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J Nutr Biochem. 2013 Jan;24(1):325-34. doi: 10.1016/j.jnutbio.2012.06.017. Epub 2012 Sep 10.

Metabolic response to green tea extract during rest and moderate-intensity exercise.

Author information

1
School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom.

Abstract

BACKGROUND:

Green tea catechins have been hypothesized to increase energy expenditure and fat oxidation by inhibiting catechol-O-methyltransferase (COMT) and thus promoting more sustained adrenergic stimulation. Metabolomics may help to clarify the mechanisms underlying their putative physiological effects.

OBJECTIVE:

The study investigated the effects of 7-day ingestion of green tea extract (GTE) on the plasma metabolite profile at rest and during exercise.

METHODS:

In a placebo-controlled, double-blind, randomized, parallel study, 27 healthy physically active males consumed either GTE (n=13, 1200 mg catechins, 240 mg caffeine/day) or placebo (n=14, PLA) drinks for 7 days. After consuming a final drink (day 8), they rested for 2 h and then completed 60 min of moderate-intensity cycling exercise (56% ± 4% VO(2)max). Blood samples were collected before and during exercise. Plasma was analyzed using untargeted four-phase metabolite profiling and targeted profiling of catecholamines.

RESULTS:

Using the metabolomic approach, we observed that GTE did not enhance adrenergic stimulation (adrenaline and noradrenaline) during rest or exercise. At rest, GTE led to changes in metabolite concentrations related to fat metabolism (3-β-hydroxybutyrate), lipolysis (glycerol) and tricarboxylic acid cycle (TCA) cycle intermediates (citrate) when compared to PLA. GTE during exercise caused reductions in 3-β-hydroxybutyrate concentrations as well as increases in pyruvate, lactate and alanine concentrations when compared to PLA.

CONCLUSIONS:

GTE supplementation resulted in marked metabolic differences during rest and exercise. Yet these metabolic differences were not related to the adrenergic system, which questions the in vivo relevance of the COMT inhibition mechanism of action for GTE.

PMID:
22974973
DOI:
10.1016/j.jnutbio.2012.06.017
[Indexed for MEDLINE]

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