Khan Serajul I, Burne John A
School of Biomedical Sciences, University of Sydney, PO Box 170, Lidcombe, NSW 1825, Australia.
J Neurophysiol. 2007 Sep;98(3):1102-7. doi: 10.1152/jn.00371.2007. Epub 2007 Jul 18.
Muscle cramp was induced in one head of the gastrocnemius muscle (GA) in eight of thirteen subjects using maximum voluntary contraction when the muscle was in the shortened position. Cramp in GA was painful, involuntary, and localized. Induction of cramp was indicated by the presence of electromyographic (EMG) activity in one head of GA while the other head remained silent. In all cramping subjects, reflex inhibition of cramp electrical activity was observed following Achilles tendon electrical stimulation and they all reported subjective relief of cramp. Thus muscle cramp can be inhibited by stimulation of tendon afferents in the cramped muscle. When the inhibition of cramp-generated EMG and voluntary EMG was compared at similar mean EMG levels, the area and timing of the two phases of inhibition (I(1), I(2)) did not differ significantly. This strongly suggests that the same reflex pathway was the source of the inhibition in both cases. Thus the cramp-generated EMG is also likely to be driven by spinal synaptic input to the motorneurons. We have found that the muscle conditions that appear necessary to facilitate cramp, a near to maximal contraction of the shortened muscle, are also the conditions that render the inhibition generated by tendon afferents ineffective. When the strength of tendon inhibition in cramping subjects was compared with that in subjects that failed to cramp, it was found to be significantly weaker under the same experimental conditions. It is likely that reduced inhibitory feedback from tendon afferents has an important role in generating cramp.
在13名受试者中的8名中,当腓肠肌处于缩短位置时,通过最大自主收缩在腓肠肌(GA)的一个头诱发肌肉痉挛。GA中的痉挛是疼痛的、不自主的且局限的。GA一个头中存在肌电图(EMG)活动而另一个头保持静息表明痉挛被诱发。在所有发生痉挛的受试者中,跟腱电刺激后观察到痉挛电活动的反射性抑制,并且他们都报告痉挛主观缓解。因此,肌肉痉挛可通过刺激痉挛肌肉中的腱传入纤维来抑制。当在相似的平均EMG水平下比较痉挛产生的EMG和自主EMG的抑制情况时,两个抑制阶段(I(1),I(2))的面积和时间没有显著差异。这强烈表明相同的反射通路是两种情况下抑制的来源。因此,痉挛产生的EMG也可能由运动神经元的脊髓突触输入驱动。我们发现,促进痉挛所需的肌肉状态,即缩短肌肉的近最大收缩,也是使腱传入纤维产生的抑制无效的状态。当比较痉挛受试者与未发生痉挛受试者的腱抑制强度时,发现在相同实验条件下前者明显较弱。腱传入纤维的抑制性反馈减少可能在产生痉挛中起重要作用。