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Skeletal muscle interstitial O 2 pressures: bridging the gap between the capillary and myocyte
Author(s) -
Hirai Daniel M.,
Colburn Trenton D.,
Craig Jesse C.,
Hotta Kazuki,
Kano Yutaka,
Musch Timothy I.,
Poole David C.
Publication year - 2019
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1111/micc.12497
Subject(s) - skeletal muscle , myocyte , chemistry , biophysics , capillary action , flux (metallurgy) , medicine , materials science , biology , organic chemistry , composite material
The oxygen transport pathway from air to mitochondria involves a series of transfer steps within closely integrated systems (pulmonary, cardiovascular, and tissue metabolic). Small and finite O 2 stores in most mammalian species require exquisitely controlled changes in O 2 flux rates to support elevated ATP turnover. This is especially true for the contracting skeletal muscle where O 2 requirements may increase two orders of magnitude above rest. This brief review focuses on the mechanistic bases for increased microvascular blood‐myocyte O 2 flux (V̇O 2 ) from rest to contractions. Fick's law dictates that V̇O 2 elevations driven by muscle contractions are produced by commensurate changes in driving force (ie, O 2 pressure gradients; Δ PO 2 ) and/or effective diffusing capacity ( DO 2 ). While previous evidence indicates that increased DO 2 helps modulate contracting muscle O 2 flux, up until recently the role of the dynamic Δ PO 2 across the capillary wall was unknown. Recent phosphorescence quenching investigations of both microvascular and novel interstitial PO 2 kinetics in health have resolved an important step in the O 2 cascade between the capillary and myocyte. Specifically, the significant transmural Δ PO 2 at rest was sustained (but not increased) during submaximal contractions. This supports the contention that the blood‐myocyte interface provides a substantial effective resistance to O 2 diffusion and underscores that modulations in erythrocyte hemodynamics and distribution ( DO 2 ) are crucial to preserve the driving force for O 2 flux across the capillary wall (Δ PO 2 ) during contractions. Investigation of the O 2 transport pathway close to muscle mitochondria is key to identifying disease mechanisms and develop therapeutic approaches to ameliorate dysfunction and exercise intolerance.