MiP2005: Session 1
Mitochondrial Physiology Network 10.9: 13 (2005) - download pdf
Kent Sahlin1, 2, 3, M Mogensen2, JS Nielsen2, M Tonkonogi1, 3, 4
1 Stockholm University College of Physical Education and Sports, Sthlm Sweden; 2 Inst. of Sport Sciences and Clinical Biomec., Univ. of Southern Denmark, Odense; 3 Dept. of Physiology and Pharmacology, Karolinska Intitutet, Stockholm, Sweden; 4Dept. of Health and Social Sciences, Dalarna University, Falun, Sweden. - firstname.lastname@example.org
The effect of repeated static exercise (RSC) on mitochondrial function and SR Ca2+ kinetics was investigated in human muscle. Ten male subjects performed 5 sustained static contractions at 66 % of maximal voluntary contraction force (MVC) to fatigue with 10 min rest in between. Muscle contractility was measured pre- and post-exercise with MVC and transcutaneous electrical stimulation. Mitochondria isolated from muscle biopsies (pre-, 0 and 24 h post-exercise) were analyzed for respiratory function (with and without prior exposure to H2O2 (ROS)), mitochondrial resistance to Ca2+ induced pore opening (MCaR) and in vitro sarcoplasmatic reticulum (SR) Ca2+ uptake and release.
RSC had no effect on mitochondrial function. However, mitochondria isolated from muscle samples taken after RSC were more vulnerable to ROS as demonstrated by reduced respiratory control index (RCI=state 3/state 4), reduced P/O ratio and reduced maximal rate of oxidative phosphorylation (oxphos) (P<0.05). After 24 h recovery P/O ratio and oxphos were restored, whereas RCI remained depressed and uncoupled respiration was elevated. MCaR was related to % type II fibres (myosine heavy chain II) but was not affected by RSC. RSC resulted in altered muscle contractility (reduced MVC, twitch force, 20/50 Hz force ratio and faster force relaxation) which remained 3 h post-exercise. SR Ca2+ uptake rate was lower 0 h post-exercise (P<0.01 vs. 24 h post-exercise) and could not explain the faster force relaxation.
It is concluded that RSC does not affect mitochondrial function but increases the vulnerability of mitochondria towards ROS. It is suggested that this is a consequence of augmented ROS formation and associated depression of scavenger substances during RSC, which is an ischemia-reperfusion type of exercise. The depressed 20/50 Hz force ratio and the slow recovery of muscle contractile function suggest that fatigue is related to non-metabolic factors e.g. failure of excitation-contraction coupling.