4.2 Article

Corticospinal excitability for flexor carpi radialis decreases with baroreceptor unloading during intentional co-contraction with opposing forearm muscles

期刊

EXPERIMENTAL BRAIN RESEARCH
卷 237, 期 8, 页码 1947-1958

出版社

SPRINGER
DOI: 10.1007/s00221-019-05563-6

关键词

Transcranial magnetic stimulation; Motor cortex; Orthostatic stress; Baroreflex

资金

  1. National Institute of Neurological Disorders and Stroke [1R03NS106088-01A1] Funding Source: Medline

向作者/读者索取更多资源

Concurrent activation of antagonistic muscles (co-contraction) is used for stiffening a joint, whereas its neural control under hemodynamic stress (e.g., posture change, high gravity, and hemorrhage) is unknown. Corticospinal excitability during co-contraction may be altered with baroreceptor unloading due to potential modulations in spinal and/or inhibitory pathways (e.g., disynaptic group I inhibition and GABA-mediated intracortical inhibition). The purpose of this study was to understand the effect of baroreceptor unloading on corticospinal excitability during co-contraction in humans. Motor evoked potential and cortical silent period in a wrist flexor muscle were examined using transcranial magnetic stimulation in two groups of healthy young adults. All subjects performed isometric contraction of the wrist flexors (flexion) and co-contraction of the wrist flexors and extensors (co-contraction). Spinal disynaptic inhibition was also assessed with the ratio of H-reflex responses to unconditioned and conditioned electrical stimulations of the peripheral nerves for the muscles. In one of the groups, baroreflex unloading was induced by applying lower body negative pressure. There was no significant effect of baroreflex unloading on cortical silent period or H-reflex measure of disynaptic inhibition. With baroreflex unloading, motor evoked potential area in the flexor carpi radialis was decreased during co-contraction but not during flexion. The results indicated that baroreceptor unloading decreases corticospinal excitability during co-contraction of antagonistic muscles, apparently by influencing neural pathways that were not probed with cortical silent period or spinal disynaptic inhibition.

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