AENDO June 39/6

Galassetti, Pietro, Robert H. Coker, Drury B. Lacy, Alan D. Cherrington, and David H. Wasserman. Prior exercise increases net hepatic glucose uptake during a glucose load. Am. J. Physiol. 276 (Endocrinol. Metab. 39): E1022–E1029, 1999.—The aim of these studies was to determine whether prior exercise enhances net hepatic glucose uptake (NHGU) during a glucose load. Sampling catheters (carotid artery, portal, hepatic, and iliac veins), infusion catheters (portal vein and vena cava), and Doppler flow probes (portal vein, hepatic and iliac arteries) were implanted. Exercise (150 min; n 5 6) or rest (n 5 6) was followed by a 30-min control period and a 100-min experimental period (3.5 mg·kg21 ·min21 of glucose in portal vein and as needed in vena cava to clamp arterial blood glucose at ,130 mg/dl). Somatostatin was infused, and insulin and glucagon were replaced intraportally at fourfold basal and basal rates, respectively. During experimental period the arterial-portal venous (a-pv) glucose gradient (mg/dl) was 218 6 1 in sedentary and 219 6 1 in exercised dogs. Arterial insulin and glucagon were similar in the two groups. Net hepatic glucose balance (mg·kg21 ·min21) shifted from 1.9 6 0.2 in control period to 21.8 6 0.2 (negative rates represent net uptake) during experimental period in sedentary dogs (D3.7 6 0.5); with prior exercise it shifted from 4.1 6 0.3 (P , 0.01 vs. sedentary) in control period to 23.2 6 0.4 (P , 0.05 vs. sedentary) during experimental period (D7.3 6 0.7, P , 0.01 vs. sedentary). Net hindlimb glucose uptake (mg/min) was 4 6 1 in sedentary animals in control period and 13 6 2 during experimental period; in exercised animals it was 7 6 1 in control period (P , 0.01 vs. sedentary) and 32 6 4 (P , 0.01 vs. sedentary) during experimental period. As the total glucose infusion rate (mg·kg21 ·min21) was 7 6 1 in sedentary and 11 6 1 in exercised dogs, ,30% of the added glucose infusion due to prior exercise could be accounted for by the greater NHGU. In conclusion, when determinants of hepatic glucose uptake (insulin, glucagon, a-pv glucose gradient, glycemia) are controlled, prior exercise increases NHGU during a glucose load due to an effect that is intrinsic to the liver. Increased glucose disposal in the postexercise state is therefore due to an improved ability of both liver and muscle to take up glucose.