Dynamics of muscle microcirculatory and blood–myocyte O2flux during contractions

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Abstract
The O2requirements 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 O2flux. 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 O2flux 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 recruitmentper se, increased RBC flux and haematocrit within already‐flowing capillaries probably elevate perfusive and diffusive O2conductances and hence blood–myocyte O2flux. Additional surface area for O2exchange 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 O2and substrate delivery to contracting skeletal muscle. Indeed, the presence of very low intramyocyte O2partial pressures (PO2s) and the absence of intramyocytePO2gradients, 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‐emphasizingde novo‘capillary recruitment’. Diseases such as heart failure impair blood–myocyte O2flux, 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.

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