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Skeletal muscle microvascular (capillary) blood flow increases in the post-prandial state or during insulin infusion due to dilation of pre-capillary arterioles to augment glucose disposal. This effect occurs independent of changes in large artery function. However, acute hyperglycemia impairs vascular function, causes insulin to vasoconstrict pre-capillary arterioles, and causes muscle insulin resistance in vivo. We hypothesize that acute hyperglycemia impairs post-prandial muscle microvascular perfusion, without disrupting normal large artery hemodynamics, in healthy humans. Fifteen healthy people (5F/10M) underwent an oral glucose challenge (50g glucose) and a mixed meal challenge (MMC) on two separate occasions (randomised, cross-over design). At 1 hr, both challenges produced a comparable increase (6-fold) in plasma insulin levels. However, the OGC produced a 1.5-fold higher increase in blood glucose when compared to the MMC 1-hr post ingestion. Forearm muscle microvascular blood volume and flow (contrast-enhanced ultrasound) were increased during the MMC (1.3- and 1.9-fold from baseline, respectively, p<0.05 for both) but decreased during the OGC (0.7- and 0.6-fold from baseline, respectively, p<0.05 for both) despite a similar hyperinsulinemia. Both challenges stimulated brachial artery flow (ultrasound), and heart rate to a similar extent, as well as yielding comparable decreases in diastolic blood pressure and total vascular resistance. Systolic blood pressure and aortic stiffness remained unaltered by either challenge. Independent of large artery hemodynamics, hyperglycemia impairs muscle microvascular blood flow, potentially limiting glucose disposal into skeletal muscle. The OGC reduced microvascular blood flow in muscle peripherally, and therefore may underestimate the importance of skeletal muscle in postprandial glucose disposal.
This article was published in the following journal.
Name: American journal of physiology. Endocrinology and metabolism
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