Format

Send to

Choose Destination
Exp Brain Res. 2016 Dec;234(12):3669-3676. Epub 2016 Sep 2.

Acute aerobic exercise modulates primary motor cortex inhibition.

Author information

1
Movement Neuroscience Laboratory, The University of Auckland, Auckland, New Zealand.
2
Centre for Brain Research, The University of Auckland, Auckland, New Zealand.
3
School of Psychological Sciences and Monash Institute of Cognitive and Clinical Neurosciences, Monash University, Melbourne, VIC, Australia.
4
Exercise Neurometabolism Laboratory, Department of Exercise Sciences, The University of Auckland, Auckland, New Zealand.
5
Movement Neuroscience Laboratory, The University of Auckland, Auckland, New Zealand. w.byblow@auckland.ac.nz.
6
Centre for Brain Research, The University of Auckland, Auckland, New Zealand. w.byblow@auckland.ac.nz.

Abstract

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 (VO2 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 GABAB-mediated intracortical inhibition may be down-regulated after acute aerobic exercise. The potential effects this may have on M1 plasticity remain to be determined.

KEYWORDS:

Aerobic exercise; Intracortical inhibition; Motor cortex; Transcranial magnetic stimulation

PMID:
27590480
DOI:
10.1007/s00221-016-4767-5
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center