Passive leg movement and nitric oxide-mediated vascular function: the impact of age

• Published in: American Journal of Physiology: Cell Physiology Vol. 308; no. 6; pp. H672 - H679
• Main Authors: Trinity, Joel D., Groot, H. Jonathan, Layec, Gwenael, Rossman, Matthew J., Ives, Stephen J., Morgan, David E., Gmelch, Ben S., Bledsoe, Amber, Richardson, Russell S.
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 15.03.2015
• Subjects: Adult; Age; Age Factors; Aged; Arterial Pressure; Blood Flow Velocity; Cardiovascular system; Enzyme Inhibitors - administration & dosage; Femoral Artery - diagnostic imaging; Femoral Artery - metabolism; Heart Rate; Humans; Impact analysis; Infusions, Intra-Arterial; Integrative Cardiovascular Physiology and Pathophysiology; Legs; Lower Extremity; Male; Movement; Muscle Contraction; Muscle, Skeletal - blood supply; Muscle, Skeletal - metabolism; Nitric oxide; Nitric Oxide - metabolism; Nitric Oxide Synthase - antagonists & inhibitors; Nitric Oxide Synthase - metabolism; omega-N-Methylarginine - administration & dosage; Regional Blood Flow; Stroke Volume; Ultrasonography; Vasodilation - drug effects; Young Adult; endothelial function; nitric oxide; flow-mediated dilation; leg blood flow; aging
• ISSN: 0363-6135; 1522-1539; 0363-6143; 1522-1539
• DOI: 10.1152/ajpheart.00806.2014

In young healthy men, passive leg movement (PLM) elicits a robust nitric oxide (NO)-dependent increase in leg blood flow (LBF), thus providing a novel approach to assess NO-mediated vascular function. While the magnitude of the LBF response to PLM is markedly reduced with age, the role of NO in this attenuated response in the elderly is unknown. Therefore, this study sought to determine the contribution of NO in the PLM-induced LBF with age. Fourteen male subjects (7 young, 24 ± 1 yr; and 7 old, 75 ± 3 yr) underwent PLM with and without NO synthase (NOS) inhibition achieved by intra-arterial infusion of N G -monomethyl-l-arginine (l-NMMA). LBF was determined second-by-second by Doppler ultrasound, and central hemodynamics were measured by finger photoplethysmography. NOS inhibition blunted the PLM-induced peak increase in LBF in the young (control: 668 ± 106; l-NMMA: 431 ± 95 Δml/min; P = 0.03) but had no effect in the old (control: 266 ± 98; l-NMMA: 251 ± 92 Δml/min; P = 0.59). Likewise, the magnitude of the reduction in the overall (i.e., area under the curve) PLM-induced LBF response to NOS inhibition was less in the old (LBF: −31 ± 18 ml) than the young (LBF: −129 ± 21 ml; P < 0.01). These findings suggest that the age-associated reduction in PLM-induced LBF in the elderly is primarily due to a reduced contribution to vasodilation from NO and therefore support the use of PLM as a novel approach to assess NO-mediated vascular function across the lifespan.