Insulin stimulates nerve arterial vasodilation through a nitric-oxide synthase (NOS) mechanism. Experimental diabetes reduces vasa nervorum NO-reactivity. Studies investigating hyperglycemia and nerve arterial vasodilation typically omit insulin-treatment and use sedentary rats resulting in severe hyperglycemia. We tested the hypotheses that i) insulin-treated experimental diabetes and inactivity (DS) will attenuate insulin-mediated nerve arterial vasodilation and ii) deficits in vasodilation in DS rats will be overcome by concurrent exercise training (DX; 75-85% VO2max, 1 h/d, 5 d/week, for 10 weeks). The baseline index of vascular conductance values (iVC = nerve blood flow velocity/mean arterial blood pressure) were similar (P≥0.68), but peak iVC and the area under the curve (AUCi) for the iVC during a euglycemic hyperinsulinemic clamp (EHC; 10 mU/kg/min), were lower in DS rats vs. control sedentary (CS) rats and DX rats (P≤0.01). Motor nerve conduction velocity (MNCV) was lower in DS rats vs. CS rats and DX rats (P≤0.01). Compared with DS rats, DX rats expressed greater nerve endothelial NOS (eNOS) protein content (P=0.04). In a separate analysis, we examined the impact of diabetes in exercise trained rats alone. Compared with exercise trained control rats (CX), DX rats had a lower AUCi during the EHC, lower MNCV values and lower sciatic nerve eNOS protein content (P≤0.03). Therefore, vasa nervorum and motor nerve function are impaired in DS rats. Such deficits in rats with diabetes can be overcome by concurrent exercise training. However, in exercise trained rats (CX and DX groups), poorly controlled blood glucose lowers vasa nervorum and nerve function.