Joyner Michael J, Wilkins Brad W
Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA.
J Physiol. 2007 Sep 15;583(Pt 3):855-60. doi: 10.1113/jphysiol.2007.135889. Epub 2007 Jul 19.
Exercise can increase skeletal muscle blood flow by 100-fold over values observed at rest. As this value was 3 to 4 times higher than so-called 'textbook' values at the time it raised a number of issues about cardiovascular control. However, there is a continuing inability to identify the factor or combination of factors that explain this substantial increase in muscle blood flow. Moreover, these governing mechanism(s) must also explain the precise matching of muscle blood flow to metabolic demand and oxygen use or need. The difficulties identifying the mechanisms for exercise hyperaemia are especially disappointing due to the essentially concurrent discovery in the 1980s that the vascular endothelium was a key site of vasomotor control and that nitric oxide (NO) potentially released from nerves, endothelial cells, directly from tissues such as skeletal muscle, or perhaps released from red blood cells, might participate in vascular control in a way that would permit blood flow and metabolism to be closely matched.
运动可使骨骼肌血流量比静息时增加100倍。由于该数值比当时所谓的“教科书”数值高出3至4倍，这引发了一些关于心血管控制的问题。然而，目前仍无法确定导致肌肉血流量大幅增加的单一因素或多种因素的组合。此外，这些调控机制还必须解释肌肉血流量与代谢需求以及氧气利用或需求之间的精确匹配。鉴于20世纪80年代基本同时发现血管内皮是血管舒缩控制的关键部位，并且从神经、内皮细胞、直接从骨骼肌等组织释放的一氧化氮（NO），或者可能从红细胞释放的NO，可能以一种使血流量与代谢紧密匹配的方式参与血管控制，因此难以确定运动性充血的机制尤其令人失望。
