Gnaiger 2011 Abstract-MonteVerita: Difference between revisions
No edit summary |
No edit summary |
||
Line 13: | Line 13: | ||
[[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]]; [[ | [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]] ย | ||
[2] [[ | [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 ย | [3] Rasmussen et al 2001 AJP. | ||
[4] [[Boushel_2011_Mitochondrion|Boushel et al 2011 Mitochondrion]] ย | [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 ย | [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 | ||
|journal=Abstract | |journal=Abstract | ||
}} | }} |
Revision as of 07:20, 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 [ยตM] (p50 [kPa]) of mt-respiration increases linearly with respiratory capacity controlled by metabolic state, from 0.2 to 1.6 ยตM 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.
[6] Richardson et al; Haseler et al JAP.
[7] Pesta et al 2011 AJP; Jacobs et al 2011 JAP.
โข O2k-Network Lab: AT Innsbruck Gnaiger E
Labels: MiParea: Respiration
Stress:Hypoxia Organism: Human
Regulation: Oxygen kinetics Coupling state: OXPHOS
HRR: Oxygraph-2k