van der Poel Chris, Stephenson D George
Department of Zoology, La Trobe University, Bundoora, Victoria 3086, Australia.
J Physiol. 2002 Nov 1;544(3):765-76. doi: 10.1113/jphysiol.2002.024968.
Exposure of relaxed rat extensor digitorum longus (EDL; predominantly fast-twitch) muscle to temperatures in the upper physiological range for mammalian skeletal muscle (43-46 degrees C) led to reversible alterations of the contractile activation properties. These properties were studied using the mechanically skinned fibre preparation activated in Ca(2+)-buffered solutions. The maximum Ca(2+)-activated force (maximum force per cross-sectional area) and the steepness of force-pCa (-log(10)[Ca(2+)]) curves as measured by the Hill coefficient (n(H)) reversibly decreased by factors of 8 and 2.5, respectively, when the EDL muscle was treated at 43 degrees C for 30 min and 5 and 2.8, respectively, with treatment at 46 degrees C for 5 min. Treatment at 47 degrees C for 5 min produced an even more marked depression in maximum specific force, which fully recovered after treatment, and in the Hill coefficient, which did not recover after treatment. After all temperature treatments there was no change in the level of [Ca(2+)] at which 50 % maximum force was generated. The temperature-induced depression in force production and steepness of the force-pCa curves were shown to be associated with superoxide (O(2)(-)) production in muscle (apparent rate of O(2)(-) production at room temperature, 0.055 +/- 0.008 nmol min(-1) (g wet weight)(-1); and following treatment to 46 degrees C for 5 min, 1.8 +/- 0.2 nmol min(-1) (g wet weight)(-1)) because 20 mM Tiron, a membrane-permeant O(2)(-) scavenger, was able to markedly suppress the net rate of O(2)(-) production and prevent any temperature-induced depression of contractile parameters. The temperature-induced depression in force production of the contractile apparatus could be reversed either by allowing the intact muscle to recover for 3-4 h at room temperature or by treatment of the skinned fibre preparation with dithiothreitol (a potent reducing agent) in the relaxing solution. These results demonstrate that mammalian skeletal muscle has the ability to uncouple force production reversibly from the activator Ca(2+) as the temperature increases in the upper physiological range through an increase in O(2)(-) production.
将松弛的大鼠趾长伸肌（EDL；主要为快肌纤维）暴露于哺乳动物骨骼肌的生理温度上限范围（43 - 46摄氏度）会导致收缩激活特性发生可逆性改变。使用在Ca(2+)缓冲溶液中激活的机械去膜纤维制备物对这些特性进行了研究。当EDL肌肉在43摄氏度下处理30分钟时，最大Ca(2+)激活力（每横截面积的最大力）和通过希尔系数（n(H)）测量的力 - pCa（-log(10)[Ca(2+)]）曲线的斜率分别可逆性降低8倍和2.5倍；在46摄氏度下处理5分钟时，分别降低5倍和2.8倍。在47摄氏度下处理5分钟会使最大比力出现更明显的降低，处理后最大比力完全恢复，但希尔系数处理后未恢复。在所有温度处理后，产生50%最大力时的[Ca(2+)]水平没有变化。温度诱导的力产生降低和力 - pCa曲线斜率降低与肌肉中超氧阴离子（O(2)(-)）的产生有关（室温下O(2)(-)产生的表观速率为0.055 ± 0.008 nmol min(-1) (g湿重)(-1)；在46摄氏度下处理5分钟后，为1.8 ± 0.2 nmol min(-1) (g湿重)(-1)），因为20 mM替诺，一种可透过膜的O(2)(-)清除剂，能够显著抑制O(2)(-)的净产生速率，并防止任何温度诱导的收缩参数降低。通过让完整肌肉在室温下恢复3 - 4小时或在松弛溶液中用二硫苏糖醇（一种有效的还原剂）处理去膜纤维制备物，温度诱导的收缩装置力产生降低可以被逆转。这些结果表明，随着温度在生理温度上限范围内升高，哺乳动物骨骼肌能够通过增加O(2)(-)的产生，使力的产生与激活剂Ca(2+)可逆性解偶联。
