Difference between revisions of "Naimi 2011 Clin Physiol Funct Imaging"
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|year=2011 | |year=2011 | ||
|journal=Clin. Physiol. Funct. Imaging | |journal=Clin. Physiol. Funct. Imaging | ||
|abstract=Evidence exists for locomotor muscle impairment in patients with chronic obstructive pulmonary disease (COPD), including fiber type alterations and reduced mitochondrial oxidative capacity. In this study high-resolution respirometry was used to quantify oxygen flux in permeabilized fibres from biopsies of the vastus lateralis muscle in patients with COPD and compared to healthy control subjects. The main findings of this study were that (i) routine | |abstract=Evidence exists for locomotor muscle impairment in patients with chronic obstructive pulmonary disease (COPD), including fiber type alterations and reduced mitochondrial oxidative capacity. In this study high-resolution respirometry was used to quantify oxygen flux in permeabilized fibres from biopsies of the vastus lateralis muscle in patients with COPD and compared to healthy control subjects. The main findings of this study were that (i) routine [[State 2]] respiration was higher in COPD; (ii) [[State 3]] respiration in the presence of ADP was similar in both groups with substrate supply of electrons to [[Complex I]] (COPD 38·28 ± 3·58 versus control 42·85 ± 3·10 pmol s(-1) mg tissue(-1) ), but O(2) flux with addition of succinate was lower in COPD patients (COPD 63·72 ± 6·33 versus control 95·73 ± 6·53 pmol s(-1) mg tissue(-1) ); (iii) excess capacity of [[cytochrome c oxidase]] in COPD patients was only ~50% that of control subjects. These results indicate that quadriceps muscle mitochondrial function is altered in patients with COPD. The regulatory mechanisms underlying these functional abnormalities remain to be uncovered. | ||
|keywords=chronic obstructive pulmonary disease, mitochondrial respiration, skeletal muscle | |keywords=chronic obstructive pulmonary disease, mitochondrial respiration, skeletal muscle | ||
|mipnetlab= | |mipnetlab=DK_Copenhagen_Boushel R, DK_Copenhagen_Dela F | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
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|tissues=Skeletal Muscle | |tissues=Skeletal Muscle | ||
|preparations=Permeabilized Cell or Tissue; Homogenate | |preparations=Permeabilized Cell or Tissue; Homogenate | ||
|enzymes=Complex I, Complex IV; Cytochrome c Oxidase | |||
|topics=Respiration; OXPHOS; ETS Capacity | |||
}} | }} | ||
Revision as of 11:58, 23 October 2011
| Naimi AI, Bourbeau J, Perrault H, Baril J, Wright-Paradis C, Rossi A, Taivassalo T, Sheel AW, Rabøl R, Dela F, Boushel R (2011) Altered mitochondrial regulation in quadriceps muscles of patients with COPD. Clin. Physiol. Funct. Imaging 31(2):124-131. |
Naimi AI, Bourbeau J, Perrault H, Baril J, Wright-Paradis C, Rossi A, Taivassalo T, Sheel AW, Rabol R, Dela F, Boushel R (2011) Clin. Physiol. Funct. Imaging
Abstract: Evidence exists for locomotor muscle impairment in patients with chronic obstructive pulmonary disease (COPD), including fiber type alterations and reduced mitochondrial oxidative capacity. In this study high-resolution respirometry was used to quantify oxygen flux in permeabilized fibres from biopsies of the vastus lateralis muscle in patients with COPD and compared to healthy control subjects. The main findings of this study were that (i) routine State 2 respiration was higher in COPD; (ii) State 3 respiration in the presence of ADP was similar in both groups with substrate supply of electrons to Complex I (COPD 38·28 ± 3·58 versus control 42·85 ± 3·10 pmol s(-1) mg tissue(-1) ), but O(2) flux with addition of succinate was lower in COPD patients (COPD 63·72 ± 6·33 versus control 95·73 ± 6·53 pmol s(-1) mg tissue(-1) ); (iii) excess capacity of cytochrome c oxidase in COPD patients was only ~50% that of control subjects. These results indicate that quadriceps muscle mitochondrial function is altered in patients with COPD. The regulatory mechanisms underlying these functional abnormalities remain to be uncovered. • Keywords: chronic obstructive pulmonary disease, mitochondrial respiration, skeletal muscle
• O2k-Network Lab: DK_Copenhagen_Boushel R, DK_Copenhagen_Dela F
Labels:
Stress:Mitochondrial Disease; Degenerative Disease and Defect"Mitochondrial Disease; Degenerative Disease and Defect" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Human Tissue;cell: Skeletal Muscle"Skeletal Muscle" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property. Preparation: Permeabilized Cell or Tissue; Homogenate"Permeabilized Cell or Tissue; Homogenate" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property. Enzyme: Complex I, Complex IV; Cytochrome c Oxidase"Complex IV; Cytochrome c Oxidase" is not in the list (Adenine nucleotide translocase, Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase, Inner mt-membrane transporter, Marker enzyme, Supercomplex, TCA cycle and matrix dehydrogenases, ...) of allowed values for the "Enzyme" property. Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property.
HRR: Oxygraph-2k
