miun.sePublikasjoner
Endre søk
RefereraExporteraLink to record
Permanent link

Direct link
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Plasticity in mitochondrial cristae density allows metabolic capacity modulation in human skeletal muscle
Univ Southern Denmark, Denmark.
Univ Southern Denmark, Denmark.
Univ Southern Denmark, Denmark.
Mittuniversitetet, Fakulteten för humanvetenskap, Avdelningen för hälsovetenskap. (Swedish Winter Sports Research Centre)ORCID-id: 0000-0002-3814-6246
Vise andre og tillknytning
2017 (engelsk)Inngår i: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 595, nr 9, s. 2839-2847Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Mitochondrial energy production involves the movement of protons down a large electrochemical gradient via ATP synthase located on the folded inner membrane, known as cristae. In mammalian skeletal muscle, the density of cristae in mitochondria is assumed to be constant. However, recent experimental studies have shown that respiration per mitochondria varies. Modelling studies have hypothesized that this variation in respiration per mitochondria depends on plasticity in cristae density, although current evidence for such a mechanism is lacking. In the present study, we confirm this hypothesis by showing that, in human skeletal muscle, and in contrast to the current view, the mitochondrial cristae density is not constant but, instead, exhibits plasticity with long-term endurance training. Furthermore, we show that frequently recruited mitochondria-enriched fibres have significantly increased cristae density and that, at the whole-body level, muscle mitochondrial cristae density is a better predictor of maximal oxygen uptake rate than muscle mitochondrial volume. Our findings establish an elevating mitochondrial cristae density as a regulatory mechanism for increasing metabolic power in human skeletal muscle. We propose that this mechanism allows evasion of the trade-off between cell occupancy by mitochondria and other cellular constituents, as well as improved metabolic capacity and fuel catabolism during prolonged elevated energy requirements.

sted, utgiver, år, opplag, sider
2017. Vol. 595, nr 9, s. 2839-2847
HSV kategori
Identifikatorer
URN: urn:nbn:se:miun:diva-30838DOI: 10.1113/JP273040ISI: 000400357800012PubMedID: 27696420Scopus ID: 2-s2.0-85006380667OAI: oai:DiVA.org:miun-30838DiVA, id: diva2:1107477
Tilgjengelig fra: 2017-06-09 Laget: 2017-06-09 Sist oppdatert: 2017-07-04bibliografisk kontrollert

Open Access i DiVA

Fulltekst mangler i DiVA

Andre lenker

Forlagets fulltekstPubMedScopus

Personposter BETA

Holmberg, Hans-ChristerØrtenblad, Niels

Søk i DiVA

Av forfatter/redaktør
Holmberg, Hans-ChristerØrtenblad, Niels
Av organisasjonen
I samme tidsskrift
Journal of Physiology

Søk utenfor DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric

doi
pubmed
urn-nbn
Totalt: 244 treff
RefereraExporteraLink to record
Permanent link

Direct link
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf