Abstract
IntroductionThis study aimed to clarify cortical circuit mechanisms contributing to corticomotor excitability during postexercise depression (PED) following repetitive nonfatiguing movement. We investigated changes in short‐latency afferent inhibition (SAI) and short‐interval intracortical inhibition (SICI) by paired‐pulse transcranial magnetic stimulation (TMS) during PED.MethodsA total of 16 healthy subjects performed repetitive abduction movements of the right index finger at 2.0 Hz for 6 min at 10% maximum voluntary contraction. We measured SAI evoked by pairing ulnar nerve stimulation with TMS (interstimulus interval, 22 ms) before and during PED (n = 10, experiment 1). We also measured SICI evoked by paired TMS (interstimulus interval, 2 ms) at 80% resting motor threshold (n = 10, experiment 2), and at 80% active motor threshold (n = 8, experiment 3) before and during PED.ResultsSingle motor evoked potential amplitude significantly decreased 1–2 min after the movement task in all experiments, indicating reliable PED induction. In experiment 1, SAI significantly decreased (disinhibited) 1–2 min during PED, whereas in experiments 2 and 3, SICI showed no significant change during PED.ConclusionThis study suggests that cholinergic inhibitory circuit activity decreases during PED following repetitive nonfatiguing movement, whereas GABAA circuit activity remains stable.
Highlights
| INTRODUCTIONCorticomotor excitability changes after voluntary muscle contraction. The excitability of the primary motor cortex (M1) decreases after exhaustive exercise, causing muscle fatigue
This study aimed to clarify cortical circuit mechanisms contributing to corticomotor excitability during postexercise depression (PED) following repetitive nonfatiguing movement
In experiment 1, short-latency afferent inhibition (SAI) was measured during PED, whereas in experiments 2 and 3, short-interval intracortical inhibition (SICI) was measured during PED using condition stimuli of 80% resting motor threshold (RMT) and 80% active motor threshold (AMT), respectively
Summary
Corticomotor excitability changes after voluntary muscle contraction. The excitability of the primary motor cortex (M1) decreases after exhaustive exercise, causing muscle fatigue. MEP amplitude decreases when a subthreshold conditioning stimulus is applied to the motor cortex a few milliseconds before a suprathreshold test stimulus, known as short-interval intracortical inhibition (SICI) This inhibition depends on GABAA receptor-mediated cortical inhibition; SICI is used as an index of local GABAA circuit activity in the cortex (Kujirai et al, 1993; Ziemann, Rothwell, & Ridding, 1996). Another study suggested that cholinergic circuits in the cortex are associated with the PED after a nonfatiguing repetitive motor task (Bonato et al, 2002) Based on these reports, we speculated that SAI decreased during PED following a nonfatiguing repetitive motor task. This study suggests that distinct contributions of cortical GABAergic and cholinergic inhibitory circuits to motor cortex excitability changes following a nonfatiguing movement task
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