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 °C, 9 mM K+ reduced force to 33 ± 5 % of control force. Increasing the temperature to 30 °C restored force to 89 ± 5 % of control force. Likewise, at 30 °C 11 mMK+ reduced force to 16 ± 4% and increasing the temperature to 35 °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 °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 °C), L-lactic acid (10 mM) and the b2-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.
Updated on July 13, 2020