Summary of Study ST001907
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001201. The data can be accessed directly via it's Project DOI: 10.21228/M8G69Q This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.
| Study ID | ST001907 |
| Study Title | Training-induced bioenergetic improvement in human skeletal muscle is associated with non-stoichiometric changes in the mitochondrial proteome without reorganisation of respiratory chain content |
| Study Type | Multi Omics |
| Study Summary | Lipidomic analysis of muscle mitochondrial isolates. 10 men with repeated measures. |
| Institute | Baker Heart and Diabetes Institute |
| Department | Meteabolomics |
| Laboratory | Meteabolomics |
| Last Name | Huynh |
| First Name | Kevin |
| Address | 75 Commercial Road |
| kevin.huynh@baker.edu.au | |
| Phone | 0385321537 |
| Submit Date | 2021-08-15 |
| Num Groups | 1 |
| Total Subjects | 10 |
| Num Males | 10 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | mzML |
| Analysis Type Detail | LC-MS |
| Release Date | 2021-10-18 |
| Release Version | 1 |
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Project:
| Project ID: | PR001201 |
| Project DOI: | doi: 10.21228/M8G69Q |
| Project Title: | Training-induced bioenergetic improvement in human skeletal muscle is associated with non-stoichiometric changes in the mitochondrial proteome without reorganisation of respiratory chain content |
| Project Type: | Multi-omics |
| Project Summary: | Defects in mitochondria have been implicated in multiple diseases and aging. Interventions to improve mitochondrial function have the potential to improve quality of life. Exercise training is a readily accessible and inexpensive intervention, however how it promotes mitochondrial adaptation in skeletal muscle remains poorly understood. Here, we describe an intricate and previously undemonstrated network of differentially prioritised training-induced adaptations in human skeletal muscle mitochondria. We show that changes in hundreds of transcripts, proteins and lipid species are not stoichiometrically linked to the increase in mitochondrial content. We demonstrate a prioritization of specific pathways at different stages of the intervention, including initial deprioritisation of oxidative phosphorylation (OXPHOS) and prioritisation of TCA cycle and fatty acid β-oxidation linked mitochondrial respiration. This indicates that enhancing electron flow to OXPHOS is more important to increase ATP production than increasing the abundance of the OXPHOS machinery. Our research unearths the elaborate and multi-layered nature of the adaptive response to exercise and provides a valuable resource that can be mined to maximise the therapeutic benefits of exercise. |
| Institute: | Baker Heart and Diabetes Institute |
| Department: | Baker Heart and Diabetes Institute |
| Laboratory: | Metabolomics |
| Last Name: | Huynh |
| First Name: | Kevin |
| Address: | 75 Commercial Road |
| Email: | kevin.huynh@baker.edu.au |
| Phone: | 0385321537 |
