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• W349597969 abstract "To gain a more complete understanding of glycemic regulation and energy substrate metabolism during exercise, we examined the effects of endurance training, exercise intensity, and plasma lactate concentration on gluconeogenesis (GNG), hepatic glycogenolysis (GLY), whole body lactate turnover, and direct versus indirect lactate oxidation rates in fasted men exercising at and just below the lactate threshold (LT), where GNG precursor lactate availability is high. The lactate threshold, characterized as the onset of rapid blood lactate accumulation during incremental exercise, marks the transition between steady and non-steady state lactate turnover. We studied six untrained (UT) and six trained (T) subjects during 60-min exercise bouts at power outputs (PO) eliciting the LT. Trained subjects performed two additional exercise bouts at a PO 10% lower (LT-10%), one of which involved a lactate clamp (LC) to match blood lactate concentration ([lactate]b) to that achieved during the LT trial. Flux rates were determined by primed continuous infusion of [6,6- 2 H2]glucose, [3- 13 C]lactate, and [ 13 C]bicarbonate tracers during 90 min of rest and 60 min of cycling. Exercise at LT corresponded to 67.6 ± 1.3 and 74.8 ± 1.7 % of peak oxygen consumption (VO2peak) in the untrained and trained subjects, respectively (P -1 ·min -1 ) compared to its corresponding LT-10% control (1.7 ± 0.4 mg·kg -1 ·min -1 , P -1 ·min -1 , respectively, P -1 ·min -1 , respectively, P -1 ·min -1 , P -1 ·min -1 , 75% VO2peak) compared to UT (13.4 ± 2.5 mg·kg -1 ·min -1 , 68% VO2peak, P -1 ·min -1 , respectively, P < 0.05). We partitioned lactate Rox into its direct versus indirect (glucose that is gluconeogenically derived from lactate and subsequently oxidized) components. Direct and indirect lactate oxidation rates increased significantly from rest to exercise and their relative partitioning remained relatively constant in all trials, but differed between T and UT: direct oxidation comprised 75% of total lactate oxidation in UT and 90% in T suggesting the presence of training-induced adaptations. We conclude that i) endurance training increases the work capacity at the lactate threshold without a significant decrease in gluconeogenesis, ii) gluconeogenesis during exercise can be augmented by increased precursor delivery, iii) the lactate threshold represents a limitation in lactate clearance, iv) endurance training increases direct oxidation of lactate (90% in trained vs. 75% in untrained), regardless of activity level, suggesting underlying training-induced adaptations independent of exercise parameters, and v) exogenous lactate infusion during exercise spares muscle glycogen utilization." @default.
• W349597969 created "2016-06-24" @default.
• W349597969 creator A5085757575 @default.
• W349597969 date "2013-01-01" @default.
• W349597969 modified "2023-09-24" @default.
• W349597969 title "Regulation of Glycemia and Energy Substrate Partitioning in Exercising Humans" @default.
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