Muscle microcirculatory O(2) exchange in health and disease.

Much of our understanding of blood-muscle O(2) and substrate exchange is predicated on the presumption that, in resting muscle, a substantial proportion of the capillary bed does not sustain red blood cell (RBC) or plasma flux. According to this notion, with contractions, more capillaries are "recruited" (i.e., begin flowing) and increased metabolic demands are supported by blood-myocyte O(2) and substrate flux in these newly recruited capillaries. This scenario is attractive because additional exchange vessels are added, and radial intercapillary diffusion distances reduced, as demands increase - but is it correct? The compelling weight of evidence gathered over the last 3 decades using intravital microscopy, phosphorescence quenching and near infrared spectroscopy (NIRS) techniques challenges conventional "wisdom" and indicates that the majority of capillaries support RBC flux at rest. Thus, at the onset of contractions blood-myocyte O(2) and substrate flux must increase in vessels that were already flowing at rest. This concept forces a radical revision of the control of blood-myocyte O(2) and substrate flux. This revision is essential if we are to understand the control of microcirculatory O(2) and substrate flux in health and resolve the mechanistic bases by which these processes are compromised in diseases such as chronic heart failure.