Contribution of nitric oxide in the contraction-induced rapid vasodilation in young and older adults

Abstract

We tested the hypothesis that reduced nitric oxide (NO) bioavailability contributes to the attenuated peak and total vasodilation following single-muscle contractions in older adults. Young ( n = 10; 24 ± 2 yr) and older ( n = 10; 67 ± 2 yr) adults performed single forearm contractions at 10, 20, and 40% of maximum during saline infusion (control) and NO synthase (NOS) inhibition via NG-monomethyl-l-arginine. Brachial artery diameters and velocities were measured using Doppler ultrasound and forearm vascular conductance (FVC; in ml·min−1·100 mmHg−1) was calculated from blood flow (ml/min) and blood pressure (mmHg). Peak and total vasodilator responses [change (Δ) in FVC from baseline] were attenuated in older adults at all intensities ( P < 0.05). NOS inhibition reduced the peak ΔFVC at 10% (88 ± 12 vs. 52 ± 9 ml·min−1·100 mmHg−1), 20% (125 ± 13 vs. 83 ± 13 ml·min−1·100 mmHg−1), and 40% (207 ± 26 vs. 133 ± 20 ml·min−1·100 mmHg−1) in young subjects, ( P < 0.05 for all) and in older adults at 10% (59 ± 5 vs. 47 ± 7 ml·min−1·100 mmHg−1, P < 0.05) and 20% (88 ± 9 vs. 68 ± 9 ml·min−1·100 mmHg−1, P < 0.05), but not 40% (128 ± 12 vs. 105 ± 11 ml·min−1·100 mmHg−1, P = 0.11). The relative (%) reduction in peak ΔFVC due to NOS inhibition was greater in young vs. older adults at 20% (−36 ± 5 vs. −23 ± 5%, P < 0.05) and 40% (−35 ± 6 vs. −16 ± 7%, P < 0.05). The reduction in the total vasodilator response (area under the curve) with NOS inhibition was also greater in young vs. older adults at all intensities. Our data suggest that contraction-induced rapid vasodilation is mediated in part by NO, and that the contribution of NO is greater in young adults.