The effect of β₂‐adrenoceptor activation on ion‐shifts and fatigue in mouse soleus muscles stimulated in vitro

The resting membrane potential (RMP), the intracellular free Na+ concentration ([Na+]i) and the intracellular free K+ concentration ([K+]i), were measured with double-barrelled ion-selective microelectrodes in mouse soleus muscles in vitro. In addition, the Na+ contents and K+ contents have been measured with the flame photometric technique. At rest the beta 2-selective adrenoceptor agonist terbutaline (10(-5) M) increased the membrane potential and [K+]i, and decreased [Na+]i when compared with control muscles. During a 5 min stimulation period the muscles, which were incubated with the beta 2-adrenoceptor agonist, showed a smaller depolarization, a smaller decrease in [K+]i and a smaller increase in [Na+]i than stimulated control muscles. This difference was probably associated with an increased rate of Na-K-pumping in the beta 2-adrenoceptor stimulated muscles. The beta 2-agonist treated muscles were more resistant to fatigue than control muscles. This effect was significant with 10(-6) M terbutaline (25 degrees C). A depolarization obtained by increasing [K+]o was shown to reduce the maximal tension. It is postulated, that the K+ shifts, which are responsible for the depolarization during muscle activity, are one of the mechanisms underlying muscle fatigue.