Noireaud J, Léoty C
Exp Neurol. 1985 Mar;87(3):495-502. doi: 10.1016/0014-4886(85)90179-7.
The strength of contractures, produced by 15 to 146 mM [K]0 (as L-glutamate), was measured in isolated small bundles of muscle fibers from the fast-twitch extensor digitorum longus and from the slow-twitch soleus of normal and dystrophic (C57 BL/6J dy2J/dy2J) mice. The analysis of the relation between the maximal amplitude of the contracture vs the membrane potential and the time constant of relaxation of the K-contractures has shown that dystrophy induced an attenuation of the differences between fast- and slow-twitch muscles. The repriming of K-contractures was more affected by changes in [Ca]0 in normal soleus than in normal extensor digitorum longus and this difference was unaffected by dystrophy. For both types of muscles, the ability of caffeine to produce contractures was reduced in dystrophic muscle and this modification was not related to a change in the fiber typing.
在正常小鼠和营养不良(C57 BL/6J dy2J/dy2J)小鼠的快肌趾长伸肌和慢肌比目鱼肌中,分离出小束肌纤维,测量由15至146 mM [K]0(以L-谷氨酸盐形式)产生的挛缩强度。对挛缩最大幅度与膜电位以及K-挛缩松弛时间常数之间关系的分析表明,营养不良导致快肌和慢肌之间的差异减弱。与正常趾长伸肌相比,正常比目鱼肌中K-挛缩的再激发受[Ca]0变化的影响更大,且这种差异不受营养不良的影响。对于这两种类型的肌肉,咖啡因在营养不良肌肉中产生挛缩的能力降低,且这种改变与纤维类型的变化无关。