Transport of oxygen in muscle.
Transport of oxygen in muscle.
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DOI：
10.1146/annurev.ph.51.030189.004233
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发表时间：
1989
影响因子：
18.2
通讯作者：
B. Wittenberg;J. Wittenberg
中科院分区：
文献类型：
--
作者：
B. Wittenberg;J. Wittenberg
尽管红色肌肉能够获得无限的空气储备并从 Po = 100 托的肺泡空气中获取氧气供应，但实际上红色肌肉在体积平均肌浆氧压接近 3 托的持续稳定状态下运行。在这些氧压下，肌浆肌红蛋白被氧部分饱和；细胞内肌红蛋白提供肌浆氧压的内源性探针。心脏和红色骨骼肌可以将其工作速率和稳态氧利用速率改变 20 倍，以响应持续的需求。肌肉消耗的大部分（至少 85%）氧气用于线粒体氧化磷酸化 (89)。从逻辑上看，线粒体 ATP 生成速率也可以变化 20 倍。在这里，我们要问的是如何在近乎恒定的低肌浆氧压下实现向肌肉线粒体提供大量且可变的氧气流。我们研究肌细胞内的细胞内事件，特别关注肌红蛋白的作用。我们报告事实，让他们尽可能贴近实验结果来说话和推断。顺便说一句，我们提到了氧传输和扩散的一些数学或数值处理，但不尝试进行批判性审查或分析。肌红蛋白在肌肉供氧中的作用由密立根 (86) 首创，其他文献对此进行了综述 (73, 125, 133, 134)。此外，细胞内肌红蛋白功能的分子机制将在即将发表的综述中进行更详细的讨论（1. B. Wittenberg，B. A. Wittenberg，准备中）。
Red muscles, despite access to an infinite reservoir of air and drawing their oxygen supply from alveolar air of Po, = 100 torr, actually operate in sustained steady states of volume-average sarcoplasmic oxygen pressure near 3 torr. At these oxygen pressures, sarcoplasmic myoglobin is partially sat urated with oxygen; intracellular myoglobin offers an endogenous probe of sarcoplasmic oxygen pressure. The heart and red skeletal muscles can vary their rate of work and their rate of steady state oxygen utilization 20-fold in response to sustained demand. Most (at least 85%) of the oxygen consumed by muscle is used for mitochondrial oxidative phosphorylation (89). That the rate of mitochondrial ATP genesis can also vary 20-fold follows logically. Here we ask how the massive and variable flow of oxygen to muscle mitochondria is achieved at near-constant low sarcoplasmic oxygen pressure. We address intracellular events within the myocyte with particular attention to the role of myoglobin. We report the facts and let them speak and draw inferences as closely as possible to the experimental findings. In passing, we allude to some mathematical or numerical treatments of oxygen transport and diffusion but do not attempt a critical review or analysis. The role of myoglo bin in oxygen supply to muscle, pioneered by Millikan (86), is reviewed elsewhere (73, 125, 133, 134). Also, the molecular mechanism of in tracellular myoglobin function is discussed in greater detail in an upcoming review (1. B. Wittenberg, B. A. Wittenberg, in preparation).