Acute aerobic exercise modulates primary motor cortex inhibition

Aerobic exercise can enhance neuroplasticity although presently the neural mechanisms underpinning these benefits remain unclear. One possible mechanism is through effects on primary motor cortex (M1) function via down-regulation of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). The...

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Bibliographic Details
Published in:Experimental brain research Vol. 234; no. 12; pp. 3669 - 3676
Main Authors: Mooney, Ronan A., Coxon, James P., Cirillo, John, Glenny, Helen, Gant, Nicholas, Byblow, Winston D.
Format: Journal Article
Language:English
Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.12.2016
Springer
Springer Nature B.V
Subjects:
Achievement tests
Adolescent
Adult
Adults
Aerobic exercise
Aerobic exercises
Aerobics
Biomedical and Life Sciences
Biomedicine
Brain
Brain research
Cortex
Disinhibition
Electromyography
Evoked Potentials, Motor - physiology
Evoked responses
Exercise
Exercise - physiology
Female
Function
Gamma-aminobutyric acid
Hand - innervation
Handedness
Heart rate
Humans
Inhibition (Neurophysiology)
Investigations
Male
Motor Cortex - physiology
Muscle, Skeletal - physiology
Neural Inhibition - physiology
Neurology
Neuroplasticity
Neurosciences
Physical fitness
Plasticity
Psychological research
Questionnaires
Research Article
Statistics, Nonparametric
Transcranial Magnetic Stimulation
Young Adult
New Zealand
Transcranial magnetic stimulation
Intracortical inhibition
Motor cortex
Aerobic exercise
ISSN:0014-4819, 1432-1106
Online Access:Get full text
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Summary:Aerobic exercise can enhance neuroplasticity although presently the neural mechanisms underpinning these benefits remain unclear. One possible mechanism is through effects on primary motor cortex (M1) function via down-regulation of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). The aim of the present study was to examine how corticomotor excitability (CME) and M1 intracortical inhibition are modulated in response to a single bout of moderate intensity aerobic exercise. Ten healthy right-handed adults were participants. Single- and paired-pulse transcranial magnetic stimulation was applied over left M1 to obtain motor-evoked potentials in the right flexor pollicis brevis . We examined CME, cortical silent period (SP) duration, short- and long-interval intracortical inhibition (SICI, LICI), and late cortical disinhibition (LCD), before and after acute aerobic exercise (exercise session) or an equivalent duration without exercise (control session). Aerobic exercise was performed on a cycle ergometer for 30 min at a workload equivalent to 60 % of maximal cardiorespiratory fitness (VO 2 peak; heart rate reserve = 75 ± 3 %, perceived exertion = 13.5 ± 0.7). LICI was reduced at 10 (52 ± 17 %, P  = 0.03) and 20 min (27 ± 8 %, P  = 0.03) post-exercise compared to baseline (13 ± 4 %). No significant changes in CME, SP duration, SICI or LCD were observed. The present study shows that GABA B -mediated intracortical inhibition may be down-regulated after acute aerobic exercise. The potential effects this may have on M1 plasticity remain to be determined.
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ISSN:0014-4819
1432-1106
DOI:10.1007/s00221-016-4767-5