The Physiological Consequences of Breathing Supplementary Oxygen in Healthy Human Subjects

Previous studies have implicated oxygen (02)-dependent substances in the vasodilator response to muscle contraction. This thesis explores the effect of breathing supplementary O2, (40% O2: hyperoxia) on the increase in forearm blood flow (FBF) and vascular conductance (functional hyperaemia) evoked by forearm contractions in healthy young male subjects. Hyperoxia given throughout the protocol did not affect resting vascular conductance, yet reduced the hyperaemia evoked by sub-maximal static and rhythmic contractions and by maximal voluntary effort contractions (100% MVE). Hyperoxia given only during two successive periods of 100% MVE to exhaustion reduced the postcontraction hyperaemia but had no affect on the shortened time to voluntary exhaustion (TVE) of Contraction 2. By contrast, hyperoxia given only during recovery did not affect the hyperaemia, but lengthened the TVE of Contraction 2. Hyperoxia given during 100% MVE also reduced forearm venous concentrations of lactate and H+ but not of K+ and the cyclooxygenase (COX) product, prostaglandin h (PGh). Given the concomitant decrease in FBF this suggests reduced efflux of lactate, H+ and K+ and PGh. Further, COX inhibition with aspirin attenuated the hyperaemia but, in the presence of aspirin, hyperoxia given during recovery had no further effect on the hyperaemia: despite the reduced FBF, the TVE of Contraction 2 was stil1 improved. It is proposed that hyperoxia and the consequent increase in arterial O2tension (Pa02) can improve O2 delivery to forearm muscle even during 100% MVE so limiting anaerobic metabolism and possibly muscle and/or endothelial efflux of PGh and K+. These results are considered in relation to the influence of Pa02 in determining the role of PGs and other metabolites in functional hyperaemia and recovery from static contraction.EThOS - Electronic Theses Online ServiceGBUnited Kingdo