Glucose administration before exercise modulates catecholaminergic responses in glycogen-depleted subjects.

In glycogen-depleted subjects (GD) a nonlinear increase in epinephrine (Epi) and norepinephrine (NE) parallels blood lactate (La) during graded exercise. The effect of glucose (Glc) supplementation and route of administration on these relationships was studied in 26 GD athletes who were randomly assigned to receive 1.3 g/kg Glc by slow intravenous infusion (IV; n = 9), oral administration (PO; n = 9), or artificially sweetened placebo in 1 liter of water (Asp; n = 8) in the 2 h preceding a graded maximal exercise. Performance and La were similar among the three groups in normal glycogen (NG) or GD conditions. However, slightly improved performances were observed in GD compared with NG and were associated with a shift to the right in La curves. Blood Glc concentrations were higher in IV and PO before exercise, but they rapidly decreased to lowest levels in IV, gradually decreased over time in PO, and remained stable in Asp or NG. Insulin concentrations were highest in IV and lowest in Asp and NG at onset of exercise, rapidly decreasing in IV and PO although remaining at higher levels than in Asp or NG. In contrast, higher serum levels of free fatty acids were measured during exercise in Asp with no significant differences in glucagon or glycerol among the three groups. Free and sulfated NE increases were smaller in IV than in PO and Asp on exhaustion. In contrast, free and conjugated Epi were most increased in IV, with smallest increases in Asp. Dopamine levels were most increased in IV at exhaustion. We conclude that the changes of Epi and NE concentrations, associated with the activation of glucoregulatory mechanisms, including hyperinsulinemia, display different magnitude and time courses during exercise in GD subjects who receive oral vs. intravenous load of Glc before exercise. We speculate that the magnitude of insulin surge after acutely increased Glc before exercise in GD subjects may exert dissociative effects on adrenal-dependent glycogenolysis and on sympathetic responses.