发展并不明显。VCO₂与VO₂增加的差异可归因于细胞中额外的二氧化碳释放，因为碳酸氢根（HCO₃⁻）缓冲了乳酸。因此，有氧二氧化碳产生的慢成分（与VO₂平行）被缓冲性VCO₂的增加所掩盖。这种二氧化碳以及产生乳酸的细胞对细胞外HCO₃⁻的消耗，使氧合血红蛋白解离曲线向右移动（波尔效应）。已观察到运动性乳酸酸中毒在达到最小毛细血管氧分压后发生。因此，乳酸酸中毒有助于促进氧合血红蛋白解离和氧气向肌肉细胞的转运，而不会使毛细血管末端氧分压进一步降低。基于这些观察结果，推测同时测量VO₂和VCO₂的动态变化，可能有助于推断特定工作任务中运动生物能量学的有氧和无氧贡献。
