Adrenodemedullation affects endurance but not hepatic fructose 2,6-bisphosphate

Sham-operated (SHAM) and saline (ADM-S)- or epinephrine (ADM-E)-infused adrenodemedullated rats were run on a treadmill (21 m/min, 15% grade) for 80 min or until exhaustion. ADM-S rats had significantly lower endurance run times (116 ± 6 min) than ADM-E rats (136 ± 8 min) and SHAM rats (150 ± 6 min). Liver glycogen content dropped from 56 ± 4 to 10 ± 2 mg/g in SHAM and from 54 ± 4 to 18 ± 5 mg/g in ADM-S and to 20 ± 8 mg/g in ADM-E rats at 80 min. Liver glycogen was depleted in all rats at exhaustion. Liver fructose 2,6-bisphosphate was decreased markedly in exercising rats, and the extent of decrease was not influenced by adrenodemedullation or by epinephrine infusion. ADM-S rats showed impaired glycogen depletion in the white vastus lateralis and soleus muscles, hypoglycemia, and low blood lactate at 80 min and at exhaustion. Infusion of epinephrine into ADM rats reversed these deficiencies. These data indicate that the adrenal medulla is unessential for normal endurance exercise as long as liver glycogen is available. After liver glycogen is depleted, epinephrine from the adrenal medulla prevents hypoglycemia and is essential for allowing continuation of exercise.