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Repeated static contractions increase mitochondrial vulnerability toward oxidative stress in human skeletal muscle

¹Institute of Sport Sciences and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark; ²Stockholm University College of Physical Education and Sports, Stockholm; ³Department of Physiology and Pharmacology, Karolinska Intitutet, Stockholm; and ⁴Department of Health and Social Sciences, Dalarna University, Falun, Sweden

Submitted 19 August 2005 ; accepted in final form 9 May 2006

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 sarcoplasmic reticulum (SR) Ca²⁺ kinetics in human muscle. Ten male subjects performed five bouts of static knee extension with 10-min rest in between. Each bout of RSC (target torque 66% of maximal voluntary contraction torque) was maintained to fatigue. Muscle biopsies were taken preexercise and 0.3 and 24 h postexercise 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 (phosphorylated ADP-to-oxygen consumed ratio), and increased noncoupled respiration (HPX/Con post- vs. preexercise). SR Ca²⁺ uptake rate was lower 0.3 vs. 24 h postexercise, whereas SR Ca²⁺ release rate was unchanged. RSC resulted in long-lasting changes in muscle contractility, including reduced maximal torque, low-frequency fatigue, and faster torque relaxation. It is concluded that RSC increases mitochondrial vulnerability toward ROS, reduces SR Ca²⁺ uptake rate, and causes low-frequency fatigue. Although conclusive evidence is lacking, we suggest that these changes are related to increased formation of ROS during RSC.

calcium homeostasis; exercise; mitochondria; oxidative phosphorylation