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Article Dans Une Revue American Journal of Respiratory and Critical Care Medicine Année : 2001

Effects of chronic hypoxemia on the afferent nerve activities from skeletal muscle

Résumé

An acute reduction of the oxygen supply to contracting muscles not only affects their metabolism but also modifies their sensorimotor control through changes in afferent discharge of the group I and group III-IV nerve fibers, the latter playing a pivotal role in the protective mechanisms against muscle fatigue. The effects of chronic hypoxemia on the muscle sensitivity are totally unknown. In the present study, group I fibers (mechanosensory afferents) and group III-IV fibers (mechanosensory and chemosensory afferents) from the anterior tibial muscle were recorded in normoxemic and chronic hypoxemic rats. Hypoxemic rats breathed for 45 d a gas mixture containing 9.5 to 10% O(2) in N(2). The data were compared with those obtained in normoxemic animals of the same age. To activate the different muscle afferents, we used different test agents, including electrically induced fatigue (EIF), KCl, lactic acid injections, as well as tendon vibrations. The conduction velocity of all nerve fibers was significantly (p \textless 0.01) higher in hypoxemic rats than in the normoxemic group. Chronic hypoxemia significantly depressed the response of the group III-IV muscle afferents to KCl injections and even abolished their response to lactic acid and EIF. However, the response to tendon vibrations of the group I afferents was similar in hypoxemic and normoxemic rats. These results suggest that chronic hypoxemia markedly alters the chemosensitivity of the group III-IV muscle afferents, which may explain the higher fatigability of hypoxemic subjects.
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Dates et versions

hal-01436194 , version 1 (16-01-2017)

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E. Dousset, P. Decherchi, L. Grélot, Y. Jammes. Effects of chronic hypoxemia on the afferent nerve activities from skeletal muscle. American Journal of Respiratory and Critical Care Medicine, 2001, 164 (8 Pt 1), pp.1476--1480. ⟨10.1164/ajrccm.164.8.2010135⟩. ⟨hal-01436194⟩

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