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Respir Physiol Neurobiol. 2014 Jan 1;190:70-5. doi: 10.1016/j.resp.2013.09.007. Epub 2013 Sep 23.

Forearm muscle oxygenation responses during and following arterial occlusion in patients with mitochondrial myopathy.

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  • 1Department of Movement and Sport Sciences, Ghent University, Watersportlaan 2, 9000 Ghent, Belgium; Center of Sports Medicine, Ghent University Hospital, De Pintelaan 185, 9000 Ghent, Belgium. Electronic address: Jan.boone@ugent.be.

Abstract

The aim was to study whether mitochondrial myopathy induces different oxygenation (deoxy[Hb+Mb] and oxy[Hb+Mb]) responses during and following arterial occlusion. In 10 mitochondrial myopathy patients (MMpatients) (age: 29±7 years; body mass: 59.9±15.7kg; heigth: 166.2±11.4cm) and age- and gender-matched healthy subjects (age: 28±9 years; body mass: 72.7±16.9kg; height: 174.4±8.7cm) arterial occlusion was performed by inflating a cuff to 240mmHg. Deoxy[Hb+Mb] and oxy[Hb+Mb] were registered during (AOoxy and AOdeoxy) and following (POdeoxy and POoxy) arterial occlusion. Amplitude of AOdeoxy did not differ (p=0.47) between MMpatients (44.9±28.0μM) and healthy subjects (38.6±22.8μM), The time constant of the exponential model was greater in MMpatients (263.4±49.1s vs. 200.3±73.7s, p=0.03). Following cuff release, in both populations a transient increase in total[Hb+Mb] was observed induced by different kinetics of POoxy and POdeoxy. The increase in POoxy (TD=6.6±2.2s and 11.9±3.5s; τ=3.8±1.4s and 6.4±2.9s for MMpatients and healthy subjects, respectively) was faster (p<0.001 for TD and τ) compared to the decrease in POdeoxy (TD=13.2±3.6s and 26.5±4.6s; τ=-6.2±2.2s and -9.6±2.4s for MMpatients and healthy subjects, respectively). POoxy and POdeoxy showed faster kinetics (p<0.001 and p<0.01 for TD and τ, respectively) in MMpatients compared to healthy subjects. MMpatients display altered oxygenation responses during and following arterial occlusion reflecting pathology related changes in the relationship between muscle blood flow and oxygen uptake.

Copyright © 2013 Elsevier B.V. All rights reserved.

KEYWORDS:

Arterial occlusion; Mitochondrial myopathy; O(2) extraction; O(2) supply; Oxygenation

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