De Havas, Jack;
Ito, Sho;
Gomi, Hiroaki;
(2020)
On Stopping Voluntary Muscle Relaxations and Contractions: Evidence for Shared Control Mechanisms and Muscle State-Specific Active Breaking.
The Journal of Neuroscience
, 40
(31)
pp. 6035-6048.
10.1523/jneurosci.0002-20.2020.
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On stopping voluntary muscle relaxations and contractions Evidence for shared control mechanisms and muscle state-specific active breaking.pdf - Published Version Download (3MB) | Preview |
Abstract
Control of the body requires inhibiting complex actions, involving contracting and relaxing muscles. However, little is known of how voluntary commands to relax a muscle are cancelled. Action inhibition causes both suppression of muscle activity and the transient excitation of antagonist muscles, the latter being termed active breaking. We hypothesized that active breaking is present when stopping muscle relaxations. Stop signal experiments were used to compare the mechanisms of active breaking for muscle relaxations and contractions in male and female human participants. In experiments 1 and 2, go signals were presented that required participants to contract or relax their biceps or triceps muscle. Infrequent Stop signals occurred after fixed delays (0–500 ms), requiring that participants cancelled go commands. In experiment 3, participants increased (contract) or decreased (relax) an existing isometric finger abduction depending on the go signal, and cancelled these force changes whenever Stop signals occurred (dynamically adjusted delay). We found that muscle relaxations were stopped rapidly, met predictions of existing race models, and had Stop signal reaction times that correlated with those observed during the stopping of muscle contractions, suggesting shared control mechanisms. However, stopped relaxations were preceded by transient increases in electromyography (EMG), while stopped contractions were preceded by decreases in EMG, suggesting a later divergence of control. Muscle state-specific active breaking occurred simultaneously across muscles, consistent with a central origin. Our results indicate that the later stages of action inhibition involve separate excitatory and inhibitory pathways, which act automatically to cancel complex body movements.
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