Prior exercise increases net hepatic glucose uptake during a glucose load

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 a rtery, portal, hepatic, and iliac veins), infusion catheters (portal vein a nd vena cava), and Doppler flow probes (portal vein, hepatic and iliac arte ries) were implanted. Exercise (150 min; it = 6) or rest (n = 6) was follow ed by a 30-min control period and a 100-min experimental period (3.5 mg.kg( -1).min(-1) of glucose in portal vein and as needed in vena cava to clamp a rterial blood glucose at similar to 130 mg/dl). Somatostatin was infused, a nd insulin and glucagon were replaced intraportally at fourfold basal and b asal rates, respectively. During experimental period the arterial-portal ve nous (a-pv) glucose gradient (mg/dl) was -18 +/- 1 in sedentary and -19 +/- 1 in exercised dogs. Arterial insulin and glucagon were similar in the two groups. Net hepatic glucose balance (mg.kg(-1).min(-1)) shifted from 1.9 /- 0.2 in control period to -1.8 +/- 0.2 (negative rates represent net upta ke) during experimental period in sedentary dogs (Delta 3.7 +/- 0.5); with prior exercise it shifted from 4.1 +/- 0.3 (P < 0.01 vs. sedentary) in cent ral period to -3.2 +/- 0.4 (P < 0.05 vs. sedentary) during experimental per iod (Delta 7.3 +/- 0.7, P < 0.01 vs, sedentary). Net hindlimb glucose uptak e (mg/min) was 4 +/- 1 in sedentary animals in control period and 13 +/- 2 during experimental period; in exercised animals it was 7 +/- 1 in control period (P < 0.01 vs, sedentary) and 32 +/- 4 (P < 0.01 vs, sedentary) durin g experimental period. As the total glucose infusion rate (mg.kg(-1).min(-1 )) was 7 +/- 1 in sedentary and 11 +/- 1 in exercised dogs, similar to 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 up take (insulin, glucagon, a-pv glucose gradient, glycemia) are controlled, p rior exercise increases NHGU during a glucose load due to an effect that is intrinsic to the liver. Increased glucose disposal in the postexercise sta te is therefore due to an improved ability of both liver and muscle to take up glucose.