REGULATION OF GLUCOSE-PRODUCTION DURING EXERCISE AT 80-PERCENT 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 dur ing 30 min of cycling at 80% of peak oxygen uptake on two occasions: o nce 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 durin g exercise to match glycemia with control levels. Glucose kinetics wer e 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 cl amp experiments, with endogenous R-a peaking at 37.2 +/- 7.9 mu mol.mi n(-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 exer cise). Thus neither decrements in insulin or increments in glucagon ar e apparently required to stimulate glucose R-a under the present condi tions. Because epinephrine levels rose only slightly it appears that e ither neurally released norepinephrine or some other, as yet unidentif ied. factor is responsible for stimulating glucose R-a during intense but submaximal exercise.