Difference between revisions of "Gnaiger 2009 Int J Biochem Cell Biol"
(new pub) |
|||
| Line 1: | Line 1: | ||
{{Publication | |||
|title=Gnaiger E (2009) Capacity of oxidative phosphorylation in human skeletal muscle. New perspectives of mitochondrial physiology. Int. J. Biochem. Cell Biol. 41: 1837-1845. | |||
|authors=Gnaiger E | |||
|year=2009 | |||
Maximal ADP-stimulated mitochondrial respiration depends on [[convergent electron flow]] through Complexes I+II to the [[Q-junction]] of the [[electron transport system]] (ETS). In most studies of respiratory control in mitochondrial preparations, however, respiration is limited artificially by supplying substrates for electron input through either Complex I or II. [[High-resolution respirometry]] with minimal amounts of tissue biopsy (1 to 3 mg wet weight of [[permeabilized muscle fibres]] per assay) provides a routine approach for multiple [[substrate-uncoupler-inhibitor titrations]]. Under physiological conditions, maximal respiratory capacity is obtained with glutamate+malate+succinate, reconstituting the operation of the [[tricarboxylic acid cycle]] and preventing depletion of key metabolites from the mitochondrial matrix. In human skeletal muscle, conventional assays with [[pyruvate+malate]] or [[glutamate+malate]] yield submaximal oxygen fluxes at 0.50 to 0.75 of capacity of oxidative phosphorylation (OXPHOS). Best estimates of muscular [[OXPHOS capacity]] at 37 °C [pmol O2∙s-1∙mg-1 wet weight] with isolated mitochondria or permeabilized fibres, suggest a range of 100 to 150 and up to 180 in healthy humans with normal [[body mass index]] and top endurance athletes, but reduction to 60 to 120 in overweight healthy adults with predominantly sedentary life style. The apparent ETS excess capacity (uncoupled respiration) over ADP-stimulated OXPHOS capacity is high in skeletal muscle of active and sedentary humans, but absent in mouse skeletal muscle. Such differences of mitochondrial quality in skeletal muscle are unexpected and cannot be explained at present. A comparative data base of mitochondrial physiology may provide the key for understanding the functional implications of mitochondrial diversity from mouse to man, and evaluation of altered mitochondrial respiratory control patterns in health and disease. | |journal=Int. J. Biochem. Cell Biol. | ||
|mipnetlab=AT_Innsbruck_GnaigerE | |||
|abstract=Maximal ADP-stimulated mitochondrial respiration depends on [[convergent electron flow]] through Complexes I+II to the [[Q-junction]] of the [[electron transport system]] (ETS). In most studies of respiratory control in mitochondrial preparations, however, respiration is limited artificially by supplying substrates for electron input through either Complex I or II. [[High-resolution respirometry]] with minimal amounts of tissue biopsy (1 to 3 mg wet weight of [[permeabilized muscle fibres]] per assay) provides a routine approach for multiple [[substrate-uncoupler-inhibitor titrations]]. Under physiological conditions, maximal respiratory capacity is obtained with glutamate+malate+succinate, reconstituting the operation of the [[tricarboxylic acid cycle]] and preventing depletion of key metabolites from the mitochondrial matrix. In human skeletal muscle, conventional assays with [[pyruvate+malate]] or [[glutamate+malate]] yield submaximal oxygen fluxes at 0.50 to 0.75 of capacity of oxidative phosphorylation (OXPHOS). Best estimates of muscular [[OXPHOS capacity]] at 37 °C [pmol O2∙s-1∙mg-1 wet weight] with isolated mitochondria or permeabilized fibres, suggest a range of 100 to 150 and up to 180 in healthy humans with normal [[body mass index]] and top endurance athletes, but reduction to 60 to 120 in overweight healthy adults with predominantly sedentary life style. The apparent ETS excess capacity (uncoupled respiration) over ADP-stimulated OXPHOS capacity is high in skeletal muscle of active and sedentary humans, but absent in mouse skeletal muscle. Such differences of mitochondrial quality in skeletal muscle are unexpected and cannot be explained at present. A comparative data base of mitochondrial physiology may provide the key for understanding the functional implications of mitochondrial diversity from mouse to man, and evaluation of altered mitochondrial respiratory control patterns in health and disease. | |||
Mitochondrial respiratory control, high-resolution respirometry, skeletal muscle, Q-cycle, Q-junction, electron transport, maximal oxygen consumption, pyruvate, glutamate, succinate, tricarboxylic acid cycle | |keywords=Mitochondrial respiratory control, high-resolution respirometry, skeletal muscle, Q-cycle, Q-junction, electron transport, maximal oxygen consumption, pyruvate, glutamate, succinate, tricarboxylic acid cycle | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19467914 PMID: 19467914] | |||
=== | }} | ||
{{Labeling | |||
|instruments=Oxygraph-2k | |||
|discipline=Mitochondrial Physiology, Biomedicine | |||
|organism=Human | |||
|tissues=Skeletal Muscle | |||
|preparations=Permeabilized Cell or Tissue; Homogenate | |||
|injuries=Mitochondrial Disease; Degenerative Disease and Defect, Aging; Senescence | |||
|topics=Respiration; OXPHOS; ETS Capacity, Flux Control; Additivity; Threshold; Excess Capacity, Coupling; Membrane Potential, Mitochondrial Biogenesis; Mitochondrial Density, Substrate; Glucose; TCA Cycle | |||
}} | |||
Revision as of 10:16, 13 September 2010
| Gnaiger E (2009) Capacity of oxidative phosphorylation in human skeletal muscle. New perspectives of mitochondrial physiology. Int. J. Biochem. Cell Biol. 41: 1837-1845. |
Gnaiger E (2009) Int. J. Biochem. Cell Biol.
Abstract: Maximal ADP-stimulated mitochondrial respiration depends on convergent electron flow through Complexes I+II to the Q-junction of the electron transport system (ETS). In most studies of respiratory control in mitochondrial preparations, however, respiration is limited artificially by supplying substrates for electron input through either Complex I or II. High-resolution respirometry with minimal amounts of tissue biopsy (1 to 3 mg wet weight of permeabilized muscle fibres per assay) provides a routine approach for multiple substrate-uncoupler-inhibitor titrations. Under physiological conditions, maximal respiratory capacity is obtained with glutamate+malate+succinate, reconstituting the operation of the tricarboxylic acid cycle and preventing depletion of key metabolites from the mitochondrial matrix. In human skeletal muscle, conventional assays with pyruvate+malate or glutamate+malate yield submaximal oxygen fluxes at 0.50 to 0.75 of capacity of oxidative phosphorylation (OXPHOS). Best estimates of muscular OXPHOS capacity at 37 °C [pmol O2∙s-1∙mg-1 wet weight] with isolated mitochondria or permeabilized fibres, suggest a range of 100 to 150 and up to 180 in healthy humans with normal body mass index and top endurance athletes, but reduction to 60 to 120 in overweight healthy adults with predominantly sedentary life style. The apparent ETS excess capacity (uncoupled respiration) over ADP-stimulated OXPHOS capacity is high in skeletal muscle of active and sedentary humans, but absent in mouse skeletal muscle. Such differences of mitochondrial quality in skeletal muscle are unexpected and cannot be explained at present. A comparative data base of mitochondrial physiology may provide the key for understanding the functional implications of mitochondrial diversity from mouse to man, and evaluation of altered mitochondrial respiratory control patterns in health and disease. • Keywords: Mitochondrial respiratory control, high-resolution respirometry, skeletal muscle, Q-cycle, Q-junction, electron transport, maximal oxygen consumption, pyruvate, glutamate, succinate, tricarboxylic acid cycle
• O2k-Network Lab: AT_Innsbruck_GnaigerE
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., Aging; Senescence"Aging; Senescence" 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.
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., Flux Control; Additivity; Threshold; Excess Capacity"Flux Control; Additivity; Threshold; Excess 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., Coupling; Membrane Potential"Coupling; Membrane Potential" 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., Mitochondrial Biogenesis; Mitochondrial Density"Mitochondrial Biogenesis; Mitochondrial Density" 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., Substrate; Glucose; TCA Cycle"Substrate; Glucose; TCA Cycle" 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
