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Hypoxia transiently affects skeletal muscle hypertrophy in a functional overload model
Örebro University, School of Health Sciences. Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.ORCID iD: 0000-0002-5322-4150
Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.
Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.
Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.
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2012 (English)In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 302, p. R643-R654Article in journal (Refereed) Published
Abstract [en]

Hypoxia induces a loss of skeletal muscle mass, but the signaling pathways and molecular mechanisms involved remain poorly understood. We hypothesized that hypoxia could impair skeletal muscle hypertrophy induced by functional overload (Ov). To test this hypothesis, plantaris muscles were overloaded during 5, 12, and 56 days in female rats exposed to hypobaric hypoxia (5,500 m), and then, we examined the responses of specific signaling pathways involved in protein synthesis (Akt/mTOR) and breakdown (atrogenes). Hypoxia minimized the Ov-induced hypertrophy at days 5 and 12 but did not affect the hypertrophic response measured at day 56. Hypoxia early reduced the phosphorylation levels of mTOR and its downstream targets P70(S6K) and rpS6, but it did not affect the phosphorylation levels of Akt and 4E-BP1, in Ov muscles. The role played by specific inhibitors of mTOR, such as AMPK and hypoxia-induced factors (i.e., REDD1 and BNIP-3) was studied. REDD1 protein levels were reduced by overload and were not affected by hypoxia in Ov muscles, whereas AMPK was not activated by hypoxia. Although hypoxia significantly increased BNIP-3 mRNA levels at day 5, protein levels remained unaffected. The mRNA levels of the two atrogenes MURF1 and MAFbx were early increased by hypoxia in Ov muscles. In conclusion, hypoxia induced a transient alteration of muscle growth in this hypertrophic model, at least partly due to a specific impairment of the mTOR/P70(S6K) pathway, independently of Akt, by an undefined mechanism, and increased transcript levels for MURF1 and MAFbx that could contribute to stimulate the proteasomal proteolysis.

Place, publisher, year, edition, pages
HighWire Press , 2012. Vol. 302, p. R643-R654
Keywords [en]
Akt/mammalian target of rapamycin pathway, BCL2 and adenovirus E1B 19-kDa-interacting protein 3, REDD1, atrogenes
National Category
Medical and Health Sciences Physiology
Identifiers
URN: urn:nbn:se:oru:diva-66016DOI: 10.1152/ajpregu.00262.2011ISI: 000301279100019PubMedID: 22189670Scopus ID: 2-s2.0-84857834887OAI: oai:DiVA.org:oru-66016DiVA, id: diva2:1192514
Note

Funding Agency:

Ministere de I'Enseignement Superieur et de la Recherche

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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