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Difference between revisions of "Gnaiger 2009 Int J Biochem Cell Biol"

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|year=2009
|year=2009
|journal=Int J Biochem Cell Biol
|journal=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 O<sub>2</sub>∙s­<sup>-1</sup>∙mg<sup>-1</sup> 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.
|abstract=[[File:Q-junction Gnaiger 2009.jpg|right|400px]] 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 O<sub>2</sub>∙s­<sup>-1</sup>∙mg<sup>-1</sup> 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=[[Q-junction]], Q-cycle, Pyruvate, Glutamate, Succinate, Tricarboxylic acid cycle
|keywords=[[Q-junction]], Q-cycle, Pyruvate, Glutamate, Succinate, Tricarboxylic acid cycle
|mipnetlab=AT_Innsbruck_Gnaiger E, AT Innsbruck OROBOROS
|mipnetlab=AT_Innsbruck_Gnaiger E, AT Innsbruck OROBOROS

Revision as of 16:37, 22 June 2014

Publications in the MiPMap
Gnaiger E (2009) Capacity of oxidative phosphorylation in human skeletal muscle. New perspectives of mitochondrial physiology. Int J Biochem Cell Biol 41: 1837-1845.

» PMID: 19467914

Gnaiger E (2009) Int J Biochem Cell Biol

Abstract:

Q-junction Gnaiger 2009.jpg

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: Q-junction, Q-cycle, Pyruvate, Glutamate, Succinate, Tricarboxylic acid cycle

O2k-Network Lab: AT_Innsbruck_Gnaiger E, AT Innsbruck OROBOROS


Labels: MiParea: Respiration, mt-Biogenesis;mt-density, Exercise physiology;nutrition;life style, mt-Medicine  Pathology: Aging; senescence"Aging; senescence" is not in the list (Aging;senescence, Alzheimer's, Autism, Cancer, Cardiovascular, COPD, Diabetes, Inherited, Infectious, Myopathy, ...) of allowed values for the "Diseases" property., Obesity 

Organism: Human, Mouse  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue, Isolated Mitochondria"Isolated Mitochondria" 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: Marker Enzyme"Marker Enzyme" 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: Coupling efficiency;uncoupling  Coupling state: LEAK, OXPHOS, ETS"ETS" is not in the list (LEAK, ROUTINE, OXPHOS, ET) of allowed values for the "Coupling states" property. 

HRR: Oxygraph-2k 

BMI 

Further references