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Dynamics of muscle microcirculatory and blood–myocyte O 2 flux during contractions
Author(s) -
Poole D. C.,
Copp S. W.,
Hirai D. M.,
Musch T. I.
Publication year - 2011
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2010.02246.x
Subject(s) - myocyte , skeletal muscle , flux (metallurgy) , capillary action , biophysics , chemistry , contraction (grammar) , red blood cell , medicine , anatomy , cardiology , biology , biochemistry , physics , thermodynamics , organic chemistry
The O 2 requirements of contracting skeletal muscle may increase 100‐fold above rest. In 1919, August Krogh’s brilliant insights recognized the capillary as the principal site for this increased blood–myocyte O 2 flux. Based on the premise that most capillaries did not sustain RBC flux at rest, Krogh proposed that capillary recruitment [i.e. initiation of red blood cell (RBC) flux in previously non‐flowing capillaries] increased the capillary surface area available for O 2 flux and reduced mean capillary‐to‐mitochondrial diffusion distances. More modern experimental approaches reveal that most muscle capillaries may support RBC flux at rest. Thus, rather than contraction‐induced capillary recruitment per se , increased RBC flux and haematocrit within already‐flowing capillaries probably elevate perfusive and diffusive O 2 conductances and hence blood–myocyte O 2 flux. Additional surface area for O 2 exchange is recruited but, crucially, this may occur along the length of already‐flowing capillaries (i.e. longitudinal recruitment). Today, the capillary is still considered the principal site for O 2 and substrate delivery to contracting skeletal muscle. Indeed, the presence of very low intramyocyte O 2 partial pressures ( P O 2 s) and the absence of intramyocyte P O 2 gradients, whilst refuting the relevance of diffusion distances, place an even greater importance on capillary hemodynamics. This emergent picture calls for a paradigm‐shift in our understanding of the function of capillaries by de‐emphasizing de novo ‘capillary recruitment’. Diseases such as heart failure impair blood–myocyte O 2 flux, in part, by decreasing the proportion of RBC‐flowing capillaries. Knowledge of capillary function in healthy muscle is requisite for identification of pathology and efficient design of therapeutic treatments.