Literature DB >> 29771607

Mechanistic insights into the modulatory role of the mechanoreflex on central hemodynamics using passive leg movement in humans.

Nicholas T Kruse1,2, William E Hughes1, Darren P Casey1,2,3.   

Abstract

The aim of this study was to examine the independent contributions of joint range of motion (ROM), muscle fascicle length (MFL), and joint angular velocity on mechanoreceptor-mediated central cardiovascular dynamics using passive leg movement (PLM) in humans. Twelve healthy men (age: 23 ± 2 yr, body mass index: 23.7 kg/m2) performed continuous PLM at various randomized joint angle ROMs (0°-50° vs. 50°-100° vs. 0°-100°) and joint angular velocities ("fast": 200°/s vs. "slow": 100°/s). Measures of heart rate (HR), cardiac output (CO), and mean arterial pressure (MAP) were recorded during baseline and during 60 s of PLM. MFL was calculated from muscle architectural measurements of fascicle pennation angle and tissue thickness (Doppler ultrasound). Percent change in MFL increased across the transition of PLM from 0° to 50° (15 ± 3%; P < 0.05) and from 0° to 100° knee flexion (27 ± 4%; P < 0.05). The average peak percent change in HR (increased, approx. +5 ± 2%; P < 0.05), CO (increased, approx. +5 ± 3%; P < 0.05), and MAP (decreased, approx. -2 ± 2%; P < 0.05) were similar between fast versus slow angular velocities when compared against shorter absolute joint ROMs (i.e., 0°-50° and 50°-100°). However, the condition that exhibited the greatest angular velocity in combination with ROM (0°-100° at 200°/s) elicited the greatest increases in HR (+13 ± 2%; P < 0.05) and CO (+12 ± 2%; P < 0.05) compared with all conditions. Additionally, there was a significant relationship between MFL and HR within 0°-100° at 200°/s condition ( r2 = 0.59; P < 0.05). These findings suggest that increasing MFL and joint ROM in combination with increased angular velocity via PLM are important components that activate mechanoreflex-mediated cardioacceleration and increased CO. NEW &amp; NOTEWORTHY The mechanoreflex is an important autonomic feedback mechanism that serves to optimize skeletal muscle perfusion during exercise. The present study sought to explore the mechanistic contributions that initiate the mechanoreflex using passive leg movement (PLM). The novel findings show that progressively increasing joint angle range of motion and muscle fascicle length via PLM, in combination with increased angular velocity, are important components that activate mechanoreflex-mediated cardioacceleration and increase cardiac output in humans.

Entities:  

Keywords:  angular velocity; fascicle length; hemodynamics; mechanoreflex; passive leg movement

Mesh:

Year:  2018        PMID: 29771607      PMCID: PMC6139517          DOI: 10.1152/japplphysiol.01085.2017

Source DB:  PubMed          Journal:  J Appl Physiol (1985)        ISSN: 0161-7567


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