Caruana Hannah, Marshall Janice M
School of Clinical and Experimental Medicine, Centre for Cardiovascular Science, College of Medical and Dental Sciences, University of Birmingham, Birmingham, B15 2TT, UK.
Eur J Appl Physiol. 2015 Sep;115(9):1995-2006. doi: 10.1007/s00421-015-3182-0. Epub 2015 May 12.
We have argued that breathing 40 % O2 attenuates exercise hyperaemia by decreasing production of O2-dependent vasodilators. However, breathing 100 % O2 attenuated endothelium-dependent vasodilatation evoked by acetylcholine and this effect was prevented by vitamin C, implicating reactive oxygen species (ROS). We have therefore used vitamin C to test the hypothesis that 40 % O2 modulates exercise hyperaemia and reactive hyperaemia independently of ROS.
In a cross-over study on 10 male subjects (21.1 ± 0.84 years), we measured forearm blood flow (venous occlusion plethysmography) and calculated forearm vascular conductance (FVC) at rest and following static handgrip at 60 % maximum voluntary contraction for 2 min and following arterial occlusion for 2 min, after placebo or oral vitamin C (2000 mg), and when breathing air or 40 % O2.
During air breathing, vitamin C augmented the peak increase in FVC following static contraction, or release of arterial occlusion, by ~50 or 60 %, respectively (P < 0.05). Breathing 40 % O2 in the presence of placebo attenuated post-contraction hyperaemia by ~25 % (P < 0.05), but had no effect on reactive hyperaemia. By contrast, in the presence of vitamin C, 40 % O2 attenuated the peak increase in FVC following static contraction, or release of arterial occlusion by ~25 and 50 %, respectively (P < 0.05).
These results indicate that in young men, exercise hyperaemia following strenuous muscle contraction and reactive hyperaemia are blunted by ROS. However, they are also consistent with the view that modest hyperoxia induced by breathing 40 % O2 acts independently of ROS to attenuate not only post-contraction hyperaemia, but also reactive hyperaemia, by decreasing release of O2-dependent vasodilators.
我们曾提出，呼吸40%的氧气可通过减少氧依赖性血管舒张剂的产生来减弱运动性充血。然而，呼吸100%的氧气会减弱乙酰胆碱诱发的内皮依赖性血管舒张，且维生素C可预防这种效应，这表明活性氧（ROS）起了作用。因此，我们使用维生素C来检验这一假设，即40%的氧气独立于ROS调节运动性充血和反应性充血。
在一项针对10名男性受试者（21.1±0.84岁）的交叉研究中，我们测量了前臂血流量（静脉阻塞体积描记法），并在静息状态下、以最大自主收缩的60%进行2分钟静态握力后以及动脉阻塞2分钟后，在服用安慰剂或口服维生素C（2000毫克）后，以及呼吸空气或40%氧气时，计算前臂血管传导率（FVC）。
在呼吸空气时，维生素C使静态收缩或动脉阻塞解除后FVC的峰值增加分别提高了约50%或60%（P<0.05）。在服用安慰剂的情况下呼吸40%的氧气使收缩后充血减弱了约25%（P<0.05），但对反应性充血没有影响。相比之下，在服用维生素C的情况下，40%的氧气使静态收缩或动脉阻塞解除后FVC的峰值增加分别减弱了约25%和50%（P<0.05）。
这些结果表明，在年轻男性中，剧烈肌肉收缩后的运动性充血和反应性充血会被ROS减弱。然而，它们也与以下观点一致，即呼吸40%的氧气所诱发的适度高氧独立于ROS发挥作用，通过减少氧依赖性血管舒张剂的释放，不仅减弱收缩后充血，还减弱反应性充血。
