Lemieux 2017 Sci Rep

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Lemieux H, Blier PU, Gnaiger E (2017) Remodeling pathway control of mitochondrial respiratory capacity by temperature in mouse heart: electron flow through the Q-junction in permeabilized fibers. Sci Rep 7:2840, DOI:10.1038/s41598-017-02789-8.

» PMID: 28588260 Sci Rep Open Access

Lemieux H, Blier PU, Gnaiger E (2017) Sci Rep

Abstract: Fuel substrate supply and oxidative phosphorylation are key determinants of muscle performance. Numerous studies of mammalian mitochondria are carried out (i) with substrate supply that limits electron flow, and (ii) far below physiological temperature. To analyze potentially implicated biases, we studied mitochondrial respiratory control in permeabilized mouse myocardial fibers using high-resolution respirometry. The capacity of oxidative phosphorylation at 37 °C was nearly two-fold higher when fueled by physiological substrate combinations reconstituting tricarboxylic acid cycle function, compared with electron flow measured separately through NADH to Complex I or succinate to Complex II. The relative contribution of the NADH pathway to physiological respiratory capacity increased with a decrease in temperature from 37 to 25 ºC. The apparent excess capacity of cytochrome c oxidase above physiological pathway capacity increased sharply under hypothermia due to limitation by NADH-linked dehydrogenases. This mechanism of mitochondrial respiratory control in the hypothermic mammalian heart is comparable to the pattern in ectotherm species, pointing towards NADH-linked mt-matrix dehydrogenases and the phosphorylation system rather than electron transfer complexes as the primary drivers of thermal sensitivity at low temperature. Delineating the link between stress and remodeling of oxidative phosphorylation is important for understanding metabolic perturbations in disease evolution and cardiac protection.

Bioblast editor: Gnaiger E O2k-Network Lab: AT Innsbruck Gnaiger E, AT Innsbruck Oroboros, CA Rimouski Blier PU, CA Edmonton Lemieux H

Labels: MiParea: Respiration, Comparative MiP;environmental MiP 

Organism: Mouse  Tissue;cell: Heart  Preparation: Permeabilized tissue  Enzyme: Marker enzyme  Regulation: Cyt c, Inhibitor, Temperature, Threshold;excess capacity, Uncoupler  Coupling state: LEAK, OXPHOS, ET  Pathway: N, S, NS  HRR: Oxygraph-2k, O2k-Protocol 

1PM;2D;3G;4S;5U;6Rot-, SUIT-008, 1GM;2D;3P;4S;5U;6Rot-, SUIT-014, SUIT-008 O2 pce D025, MitoFitPublication, 2017-06 

Preprints for Gentle Science

Lemieux H, Blier PU, Gnaiger E (2017) Remodeling pathway control of oxidative phosphorylation by temperature in the heart. bioRxiv doi: https://doi.org/10.1101/103457. - »Bioblast link«
» Preprints for Gentle Science

COST Action MitoEAGLE In the spirit of COST Action MitoEAGLE WG1

SUIT protocols

1PM;2D;3G;3c;4S;5U;6Rot;7Ama.png 1PM;2D;3G;4S;5U;6Rot-

1GM;2D;2c;3P;4S;5U;6Rot;7Ama.png 1GM;2D;3P;4S;5U;6Rot-


  • NADH-linked or N-pathways (CI-entry into Q); succinate-linked or S-pathway (CII-entry into Q); NS-pathway (convergent CI&II-entry into Q)

MitoFit Contribution to K-Regio MitoFit

Further references

  1. Li P, Wang B, Sun F, Li Y, Li Q, Lang H, Zhao Z, Gao P, Zhao Y, Shang Q, Liu D, Zhu Z (2015) Mitochondrial respiratory dysfunctions of blood mononuclear cells link with cardiac disturbance in patients with early-stage heart failure. Sci Rep 5:10229. - »Bioblast link«