**Background:** Green tea catechins, particularly epigallocatechin gallate (EGCG), have been shown to alter resting energy metabolism and lipid oxidation, though results are inconsistent. The sympatho-adrenal system plays a key role in regulating metabolism during exercise via circulating catecholamines, which stimulate hormone-sensitive lipase and promote lipid combustion. It has been hypothesized that catechins may regulate this system through inhibition of catechol-O-methyltransferase (COMT), but in vivo evidence is limited. This study aimed to investigate the impact of acute EGCG ingestion on catecholamine metabolism, catecholamine metabolites, and systemic metabolic variables across a range of exercise intensities during graded cycle exercise.
**Methods:** Eight healthy males (age 22.4 ± 3.3 years, BMI 25.7 ± 2.4 kg/m², estimated body fat 15 ± 5.2%) completed a randomized, placebo-controlled, single-blind, cross-over trial. After an overnight fast, participants ingested either 1450 mg EGCG (minimum 94% EGCG, < 0.1% caffeine) or 1450 mg corn flour placebo. Following a 2-hour monitoring period, participants performed a continuous graded cycle exercise test to volitional exhaustion (starting at 60 W, increasing by 30 W every 3 minutes, cadence 60–70 rpm). Venous blood samples were collected at rest, 2 hours post-ingestion, and during the last 30 seconds of each 3-minute stage. Blood was analyzed for adrenaline, noradrenaline, metanephrine, normetanephrine (ELISA), lactate, and glucose. Respiratory gases were measured continuously for indirect calorimetry. Data were grouped into five metabolic domains: rest, 2 h post-ingestion (POST-ING), peak lipid oxidation rate (FATpeak), lactate threshold (LT), and peak oxygen consumption (VO₂peak). Statistical analysis used two-way repeated measures ANOVA with post hoc dependent t-tests and Bonferroni corrections.
**Key Results:** Resting catecholamine and metanephrine concentrations were similar between trials. Plasma adrenaline was significantly lower in the EGCG trial at FATpeak (EGCG 0.18 ± 0.11 vs. PLAC 0.37 ± 0.27 nmol/L, P < 0.05), LT (EGCG 0.35 ± 0.16 vs. PLAC 1.59 ± 0.49 nmol/L, P < 0.001), and VO₂peak (EGCG 0.91 ± 0.58 vs. PLAC 4.39 ± 2.42 nmol/L, P < 0.001). Noradrenaline was significantly lower under EGCG at POST-ING (P < 0.05), FATpeak (EGCG 0.93 ± 0.72 vs. PLAC 2.43 ± 1.04 nmol/L, P < 0.05), LT (EGCG 3.41 ± 2.27 vs. PLAC 7.12 ± 7.00 nmol/L, P < 0.01), and VO₂peak (EGCG 12.52 ± 6.53 vs. PLAC 21.90 ± 2.66 nmol/L, P < 0.05). Despite lower catecholamines, metanephrine and normetanephrine concentrations increased similarly with exercise in both trials (NS). Lipid oxidation rate at FATpeak was 32% lower in the EGCG trial (EGCG 0.33 ± 0.14 vs. PLAC 0.49 ± 0.11 g/min, P < 0.05), with a compensatory increase in carbohydrate oxidation (EGCG 0.87 ± 0.39 vs. PLAC 0.44 ± 0.34 g/min, P < 0.05). Blood lactate and glucose increased similarly with exercise intensity in both trials, though post-ingestion glucose was slightly lower under EGCG (EGCG Rest 4.39 ± 0.30 vs. Post-Ingestion 4.15 ± 0.30 mmol/L, P ≤ 0.05). Cycle time to exhaustion (EGCG 1370 ± 152 vs. PLAC 1377 ± 150 s, NS) and peak power output (EGCG 270 ± 32 vs. PLAC 266 ± 25 W, NS) were similar between conditions. Cardiorespiratory variables (heart rate, ventilation, VO₂, VCO₂, RER, RPE) showed no between-group differences.
**Clinical Implications:** This study provides the first in vivo evidence in humans that acute EGCG supplementation significantly lowers circulating catecholamine concentrations during exercise, contrary to the hypothesis that EGCG inhibits COMT (which would be expected to sustain or elevate catecholamines). The 32% reduction in lipid oxidation at FATpeak, occurring at the same relative exercise intensity in both trials, suggests that lower catecholamine concentrations may reduce stimulation of hormone-sensitive lipase, thereby decreasing intramuscular triglyceride utilization. The lack of difference in metanephrine/normetanephrine between trials indicates similar COMT activity, questioning the proposed COMT-inhibition mechanism. Alternative mechanisms, such as EGCG inhibition of DOPA decarboxylase or effects on chromaffin cell catecholamine secretion, warrant further investigation. The absence of any change in exercise performance or perceived exertion suggests that despite altered substrate metabolism and reduced sympatho-adrenal activity, compensatory mechanisms maintain functional capacity. These findings have implications for understanding how green tea catechins influence energy metabolism and may inform future research on metabolic modulation during exercise.