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Permanent link (DOI): https://doi.org/10.7939/R3GH9BP78

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Decreases in the excitability of motor axons contribute substantially to contraction fatigability during neuromuscular electrical stimulation Open Access

Descriptions

Other title
Subject/Keyword
contraction fatigability
threshold tracking
neuromuscular electrical stimulation
Type of item
Thesis
Degree grantor
University of Alberta
Author or creator
Luu, Minh J
Supervisor and department
Collins, David (Physical Education and Recreation, Neuroscience)
Jones, Kelvin (Physical Education and Recreation, Neuroscience)
Examining committee member and department
Chan, Ming (Department of Medicine)
Ali, Declan (Department of Physiology)
Department
Neuroscience
Physical Education and Recreation
Specialization

Date accepted
2017-09-12T16:10:31Z
Graduation date
2017-11:Fall 2017
Degree
Master of Science
Degree level
Master's
Abstract
Activity-dependent changes in axonal excitability are well-documented, yet the contribution to contraction fatigability during neuromuscular electrical stimulation (NMES) is unclear. The present study was designed to: 1) characterize the magnitude and time course of changes in motor axon excitability before, during and after contractions produced at three stimulation frequencies, and 2) determine the relationship between changes at the axon, neuromuscular junction and muscle to the decline in torque observed at each frequency. Eight neurologically-intact participants attended three sessions during which NMES was delivered to the common peroneal nerve at 20, 40, or 60 Hz for 8 min (0.3 s “on”, 0.7 s “off”). Decreases in axonal excitability were measured as increases in current needed to produce an M-wave of 30% maximal (threshold current). Supramaximal stimuli were delivered over the nerve trunk or muscle belly to assess neuromuscular transmission and the force-generating capacity of the muscle, respectively. Torque decreased by 51 and 64% during 40 and 60 Hz NMES, respectively, but did not decrease significantly during 20 Hz NMES. The current required to produce the target M-wave increased 14, 27, and 35% during, and returned to baseline 1, 3, and 5 min following, 20, 40 and 60 Hz NMES, respectively. There was no other evidence of impaired neuromuscular transmission. Reduction in the force-generating capacity of the muscle was evident at 40 and 60 Hz NMES. Regression analysis showed decreases in torque were best predicted by decreases in axonal excitability overall, but were equally dependent on changes in the axon and muscle at each frequency. The present study demonstrates that activity-dependent decreases in axonal excitability contributes substantially to contraction fatigability during NMES.
Language
English
DOI
doi:10.7939/R3GH9BP78
Rights
This thesis is made available by the University of Alberta Libraries with permission of the copyright owner solely for the purpose of private, scholarly or scientific research. This thesis, or any portion thereof, may not otherwise be copied or reproduced without the written consent of the copyright owner, except to the extent permitted by Canadian copyright law.
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