The Effect of Physical Activity on Passive Leg Movement-Induced Vasodilation with Age.

Abstract

Because of reduced nitric oxide (NO) bioavailability with age, passive leg movement (PLM)-induced vasodilation is attenuated in older sedentary subjects and, unlike the young subjects, cannot be augmented by posture-induced elevations in femoral perfusion pressure. However, whether vasodilator function assessed with PLM, and therefore NO bioavailability, is preserved in older individuals with greater physical activity and fitness is unknown. PLM was performed on four subject groups: young sedentary (Y, 23 ± 1 yr, n = 12), old sedentary (OS, 73 ± 2 yr, n = 12), old active (OA, 71 ± 2 yr, n = 10), and old endurance trained (OT, 72 ± 1 yr, n = 10) in the supine and upright-seated posture. Hemodynamics were measured using ultrasound Doppler and finger photoplethysmography. In the supine posture, PLM-induced peak change in leg vascular conductance was significantly attenuated in the OS compared with the young subjects (OS = 4.9 ± 0.5, Y = 6.9 ± 0.7 mL·min·mm Hg) but was not different from the young in the OA and OT (OA = 5.9 ± 1.0, OT = 5.4 ± 0.4 mL·min·mm Hg). The upright-seated posture significantly augmented peak change in leg vascular conductance in all but the OS (OS = 4.9 ± 0.5, Y = 11.8 ± 1.3, OA = 7.3 ± 0.8, OT = 8.1 ± 0.8 mL·min·mm Hg), revealing a significant vasodilatory reserve capacity in the other groups (Y = 4.92 ± 1.18, OA = 1.37 ± 0.55, OT = 2.76 ± 0.95 mL·min·mm Hg). As PLM predominantly reflects NO-mediated vasodilation, these findings support the idea that augmenting physical activity and fitness can protect NO bioavailability, attenuating the deleterious effects of advancing age on vascular function.