Fibre-specific mitochondrial protein abundance is linked to resting and post-training mitochondrial content in the muscle of men

被引:3
|
作者
Elizabeth G. Reisman [1 ]
Javier Botella [2 ]
Cheng Huang [1 ]
Ralf B. Schittenhelm [3 ]
David A. Stroud [4 ]
Cesare Granata [4 ]
Owala S. Chandrasiri [5 ]
Georg Ramm [6 ]
Viola Oorschot [7 ]
Nikeisha J. Caruana [1 ]
David J. Bishop [8 ]
机构
[1] Victoria University,Institute for Health and Sport (IHES)
[2] Australian Catholic University,Mary MacKillop Institute for Health Research
[3] Deakin University,Metabolic Research Unit, School of Medicine and Institute for Mental and Physical Health and Clinical Translation (IMPACT)
[4] Monash University,Monash Proteomics & Metabolomics Facility, Biomedicine Discovery Institute and Department of Biochemistry and Molecular Biology
[5] The University of Melbourne,Department of Biochemistry and Pharmacology, Bio21 Molecular Science and Biotechnology Institute
[6] Royal Children’s Hospital,Murdoch Children’s Research Institute
[7] Royal Children’s Hospital,Victorian Clinical Genetics Services
[8] Monash University,Department of Diabetes, Central Clinical School
[9] Leibniz Center for Diabetes Research at Heinrich-Heine-University,Institute for Clinical Diabetology, German, Diabetes Center
[10] Düsseldorf,Ramaciotti Centre for Cryo EM, Biomedicine Discovery Institute and Department of Biochemistry and Molecular Biology
[11] German Center for Diabetes Research,Electron Microscopy Core Facility
[12] Partner Düsseldorf,undefined
[13] Monash University,undefined
[14] European Molecular Biology Laboratory,undefined
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D O I
10.1038/s41467-024-50632-2
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摘要
Analyses of mitochondrial adaptations in human skeletal muscle have mostly used whole-muscle samples, where results may be confounded by the presence of a mixture of type I and II muscle fibres. Using our adapted mass spectrometry-based proteomics workflow, we provide insights into fibre-specific mitochondrial differences in the human skeletal muscle of men before and after training. Our findings challenge previous conclusions regarding the extent of fibre-type-specific remodelling of the mitochondrial proteome and suggest that most baseline differences in mitochondrial protein abundances between fibre types reported by us, and others, might be due to differences in total mitochondrial content or a consequence of adaptations to habitual physical activity (or inactivity). Most training-induced changes in different mitochondrial functional groups, in both fibre types, were no longer significant in our study when normalised to changes in markers of mitochondrial content.
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