Walker, Branton

We tested the hypothesis that aging would be associated with slowed vasodilator kinetics in contracting muscle in part due to a reduced nitric oxide (NO) bioavailability. Young (n=10; 24 ± 2 yr) and older (n=10; 67 ± 2 yr) adults performed rhythmic forearm exercise (4 min each) at 10, 20 and 30% of max during saline infusion (control) and NO synthase (NOS) inhibition. Brachial artery diameter and velocities were measured using Doppler ultrasound. Forearm vascular conductance (FVC) was calculated for each duty cycle (1s contraction/2s relaxation) from blood flow (ml/min) and blood pressure (mmHg) and fit with a monoexponential model. The main parameters derived from the model were the amplitude (Amp) of the FVC response and the number of duty cycles for FVC to change 63% of the steady‐state amplitude (τFVC). Under control conditions 1) the Amp of the response at 20 and 30% MVC was lower in older (240 ± 24 and 319 ± 33 ml/min/100mmHg) compared to young adults (338 ± 45 and 462 ± 52 ml/min/100mmHg; P < 0.05) and 2) τFVC was slower in older (10 ± 1, 13 ± 1 and 15 ± 1 duty cycles) compared to young (6 ± 1, 9 ± 1 and 11 ± 1 duty cycles) adults at all intensities ( P < 0.05). NOS inhibition blunted the Amp and slowed the τFVC in young, at all intensities (10 ± 2, 12 ± 1 and 16 ± 2 duty cycles; P < 0.05), whereas it did not change in older adults. Our data indicate that the vasodilator kinetics in exercising muscle are altered with aging likely due to blunted NO signaling. Grant Funding Source : Supported by NIH grants HL105467 (DPC), HL46493 (MJJ) and by CTSA UL1 TR000135