Indexed on: 01 Apr '16Published on: 01 Apr '16Published in: Medicine and science in sports and exercise
Due to reduced nitric oxide (NO) bioavailability with age, passive leg movement (PLM)-induced vasodilation is attenuated in older sedentary subjects and, unlike the young, 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 yrs, n = 12); old sedentary (OS, 73±2 yrs, n = 12); old active (OA, 71±2 yrs, n = 10); old endurance trained (OT, 72±1 yrs, n = 10)) in the supine and upright-seated posture. Hemodynamics were measured utilizing ultrasound Doppler and finger photoplethysmography.In the supine posture, PLM-induced peak change in leg vascular conductance (ΔLVCpeak) was significantly attenuated in the OS compared to the young (OS: 4.9±0.5, Y: 6.9±0.7 ml/min/mmHg), but was not different from the young in the OA and OT (OA: 5.9±1.0, OT: 5.4±0.4 ml/min/mmHg). The upright-seated posture significantly augmented ΔLVCpeak 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/mmHg), 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/mmHg).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.