TY - JOUR
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.
KW - Bioenergetics
KW - Mitochondrial P
KW - Mitochondrial respiration
KW - Oxygen transport
KW - V̇max
UR - http://www.scopus.com/inward/record.url?scp=84888025865&partnerID=8YFLogxK
U2 - 10.1016/j.resp.2013.08.020
DO - 10.1016/j.resp.2013.08.020
M3 - Article
C2 - 24012990
AN - SCOPUS:84888025865
SN - 1569-9048
VL - 189
SP - 477
EP - 483
JO - Respiratory Physiology and Neurobiology
JF - Respiratory Physiology and Neurobiology
IS - 3
ER -