Endurance training improves endothelium-dependent vasodilation, yet it does not increase basal blood flow in the legs. We determined the effects of a 3-month aerobic exercise intervention on basal leg blood flow, and -adrenergic vasoconstriction and nitric oxide (NO) release in seven apparently healthy middle-aged and older adults (60±3 yr). Basal femoral artery blood flow (via Doppler ultrasound) (pre-training: 354±29; post-training: 335±34 ml/min) and vascular conductance did not change significantly with the exercise training. Before the exercise intervention, femoral artery blood flow increased 32±16% with systemic -adrenergic blockade (with phentolamine) (P<0.05), and the addition of nitric oxide synthase (NOS) inhibition using N^G-monomethyl-L-arginine (L-NMMA) did not affect femoral artery blood flow. After training, femoral artery blood flow increased 47±7% with -adrenergic blockade (P<0.01) and then decreased 18±7% with the subsequent administration of L-NMMA (P<0.05). Leg vascular conductance showed a greater -adrenergic blockade-induced vasodilation (+1.7±0.5 to +3.0±0.5 U, P<0.05) as well as NOS inhibition-induced vasoconstriction (-0.8±0.4 to -2.7±0.7 U, P<0.05) after the exercise intervention. Resting plasma norepinephrine concentration significantly increased after the training. These results suggest that regular aerobic exercise training enhances NO bioavailability in middle-aged and older adults and that basal limb blood flow does not change with exercise training because of the contrasting influences of sympathetic nervous system activity and endothelium-derived vasodilation on the vasculature.