Wasserman K
Department of Medicine, Harbor-UCLA Medical Center, Torrance 90509.
Circulation. 1988 Oct;78(4):1060-71. doi: 10.1161/01.cir.78.4.1060.
The primary role of the heart is to provide energy for the circulatory transport of oxygen (O2) to cells at rates commensurate with their metabolic activity. At rest, even a "sick" heart may be capable of transporting O2 adequately. But during exercise, the increase in O2 required by muscle cells demands that their blood flow be increased. The supply of O2 needed to meet the O2 requirement for muscle mitochondrial high-energy phosphate generation during exercise is a critical function of the circulation. Thus, the adequacy of cardiovascular function can be estimated, noninvasively, from the pattern of O2 uptake in response to an exercise stimulus. While arterial O2 tension (PaO2) is dependent on pulmonary function (except for intracardiac right-to-left shunt), the mass transfer of O2 (VO2) between the cells and lungs depends on pulmonary blood flow (i.e., cardiac output) and O2 concentration difference between the pulmonary arterial and pulmonary venous blood, C(a-v)O2 (Fick principle). Thus, VO2 in the first 15 seconds of exercise can be used to describe the initial increase in pulmonary blood flow and stroke volume, while the subsequent rise in VO2 results from the further increase in VO2 in response to work rate increase are used to detect circulatory disturbances. Also, the rate of CO2 output (VCO2) has been valuable in the assessment of cardiovascular function when related to VO2. Inadequate O2 availability results in anaerobic metabolism, causing increased muscle lactic acid production. At the pH of cell water, most of the hydrogen ions produced with lactate are buffered by bicarbonate. The CO2 generated by the buffering reaction (22 ml for each milliequivalent) causes a net increase in VCO2 relative to VO2 at the work rate at which buffering begins. This provides a useful estimate of the anaerobic threshold. Thus, study of the dynamic coupling of external to cellular respiration during a work rate stimulus provides valuable, direct, and noninvasive information about cardiovascular mechanisms in health and disease.
心脏的主要作用是为将氧气（O₂）循环输送到细胞提供能量，输送速率要与细胞的代谢活动相匹配。在静息状态下，即使是“患病”的心脏也可能有能力充分输送O₂。但在运动期间，肌肉细胞对O₂需求的增加要求其血流量增加。在运动期间，为满足肌肉线粒体高能磷酸生成所需的O₂供应是循环系统的一项关键功能。因此，可以根据对运动刺激的O₂摄取模式，以非侵入性方式估计心血管功能是否充足。虽然动脉血氧分压（PaO₂）取决于肺功能（心内右向左分流除外），但细胞与肺之间的O₂质量转移（VO₂）取决于肺血流量（即心输出量）以及肺动脉血与肺静脉血之间的O₂浓度差，即C(a-v)O₂（菲克原理）。因此，运动开始后15秒内的VO₂可用于描述肺血流量和每搏输出量的初始增加，而随后VO₂的升高是由于工作负荷增加导致VO₂进一步升高，可用于检测循环系统紊乱。此外，当与VO₂相关时，二氧化碳排出率（VCO₂）在评估心血管功能方面也很有价值。O₂供应不足会导致无氧代谢，从而增加肌肉乳酸生成。在细胞内水的pH值下，与乳酸一起产生的大多数氢离子由碳酸氢盐缓冲。缓冲反应产生的CO₂（每毫当量产生22毫升）会导致在缓冲开始的工作负荷下，VCO₂相对于VO₂净增加。这为无氧阈值提供了有用的估计。因此，在工作负荷刺激期间研究外部呼吸与细胞呼吸的动态耦合，可为健康和疾病状态下的心血管机制提供有价值、直接且非侵入性的信息。
