Influence of hypoglucagonemia on splanchnic glucose output during leg exercise in man

Summary. The present study was undertaken to examine the role of glucagon in the regulation of hepatic glucose production during exercise. Using the hepatic vein catheter technique, the influence of somatostatin-induced hypoglucagonemia on splanchnic exchange of glucose and glucose precursors during exercise was studied in normal postabsorptive man. In the experiments hypoglucagonemia was induced 10 min before and during 40 min of supine bicycle exercise (series 1), or 1–2 h before, and during, 40 min of upright bicycle exercise (series 2). The relative work intensities were 50% (series 1) and 55% (series 2) of maximal oxygen uptake. Control studies without somatostatin were conducted in both series. In both series, insulin and glucagon levels were suppressed by 40–50% throughout the period of somatostatin infusion. In series 1, somatostatin infusion at rest resulted in a 50 % fall in splanchnic glucose output. Onset of exercise during suppressed glucose production was followed by a rise in splanchnic glucose output similar to that seen in control subjects, but the absolute rate of glucose production was 5–25 % lower than in controls. In contrast to the euglycemia observed in the control experiment, exercise during somatostatin administration was accompanied by a 1–2 mmol/1 fall in blood glucose concentration due to the lower rate of glucose production. In series 2, a variable glucose infusion was added to the somatostatin administration before exercise to maintain euglycemia. After 1–2 h of somatostatin administration, glucose infusion was no longer required to prevent hypoglycemia, and splanchnic glucose output had returned to the basal level. At this time exercise was started. Both the rise in splanchnic glucose production and the absolute rate of splanchnic glucose output during exercise were similar to those observed without somatostatin. However, exercise during prolonged somatostatin infusion was accompanied by a gradual 50% rise in arterial glucose concentration, whereas no change in blood glucose during exercise was seen in controls.