Diaphragm muscle adaptation to sustained hypoxia: lessons from animal models with relevance to high altitude and chronic respiratory diseases

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dc.contributor.author O'Halloran, Ken D.
dc.contributor.author Lewis, Philip
dc.date.accessioned 2017-01-04T15:28:17Z
dc.date.available 2017-01-04T15:28:17Z
dc.date.issued 2016-12-12
dc.identifier.citation Lewis, P. and O'Halloran, K. D. (2016) 'Diaphragm Muscle Adaptation to Sustained Hypoxia: Lessons from Animal Models with Relevance to High Altitude and Chronic Respiratory Diseases', Frontiers in Physiology, 7, 623 (11pp). doi:10.3389/fphys.2016.00623 en
dc.identifier.volume 7 en
dc.identifier.startpage 623-1 en
dc.identifier.endpage 623-11 en
dc.identifier.issn 1664-042X
dc.identifier.uri http://hdl.handle.net/10468/3425
dc.identifier.doi 10.3389/fphys.2016.00623
dc.description.abstract The diaphragm is the primary inspiratory pump muscle of breathing. Notwithstanding its critical role in pulmonary ventilation, the diaphragm like other striated muscles is malleable in response to physiological and pathophysiological stressors, with potential implications for the maintenance of respiratory homeostasis. This review considers hypoxic adaptation of the diaphragm muscle, with a focus on functional, structural, and metabolic remodeling relevant to conditions such as high altitude and chronic respiratory disease. On the basis of emerging data in animal models, we posit that hypoxia is a significant driver of respiratory muscle plasticity, with evidence suggestive of both compensatory and deleterious adaptations in conditions of sustained exposure to low oxygen. Cellular strategies driving diaphragm remodeling during exposure to sustained hypoxia appear to confer hypoxic tolerance at the expense of peak force-generating capacity, a key functional parameter that correlates with patient morbidity and mortality. Changes include, but are not limited to: redox-dependent activation of hypoxia-inducible factor (HIF) and MAP kinases; time-dependent carbonylation of key metabolic and functional proteins; decreased mitochondrial respiration; activation of atrophic signaling and increased proteolysis; and altered functional performance. Diaphragm muscle weakness may be a signature effect of sustained hypoxic exposure. We discuss the putative role of reactive oxygen species as mediators of both advantageous and disadvantageous adaptations of diaphragm muscle to sustained hypoxia, and the role of antioxidants in mitigating adverse effects of chronic hypoxic stress on respiratory muscle function. en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher Frontiers Media en
dc.rights © 2016 Lewis and O’Halloran. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. en
dc.rights.uri https://creativecommons.org/licenses/by/4.0/ en
dc.subject Redox en
dc.subject Diaphragm muscle en
dc.subject Reactive oxygen species en
dc.subject COPD en
dc.subject Atrophy en
dc.title Diaphragm muscle adaptation to sustained hypoxia: lessons from animal models with relevance to high altitude and chronic respiratory diseases en
dc.type Article (peer-reviewed) en
dc.internal.authorcontactother Ken O'Halloran, Physiology, University College Cork, Cork, Ireland. +353-21-490-3000 Email: k.ohalloran@ucc.ie en
dc.internal.availability Full text available en
dc.date.updated 2017-01-04T15:21:10Z
dc.description.version Published Version en
dc.internal.rssid 372727925
dc.contributor.funder Health Research Board en
dc.description.status Peer reviewed en
dc.identifier.journaltitle Frontiers in Physiology en
dc.internal.copyrightchecked Yes !!CORA!! en
dc.internal.licenseacceptance Yes en
dc.internal.IRISemailaddress k.odonoghue@ucc.ie en


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© 2016 Lewis and O’Halloran. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. Except where otherwise noted, this item's license is described as © 2016 Lewis and O’Halloran. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
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