School of Biological Sciences, Georgia Institute of Technology, 555 14th Street NW, Atlanta, GA, 30332-0356, USA.
Activ Surgical, 840 Summer Street, Suite 108, Boston, MA, 02127, USA.
Exp Brain Res. 2019 Aug;237(8):1947-1958. doi: 10.1007/s00221-019-05563-6. Epub 2019 May 25.
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.
拮抗肌同时收缩（协同收缩）用于使关节僵硬，但其在血流动力学应激下（例如姿势改变、高重力和出血）的神经控制尚不清楚。由于脊髓和/或抑制性通路（例如，双突触 I 型抑制和 GABA 介导的皮质内抑制）的潜在调制，协同收缩期间皮质脊髓兴奋性可能会因压力感受器去负荷而改变。本研究的目的是了解压力感受器去负荷对人类协同收缩期间皮质脊髓兴奋性的影响。使用经颅磁刺激在两组健康年轻成年人中检查了腕屈肌的运动诱发电位和皮质静息期。所有受试者均进行腕屈肌等长收缩（屈曲）和腕屈肌与伸肌协同收缩（协同收缩）。还通过测量肌肉的外周神经未条件和条件电刺激的 H 反射反应比评估了脊髓双突触抑制。在其中一组中，通过施加下体负压来诱导压力感受器去负荷。压力感受器去负荷对皮质静息期或双突触抑制的 H 反射测量无明显影响。在压力感受器去负荷时，桡侧腕屈肌的运动诱发电位面积在协同收缩期间减小，但在屈曲期间没有减小。结果表明，压力感受器去负荷降低了拮抗肌协同收缩期间的皮质脊髓兴奋性，显然是通过影响皮质静息期或脊髓双突触抑制未探测到的神经通路。
