Decreased blood flow but unaltered insulin sensitivity of glucose uptake in skeletal muscle of chronic smokers

Chronic cigarette smoking is associated with dysfunction of the vascular en dothelium. Smokers have also been shown to be insulin-resistant, at least i n some studies. Since insulin-induced vasodilation is dependent on endothel ial cell nitric oxide (NO) synthesis, we tested the hypothesis that decreas ed skeletal muscle blood flow causes insulin resistance in smokers. We stud ied 37 young normotensive normolipidemic nondiabetic men, of which 14 were smokers and 23 lifelong nonsmokers, The groups were similar with respect to age, body mass index (BMI), and maximal oxygen uptake (VO(2)max). Basal an d insulin-stimulated femoral muscle blood flow was measured using [O-15]H2O and insulin-stimulated muscle glucose uptake using [F-18]fluoro-2-deoxy-D- glucose ([F-18]FDG) and positron emission tomography (PET), Whole-body gluc ose uptake was measured using the hyperinsulinemic (insulin infusion 5 mU/k g . min)-euglycemic clamp technique. In the basal state, muscle blood Row w as 51 % lower in smokers (17 +/- 3 mL/kg muscle . min) versus nonsmokers (3 5 +/- 17 mL/kg . min, P < .0001). Insulin increased muscle blood flow compa rably in both groups; the mean rate of insulin-stimulated blood flow was 30 +/- 10 and 55 +/- 38 mL/kg . min (P = .049), respectively. Whole-body and skeletal muscle glucose uptake were similar in both groups during insulin i nfusion. We conclude that muscle blood flow is lower in chronic smokers com pared with nonsmokers under both fasting end hyperinsulinemic conditions. T he insulin-induced increase in muscle blood flow and insulin-stimulated glu cose uptake appear normal, suggesting that the vasodilatory and metabolic e ffects of insulin are intact in smokers and the reduced muscle blood flow p er se does not cause insulin resistance in these subjects. Copyright (C) 19 99 by W.B. Saunders Company.