Key points : Passive limb movement elicits a robust increase in limb blood flow (LBF) and limb vascular conductance (LVC) without a concomitant increase in skeletal muscle metabolism. The peripheral vascular mechanisms associated with the increase in LBF and LVC are unknown. Using an intra‐arterial infusion of N^G‐monomethyl‐l‐arginine (l‐NMMA) to inhibit nitric oxide synthase (NOS) the hyperaemic and vasodilatory response to passive limb movement was attenuated by nearly 80%. This finding demonstrates that the increases in LBF and LVC during passive limb movement are primarily NO dependent. Passive limb movement appears to have significant promise as a new approach to assess NO‐mediated vascular function, an important predictor of cardiovascular disease risk.

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.

The purpose of this investigation was to partially remove feedback from type III/IV skeletal muscle afferents and determine how this feedback influences the central and peripheral hemodynamic responses to passive leg movement. Heart rate (HR), stroke volume (SV), cardiac output (CO), mean arterial pressure, leg vascular conductance (LVC), and leg blood flow (LBF) were measured during 2 min of passive knee extension in eight young men before and after intrathecal fentanyl injection. Passive movement increased HR by 14 beats/min from baseline to maximal response during control (CON) (65 ± 4 to 79 ± 5 beats/min, P < 0.05), whereas HR did not significantly increase with the fentanyl block (BLK). LBF and LVC increased in both conditions; however, these increases were attenuated and delayed during BLK [%change from baseline to maximum, LBF: CON 295 ± 109 vs. BLK 210 ± 86%, (P < 0.05); LVC: CON 322 ± 40% vs. BLK 231 ± 32%, (P < 0.04)]. In CON, HR, SV, CO, and LVC increased contributing to the hyperemic response. However, under BLK conditions, statistically insignificant increases in HR and SV combined to yield a small, but significant, increase in CO and an attenuated hyperemic response. Therefore, partially blocking skeletal muscle afferent feedback blunts the central hemodynamic response due to passive limb movement, which then results in an attenuated and delayed movement-induced hyperemia. In combination, these findings provide evidence that limb movement-induced hyperemia has a significant central hemodynamic component induced by peripheral nerve activation.

An exaggerated blood pressure (BP) response to exercise has been linked to cardiovascular disease, but little is known about the impact of age and sex on this response. Therefore, this study examined the hemodynamic and skeletal muscle metabolic response to dynamic plantar flexion exercise, at 40% of maximum plantar flexion work rate, in 40 physical activity-matched young (23 ± 1 yr, n = 20) and old (73 ± 2 yr, n = 20), equally distributed, male and female subjects. Central hemodynamics and BP (finometer), popliteal artery blood flow (Doppler ultrasound), and skeletal muscle metabolism (³¹P-magnetic resonance spectroscopy) were measured during 5 min of plantar flexion exercise. Popliteal artery blood flow and high-energy phosphate responses to exercise were not affected by age or sex, whereas aging, independent of sex, attenuated stroke volume and cardiac output responses. Systolic BP and mean arterial pressure responses were exaggerated in old women (Δ42 ± 4 and Δ28 ± 3 mmHg, respectively), with all other groups exhibiting similar increases in systolic BP (old men: Δ27 ± 8 mmHg, young men: Δ27 ± 3 mmHg, and young women: Δ22 ± 3 mmHg) and mean arterial pressure (old men: Δ15 ± 4 mmHg, young men: Δ19 ± 2 mmHg, and young women: Δ17 ± 2 mmHg). Interestingly, the exercise-induced change in systemic vascular resistance in old women (∆0.8 ± 1.0 mmHg·l⁻¹·min⁻¹) was augmented compared with young women and young and old men (∆−2.8 ± 0.5, ∆−1.6 ± 0.6, and ∆−3.18 ± 1.4 mmHg·l⁻¹·min⁻¹, respectively, P < 0.05). Thus, in combination, advancing age and female sex results in an exaggerated BP response to exercise, likely the result of a failure to reduce systemic vascular resistance. NEW & NOTEWORTHY An exaggerated blood pressure response to exercise has been linked to cardiovascular disease; however, little is known about how age and sex impact this response in healthy individuals. During dynamic exercise, older women exhibited an exaggerated blood pressure response driven by an inability to lower systemic vascular resistance.