Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Repeated static contractions increase mitochondrial vulnerability towards oxidative stress in human skeletal muscle
Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
2007 (English)In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 101, 833-839 p.Article in journal (Refereed) Published
Abstract [en]

Repeated static contractions (RSC) induce large fluctuations in tissue oxygen tension and increase the generation of reactive oxygen species (ROS). This study investigated the effect of RSC on muscle contractility, mitochondrial respiratory function, and in vitro sarcoplasmatic reticulum (SR) Ca2+-kinetics in human muscle. Ten male subjects performed 5 bouts of static knee extension with 10 min rest in between. Each bout of RSC (target torque 66% of maximal voluntary contraction torque, MVC) was maintained to fatigue. Muscle biopsies were taken pre-exercise and 0.3 and 24 h post-exercise from vastus lateralis. Mitochondria were isolated and respiratory function measured after incubation with H2O2 (HPX) or control medium (CON). Mitochondrial function was not affected by RSC during CON. However, RSC exacerbated mitochondrial dysfunction during HPX resulting in decreased respiratory control index, decreased mitochondrial efficiency (P/O ratio) and increased non-coupled respiration (HPX/CON post vs. pre-exercise). SR Ca2+ uptake rate was lower 0.3 h vs. 24 h post-exercise, whereas SR Ca2+ release rate was unchanged. RSC resulted in long-lasting changes in muscle contractility including reduced maximal torque, low frequency fatigue (LFF) and faster torque relaxation. It is concluded that RSC increases mitochondrial vulnerability towards ROS, reduces SR Ca2+ uptake rate and causes LFF. Although conclusive evidence is lacking we suggest that these changes are related to increased formation of ROS during RSC.

Place, publisher, year, edition, pages
2007. Vol. 101, 833-839 p.
National Category
Medical Bioscience
Identifiers
URN: urn:nbn:se:gih:diva-300OAI: oai:DiVA.org:gih-300DiVA: diva2:661
Available from: 2007-09-25 Created: 2007-09-25 Last updated: 2011-05-06

Open Access in DiVA

fulltext(173 kB)434 downloads
File information
File name FULLTEXT01.pdfFile size 173 kBChecksum SHA-1
4c0a3eb6d5e93502b534db9f28264c43d10dc6d97bac46ff989b7bdf415d2ab4beea3d95
Type fulltextMimetype application/pdf

Search in DiVA

By author/editor
Sahlin, Kent
By organisation
Department of Sport and Health Sciences
In the same journal
Journal of applied physiology
Medical Bioscience

Search outside of DiVA

GoogleGoogle Scholar
Total: 434 downloads
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Total: 384 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf