Nitric oxide‐mediated vascular function in response to limb movement: the impact of age

Abstract

In young men passive movement‐induced increases in leg blood flow (LBF) and leg vascular conductance (LVC) are predominantly nitric oxide (NO)‐dependent, however the contribution of NO to the attenuated response with age remains unknown. Therefore, this study sought to determine the contribution of NO to movement‐induced hyperemia and vasodilation in the elderly. Fourteen male subjects (7 young, 24 ± 1 yrs, and 7 old, 75 ± 3 yrs) underwent passive knee extension with and without NO synthase (NOS) inhibition via intra‐arterial infusion of NG‐monomethyl‐L‐arginine (L‐NMMA). Leg blood flow (LBF) and central hemodynamics were determined by Doppler ultrasound and finger photoplethysmography, respectively. NOS inhibition blunted the peak increase in LBF in the young (control; 668 ± 106, L‐NMMA; 431 ± 95 ml/min, p = 0.03), but had no effect on the already attenuated hyperemic response of the old (control; 266 ± 98, L‐NMMA; 251 ± 92 ml/min, p = 0.59). Similarly, the magnitude of change in the area under the curve over time for the LBF and LVC responses to NOS inhibition was less in the old (LBF; −31 ± 18 ml, LVC; −0.4 ± 0.2 ml/mmHg) than the young (LBF; −129 ± 21 ml, p < 0.01, LVC; − 1.5 ± 0.2 < 0.01). Thus, age‐associated reductions in hyperemia and vasodilation in the elderly are primarily due to a reduced contribution of NO and support passive limb movement as a novel approach to assess NO‐mediated vascular function across the lifespan.