Abstract

Several thousand capillaries are small enough to fit comfortably on the period at the end of this sentence and yet, within skeletal muscle, thousands of miles of capillaries combine to provide a vast surface, some hundreds of square metres, that is essential for blood–myocyte flux of O2, glucose and free fatty acids. As dictated by muscle metabolic demands and a complex array of neural, humoral and local controllers, muscular arterioles function as ‘gatekeepers’, regulating capillary red blood cell (RBC) and plasma flow. The issue considered here is whether or not most capillaries support RBC and/or plasma flux in resting skeletal muscle. If such is the case, this dismisses de novo recruitment of capillaries as a requirement for increased blood–myocyte flux either at rest or during muscle contractions. Resolution of this problem is fundamental to understanding muscle metabolic function in health and the mechanistic bases for dysfunction in diseases such as diabetes, sepsis and heart failure (Lemkes et al. 2012; Poole et al. 2012; Eskens et al. 2013).

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