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Updated: Jan 10, 2026

A Model to Simulate Clinically Relevant Hypoxia in Humans
Published on: December 22, 2016
[The muscle out of breath: limitations and adaptations to hypoxia]
Angèle N Merlet1, Laurent A Messonnier2, Léonard Féasson1
1Unité de myologie, Service de physiologie clinique et de l'exercice, Centre référent maladies neuromusculaires rares - Euro-NmD, Hôpital universitaire de Saint-Etienne, Saint-Etienne, France - Laboratoire interuniversitaire de biologie de la motricité, EA 7424, F-42023, Université de Lyon, UJM-Saint-Etienne, France.
Abstract:
Skeletal muscle undergoes and also adapts to hypoxia caused by certain chronic diseases, whether it is chronic (chronic obstructive pulmonary disease [COPD], chronic heart failure [CHF]), intermittent (obstructive sleep apnea syndrome [OSAS]), or mixed (sickle cell disease [SCD]). This review reports the associated muscle remodeling. In COPD and CHF, muscle atrophy, fiber type redistribution, reduced microvascularization, and impaired oxidative metabolism are observed. SCD induces similar abnormalities as seen in COPD and CHF but with a specific microvascular remodeling. Conversely, OSAS improves microvascularization and oxidative metabolism, without a notable effect on muscle fiber type or trophicity. These differences likely reflect the nature and severity of hypoxia, as well as the degree of patient deconditioning.
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