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Contribution of non-endothelium-dependent substances to exercise hyperaemia: are they O2 dependent?

Authors

  • Janice M. Marshall,

    1. School of Clinical & Experimental Medicine, College of Medical & Dental Sciences, The Medical School, Vincent Drive, University of Birmingham, Birmingham B15 2TT, UK
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  • Clare J. Ray

    1. School of Clinical & Experimental Medicine, College of Medical & Dental Sciences, The Medical School, Vincent Drive, University of Birmingham, Birmingham B15 2TT, UK
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  • This report was presented at The Journal of Physiology Symposium on Blood flow regulation: from rest to maximal exercise, which took place at the Main Meeting of The Physiological Society, Edinburgh, UK on 3 July 2012. It was commissioned by the Editorial Board and reflects the views of the authors.

J. M. Marshall: School of Clinical & Experimental Medicine, College of Medical & Dental Sciences, The Medical School, Vincent Drive, University of Birmingham, Birmingham B15 2TT, UK. Email: j.m.marshall@bham.ac.uk

Abstract

Abstract  This review considers the contributions to exercise hyperaemia of substances released into the interstitial fluid, with emphasis on whether they are endothelium dependent or O2 dependent. The early phase of exercise hyperaemia is attributable to K+ released from contracting muscle fibres and acting extraluminally on arterioles. Hyperpolarization of vascular smooth muscle and endothelial cells induced by K+ may also facilitate the maintained phase, for example by facilitating conduction of dilator signals upstream. ATP is released into the interstitium from muscle fibres, at least in part through cystic fibrosis transmembrane conductance regulator-associated channels, following the fall in intracellular H+. ATP is metabolized by ectonucleotidases to adenosine, which dilates arterioles via A2A receptors, in a nitric oxide-independent manner. Evidence is presented that the rise in arterial inline image achieved by breathing 40% O2 attenuates efflux of H+ and lactate, thereby decreasing the contribution that adenosine makes to exercise hyperaemia; efflux of inorganic phosphate and its contribution may likewise be attenuated. Prostaglandins (PGs), PGE2 and PGI2, also accumulate in the interstitium during exercise, and breathing 40% O2 abolished the contribution of PGs to exercise hyperaemia. This suggests that PGE2 released from muscle fibres and PGI2 released from capillaries and venular endothelium by a fall in their local inline image act extraluminally to dilate arterioles. Although modest hyperoxia attenuates exercise hyperaemia by improving O2 supply, limiting the release of O2-dependent adenosine and PGs, higher O2 concentrations may have adverse effects. Evidence is presented that breathing 100% O2 limits exercise hyperaemia by generating O2, which inactivates nitric oxide and decreases PG synthesis.

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