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Exp Brain Res. 2012 Sep;221(3):299-308. doi: 10.1007/s00221-012-3173-x. Epub 2012 Jul 13.

Contribution of intracortical inhibition in voluntary muscle relaxation.

Author information

1
Industrial and Manufacturing Engineering, University of Wisconsin-Milwaukee, 3200 N Cramer St., Milwaukee, WI 53211, USA. bmotawar@uwm.edu

Abstract

Terminating a voluntary muscle contraction is an important aspect of motor control, and yet, its neurophysiology is unclear. The objective of this study was to determine the role of short-interval intracortical inhibition (SICI) by comparing SICIs during relaxation from a power grip versus during a sustained power grip at the matching muscle activity level. Right-handed healthy young adults gripped and relaxed from power grip following auditory cues. The relaxation period was determined as the time for the flexor digitorum superficialis (FDS) muscle to reach its pre-contraction baseline level after the cue to relax. SICI during relaxation was obtained at different times into the relaxation period in two separate studies (70, 80, 90 % into relaxation in Study 1; 25, 50, 75 % into relaxation in Study 2). In addition, SICI during sustained contraction was assessed while subjects maintained a power grip at the matching FDS EMG levels (obtained during relaxation, for both Studies). Results showed that the mean SICI was greater during relaxation than during sustained contraction at the matching muscle activity level in both Studies (p < 0.05), indicating increased activation of intracortical inhibitory circuits for muscle relaxation. SICI gradually increased from 25 to 50 and 75 % into relaxation (Study 2, p < 0.05), but did not change from 70 to 80 and 90 % into relaxation (Study 1). MEP decreased with progression of relaxation (p < 0.05) in both Studies, reflecting gradual decreases in corticomotor excitability. This work supports the hypothesis that relaxation from a voluntary muscle contraction involves inhibitory activity in the primary motor cortex.

PMID:
22791231
DOI:
10.1007/s00221-012-3173-x
[Indexed for MEDLINE]

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