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Vasodilation and Hyperemia during Passive Limb Movement: Impact of Acute Sympathetic Activation
Author(s) -
Trinity Joel Douglas,
Lee Joshua F,
Garten Ryan S,
O'Keefe Zachary Barrett,
Layec Gwenael,
Wray David Walter,
Richardson Russell S
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.752.5
Subject(s) - microneurography , medicine , vasodilation , isometric exercise , cardiology , hemodynamics , anesthesia , heart rate , blood pressure , baroreflex
Heightened muscle sympathetic nerve activity (MSNA) is associated with impaired vasodilatory capacity and vascular dysfunction linked to aging and cardiovascular disease. The contribution of elevated MSNA to the vasodilatory response during continuous passive limb movement (PLM), a novel method to assess vascular function, has not been determined. This study sought to test the hypothesis that elevated MSNA will negatively impact the vasodilatory response to PLM in healthy young men (n=11, 25±2 yr). Post exercise circulatory occlusion (PECO) following 2 min of isometric handgrip (HG) exercise performed at 25% (PECO‐25%) and 40% (PECO‐40%) of maximum voluntary contraction (MVC) was utilized to incrementally engage the metaboreceptors and augment MSNA. Control (CON‐25% and CON‐40%) trials, without PECO, were performed to account for changes due to HG exercise. PLM was performed 2 min after the cessation of exercise and central (photoplethysmography) and peripheral hemodynamics (Doppler ultrasound) were assessed. MSNA was directly recorded by microneurography (n=8). MSNA was incrementally augmented during PECO‐25% (+ 8±3 burst/min) and PECO‐40% (+ 15±4 burst/min) and returned to pre‐HG levels during CON trials. Vasodilation, assessed by the overall change in leg vascular conductance (LVC) during PLM, was reduced following HG exercise in all conditions (Δ in peak LVC range; −15 to −41%). The peak change in LVC was not different between CON‐25% (7.2±1 ml/min/mmHg) and PECO‐25% (8.1±1.4 ml/min/mmHg, p <0.05) while the peak change in LVC during PECO‐40% (5.4±1.1 ml/min/mmHg) was significantly attenuated compared to PECO‐25% (p < 0.05). These findings indicate that alterations in MSNA can modify the vasodilatory response to PLM and that the magnitude of reduction in vasodilation during PLM appears to be graded in relation to the elevation in MSNA. In conclusion, elevations in MSNA that are typically exhibited with aging a cardiovascular disease, impact the vasodilatory response to PLM. Thus, basal sympathetic tone is important to consider when comparing vasodilatory capacity across heterogeneous groups. Support or Funding Information AHA SDG (1850039), VA RR&D CDA2 (1215)