title: Effects of modest hyperoxia and oral vitamin C on exercise hyperaemia and reactive hyperaemia in healthy young men.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: School of Clinical and Experimental Medicine, Centre for Cardiovascular Science, College of Medical and Dental Sciences, University of Birmingham, Birmingham, B15 2TT, UK.
authors.forename: Hannah
authors.initials: H
authors.lastname: Caruana
authors.forename: Janice M
authors.initials: JM
authors.lastname: Marshall
mesh_terms: D000284:Administration, Oral; D000328:Adult; D001205:Ascorbic Acid / Q000008:administration & dosage*; D019587:Dietary Supplements; D004305:Dose-Response Relationship, Drug; D015444:Exercise; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology* / Q000517:prevention & control*; D018496:Hyperoxia / Q000503:physiopathology*; D008297:Male; D010101:Oxygen Consumption / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000097:blood; D012016:Reference Values
chemical_list: D017382:Reactive Oxygen Species; D001205:Ascorbic Acid