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Research Article Free access | 10.1172/JCI118826

Differential sympathetic neural control of oxygenation in resting and exercising human skeletal muscle.

J Hansen, G D Thomas, S A Harris, W J Parsons, and R G Victor

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75235-8573, USA.

Find articles by Hansen, J. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75235-8573, USA.

Find articles by Thomas, G. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75235-8573, USA.

Find articles by Harris, S. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75235-8573, USA.

Find articles by Parsons, W. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75235-8573, USA.

Find articles by Victor, R. in: JCI | PubMed | Google Scholar

Published July 15, 1996 - More info

Published in Volume 98, Issue 2 on July 15, 1996
J Clin Invest. 1996;98(2):584–596. https://doi.org/10.1172/JCI118826.
© 1996 The American Society for Clinical Investigation
Published July 15, 1996 - Version history
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Abstract

Metabolic products of skeletal muscle contraction activate metaboreceptor muscle afferents that reflexively increase sympathetic nerve activity (SNA) targeted to both resting and exercising skeletal muscle. To determine effects of the increased sympathetic vasoconstrictor drive on muscle oxygenation, we measured changes in tissue oxygen stores and mitochondrial cytochrome a,a3 redox state in rhythmically contracting human forearm muscles with near infrared spectroscopy while simultaneously measuring muscle SNA with microelectrodes. The major new finding is that the ability of reflex-sympathetic activation to decrease muscle oxygenation is abolished when the muscle is exercised at an intensity > 10% of maximal voluntary contraction (MVC). During high intensity handgrip, (45% MVC), contraction-induced decreases in muscle oxygenation remained stable despite progressive metaboreceptor-mediated reflex increases in SNA. During mild to moderate handgrips (20-33% MVC) that do not evoke reflex-sympathetic activation, experimentally induced increases in muscle SNA had no effect on oxygenation in exercising muscles but produced robust decreases in oxygenation in resting muscles. The latter decreases were evident even during maximal metabolic vasodilation accompanying reactive hyperemia. We conclude that in humans sympathetic neural control of skeletal muscle oxygenation is sensitive to modulation by metabolic events in the contracting muscles. These events are different from those involved in either metaboreceptor muscle afferent activation or reactive hyperemia.

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