OBJECTIVE: To determine the metabolic effects of catecholamines released at sympathetic nerves ending in the postabsorptive and postprandial states. DESIGN: Sympathetic activity was acutely increased by lower body negative pressure (LBNP; -15 mmHg) on two occasions in a group of eight healthy volunteers: (1) in the postabsorptive state; and (2) after glucose ingestion. MEASUREMENTS: Plasma norepinephrine concentrations were determined by HPLC and energy expenditure and substrate oxidation rates were assessed with indirect calorimetry. RESULTS: After glucose, LBNP increased plasma norepinephrine by 27% and lipid oxidation by 72% and decreased glucose oxidation by 14%. Energy expenditure was not altered. In the postabsorptive state, LBNP increased plasma norepinephrine by 34%, but had no significant effect on energy or substrate metabolism. CONCLUSIONS: In healthy humans, LBNP-induced activation of the sympathetic nervous system decreases glucose oxidation and increases lipid oxidation after oral glucose, but does not quantitatively affect energy expenditure.
OBJECTIVE: To determine the metabolic effects of catecholamines released at sympathetic nerves ending in the postabsorptive and postprandial states. DESIGN: Sympathetic activity was acutely increased by lower body negative pressure (LBNP; -15 mmHg) on two occasions in a group of eight healthy volunteers: (1) in the postabsorptive state; and (2) after glucose ingestion. MEASUREMENTS: Plasma norepinephrine concentrations were determined by HPLC and energy expenditure and substrate oxidation rates were assessed with indirect calorimetry. RESULTS: After glucose, LBNP increased plasma norepinephrine by 27% and lipid oxidation by 72% and decreased glucose oxidation by 14%. Energy expenditure was not altered. In the postabsorptive state, LBNP increased plasma norepinephrine by 34%, but had no significant effect on energy or substrate metabolism. CONCLUSIONS: In healthy humans, LBNP-induced activation of the sympathetic nervous system decreases glucose oxidation and increases lipid oxidation after oral glucose, but does not quantitatively affect energy expenditure.
Authors: Sammy Bedoui; Elena Velkoska; Steve Bozinovski; Jessica E Jones; Gary P Anderson; Margaret J Morris Journal: J Inflamm (Lond) Date: 2005-03-21 Impact factor: 4.981