Petersen N, Morita H, Nielsen J
Department of Medical Physiology, Panum Institute, University of Copenhagen, Denmark.
J Neurosci Methods. 1998 Oct 1;84(1-2):1-8. doi: 10.1016/s0165-0270(98)00044-2.
Changes in reciprocal inhibition from ankle dorsiflexors to ankle plantar flexors were evaluated at increasing levels of tonic plantar flexion in 11 healthy subjects. Stimulation of the common peroneal nerve (CPN) evoked a short-latency depression of the rectified and averaged soleus electromyogram (average latency of depression: 40 ms) and a short-latency inhibition of the soleus H-reflex (conditioning-test interval: 2-3 ms). When the intensity of the CPN stimulation was below approximately 1.2 x motor threshold (x MT) the inhibition of both the soleus EMG (expressed as the amount of EMG during the inhibition as percentage of the background EMG) and the soleus H-reflex (expressed as the size of the conditioned reflex as percentage of the control H-reflex size) were seen to decrease with increasing levels of plantar flexion. At intensities of stimulation higher than approximately 1.2 x MT the inhibition of the EMG and the H-reflex was very strong and was not modulated with contraction. It is suggested that the decrease of reciprocal inhibition with increasing levels of plantar flexion is due to a decreased excitability of the Ia inhibitory interneurones which are responsible for the inhibition. It is emphasized that submaximal stimulation is necessary to demonstrate this modulation of inhibition and that the functional contribution of reciprocal inhibition to motor performance cannot be revealed from the amount of inhibition evoked by artificial electrical stimulation of a peripheral nerve.
在11名健康受试者中，随着跖屈张力水平的升高，评估了从踝背屈肌到踝跖屈肌的交互抑制变化。刺激腓总神经（CPN）可引起比目鱼肌整流平均肌电图的短潜伏期抑制（抑制的平均潜伏期：40毫秒）和比目鱼肌H反射的短潜伏期抑制（条件刺激-测试间隔：2-3毫秒）。当CPN刺激强度低于约1.2倍运动阈值（x MT）时，随着跖屈水平的升高，比目鱼肌肌电图的抑制（表示为抑制期间肌电图量占背景肌电图的百分比）和比目鱼肌H反射的抑制（表示为条件反射大小占对照H反射大小的百分比）均降低。当刺激强度高于约1.2 x MT时，肌电图和H反射的抑制非常强烈，且不受收缩调节。提示随着跖屈水平升高，交互抑制降低是由于负责抑制的Ia抑制性中间神经元兴奋性降低所致。需要强调的是，必须进行次最大刺激才能证明这种抑制调节，并且从外周神经人工电刺激诱发的抑制量无法揭示交互抑制对运动表现的功能贡献。
