Kd. Sumida et Cm. Donovan, ENHANCED HEPATIC GLUCONEOGENIC CAPACITY FOR SELECTED PRECURSORS AFTERENDURANCE TRAINING, Journal of applied physiology, 79(6), 1995, pp. 1883-1888
The effects of endurance training (running 90 min/day, 30 m/min, simil
ar to 10% grade) on hepatic gluconeogenesis were studied in 24-h-faste
d rats by using the isolated liver perfusion technique. After isolatio
n, livers were perfused (single pass) for 30 min with Krebs-Henseleit
bicarbonate buffer and fresh bovine red blood cells (hematocrit 20-24%
) with no added substrate. Alanine (10 mM), dihydroxyacetone (20 mM),
or glutamine (10 mM) was then added to the reservoir, and perfusions c
ontinued for 60 min. No significant differences were observed in perfu
sate pH, hematocrit, bile production, or serum alanine aminotransferas
e effluxing from livers from trained or control animals for any perfus
ion. Livers from trained animals that were perfused with 10 mM alanine
demonstrated significantly higher rates of glucose production compare
d with livers from control animals (0.51 +/- 0.04 vs. 0.40 +/- 0.02 mu
mol . min(-1). g liver(-1), respectively). Elevations of a similar ma
gnitude were observed for rates of [C-14]alanine incorporation into [C
-14]glucose in livers from trained vs. control animals (8,797 +/- 728
vs. 6,962 +/- 649 dpm . min(-1). g liver(-1), respectively). Significa
nt increases were also observed in hepatic alanine uptake (30%), oxyge
n consumption (23%), urea release (22%), and (CO2)-C-14 production (29
%) oflivers of endurance-trained animals. In contrast, no significant
differences between groups were observed for hepatic glucose output af
ter perfusions with either dihydroxyacetone (1.75 +/- 0.06 mu mol . mi
n(-1). g liver(-1)) or glutamine (0.62 +/- 0.04 mu mol . min(-1). g li
ver(-1)). Further, during perfusions with dihydroxyacetone and glutami
ne, training had no significant impact on precursor uptake, oxygen con
sumption, or urea output. The current findings indicate a training-ind
uced adaptation for hepatic gluconeogenesis located below the level of
the triose phosphates.