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1 University of Tasmania
* To whom correspondence should be addressed. E-mail: michael.clark{at}utas.edu.au.
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 current status of these observations, techniques available to measure such changes, as well as the possible under-pinning 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 non-nutritive route to the nutritive route with flow becoming dominant in the non-nutritive 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, accounting 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.
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