Locomotor exercise induces long-lasting impairments in the capacity of the human motor cortex to voluntarily activate knee extensor muscles

Sidhu, S. K., Bentley, D. J. and Carroll, T. J. (2009) Locomotor exercise induces long-lasting impairments in the capacity of the human motor cortex to voluntarily activate knee extensor muscles. Journal of Applied Physiology, 106 2: 556-565. doi:10.1152/japplphysiol.90911.2008


Author Sidhu, S. K.
Bentley, D. J.
Carroll, T. J.
Title Locomotor exercise induces long-lasting impairments in the capacity of the human motor cortex to voluntarily activate knee extensor muscles
Journal name Journal of Applied Physiology   Check publisher's open access policy
ISSN 8750-7587
Publication date 2009-02-01
Year available 2008
Sub-type Article (original research)
DOI 10.1152/japplphysiol.90911.2008
Open Access Status DOI
Volume 106
Issue 2
Start page 556
End page 565
Total pages 10
Editor J. A. Dempsey
Place of publication Bethesda, U.S.
Publisher American Psysiological Society
Language eng
Subject C1
970117 Expanding Knowledge in Psychology and Cognitive Sciences
110603 Motor Control
170112 Sensory Processes, Perception and Performance
1106 Human Movement and Sports Science
Abstract Sidhu SK, Bentley DJ, Carroll TJ. Locomotor exercise induces long-lasting impairments in the capacity of the human motor cortex to voluntarily activate knee extensor muscles. J Appl Physiol 106: 556-565, 2009. First published December 4, 2008; doi: 10.1152/japplphysiol.90911.2008.-Muscle fatigue is a reduction in the capacity to exert force and may involve a "central" component originating in the brain and/or spinal cord. Here we examined whether supraspinal factors contribute to impaired central drive after locomotor endurance exercise. On 2 separate days, 10 moderately active individuals completed a locomotor cycling exercise session or a control session. Brief (2 s) and sustained (30 s) isometric knee extension contractions were completed before and after locomotor exercise consisting of eight, 5-min bouts of cycling at 80% of maximum workload. In the control session, subjects completed the isometric contractions in a rested state. Twitch responses to supra-maximal motor nerve stimulation and transcranial magnetic stimulation were obtained to assess peripheral force-generating capacity and voluntary activation. Maximum voluntary contraction (MVC) force during brief contractions decreased by 23 +/- 6.3% after cycling exercise and remained 12 +/- 2.8% below baseline 45 min later (F(1,9) > 15.5; P < 0.01). Resting twitch amplitudes declined by similar to 45% (F(1,9) = 28.3; P < 0.001). Cortical voluntary activation declined from 90.6 +/- 1.6% at baseline to 80.6 +/- 2.1% after exercise (F(1,9) = 28.0; P < 0.001) and remained significantly reduced relative to control 30- 45 min later (80.6 +/- 3.4%; F(1,9) = 10.7; P < 0.01). Thus locomotor exercise caused a long-lasting impairment in the capacity of the motor cortex to drive the knee extensors. Force was reduced more during sustained MVC after locomotor exercise than in the control session. Peripheral mechanisms contributed relatively more to this force reduction in the control session, whereas supraspinal fatigue played a greater role in sustained MVC reduction after locomotor exercise.
Formatted abstract
Muscle fatigue is a reduction in the capacity to exert force and may involve a "central" component originating in the brain and/or spinal cord. Here we examined whether supraspinal factors contribute to impaired central drive after locomotor endurance exercise. On 2 separate days, 10 moderately active individuals completed a locomotor cycling exercise session or a control session. Brief (2 s) and sustained (30 s) isometric knee extension contractions were completed before and after locomotor exercise consisting of eight, 5-min bouts of cycling at 80% of maximum workload. In the control session, subjects completed the isometric contractions in a rested state. Twitch responses to supramaximal motor nerve stimulation and transcranial magnetic stimulation were obtained to assess peripheral force-generating capacity and voluntary activation. Maximum voluntary contraction (MVC) force during brief contractions decreased by 23 ± 6.3% after cycling exercise and remained 12 ± 2.8% below baseline 45 min later (F1,9 > 15.5; P < 0.01). Resting twitch amplitudes declined by 45% (F1,9 = 28.3; P < 0.001). Cortical voluntary activation declined from 90.6 ± 1.6% at baseline to 80.6 ± 2.1% after exercise (F1,9 = 28.0; P < 0.001) and remained significantly reduced relative to control 30–45 min later (80.6 ± 3.4%; F1,9 = 10.7; P < 0.01). Thus locomotor exercise caused a long-lasting impairment in the capacity of the motor cortex to drive the knee extensors. Force was reduced more during sustained MVC after locomotor exercise than in the control session. Peripheral mechanisms contributed relatively more to this force reduction in the control session, whereas supraspinal fatigue played a greater role in sustained MVC reduction after locomotor exercise.
Keyword Central fatigue
Maximal voluntary contraction
Twitch interpolation
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ
Additional Notes First published online December 4, 2008.

 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 70 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 74 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Sun, 22 Mar 2009, 20:15:28 EST by Deborah Noon on behalf of School of Human Movement and Nutrition Sciences