Asymmetrical modulation of corticospinal excitability in the contracting and resting contralateral wrist flexors during unilateral shortening, lengthening and isometric contractions
- PMID: 20730420
- DOI: 10.1007/s00221-010-2397-x
Asymmetrical modulation of corticospinal excitability in the contracting and resting contralateral wrist flexors during unilateral shortening, lengthening and isometric contractions
Abstract
Unilateral isometric muscle contractions increase motor-evoked potentials (MEPs) produced by transcranial magnetic stimulation not only in the contracting muscle but also in the resting contralateral homologous muscle. Corticospinal excitability in the M1 contralateral to the contracting muscle changes depending on the type of muscle contraction. Here, we investigated the possibility that corticospinal excitability in M1 ipsilateral to the contracting muscle is modulated in a contraction-type-dependent manner. To this end, we evaluated MEPs in the resting left flexor carpi radialis (FCR) during unilateral shortening, lengthening, and isometric muscle contractions of the right wrist flexors at 10, 20, and 30% of maximal isometric contraction force. To compare the effects of different unilateral contractions on MEPs between the contracting and resting sides, MEPs in the right FCR were recorded on two separate days. In a separate experiment, we investigated the contraction specificity of the crossed effect at the spinal level by recording H-reflexes from the resting left FCR during contraction of the right wrist flexors. The results showed that MEPs in the contracting right FCR were the smallest during lengthening contraction. By contrast, MEPs in the resting left FCR were the largest during lengthening contraction, whereas the H-reflex was similar in the resting left FCR during the three types of muscle contraction. These results suggest that different types of unilateral muscle contraction asymmetrically modulate MEP size in the resting contralateral homologous muscle and in the contracting muscle and that this regulation occurs at the supraspinal level.
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