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- Sahlin, Kent, et al.
(författare)
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Repeated static contractions increase mitochondrial vulnerability toward oxidative stress in human skeletal muscle.
- 2006
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Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 101:3, s. 833-839
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- 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.
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- Seppet, E. K., et al.
(författare)
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Functional complexes of mitochondria with MgATPase of myofibrils and sarcoplasmic reticulum in muscle cells
- 2001
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Ingår i: Biochimica et Biophysica Acta - Bioenergetics. - Amsterdam : Elsevier. - 0005-2728 .- 1879-2650. ; 1504:2-3, s. 379-395
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Tidskriftsartikel (refereegranskat)abstract
- Regulation of mitochondrial respiration in situ in the muscle cells was studied by using fully permeabilized muscle fibers and cardiomyocytes. The results show that the kinetics of regulation of mitochondrial respiration in situ by exogenous ADP are very different from the kinetics of its regulation by endogenous ADP. In cardiac and m. soleus fibers apparent Km for exogenous ADP in regulation of respiration was equal to 300–400 µM. However, when ADP production was initiated by intracellular ATPase reactions, the ADP concentration in the medium leveled off at about 40 µM when about 70% of maximal rate of respiration was achieved. Respiration rate maintained by intracellular ATPases was suppressed about 20–30% during exogenous trapping of ADP with excess pyruvate kinase (PK, 20 IU/ml) and phosphoenolpyruvate (PEP, 5 mM). ADP flux via the external PK+PEP system was decreased by half by activation of mitochondrial oxidative phosphorylation. Creatine (20 mM) further activated the respiration in the presence of PK+PEP. It is concluded that in oxidative muscle cells mitochondria behave as if they were incorporated into functional complexes with adjacent ADP producing systems – with the MgATPases in myofibrils and Ca,MgATPases of sarcoplasmic reticulum.
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- Svensson, M, et al.
(författare)
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Effect of Q10 supplementation on tissue Q10 levels and adenine nucleotide catabolism during high-intensity exercise.
- 1999
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Ingår i: International Journal of Sport Nutrition. - : Human Kinetics. - 1050-1606. ; 9, s. 166-180
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Tidskriftsartikel (refereegranskat)abstract
- The aim of the present study was to investigate the concentration of ubiquinone-10 (Q10), at rest, in human skeletal muscle and blood plasma before and after a period of high-intensity training with or without Q10 supplementation. Another aim was to explore whether adenine nucleotide catabolism, lipid peroxidation, and mitochondrial function were affected by Q10 treatment. Seventeen young healthy men were assigned to either a control (placebo) or Q10-supplementation (120 mg/day) group. Q10 supplementation resulted in a significantly higher plasma Q10/total cholesterol level on Days 11 and 20 compared with Day 1. There was no significant change in the concentration of Q10 in skeletal muscle or in isolated skeletal muscle mitochondria in either group. Plasma hypoxanthine and uric acid concentrations increased markedly after each exercise test session in both groups. After the training period, the postexercise increase in plasma hypoxanthine was markedly reduced in both groups, but the response was partially reversed after the recovery period. It was concluded that Q10 supplementation increases the concentration of Q10 in plasma but not in skeletal muscle.
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