ArticleAutonomic neuroscience : basic & clinical2022
Passive leg movement-induced vasodilation and exercise-induced sympathetic vasoconstriction.
Article in Autonomic neuroscience : basic & clinical, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Effects of ischemic conditioning on microvascular reactivity to single passive limb movement in young adults: a pilot study.European journal of applied physiology · 2025Trial
- Cold pressor-induced sympathetic activation blunts the femoral but not carotid artery vascular responsiveness.Physiological reports · 2025Trial
- The Acute Ingestion of Yerba Mate (Ilex paraguariensis) Infusion Does Not Modify Endothelial Function, Hemodynamics, or Heart Rate Variability: A Randomized Crossover Clinical Trial.Plant foods for human nutrition (Dordrecht, Netherlands) · 2024Trial
- Oxidative stress and impaired cardiovagal baroreflex sensitivity in young adults with post-traumatic stress disorder.Experimental physiology · 2026Article
- Acute sympathetic activation blunts the hyperemic and vasodilatory response to passive leg movement in young healthy males.Physiological reports · 2025Article
- The relationship between muscle sympathetic nerve activity and serum fatty acid binding protein 4 at rest and during isometric handgrip exercise.Physiological reports · 2024Article
- Acute sympathetic activation blunts the hyperemic and vasodilatory response to passive leg movement.Research square · 2024Article
- Pharmacological modulation of adrenergic tone alters the vasodilatory response to passive leg movement in young but not in old adults.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The role of nitric oxide (NO) as a modulator of functional sympatholysis has been debated in the literature, but the preponderance of evidence suggests that the magnitude of NO-mediated dilation is restrained by sympathetic vasoconstriction. Therefore, we hypothesized that passive leg movement (PLM)-induced vasodilation, which is predominantly NO-mediated, would be attenuated by an exercise-induced increase in muscle sympathetic nerve activity (MSNA). To test this hypothesis, MSNA, leg blood flow (LBF), and mean arterial blood pressure (MAP) were measured and leg vascular conductance (LVC) calculated in 9 healthy subjects (30 ± 3 yr), during PLM with and without sympathoexcitation evoked by arm-cranking exercise (ACE), at 25, 50, and 75% of maximal capacity. During this incremental intensity ACE, MSNA increased significantly (26 ± 2, 34 ± 3, and 41 ± 5 bursts/100 HB, respectively). LVC during PLM fell markedly (~1.2 ml/min/mmHg) with each increase in ACE intensity, and there was a strong relationship (r = 0.92; p < 0.05) between ∆MSNA and ∆Peak LVC induced by the three intensities of ACE. Thus, as anticipated, this study reveals that the, NO-mediated, PLM-induced vasodilation, is significantly and proportionally attenuated by exercise-induced MSNA. This finding highlights the dominant role of MSNA in regulating skeletal muscle vascular conductance.
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Registered trials
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