Adrenaline increases skeletal muscle glycogenolysis, pyruvate dehydrogenase activation and carbohydrate oxidation during moderate exercise in humans

1. To evaluate the role of adrenaline in regulating carbohydrate metabolism during moderate exercise, 10 moderately trained men completed two 20 min e xercise bouts at 58 +/- 2% peak pulmonary oxygen uptake ((V) over dot (O2,p eak)). On one occasion saline was infused. (CON), and on the other adrenali ne was infused intravenously for 5 min prior to and throughout exercise (AD R). Glucose kinetics were measured by a primed, continuous infusion of 6,6- [H-2]glucose and muscle samples were obtained prior to and at 1 and 20 min of exercise. 2. The infusion of adrenaline elevated (P < 0.01) plasma adrenaline concent rations at rest (pre infusion, 0.28 +/- 0.09; post-infusion, 1.70 +/- 0.45 nmol l(-1); means +/- S.E.M.) and this effect was maintained throughout exe rcise. Total carbohydrate oxidation increased by 18% and this effect was du e to greater skeletal muscle glycogenolysis (P < 0.05) and pyruvate dehydro genase (PDH) activation (P < 0.05, treatment effect). Glucose rate of appea rance was not different between trials, but the infusion of adrenaline decr eased (P < 0.05, treatment effect) skeletal muscle glucose uptake in ADR. 3. During exercise muscle glucose B-phosphate (G-6-P) (P = 0.055, treatment effect) and lactate (P <less than> 0.05) were elevated in ADR compared wit h CON and no changes were observed for pyruvate, creatine, phosphocreatine, ATP and the calculated free concentrations of ADP and AMP. 4. The data demonstrate that elevated plasma adrenaline levels during moder ate exercise in untrained men increase skeletal muscle glycogen breakdown a nd PDH activation, which results in greater carbohydrate oxidation. The gre ater muscle glycogenolysis appears to be clue to increased glycogen phospho rylase transformation whilst the increased PDH activity cannot be readily e xplained. Finally, the decreased glucose uptake observed during exercise in ADR is likely to be due to the increased intracellular G-6-P and a subsequ ent decrease in glucose phosphorylation.