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Effect of hypoxia exposure on the recovery of skeletal muscle phenotype during regeneration
Département Environnements Opérationnels, Institut de Recherche Biomédicale des Armées Antenne de la Tronche, La Tronche cedex, France.ORCID iD: 0000-0002-5322-4150
Département Environnements Opérationnels, Institut de Recherche Biomédicale des Armées Antenne de la Tronche, La Tronche cedex, France; Ecole du Val-de-Grâce, Paris, France.
Département Environnements Opérationnels, Institut de Recherche Biomédicale des Armées Antenne de la Tronche, La Tronche cedex, France.
Département Environnements Opérationnels, Institut de Recherche Biomédicale des Armées Antenne de la Tronche, La Tronche cedex, France.
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2014 (English)In: Molecular and Cellular Biochemistry, ISSN 0300-8177, E-ISSN 1573-4919, Vol. 390, no 1-2, p. 31-40Article in journal (Refereed) Published
Abstract [en]

Hypoxia impairs the muscle fibre-type shift from fast-to-slow during post-natal development; however, this adaptation could be a consequence of the reduced voluntary physical activity associated with hypoxia exposure rather than the result of hypoxia per se. Moreover, muscle oxidative capacity could be reduced in hypoxia, particularly when hypoxia is combined with additional stress. Here, we used a model of muscle regeneration to mimic the fast-to-slow fibre-type conversion observed during post-natal development. We hypothesised that hypoxia would impair the recovery of the myosin heavy chain (MHC) profile and oxidative capacity during muscle regeneration. To test this hypothesis, the soleus muscle of female rats was injured by notexin and allowed to recover for 3, 7, 14 and 28 days under normoxia or hypobaric hypoxia (5,500 m altitude) conditions. Ambient hypoxia did not impair the recovery of the slow MHC profile during muscle regeneration. However, hypoxia moderately decreased the oxidative capacity (assessed from the activity of citrate synthase) of intact muscle and delayed its recovery in regenerated muscle. Hypoxia transiently increased in both regenerated and intact muscles the content of phosphorylated AMPK and Pgc-1α mRNA, two regulators involved in mitochondrial biogenesis, while it transiently increased in intact muscle the mRNA level of the mitophagic factor BNIP3. In conclusion, hypoxia does not act to impair the fast-to-slow MHC isoform transition during regeneration. Hypoxia alters the oxidative capacity of intact muscle and delays its recovery in regenerated muscle; however, this adaptation to hypoxia was independent of the studied regulators of mitochondrial turn-over.

Place, publisher, year, edition, pages
Kluwer Academic Publishers, 2014. Vol. 390, no 1-2, p. 31-40
National Category
Medical and Health Sciences Cell Biology
Identifiers
URN: urn:nbn:se:oru:diva-66013DOI: 10.1007/s11010-013-1952-8ISI: 000334267800004PubMedID: 24385110Scopus ID: 2-s2.0-84898862978OAI: oai:DiVA.org:oru-66013DiVA, id: diva2:1192497
Note

Funding Agencies:

Ministere de I'Enseignement Superieur et de la Recherche 

Association Francaise contre les Myopathies, 13955

Available from: 2018-03-22 Created: 2018-03-22 Last updated: 2018-03-26Bibliographically approved

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Chaillou, Thomas

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