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Department of Molecular Physiology and Biophysics, and Diabetes Research and Training Center, Vanderbilt University, Nashville, Tennessee 37232-0615
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 = 6) or rest
(n = 6) was followed 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 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
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 uptake) during experimental period in
sedentary dogs (
3.7 ± 0.5); with prior exercise it shifted from
4.1 ± 0.3 (P < 0.01 vs.
sedentary) in control period to
3.2 ± 0.4 (P < 0.05 vs. sedentary) during
experimental period (
7.3 ± 0.7, P < 0.01 vs. sedentary). Net
hindlimb glucose uptake (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) during experimental period. As the total glucose infusion rate (mg · kg
1 · min
1)
was 7 ± 1 in sedentary and 11 ± 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.
carbohydrates; glucose balance; portal vein; exertion; dog
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