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Am J Physiol Endocrinol Metab 295: E732-E750, 2008. First published July 8, 2008; doi:10.1152/ajpendo.90477.2008
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REVIEWS

Impaired microvascular perfusion: a consequence of vascular dysfunction and a potential cause of insulin resistance in muscle

Michael G. Clark

Menzies Research Institute, University of Tasmania, Hobart, Australia

Submitted 29 May 2008 ; accepted in final form 7 July 2008

ABSTRACT

Insulin has an exercise-like action to increase microvascular perfusion of skeletal muscle and thereby enhance delivery of hormone and nutrient to the myocytes. With insulin resistance, insulin's action to increase microvascular perfusion is markedly impaired. This review examines the present status of these observations and techniques available to measure such changes as well as the possible underpinning mechanisms. Low physiological doses of insulin and light exercise have been shown to increase microvascular perfusion without increasing bulk blood flow. In these circumstances, blood flow is proposed to be redirected from the nonnutritive route to the nutritive route with flow becoming dominant in the nonnutritive route when insulin resistance has developed. Increased vasomotion controlled by vascular smooth muscle may be part of the explanation by which insulin mediates an increase in microvascular perfusion, as seen from the effects of insulin on both muscle and skin microvascular blood flow. In addition, vascular dysfunction appears to be an early development in the onset of insulin resistance, with the consequence that impaired glucose delivery, more so than insulin delivery, accounts for the diminished glucose uptake by insulin-resistant muscle. Regular exercise may prevent and ameliorate insulin resistance by increasing "vascular fitness" and thereby recovering insulin-mediated capillary recruitment.



Address for reprint requests and other correspondence: M. G. Clark, Menzies Research Institute, Univ. of Tasmania, Private Bag 58, Hobart 7001, Australia (e-mail: Michael.Clark{at}utas.edu.au)




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