REGULATION OF HEPATIC GLUCOSE-PRODUCTION DURING EXERCISE IN HUMANS - ROLE OF SYMPATHOADRENERGIC ACTIVITY

To investigate the role of sympathoadrenergic activity on glucose production (R(a)) during exercise, eight healthy males bicycled 20 min at 41 +/- 2 and 74 +/- 4% maximal O2 uptake (VO2max; mean +/- SE) either without (control; Co) or with blockade of sympathetic nerve activity to liver and adrenal medulla by local anesthesia of the celiac ganglion (BI). Epinephrine (Epi) was in some experiments infused during blockade to match (normal Epi) or exceed (high Epi) Epi levels during Co. A constant infusion of somatostatin and glucagon was given before and during exercise. At rest, insulin was infused at a rate maintaining euglycemia. During intense exercise, insulin infusion was halved to mimic physiological conditions. During exercise, R(a) increased in Co from 14.4 +/- 1.0 to 27.8 +/- 3.0 mumol . min-1 . kg-1 (41% VO2max) and to 42.3 +/- 5.2 (74% VO2max; P < 0.05). At 41% VO2max, plasma glucose decreased, whereas it increased during 74% VO2max. R(a) was not influenced by Bl. In high Epi, R(a) rose more markedly compared with control (P < 0.05), and plasma glucose did not fall during mild exercise and increased more during intense exercise (P < 0.05). Free fatty acid and glycerol concentrations were always lower during exercise with than without celiac blockade. We conclude that high physiological concentrations of Epi can enhance R(a) in exercising humans, but normally Epi is not a major stimulus. The study suggests that neither sympathetic liver nerve activity is a major stimulus for R(a) during exercise. The R. response is enhanced by a decrease in insulin and probably by unknown stimuli. Finally, splanchnic fat stores may be mobilized by sympathetic nerve activity during exercise.