Show simple item record

dc.contributor.authorAffourtit, C
dc.contributor.authorCarré, JE
dc.date.accessioned2024-02-05T11:32:27Z
dc.date.available2024-02-05T11:32:27Z
dc.date.issued2024-02-02
dc.identifier.issn1748-1708
dc.identifier.issn1748-1716
dc.identifier.urihttps://pearl.plymouth.ac.uk/handle/10026.1/22018
dc.description.abstract

Sarcopenia lowers the quality‐of‐life for millions of people across the world, as accelerated loss of skeletal muscle mass and function contributes to both age‐ and disease‐related frailty. Physical activity remains the only proven therapy for sarcopenia to date, but alternatives are much sought after to manage this progressive muscle disorder in individuals who are unable to exercise. Mitochondria have been widely implicated in the etiology of sarcopenia and are increasingly suggested as attractive therapeutic targets to help restore the perturbed balance between protein synthesis and breakdown that underpins skeletal muscle atrophy. Reviewing current literature, we note that mitochondrial bioenergetic changes in sarcopenia are generally interpreted as intrinsic dysfunction that renders muscle cells incapable of making sufficient ATP to fuel protein synthesis. Based on the reported mitochondrial effects of therapeutic interventions, however, we argue that the observed bioenergetic changes may instead reflect an adaptation to pathologically decreased energy expenditure in sarcopenic muscle. Discrimination between these mechanistic possibilities will be crucial for improving the management of sarcopenia.

dc.format.extente14107-
dc.format.mediumPrint-Electronic
dc.languageen
dc.publisherWiley
dc.subjectcellular bioenergetics
dc.subjectsarcopenia
dc.subjectskeletal muscle mitochondria
dc.titleMitochondrial involvement in sarcopenia
dc.typejournal-article
dc.typeReview
dc.typeEarly Access
plymouth.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/38304924
plymouth.issue3
plymouth.volume240
plymouth.publisher-urlhttp://dx.doi.org/10.1111/apha.14107
plymouth.publication-statusPublished
plymouth.journalActa Physiologica
dc.identifier.doi10.1111/apha.14107
plymouth.organisational-group|Plymouth
plymouth.organisational-group|Plymouth|Research Groups
plymouth.organisational-group|Plymouth|Faculty of Health
plymouth.organisational-group|Plymouth|Research Groups|Institute of Translational and Stratified Medicine (ITSMED)
plymouth.organisational-group|Plymouth|Research Groups|Institute of Translational and Stratified Medicine (ITSMED)|CBR
plymouth.organisational-group|Plymouth|REF 2021 Researchers by UoA
plymouth.organisational-group|Plymouth|Users by role
plymouth.organisational-group|Plymouth|Users by role|Academics
plymouth.organisational-group|Plymouth|REF 2021 Researchers by UoA|UoA03 Allied Health Professions, Dentistry, Nursing and Pharmacy
plymouth.organisational-group|Plymouth|Faculty of Health|School of Biomedical Sciences
plymouth.organisational-group|Plymouth|REF 2028 Researchers by UoA
plymouth.organisational-group|Plymouth|REF 2028 Researchers by UoA|UoA03 Allied Health Professions, Dentistry, Nursing and Pharmacy
dc.publisher.placeEngland
dcterms.dateAccepted2024-01-22
dc.date.updated2024-02-05T11:32:27Z
dc.rights.embargodate2024-2-6
dc.identifier.eissn1748-1716
rioxxterms.versionofrecord10.1111/apha.14107


Files in this item

Thumbnail
Thumbnail

This item appears in the following Collection(s)

Show simple item record


All items in PEARL are protected by copyright law.
Author manuscripts deposited to comply with open access mandates are made available in accordance with publisher policies. Please cite only the published version using the details provided on the item record or document. In the absence of an open licence (e.g. Creative Commons), permissions for further reuse of content should be sought from the publisher or author.
Theme by 
Atmire NV