Pedersen Thomas Holm, Clausen Torben, Nielsen Ole Baekgaard
Department of Physiology, University of Aarhus, DK-8000 Aarhus C, Denmark.
J Physiol. 2003 Aug 15;551(Pt 1):277-86. doi: 10.1113/jphysiol.2003.041418. Epub 2003 Jun 17.
Loss of K+ from active muscles, leading to increased [K+]o, has been proposed to cause muscle fatigue by reducing excitability. Since exercise increases muscle temperature, we investigated the influence of temperature on muscle [K+]o sensitivity. Intact rat soleus or extensor digitorum longus (EDL) muscles were mounted on force transducers and stimulated electrically to evoke short isometric tetani at regular intervals. In each experiment, control force at 4 mM K+ was initially determined at every temperature used. In soleus muscles at 20 degrees C, 9 mM K+ reduced force to 33 +/- 5 % of control force. Increasing the temperature to 30 degrees C restored force to 89 +/- 5 % of control force. Likewise, at 30 degrees C 11 mM K+ reduced force to 16 +/- 4 % and increasing the temperature to 35 degrees C restored force to 35 +/- 5 %. Similar results were obtained using EDL. The force recovery induced by elevating temperature, reflecting reduced [K+]o sensitivity, was associated with improved excitability assessed from compound action potentials. Force recovery induced by a temperature elevation from 20 to 30 degrees C was associated with hyperpolarization (5 mV), reduced [Na+]i and a 93 % increase in Na+-K+ pump activity. The force recovery was blocked by ouabain. Since intensive exercise leads to lactic acidosis and increased plasma catecholamines, the effect of these two factors was also investigated. At 11 mM K+, force was completely restored by combining temperature elevation (30 to 35 degrees C), L-lactic acid (10 mM) and the beta2-agonist salbutamol (10-5 M). We suggest an exercise scenario where the depressing action of exercise-induced hyperkalaemia is counteracted by elevated muscle temperature, lactic acidosis and catecholamines.
活跃肌肉中钾离子（K⁺）的流失会导致细胞外钾离子浓度（[K⁺]o）升高，有人提出这会通过降低兴奋性而导致肌肉疲劳。由于运动可使肌肉温度升高，我们研究了温度对肌肉[K⁺]o敏感性的影响。将完整的大鼠比目鱼肌或趾长伸肌（EDL）安装在力传感器上，并定期进行电刺激以诱发短时间等长强直收缩。在每个实验中，首先在每个使用的温度下测定4 mM K⁺时的对照力。在20℃的比目鱼肌中，9 mM K⁺可使力降低至对照力的33±5%。将温度升至30℃时，力恢复至对照力的89±5%。同样，在30℃时，11 mM K⁺可使力降低至16±4%，将温度升至35℃时，力恢复至35±5%。使用EDL也得到了类似结果。温度升高引起的力恢复反映了[K⁺]o敏感性降低，这与通过复合动作电位评估的兴奋性改善有关。温度从20℃升高到30℃引起的力恢复与超极化（5 mV）、细胞内钠离子浓度（[Na⁺]i）降低以及钠钾泵活性增加93%有关。力恢复被哇巴因阻断。由于剧烈运动导致乳酸酸中毒和血浆儿茶酚胺增加，我们还研究了这两个因素的作用。在11 mM K⁺时，通过联合温度升高（30℃至35℃）、L-乳酸（10 mM）和β2-肾上腺素能激动剂沙丁胺醇（10⁻⁵ M），力可完全恢复。我们提出了一种运动场景，即运动诱导的高钾血症的抑制作用可被升高的肌肉温度、乳酸酸中毒和儿茶酚胺所抵消。
