疲劳对去极化和咖啡因诱导的皮肤纤维挛缩的影响。
Effects of fatigue on depolarization- and caffeine-induced contractures of skinned fibres.
作者信息
Williams J H
机构信息
Muscular Function Laboratory, Department of Human Nutrition, Foods and Exercise, Virginia Polytechnic Institute and State University, Blacksburg, VA, USA.
出版信息
Acta Physiol Scand. 2004 Mar;180(3):265-9. doi: 10.1046/j.0001-6772.2003.01243.x.
AIMS
Fatigue has been shown to cause intrinsic alterations in sarcoplasmic reticulum (SR) Ca2+ release.
METHODS
In this investigation, frog semitendinosus muscles were stimulated to fatigue, in vitro (80 Hz, 100 ms, 1 train s-1, 5 min). Immediately after stimulation, single fibres were removed and skinned using either chemically or mechanically skinning. Contralateral muscle were treated similarly but were not stimulated.
RESULTS
In fatigued, saponin skinned fibres, contracture responses to low [caffeine] (4-8 mm) were depressed compared with control. However, responses to high concentrations (10-15 mm) were not different between conditions. In the fatigued, mechanically skinned fibres, responses to chloride depolarization were depressed at all [chloride] (20-100 mm) compared with control.
CONCLUSIONS
These results suggest that fatigue causes intrinsic alterations in both the SR Ca2+ release channel as well as communication between the transverse-tubule and the SR.
目的
疲劳已被证明会导致肌浆网（SR）钙释放的内在改变。
方法
在本研究中，对青蛙半腱肌进行体外疲劳刺激（80赫兹，100毫秒，每秒1次训练，5分钟）。刺激后立即取出单根肌纤维，采用化学或机械去膜方法进行去膜处理。对侧肌肉进行同样处理但不进行刺激。
结果
在疲劳的、经皂角苷去膜的肌纤维中，与对照组相比，对低浓度咖啡因（4 - 8毫摩尔）的挛缩反应受到抑制。然而，在不同条件下，对高浓度咖啡因（10 - 15毫摩尔）的反应并无差异。在疲劳的、经机械去膜的肌纤维中，与对照组相比，在所有氯化物浓度（20 - 100毫摩尔）下，对氯化物去极化的反应均受到抑制。
结论
这些结果表明，疲劳会导致肌浆网钙释放通道以及横管与肌浆网之间的通讯发生内在改变。
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