Dynamics of muscle microcirculatory and blood-myocyte O2 flux during contractions

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 (PO(2)s) and the absence of intramyocyte PO2 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.