Attenuated Postprandial Insulin Concentrations With Endurance Training Are Not Mediated By Reductions In Incretin Hormones

Abstract

The incretin hormones, glucagon-like peptide-1 (GLP1) and glucose-dependent insulinotropic polypeptide (GIP), are released from the intestine after food ingestion and stimulate the pancreas to secrete insulin. Together, these hormones account for approximately half of the postprandial rise in plasma insulin concentrations. Although endurance exercise training improves insulin action on glucose disposal in skeletal muscle and results in a concomitant decrease in postprandial insulin secretion from the pancreas, it is not known if a reduction in incretin hormones contributes to the lower insulin response. PURPOSE: To determine if long-term endurance training is associated with lower plasma GLP1 and GIP responses to oral glucose ingestion. METHODS: Fifteen master endurance athletes (56 ± 2y) and 14 healthy non-exercising control subjects (57 ± 2y) underwent 2h, 75 g oral glucose tolerance tests (OGTTs) during which blood samples were acquired every 30 minutes to assess glucose, insulin, GLP1, and GIP concentrations by using commercially available assays. An index of insulin action (ISI) was calculated based on glucose and insulin concentration from the OGTT. VO2max was assessed using indirect calorimetry and body fat was quantified using DXA. RESULTS: Athletes had higher VO2max (54 ± 2 vs 34 ± 2 mL/kg/min; P < 0.0001) and lower body fat (14 ± 1 vs 23 ± 1%; P <0.0001) than controls. While the area under the curve (AUC) for glucose from the OGTT did not differ between groups (P = 0.12), athletes had 41% lower insulin AUC (P = 0.02) and two-fold greater ISI (0.001). Athletes and controls did not differ in terms of GLP1 AUC (346 ± 65 vs. 414 ± 80 pM·min, p= 0.52) or GIP AUC (19.4 ± 1.3 vs. 18.0 ± 1.4 ng/mL·min, P = 0.49). CONCLUSIONS: These findings suggest the lower postprandial insulin responses that occur in athletes are not modulated by reductions in postprandial concentrations of the intestinally derived incretin hormones, GLP1 and GIP. Supported by NIH General Clinical Research Center RR00036, NIH Clinical Nutrition Research Unit DK56341, Saint Louis University Beaumont Award, and the Longer Life Foundation.