Background: Green tea consumption is reportedly associated with various health-promoting properties. For example, it has been shown to promote fat oxidation in humans at rest and to prevent obesity and improve insulin sensitivity in mice. Objective: We investigated the effects of acute ingestion of green tea extract (GTE) on glucose tolerance and fat oxidation during moderate-intensity exercise in humans. Design: Two studies were performed, both with a counter-balanced crossover design. In study A, 12 healthy men performed a 30-min cycling exercise at 60% of maximal oxygen consumption (V̇O₂max) before and after supplementation. In study B, 11 healthy men took an oral-glucose-tolerance test before and after supplementation. In the 24-h period before the experimental trials, participants ingested 3 capsules containing either GTE (total: 890 ± 13 mg polyphenols and 366 ± 5 mg EGCG) or a corn-flour placebo (total: 1729 ± 22 mg). Results: Average fat oxidation rates were 17% higher after ingestion of GTE than after ingestion of placebo (0.41 ± 0.03 and 0.35 ± 0.03 g/min, respectively; P < 0.05). Moreover, the contribution of fat oxidation to total energy expenditure was also significantly higher, by a similar percentage, after GTE supplementation. The insulin area under the curve decreased in both the GTE and placebo trials (3612 ± 301 and 4280 ± 309 μIU/dL · 120 min, respectively; P < 0.01), and there was a concomitant increase of 13% in insulin sensitivity. Conclusions: Acute GTE ingestion can increase fat oxidation during moderate-intensity exercise and can improve insulin sensitivity and glucose tolerance in healthy young men.

To determine the effects of training with low muscle glycogen on exercise performance, substrate metabolism, and skeletal muscle adaptation. Fourteen well-trained cyclists were pair-matched and randomly assigned to HIGH- or LOW-glycogen training groups. Subjects performed nine aerobic training (AT; 90 min at 70% VO2max) and nine high-intensity interval training sessions (HIT; 8 × 5-min efforts, 1-min recovery) during a 3-wk period. HIGH trained once daily, alternating between AT on day 1 and HIT the following day, whereas LOW trained twice every second day, first performing AT and then, 1 h later, performing HIT. Pretraining and posttraining measures were a resting muscle biopsy, metabolic measures during steady-state cycling, and a time trial. Power output during HIT was 297 ± 8 W in LOW compared with 323 ± 9 W in HIGH (P < 0.05); however, time trial performance improved by ∼10% in both groups (P < 0.05). Fat oxidation during steady-state cycling increased after training in LOW (from 26 ± 2 to 34 ± 2 μmol·kg−¹·min−¹, P < 0.01). Plasma free fatty acid oxidation was similar before and after training in both groups, but muscle-derived triacylglycerol oxidation increased after training in LOW (from 16 ± 1 to 23 ± 1 μmol·kg−¹·min−¹, P < 0.05). Training with low muscle glycogen also increased β-hydroxyacyl-CoA-dehydrogenase protein content (P < 0.01). Training with low muscle glycogen reduced training intensity and, in performance, was no more effective than training with high muscle glycogen. However, fat oxidation was increased after training with low muscle glycogen, which may have been due to the enhanced metabolic adaptations in skeletal muscle.

Neutrophils are implicated in the pathogenesis of atherosclerosis but are seldom detected in atherosclerotic plaques. We investigated whether neutrophil-derived microvesicles may influence arterial pathophysiology. Here we report that levels of circulating neutrophil microvesicles are enhanced by exposure to a high fat diet, a known risk factor for atherosclerosis. Neutrophil microvesicles accumulate at disease-prone regions of arteries exposed to disturbed flow patterns, and promote vascular inflammation and atherosclerosis in a murine model. Using cultured endothelial cells exposed to disturbed flow, we demonstrate that neutrophil microvesicles promote inflammatory gene expression by delivering miR-155, enhancing NF-κB activation. Similarly, neutrophil microvesicles increase miR-155 and enhance NF-κB at disease-prone sites of disturbed flow in vivo. Enhancement of atherosclerotic plaque formation and increase in macrophage content by neutrophil microvesicles is dependent on miR-155. We conclude that neutrophils contribute to vascular inflammation and atherogenesis through delivery of microvesicles carrying miR-155 to disease-prone regions.

The purpose of the present study was to determine whether probiotic supplementation (Lactobacillus casei Shirota (LcS)) prevents diet-induced insulin resistance in human subjects. A total of seventeen healthy subjects were randomised to either a probiotic (n 8) or a control (n 9) group. The probiotic group consumed a LcS-fermented milk drink twice daily for 4 weeks, whereas the control group received no supplementation. Subjects maintained their normal diet for the first 3 weeks of the study, after which they consumed a high-fat (65 % of energy), high-energy (50 % increase in energy intake) diet for 7 d. Whole-body insulin sensitivity was assessed by an oral glucose tolerance test conducted before and after overfeeding. Body mass increased by 0·6 (se 0·2) kg in the control group (P< 0·05) and by 0·3 (se 0·2) kg in the probiotic group (P>0·05). Fasting plasma glucose concentrations increased following 7 d of overeating (control group: 5·3 (se 0·1) v. 5·6 (se 0·2) mmol/l before and after overfeeding, respectively, P< 0·05), whereas fasting serum insulin concentrations were maintained in both groups. Glucose AUC values increased by 10 % (from 817 (se 45) to 899 (se 39) mmol/l per 120 min, P< 0·05) and whole-body insulin sensitivity decreased by 27 % (from 5·3 (se 1·4) to 3·9 (se 0·9), P< 0·05) in the control group, whereas normal insulin sensitivity was maintained in the probiotic group (4·4 (se 0·8) and 4·5 (se 0·9) before and after overeating, respectively (P>0·05). These results suggest that probiotic supplementation may be useful in the prevention of diet-induced metabolic diseases such as type 2 diabetes.

1) To investigate the effect of caffeine on exogenous carbohydrate (CHO) oxidation and glucose kinetics during exercise; and 2) to determine whether combined ingestion of caffeine and CHO enhanced cycling performance compared with CHO alone. Ten endurance-trained cyclists performed three experimental trials consisting of 105 min steady-state (SS) cycling at 62% VO2max followed by a time trial (TT) lasting approximately 45 min. During exercise, subjects ingested either of the following: a 6.4% glucose solution (GLU), a 6.4% glucose plus caffeine solution providing 5.3 mg kg(-1) of caffeine (GLU + CAF), or a placebo (PLA). Glucose solutions contained a trace amount of [U-C]glucose, and eight subjects received a primed continuous [6,6-H2]glucose infusion. Peak exogenous CHO oxidation rates were not significantly different between GLU and GLU + CAF trials (52.6 +/- 2.7 and 49.1 +/- 2.1 micromol kg.min(-1), respectively). Rates of appearance (Ra) and disappearance (Rd) of glucose were significantly higher with CHO ingestion than PLA (P < 0.01) but were not significantly different between GLU and GLU + CAF trials. Performance times were 43.45 +/- 0.86, 45.45 +/- 1.07, and 47.40 +/- 1.30 min for GLU + CAF, GLU, and PLA, respectively. Therefore, GLU + CAF ingestion enhanced TT performance by 4.6% (P < 0.05) compared with GLU and 9% (P < 0.05) compared with PLA. The coingestion of caffeine (5.3 mg kg(-1)) with CHO during exercise enhanced TT performance by 4.6% compared with CHO and 9.0% compared with water placebo. However, caffeine did not influence exogenous CHO oxidation or glucose kinetics during SS exercise.