Insulin has been shown to regulate its own delivery to skeletal muscle interstitium via actions on the microvasculature (1,2,3). In fact, these vascular effects are thought to be rate-limiting for insulin-stimulated glucose uptake by skeletal muscle (1). Insulin’s influence on microvascular vasomotion – a rhythmic change in vascular diameter (4) – is one of the suggested levels of modulation. Insulin-induced changes in pre-capillary arteriolar vasomotion would result in a rhythmical variation in blood flow downstream (flowmotion). An increase in such preferential blood flow towards a particular capillary bed i.e. capillary recruitment will increase local capillary endothelial surface area for solute exchange. Although inferred upon several times (2,5), a direct link between changes in vasomotion and changes in capillary recruitment had yet to be demonstrated. We therefore addressed this very relationship within a group of healthy volunteers displaying a wide, continuous range in BMI and, as it turned out, insulin-sensitivity. Changes in vasomotion and capillary density were determined by laser Doppler flowmetry (LDF with spectral analysis) and capillary videomicroscopy in skin, respectively, before and during a hyperinsulinemic euglycemic clamp in 19 healthy volunteers. An insulin-induced increase in the neurogenic vasomotion domain was positively related to insulin-augmented capillary recruitment (r=0.51, P=0.04), and both parameters were related to insulin-mediated glucose uptake (r=0.47, P=0.06 and r=0.73, P=0.001, respectively). Furthermore, the change in insulin-augmented capillary recruitment could, at least statistically, largely explain the association between the neurogenic domain and insulin-mediated glucose uptake in a regression analysis, supporting the suggested physiological framework.