Importance of mitochondrial PO2 in maximal O2 transport and utilization: A theoretical analysis

I. Cano; M. Mickael; D. Gomez-Cabrero; J. Tegnér; J. Roca; P. D. Wagner

doi:10.1016/j.resp.2013.08.020

Importance of mitochondrial P_O2 in maximal O₂ transport and utilization: A theoretical analysis

I. Cano^*, M. Mickael, D. Gomez-Cabrero, J. Tegnér, J. Roca, P. D. Wagner

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

26 Scopus citations

Abstract

In previous calculations of how the O₂ transport system limits V̇_O2max, it was reasonably assumed that mitochondrial P_O2 (Pm_O2) could be neglected (set to zero). However, in reality, Pm_O2 must exceed zero and the red cell to mitochondrion diffusion gradient may therefore be reduced, impairing diffusive transport of O₂ and V̇_O2max. Accordingly, we investigated the influence of Pm_O2 on these calculations by coupling previously used equations for O₂ transport to one for mitochondrial respiration relating mitochondrial V̇_O2 to P_O2. This hyperbolic function, characterized by its P₅₀ and V̇_MAX, allowed Pm_O2 to become a model output (rather than set to zero as previously). Simulations using data from exercising normal subjects showed that at V̇_O2max, Pm_O2 was usually <1mmHg, and that the effects on V̇_O2max were minimal. However, when O₂ transport capacity exceeded mitochondrial V̇_MAX, or if P₅₀ were elevated, Pm_O2 often reached double digit values, thereby reducing the diffusion gradient and significantly decreasing V̇_O2max.

Original language	English (US)
Pages (from-to)	477-483
Number of pages	7
Journal	Respiratory Physiology and Neurobiology
Volume	189
Issue number	3
DOIs	https://doi.org/10.1016/j.resp.2013.08.020
State	Published - Dec 1 2013
Externally published	Yes

Bibliographical note

Funding Information:
This research has been carried out under the Synergy-COPD research grant, funded by the Seventh Framework Program of the European Commission as a Collaborative Project with contract no.: 270086 (2011-2014), and NIH P01 HL091830.

Keywords

Bioenergetics
Mitochondrial P
Mitochondrial respiration
Oxygen transport
V̇max

ASJC Scopus subject areas

General Neuroscience
Physiology
Pulmonary and Respiratory Medicine

Access to Document

10.1016/j.resp.2013.08.020

Cite this

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title = "Importance of mitochondrial PO2 in maximal O2 transport and utilization: A theoretical analysis",

abstract = "In previous calculations of how the O2 transport system limits {\.V}O2max, it was reasonably assumed that mitochondrial PO2 (PmO2) could be neglected (set to zero). However, in reality, PmO2 must exceed zero and the red cell to mitochondrion diffusion gradient may therefore be reduced, impairing diffusive transport of O2 and {\.V}O2max. Accordingly, we investigated the influence of PmO2 on these calculations by coupling previously used equations for O2 transport to one for mitochondrial respiration relating mitochondrial {\.V}O2 to PO2. This hyperbolic function, characterized by its P50 and {\.V}MAX, allowed PmO2 to become a model output (rather than set to zero as previously). Simulations using data from exercising normal subjects showed that at {\.V}O2max, PmO2 was usually <1mmHg, and that the effects on {\.V}O2max were minimal. However, when O2 transport capacity exceeded mitochondrial {\.V}MAX, or if P50 were elevated, PmO2 often reached double digit values, thereby reducing the diffusion gradient and significantly decreasing {\.V}O2max.",

keywords = "Bioenergetics, Mitochondrial P, Mitochondrial respiration, Oxygen transport, {\.V}max",

author = "I. Cano and M. Mickael and D. Gomez-Cabrero and J. Tegn{\'e}r and J. Roca and Wagner, {P. D.}",

note = "Funding Information: This research has been carried out under the Synergy-COPD research grant, funded by the Seventh Framework Program of the European Commission as a Collaborative Project with contract no.: 270086 (2011-2014), and NIH P01 HL091830. ",

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doi = "10.1016/j.resp.2013.08.020",

language = "English (US)",

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T1 - Importance of mitochondrial PO2 in maximal O2 transport and utilization

T2 - A theoretical analysis

AU - Cano, I.

AU - Mickael, M.

AU - Gomez-Cabrero, D.

AU - Tegnér, J.

AU - Roca, J.

AU - Wagner, P. D.

N1 - Funding Information: This research has been carried out under the Synergy-COPD research grant, funded by the Seventh Framework Program of the European Commission as a Collaborative Project with contract no.: 270086 (2011-2014), and NIH P01 HL091830.

PY - 2013/12/1

Y1 - 2013/12/1

N2 - In previous calculations of how the O2 transport system limits V̇O2max, it was reasonably assumed that mitochondrial PO2 (PmO2) could be neglected (set to zero). However, in reality, PmO2 must exceed zero and the red cell to mitochondrion diffusion gradient may therefore be reduced, impairing diffusive transport of O2 and V̇O2max. Accordingly, we investigated the influence of PmO2 on these calculations by coupling previously used equations for O2 transport to one for mitochondrial respiration relating mitochondrial V̇O2 to PO2. This hyperbolic function, characterized by its P50 and V̇MAX, allowed PmO2 to become a model output (rather than set to zero as previously). Simulations using data from exercising normal subjects showed that at V̇O2max, PmO2 was usually <1mmHg, and that the effects on V̇O2max were minimal. However, when O2 transport capacity exceeded mitochondrial V̇MAX, or if P50 were elevated, PmO2 often reached double digit values, thereby reducing the diffusion gradient and significantly decreasing V̇O2max.

AB - In previous calculations of how the O2 transport system limits V̇O2max, it was reasonably assumed that mitochondrial PO2 (PmO2) could be neglected (set to zero). However, in reality, PmO2 must exceed zero and the red cell to mitochondrion diffusion gradient may therefore be reduced, impairing diffusive transport of O2 and V̇O2max. Accordingly, we investigated the influence of PmO2 on these calculations by coupling previously used equations for O2 transport to one for mitochondrial respiration relating mitochondrial V̇O2 to PO2. This hyperbolic function, characterized by its P50 and V̇MAX, allowed PmO2 to become a model output (rather than set to zero as previously). Simulations using data from exercising normal subjects showed that at V̇O2max, PmO2 was usually <1mmHg, and that the effects on V̇O2max were minimal. However, when O2 transport capacity exceeded mitochondrial V̇MAX, or if P50 were elevated, PmO2 often reached double digit values, thereby reducing the diffusion gradient and significantly decreasing V̇O2max.

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