An intact central nervous system is not necessary for insulin-mediated increases in leg blood flow in humans.

Insulin mediates an increase in blood flow in the skeletal muscle. This may be brought about through recruitment of sympathetic vasodilatory nervous activity in the central nervous system (CNS). Insulin may also mediate the vasodilatation by locally acting mechanisms in the skeletal muscle, which in turn could be modulated by vasoconstrictive sympathetic nervous activity. Five men with complete motoric lesions of their cervical spinal cord (SCI) and nine healthy (H) men underwent a hyperinsulinemic (480 mU x min(-1) x m(-2)), euglycemic clamp combined with arterio-venous catheterization of one leg and microdialysis of the thigh muscle. In response to hyperinsulinemia leg blood flow increased similarly in the two groups. Leg glucose extraction and uptake were significantly lower in SCI compared with H. Two hours post clamp, leg glucose uptake rates had not yet returned to basal values. Norepinephrine concentrations in arterial plasma and in the dialysate (reflecting extracellular fluid) did not change in response to insulin in either group, but increased in response to suprapubic bladder tapping in the SCI. Potassium balance measured by microdialysis shifted from a net release to a net uptake in response to insulin, with no difference between SCI and H. In conclusion, the mechanism by which insulin mediates an increase in skeletal muscle blood flow is not due to a CNS recruitment of sympathetic vasodilatory nervous activity. Nor is the insulin-mediated vasodilatation modulated by vasoconstrictive sympathetic nervous activity. The vasodilatation seen in response to hyperinsulinemia is a locally acting mechanism. People with SCI are markedly insulin resistant compared with able-bodied individuals.