Regulation of glucose production during exercise at 80% of VO2peak in untrained humans

To determine whether alterations in insulin and/or glucagon secretion play an important role in stimulating glucose production (R-a) during intense but submaximal exercise, we studied six untrained subjects during 30 min of cycling at 80% of peak oxygen uptake on two occasions: once under control conditions and once when alterations in insulin and glucagon secretion were prevented with the use of the pancreatic islet clamp technique. In the latter experiments. glucose was infused during exercise to match glycemia with control levels. Glucose kinetics were measured in both trials using a primed, continuous infusion of [6,6-H-2]glucose. In the control trial, glucose R-a rose from 11.9 +/- 0.8 mu mol.min(-1).kg(-1) at rest to 42.5 +/- 4.3 mu mol.min(-1).kg(-1) by the end of exercise. A similar increment was observed in the islet clamp experiments, with endogenous R-a peaking at 37.2 +/- 7.9 mu mol.min(-1).kg(-1). This was true even though glucagon concentration did not change from basal and insulin concentration actually rose (the latter apparently due to a decrease in insulin clearance during intense exercise). Thus neither decrements in insulin or increments in glucagon are apparently required to stimulate glucose R-a under the present conditions. Because epinephrine levels rose only slightly it appears that either neurally released norepinephrine or some other, as yet unidentified. factor is responsible for stimulating glucose R-a during intense but submaximal exercise.