Poole D C, Richardson R S
Department of Kinesiology, Kansas State University, Manhattan, USA.
Sports Med. 1997 Nov;24(5):308-20. doi: 10.2165/00007256-199724050-00003.
For exercise modalities such as cycling which recruit a substantial muscle mass, muscle oxygen uptake (VO2) is the primary determinant of pulmonary VO2. Indeed, the kinetic complexities of pulmonary VO2 associated with exercise onset and the non-steady state of heavy (> lactate threshold) and severe [> asymptote of power-time relationship for high intensity exercise (W)] exercise reproduce with close temporal and quantitative fidelity those occurring across the exercising muscles. For moderate (< lactate threshold) exercise and also rapidly incremental work tests, pulmonary (and muscle) VO2 increases as a linear function of work rate (approximately equal to 9 to 11 ml O2/W/min) in accordance with theoretical determinations of muscle efficiency (approximately equal to 30%). In contrast, for constant load exercise performed in the heavy and severe domains, a slow component of the VO2 response is manifest and pulmonary and muscle VO2 increase as a function of time as well as work rate beyond the initial transient associated with exercise onset. In these instances, muscle efficiency is reduced as the VO2 cost per unit of work becomes elevated, and in the severe domain, this VO2 slow component drives VO2 to its maximum and fatigue ensues rapidly. At pulmonary maximum oxygen uptake (VO2max) during cycling, the maximal cardiac output places a low limiting ceiling on peak muscle blood flow, O2 delivery and thus muscle VO2. However, when the exercise is designed to recruit a smaller muscle mass (e.g. leg extensors, 2 to 3kg), mass-specific muscle blood flow and VO2 at maximal exercise are 2 to 3 times higher than during conventional cycling. consequently, for any exercise which recruits more than approximately equal to 5 to 6kg of muscle at pulmonary VO2max, there exists a mitochondrial or VO2 reserve capacity within the exercising muscles which cannot be accessed due to oxygen delivery limitations. The implications of these latter findings relate to the design of exercise tests. Specifically, if the purpose of exercise testing is to evaluate the oxidative capacity of a small muscle mass (< 5 to 6kg), the testing procedure should be designed to restrict the exercise to those muscles so that a central (cardiac output, muscle O2 delivery) limitation is not invoked. It must be appreciated that exercise which recruits a greater muscle mass will not stress the maximum mass-specific muscle blood flow and VO2 but rather the integration of central (cardiorespiratory) and peripheral (muscle O2 diffusing capacity) limitations.
对于像骑行这样能调动大量肌肉群的运动方式，肌肉摄氧量（VO2）是肺VO2的主要决定因素。事实上，与运动开始相关的肺VO2的动力学复杂性以及重度（>乳酸阈）和极重度[>高强度运动（瓦特）功率 - 时间关系的渐近线]运动的非稳态，在时间和定量方面都能高度重现运动肌肉中发生的情况。对于中度（<乳酸阈）运动以及快速递增负荷试验，肺（和肌肉）VO2随工作率呈线性增加（约等于9至11毫升氧气/瓦特/分钟），这与肌肉效率的理论测定结果（约等于30%）一致。相比之下，对于在重度和极重度运动区间进行的恒负荷运动，VO2反应会出现一个缓慢成分，并且肺和肌肉VO2会随着时间以及工作率增加，超出与运动开始相关的初始瞬态阶段。在这些情况下，由于单位工作量的VO2成本升高，肌肉效率会降低，在极重度运动区间，这个VO2缓慢成分会使VO2达到最大值，随后迅速出现疲劳。在骑行过程中达到肺最大摄氧量（VO2max）时，最大心输出量对峰值肌肉血流量、氧气输送以及肌肉VO2构成了较低的限制上限。然而，当运动设计为调动较小肌肉群（如腿部伸肌，2至3千克）时，最大运动时的单位肌肉质量血流量和VO2比传统骑行时高2至3倍。因此，对于任何在肺VO2max时调动超过约5至6千克肌肉的运动，运动肌肉内存在线粒体或VO2储备能力，但由于氧气输送限制而无法利用。后一种发现的意义与运动测试的设计有关。具体而言，如果运动测试的目的是评估小肌肉群（<5至6千克）的氧化能力，测试程序应设计为将运动限制在这些肌肉上，以免引发中枢（心输出量、肌肉氧气输送）限制。必须认识到，调动较大肌肉群的运动不会使单位肌肉质量的最大血流量和VO2达到极限，而是会使中枢（心肺）和外周（肌肉氧气扩散能力）限制的综合作用达到极限。
