Stimulation of both aerobic glycolysis and Na+-K+-ATPase activity in skeletal muscle by epinephrine or amylin.

Epinephrine and amylin stimulate glycogenolysis, glycolysis, and Na+-K+-ATPase activity in skeletal muscle. However, it is not known whether these hormones stimulate glycolytic ATP production that is specifically coupled to ATP consumption by the Na+-K+pump. These studies correlated glycolysis with Na+-K+-ATPase activity in resting rat extensor digitorum longus and soleus muscles incubated at 30°C in well-oxygenated medium. Lactate production rose three- to fourfold, and the intracellular Na+-to-K+ratio (Na+/K+) fell with increasing concentrations of epinephrine or amylin. In muscles exposed to epinephrine at high concentrations (5 × 10-7 and 5 × 10-6 M), ouabain significantly inhibited glycolysis by ∼70% in either muscle and inhibited glycogenolysis by ∼40 and ∼75% in extensor digitorum longus and soleus, respectively. In the absence of ouabain, but not in its presence, statistically significant inverse correlations were observed between lactate production and intracellular Na+/K+for each hormone. Epinephrine had no significant effect on oxygen consumption or ATP content in either muscle. These results suggest for the first time that stimulation of glycolysis and glycogenolysis in resting skeletal muscle by epinephrine or amylin is closely linked to stimulation of active Na+-K+transport.