Submitted on August 19, 2005
Accepted on May 9, 2006
Repeated static contractions increase mitochondrial vulnerability towards oxidative stress in human skeletal muscle
Kent Sahlin1*, Jens Steen Nielsen2, Martin Mogensen2, and Michail Tonkonogi3
1 Institute of Sport Sciences and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark; Astrand laboratory, Stockholm University College of Physical Education and Sports, Stockholm, Sweden; Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
2 Institute of Sport Sciences and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark
3 Astrand laboratory, Stockholm University College of Physical Education and Sports, Stockholm, Sweden; Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden; Department of Health and Social Sciences, Dalarna University, Falun, Sweden
* To whom correspondence should be addressed. E-mail: kent.sahlin{at}ihs.se.
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.
