We tested the hypothesis that elevated sympathetic tone is responsible for lower peak vasodilation after single muscle contractions in older adults. Young (n = 13, 7 men and 6 women, age: 27 ± 1 yr) and older (n = 13, 7 men and 6 women, age: 69 ± 2 yr) adults performed single forearm contractions at 10%, 20%, and 40% of maximum during 1) control, 2) sympathetic activation via lower body negative pressure (LBNP; -20 mmHg), and 3) intra-arterial infusion of phentolamine (α-adrenergic antagonist). Brachial artery diameter and velocities were measured via Doppler ultrasound, and forearm vascular conductance (FVC; in ml·min(-1)·100 mmHg(-1)) was calculated from blood flow (in ml/min) and blood pressure (in mmHg). Peak vasodilator responses [change in (Δ) FVC from baseline] were attenuated in older adults at 20% and 40% of maximum (P < 0.05). LBNP reduced peak ΔFVC at 10% (98 ± 17 vs. 70 ± 12 ml·min(-1)·100 mmHg(-1)), 20% (144 ± 12 vs. 98 ± 3 ml·min(-1)·100 mmHg(-1)), and 40% (209 ± 20 vs. 161 ± 21 ml·min(-1)·100 mmHg(-1), P < 0.01 vs. control) in younger adults but not in older adults (71 ± 11 vs. 68 ± 11, 107 ± 13 vs. 106 ± 16, and 161 ± 22 vs. 144 ± 22 ml·min(-1)·100 mmHg(-1), respectively, P = 0.22-0.99). With phentolamine, peak ΔFVC was enhanced in older adults at each contraction intensity (100 ± 14, 147 ± 22, and 200 ± 26 ml·min(-1)·100 mmHg(-1), respectively, P < 0.01 vs. control) but not in younger adults (94 ± 13, 153 ± 13, and 224 ± 27 ml·min(-1)·100 mmHg(-1), respectively, P = 0.30-0.81 vs. control). Our data indicate that α-adrenergic vasoconstriction and/or blunted functional sympatholysis might contribute to the age-related decreases in skeletal muscle contraction-induced rapid vasodilation in humans.