Popov D V, Vinogradova O L
Usp Fiziol Nauk. 2012 Jan-Mar;43(1):30-47.
Oxygen delivery to muscle, its consumption and glycolytic flux, all of each affect and restrict aerobic performance, are discussed. Energy supply of intensive exercise till exhaustion lasting 3 to 4 min is provided mainly by oxidative metabolism, simultaneously glycolytic flux may be increased considerably. Other conditions being equal, capacity of oxygen delivery determines oxygen partial pressure in myoplasm of exercising/contracting muscle. With PO2 in myoplasm increasing from 0 to 1-2 mm Hg oxygen consumption (VO2) in mitochondria enhances dramatically, with further increase of PO2 its rise slows down. At the ascending part of VO2-PO2 relationship for mitochondria the increase of VO2 is noticeably restricted by oxygen delivery to contracting muscle. When PO2 approaches plateau of the VO2-PO2 relationship, an increase of VO2 is restricted by mitochondria capacity to accumulate oxygen and augmented oxygen delivery will not lead to a significant increase of muscle VO2. On the other hand considerable accumulation of glycolytic metabolites in contracting muscle causes a decrease of contractility which in its turn may restrict aerobic performance. Noteworthy no strict relationship between glycolytic flux and PO2 in myoplasm exists. That is why correct evaluation of factors limiting aerobic performance presupposes simultaneous evaluation of both glycolytic flux and oxygen consumption in muscle which in its turn depends on oxygen delivery to mitochondria and its utilization.
本文讨论了氧气向肌肉的输送、其消耗以及糖酵解通量，这些因素均会影响和限制有氧能力。持续3至4分钟直至力竭的高强度运动的能量供应主要由氧化代谢提供，同时糖酵解通量可能会显著增加。在其他条件相同的情况下，氧气输送能力决定了运动/收缩肌肉肌浆中的氧分压。随着肌浆中PO2从0增加到1-2 mmHg，线粒体中的耗氧量（VO2）急剧增加，随着PO2的进一步增加，其上升速度减缓。在线粒体VO2-PO2关系的上升部分，VO2的增加明显受到向收缩肌肉输送氧气的限制。当PO2接近VO2-PO2关系的平台期时，VO2的增加受到线粒体积累氧气能力的限制，增加氧气输送不会导致肌肉VO2显著增加。另一方面，收缩肌肉中糖酵解代谢产物的大量积累会导致收缩力下降，进而可能限制有氧能力。值得注意的是，肌浆中的糖酵解通量与PO2之间不存在严格的关系。因此，正确评估限制有氧能力的因素需要同时评估肌肉中的糖酵解通量和耗氧量，而这又取决于向线粒体的氧气输送及其利用情况。
