Abstract
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 PO(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.