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Complex I is bypassed during high intensity exercise.
Chalmers University of Technology, Gothenburg, Sweden.
Chalmers University of Technology, Gothenburg, Sweden.
Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Åstrandlaboratoriet.ORCID-id: 0000-0002-7743-9295
Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Åstrandlaboratoriet, Forskningsgruppen Mitokondriell funktion och metabolisk kontroll.ORCID-id: 0000-0002-1343-8656​
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2019 (engelsk)Inngår i: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 10, nr 1, artikkel-id 5072Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Human muscles are tailored towards ATP synthesis. When exercising at high work rates muscles convert glucose to lactate, which is less nutrient efficient than respiration. There is hence a trade-off between endurance and power. Metabolic models have been developed to study how limited catalytic capacity of enzymes affects ATP synthesis. Here we integrate an enzyme-constrained metabolic model with proteomics data from muscle fibers. We find that ATP synthesis is constrained by several enzymes. A metabolic bypass of mitochondrial complex I is found to increase the ATP synthesis rate per gram of protein compared to full respiration. To test if this metabolic mode occurs in vivo, we conduct a high resolved incremental exercise tests for five subjects. Their gas exchange at different work rates is accurately reproduced by a whole-body metabolic model incorporating complex I bypass. The study therefore shows how proteome allocation influences metabolism during high intensity exercise.

sted, utgiver, år, opplag, sider
Nature Publishing Group, 2019. Vol. 10, nr 1, artikkel-id 5072
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URN: urn:nbn:se:gih:diva-5909DOI: 10.1038/s41467-019-12934-8ISI: 000494938600006PubMedID: 31699973OAI: oai:DiVA.org:gih-5909DiVA, id: diva2:1369179
Tilgjengelig fra: 2019-11-11 Laget: 2019-11-11 Sist oppdatert: 2019-12-19

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