High-intensity training induces non-stoichiometric changes in the mitochondrial proteome of human skeletal muscle without reorganisation of respiratory chain content.

Autor: Granata C; Institute for Health and Sport (iHeS), Victoria University, Melbourne, VIC, 3011, Australia. cesare.granata@monash.edu.; Department of Diabetes, Central Clinical School, Monash University, Melbourne, VIC, 3004, Australia. cesare.granata@monash.edu.; Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research, Heinrich Heine University, 40225, Düsseldorf, Germany. cesare.granata@monash.edu., Caruana NJ; Institute for Health and Sport (iHeS), Victoria University, Melbourne, VIC, 3011, Australia.; Department of Biochemistry and Pharmacology and Bio21 Molecular Science and Biotechnology Institute, The University of Melbourne, Parkville, VIC, 3010, Australia., Botella J; Institute for Health and Sport (iHeS), Victoria University, Melbourne, VIC, 3011, Australia., Jamnick NA; Institute for Health and Sport (iHeS), Victoria University, Melbourne, VIC, 3011, Australia.; Metabolic Research Unit, School of Medicine and Institute for Mental and Physical Health and Clinical Translation (iMPACT), Deakin University, Geelong, VIC, Australia., Huynh K; Baker Heart & Diabetes Institute, Melbourne, VIC, 3004, Australia., Kuang J; Institute for Health and Sport (iHeS), Victoria University, Melbourne, VIC, 3011, Australia., Janssen HA; Institute for Health and Sport (iHeS), Victoria University, Melbourne, VIC, 3011, Australia., Reljic B; Department of Biochemistry and Pharmacology and Bio21 Molecular Science and Biotechnology Institute, The University of Melbourne, Parkville, VIC, 3010, Australia.; Department of Biochemistry and Molecular Biology, Monash Biomedicine Discovery Institute, Monash University, 3800, Melbourne, Australia., Mellett NA; Baker Heart & Diabetes Institute, Melbourne, VIC, 3004, Australia., Laskowski A; Department of Diabetes, Central Clinical School, Monash University, Melbourne, VIC, 3004, Australia., Stait TL; Murdoch Children's Research Institute, Royal Children's Hospital, Melbourne, VIC, 3052, Australia., Frazier AE; Murdoch Children's Research Institute, Royal Children's Hospital, Melbourne, VIC, 3052, Australia.; Department of Paediatrics, The University of Melbourne, Melbourne, VIC, 3052, Australia., Coughlan MT; Department of Diabetes, Central Clinical School, Monash University, Melbourne, VIC, 3004, Australia.; Baker Heart & Diabetes Institute, Melbourne, VIC, 3004, Australia., Meikle PJ; Baker Heart & Diabetes Institute, Melbourne, VIC, 3004, Australia., Thorburn DR; Murdoch Children's Research Institute, Royal Children's Hospital, Melbourne, VIC, 3052, Australia.; Department of Paediatrics, The University of Melbourne, Melbourne, VIC, 3052, Australia.; Victorian Clinical Genetics Services, Royal Children's Hospital, Melbourne, VIC, 3052, Australia., Stroud DA; Department of Biochemistry and Pharmacology and Bio21 Molecular Science and Biotechnology Institute, The University of Melbourne, Parkville, VIC, 3010, Australia. david.stroud@unimelb.edu.au.; Murdoch Children's Research Institute, Royal Children's Hospital, Melbourne, VIC, 3052, Australia. david.stroud@unimelb.edu.au., Bishop DJ; Institute for Health and Sport (iHeS), Victoria University, Melbourne, VIC, 3011, Australia. david.bishop@vu.edu.au.
Jazyk: angličtina
Zdroj: Nature communications [Nat Commun] 2021 Dec 03; Vol. 12 (1), pp. 7056. Date of Electronic Publication: 2021 Dec 03.
DOI: 10.1038/s41467-021-27153-3
Abstrakt: Mitochondrial defects are implicated in multiple diseases and aging. Exercise training is an accessible, inexpensive therapeutic intervention that can improve mitochondrial bioenergetics and quality of life. By combining multiple omics techniques with biochemical and in silico normalisation, we removed the bias arising from the training-induced increase in mitochondrial content to unearth an intricate and previously undemonstrated network of differentially prioritised mitochondrial adaptations. We show that changes in hundreds of transcripts, proteins, and lipids are not stoichiometrically linked to the overall increase in mitochondrial content. Our findings suggest enhancing electron flow to oxidative phosphorylation (OXPHOS) is more important to improve ATP generation than increasing the abundance of the OXPHOS machinery, and do not support the hypothesis that training-induced supercomplex formation enhances mitochondrial bioenergetics. Our study provides an analytical approach allowing unbiased and in-depth investigations of training-induced mitochondrial adaptations, challenging our current understanding, and calling for careful reinterpretation of previous findings.
(© 2021. The Author(s).)
Databáze: MEDLINE
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