Edwards Joshua N, Macdonald William A, van der Poel Chris, Stephenson D George
Dept of Zoology, La Trobe University, Melbourne, VIC, Australia.
Am J Physiol Cell Physiol. 2007 Aug;293(2):C650-60. doi: 10.1152/ajpcell.00037.2007. Epub 2007 Apr 25.
To find out whether the decrease in muscle performance of isolated mammalian skeletal muscle associated with the increase in temperature toward physiological levels is related to the increase in muscle superoxide (O(2)(-)) production, O(2)(-) released extracellularly by intact isolated rat and mouse extensor digitorum longus (EDL) muscles was measured at 22, 32, and 37 degrees C in Krebs-Ringer solution, and tetanic force was measured in both preparations at 22 and 37 degrees C under the same conditions. The rate of O(2)(-) production increased marginally when the temperature was increased from 22 to 32 degrees C, but increased fivefold when the temperature was increased from 22 to 37 degrees C in both rat and mouse preparations. This increase was accompanied by a marked decrease in tetanic force after 30 min incubation at 37 degrees C in both rat and mouse EDL muscles. Tetanic force remained largely depressed after return to 22 degrees C for up to 120 min. The specific maximum Ca(2+)-activated force measured in mechanically skinned fibers after the temperature treatment was markedly depressed in mouse fibers but was not significantly depressed in rat muscle fibers. The resting membrane and intracellular action potentials were, however, significantly affected by the temperature treatment in the rat fibers. The effects of the temperature treatment on tetanic force, maximum Ca(2+)-activated force, and membrane potential were largely prevented by 1 mM Tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl), a membrane-permeable superoxide dismutase mimetic, indicating that the increased O(2)(-) production at physiological temperatures is largely responsible for the observed depression in tetanic force at 37 degrees C by affecting the contractile apparatus and plasma membrane.
为了探究与温度升高至生理水平相关的离体哺乳动物骨骼肌肌肉性能下降是否与肌肉超氧化物（O₂⁻）生成增加有关，在22℃、32℃和37℃的 Krebs-Ringer 溶液中测量了完整分离的大鼠和小鼠趾长伸肌（EDL）肌肉细胞外释放的 O₂⁻，并在相同条件下于室温（22℃）下和37℃下测量了两种标本的强直收缩力。当温度从22℃升高到32℃时，O₂⁻生成速率略有增加，但在大鼠和小鼠标本中，当温度从22℃升高到37℃时，O₂⁻生成速率增加了五倍。这种增加伴随着大鼠和小鼠 EDL 肌肉在37℃孵育30分钟后强直收缩力的显著下降。回到22℃长达120分钟后，强直收缩力仍基本处于抑制状态。在温度处理后，在机械去膜纤维中测得的比最大钙激活力在小鼠纤维中显著降低，但在大鼠肌肉纤维中没有显著降低。然而，温度处理对大鼠纤维的静息膜电位和细胞内动作电位有显著影响。1 mM Tempol（4-羟基-2,2,6,6-四甲基哌啶-1-氧基）是一种可透过膜的超氧化物歧化酶模拟物，它在很大程度上阻止了温度处理对强直收缩力、最大钙激活力和膜电位的影响，这表明生理温度下 O₂⁻生成增加在很大程度上是通过影响收缩装置和质膜导致在37℃观察到的强直收缩力降低的原因。
