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Difference between revisions of "Gnaiger 2011 Abstract-MonteVerita"

From Bioblast
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[[MitoCom#Acknowledgment|Contribution to K-Regio]] ''[[MitoCom_K-Regio|MitoCom Tyrol]]''.
[[MitoCom#Acknowledgment|Contribution to K-Regio]] ''[[MitoCom_K-Regio|MitoCom Tyrol]]''.


[1] [[Gnaiger 2009 Int J Biochem Cell Biol|Gnaiger 2009]]; [[Lemieux_2011_IJBCB|Lemieux et al 2011 Int. J. Biochem. Cell Biol.]] Β 
[1] [[Gnaiger 2009 Int J Biochem Cell Biol|Gnaiger 2009]]; [[Lemieux_2011_Int J Biochem Cell Biol|Lemieux et al 2011 Int J Biochem Cell Biol]] Β 


[2] [[Gnaiger_2003_AdvExpMedBiol|Gnaiger 2003]]; [[Scandurra_2010_AdvExpMedBiol|Scandurra, Gnaiger 2010 Adv. Exp. Med. Biol.]] Β 
[2] [[Gnaiger_2003_Adv Exp Med Biol|Gnaiger 2003]]; [[Scandurra_2010_Adv Exp Med Biol|Scandurra, Gnaiger 2010 Adv Exp Med Biol]].


[3] Rasmussen et al 2001 AJP Β 
[3] Rasmussen et al 2001 AJP.


[4] [[Boushel_2011_Mitochondrion|Boushel et al 2011 Mitochondrion]] Β 
[4] [[Boushel_2011_Mitochondrion|Boushel et al 2011 Mitochondrion]].


[5] [[Gnaiger_1998_JEB|Gnaiger et al 1998 JEB]]
[5] [[Gnaiger_1998_JEB|Gnaiger et al 1998 JEB]].


[6] Richardson et al; Haseler et al JAP Β 
[6] Richardson et al; Haseler et al JAP.


[7] [[Pesta_2011_AJP|Pesta et al 2011 AJP]]; [[Jacobs_2011_JAP|Jacobs et al 2011 JAP]]
[7] [[Pesta_2011_AJP|Pesta et al 2011 AJP]]; [[Jacobs_2011_JAP|Jacobs et al 2011 JAP]].
|mipnetlab=AT Innsbruck Gnaiger E
|mipnetlab=AT Innsbruck Gnaiger E
|journal=Abstract
|journal=Abstract
}}
}}
{{Labeling
{{Labeling
|area=Respiration
|organism=Human
|injuries=Hypoxia
|topics=Oxygen kinetics
|couplingstates=OXPHOS
|substratestates=CI, CII, CI+II
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|injuries=Hypoxia
|organism=Human
|tissues=Skeletal Muscle
|kinetics=Oxygen
|journal=Abstract
|journal=Abstract
}}
}}

Revision as of 06:20, 11 August 2013

Gnaiger E (2011) Mitochondrial respiratory capacity at maximum aerobic exercise levels: Are intracellular oxygen levels limiting? Abstract Monte Verita.

Link: The impact of hypoxia on cells, mice and men

Gnaiger E (2011)

Event: Monte Verita

Mitochondrial capacity: OXPHOS capacity is evaluated in isolated mitochondria (mt) and permeabilized cells with physiological substrate cocktails to reconstitute tricarboxylic acid cycle function. As a consequence, convergent electron flow from Complexes CI+II of the electron transfer system (ETS) to the Q-junction exerts an additive effect on flux [1].

Oxygen kinetics of mt-respiration: The apparent Km,O2 or c50 [Β΅M] (p50 [kPa]) of mt-respiration increases linearly with respiratory capacity controlled by metabolic state, from 0.2 to 1.6 Β΅M determined by high-resolution respirometry. O2 gradients are significant only in large cells including cardiomyocytes. The apparent p50 increases 100-fold in permeabilized muscle fibers due to diffusion gradients [2].

mt-function at VO2max: Aerobic capacity of the human leg muscle exceeds maximum O2 uptake of isolated mitochondria [3] and v. lateralis during VO2max [4]. Therefore, oxygen supply limits aerobic performance, proportional to the apparent mt-excess capacity [5]. mt-respiration is more sensitive to average pO2 in heterogenous tissues than under homogenous conditions in vitro. Tissue heterogeneity increases the kinetic dependence of flux on average intracellular pO2. High mt-density reinforces the steepness of oxygen gradients and oxygen heterogeneity in the tissue, contributing to the O2 limitation in athletic vs sedentary individuals at VO2max [6]. This provides a functional rationale for the observation that hypoxia does not specifically trigger mt-biogenesis [7].

Contribution to K-Regio MitoCom Tyrol.

[1] Gnaiger 2009; Lemieux et al 2011 Int J Biochem Cell Biol

[2] Gnaiger 2003; Scandurra, Gnaiger 2010 Adv Exp Med Biol.

[3] Rasmussen et al 2001 AJP.

[4] Boushel et al 2011 Mitochondrion.

[5] Gnaiger et al 1998 JEB.

[6] Richardson et al; Haseler et al JAP.

[7] Pesta et al 2011 AJP; Jacobs et al 2011 JAP.


β€’ O2k-Network Lab: AT Innsbruck Gnaiger E


Labels: MiParea: Respiration 

Stress:Hypoxia  Organism: Human 


Regulation: Oxygen kinetics  Coupling state: OXPHOS 

HRR: Oxygraph-2k