ROLE OF SMALL DIAMETER AFFERENTS IN REFLEX INHIBITION DURING HUMAN MUSCLE FATIGUE
ROLE OF SMALL DIAMETER AFFERENTS IN REFLEX INHIBITION DURING HUMAN MUSCLE FATIGUE
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DOI：
10.1113/jphysiol.1991.sp018524
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发表时间：
1991-04-01
影响因子：
5.5
通讯作者：
GARLAND, SJ
中科院分区：
文献类型：
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作者：
GARLAND, SJ
1.前人的研究表明，人比目鱼肌运动神经元的H反射兴奋性在疲劳时降低，在最大自主收缩时伴随着相应的肌电活动的降低。这些发现与反射的存在相一致，在这种反射中，阿尔法运动神经元受到疲劳肌肉的感觉输入的抑制。为了阐明不同大小的传入神经在这种反射抑制中的作用，我们采用压迫坐骨神经的方法，试图在疲劳前阻断大的有髓传入神经。对10名健康受试者进行15赫兹间歇性电刺激，在缺血条件下诱发比目鱼肌疲劳。这些受试者还参加了一项对照测试，在该测试中，压迫阻断后会出现无疲劳的缺血。仅在神经压迫后，所有10名受试者的平均最大趾屈扭矩和相关的肌电都下降了18.8+/-16.2%(S.D.)分别为13.4+/-17.2%。在疲劳后，有5个受试者的大传入仍然被阻断，实验结果与疲劳过程中存在反射抑制是一致的。平均最大屈曲扭矩较压迫后进一步下降36.2+/-7.6%，而缺血组下降5.0+/-9.9%。与这些收缩相关的平均肌电也从阻断后的值在疲劳后下降了56.8+/-19.6%，仅在缺血后仅下降了6.4+/-8.0%。疲劳后，神经肌肉接头和肌肉纤维膜的外周兴奋性是足够的，这从M波(肌肉复合动作电位)的轻微变化中可见一斑。下降的运动动力被认为是足够的，因为除了两个受试者之外，所有受试者都没有任何叠加在最大自愿收缩上的大的插入式抽动。最大趾屈扭矩和相关肌电活动的下降与之前的一项研究中发现的非常相似，在该研究中，感觉输入没有改变。结果表明，疲劳时α-运动神经元池的任何反射抑制可能不是由大直径传入所介导的。更确切地说，这一反射是由来自疲劳肌肉的较小直径的传入神经所调节的。
1. Previous work has shown that the H reflex excitability of the human soleus motoneurones is reduced during fatigue and is accompanied by a corresponding decrease in electromyographic (EMG) activity during maximal voluntary contractions. These findings were consistent with the existence of a reflex whereby alpha-motoneurones are inhibited by sensory input from the fatigued muscle.2. To elucidate the contribution of different-sized afferents in such reflex inhibition, compression of the sciatic nerve was used in an attempt to block large myelinated afferents prior to fatigue.3. Fatigue of the soleus muscle was induced under ischaemic conditions by intermittent electrical stimulation at 15 Hz in ten healthy subjects. These subjects also participated in a control test in which the compression block was followed by ischaemia without fatigue.4. Following nerve compression alone, both the mean maximal plantarflexion torque and the associated EMG for all ten subjects declined by 18.8 +/- 16.2% (S.D.) and 13.4 +/- 17.2%, respectively.5. Following fatigue, there were five subjects in whom the large afferents remained blocked and the experimental findings were consistent with the existence of reflex inhibition during fatigue. The mean maximal plantarflexion torque decreased further by 36.2 +/- 7.6% from the value following the compression block compared to a decrease of 5.0 +/- 9.9% in the ischaemia control. The mean EMG associated with these contractions also decreased from post-block values by 56.8 +/- 19.6% following fatigue and by only 6.4 +/- 8.0% following ischaemia alone.6. The peripheral excitability of the neuromuscular junction and muscle fibre membrane was adequate following fatigue as evidenced by only modest changes in the M wave (muscle compound action potential). The descending motor drive was deemed sufficient because of the absence of any large interpolated twitches superimposed upon the maximal voluntary contraction in all but two subjects.7. The declines in maximal plantarflexion torque and the associated EMG activity were very similar to those found in a previous study in which the sensory input was unaltered. The findings demonstrated that any reflex inhibition of the alpha-motoneurone pool during fatigue was probably not mediated by large diameter afferents. Rather, it is suggested that the reflex is mediated by smaller diameter afferents originating from the fatigued muscle.