Mitochondrial bioenergetics are not associated with myofibrillar protein synthesis rates
dc.contributor.author | Holwerda, AM | |
dc.contributor.author | Dirks, ML | |
dc.contributor.author | Barbeau, P-A | |
dc.contributor.author | Goessens, J | |
dc.contributor.author | Gijsen, A | |
dc.contributor.author | van Loon, LJC | |
dc.contributor.author | Holloway, GP | |
dc.date.accessioned | 2024-07-22T15:11:12Z | |
dc.date.issued | 2024-07-15 | |
dc.date.updated | 2024-07-22T13:30:31Z | |
dc.description.abstract | BACKGROUND: Mitochondria represent key organelles influencing cellular homeostasis and have been implicated in the signalling events regulating protein synthesis. METHODS: We examined whether mitochondrial bioenergetics (oxidative phosphorylation and reactive oxygen species (H2O2) emission, ROS) measured in vitro in permeabilized muscle fibres represent regulatory factors for integrated daily muscle protein synthesis rates and skeletal muscle mass changes across the spectrum of physical activity, including free-living and bed-rest conditions: n = 19 healthy, young men (26 ± 4 years, 23.4 ± 3.3 kg/m2) and following 12 weeks of resistance-type exercise training: n = 10 healthy older men (70 ± 3 years, 25.2 ± 2.1 kg/m2). Additionally, we evaluated the direct relationship between attenuated mitochondrial ROS emission and integrated daily myofibrillar and sarcoplasmic protein synthesis rates in genetically modified mice (mitochondrial-targeted catalase, MCAT). RESULTS: Neither oxidative phosphorylation nor H2O2 emission were associated with muscle protein synthesis rates in healthy young men under free-living conditions or following 1 week of bed rest (both P > 0.05). Greater increases in GSSG concentration were associated with greater skeletal muscle mass loss following bed rest (r = -0.49, P < 0.05). In older men, only submaximal mitochondrial oxidative phosphorylation (corrected for mitochondrial content) was positively associated with myofibrillar protein synthesis rates during exercise training (r = 0.72, P < 0.05). However, changes in oxidative phosphorylation and H2O2 emission were not associated with changes in skeletal muscle mass following training (both P > 0.05). Additionally, MCAT mice displayed no differences in myofibrillar (2.62 ± 0.22 vs. 2.75 ± 0.15%/day) and sarcoplasmic (3.68 ± 0.35 vs. 3.54 ± 0.35%/day) protein synthesis rates when compared with wild-type mice (both P > 0.05). CONCLUSIONS: Mitochondrial oxidative phosphorylation and reactive oxygen emission do not seem to represent key factors regulating muscle protein synthesis or muscle mass regulation across the spectrum of physical activity. | en_GB |
dc.description.sponsorship | Natural Sciences and Engineering Research Council of Canada (NSERC) | en_GB |
dc.description.sponsorship | TI Food and Nutrition | en_GB |
dc.format.medium | Print-Electronic | |
dc.identifier.citation | Published online 15 July 2024 | en_GB |
dc.identifier.doi | https://doi.org/10.1002/jcsm.13532 | |
dc.identifier.grantnumber | 400362 | en_GB |
dc.identifier.uri | http://hdl.handle.net/10871/136824 | |
dc.identifier | ORCID: 0000-0002-9189-1042 (Dirks, Marlou L) | |
dc.language.iso | en | en_GB |
dc.publisher | Wiley | en_GB |
dc.relation.url | https://www.ncbi.nlm.nih.gov/pubmed/39007407 | en_GB |
dc.rights | © 2024 The Author(s). Journal of Cachexia, Sarcopenia and Muscle published by Wiley Periodicals LLC. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. | en_GB |
dc.subject | Aging | en_GB |
dc.subject | Muscle protein synthesis | en_GB |
dc.subject | Physical inactivity | en_GB |
dc.subject | Reactive oxygen species | en_GB |
dc.subject | Skeletal muscle | en_GB |
dc.title | Mitochondrial bioenergetics are not associated with myofibrillar protein synthesis rates | en_GB |
dc.type | Article | en_GB |
dc.date.available | 2024-07-22T15:11:12Z | |
dc.identifier.issn | 2190-5991 | |
exeter.place-of-publication | Germany | |
dc.description | This is the final version. Available on open access from Wiley via the DOI in this record | en_GB |
dc.description | Data availability statement: The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions. | en_GB |
dc.identifier.eissn | 2190-6009 | |
dc.identifier.journal | Journal of Cachexia, Sarcopenia and Muscle | en_GB |
dc.relation.ispartof | J Cachexia Sarcopenia Muscle | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | en_GB |
dcterms.dateAccepted | 2024-06-03 | |
rioxxterms.version | VoR | en_GB |
rioxxterms.licenseref.startdate | 2024-07-15 | |
rioxxterms.type | Journal Article/Review | en_GB |
refterms.dateFCD | 2024-07-22T15:08:54Z | |
refterms.versionFCD | VoR | |
refterms.dateFOA | 2024-07-22T15:11:22Z | |
refterms.panel | A | en_GB |
refterms.dateFirstOnline | 2024-07-15 |
Files in this item
This item appears in the following Collection(s)
Except where otherwise noted, this item's licence is described as © 2024 The Author(s). Journal of Cachexia, Sarcopenia and Muscle published by Wiley Periodicals LLC. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.