Glucose-fructose beverages do not alter the effects of training on lactate metabolism

Glucose-fructose beverages do not alter the effects of training on lactate metabolism Rosset R., Egli L., Cros J., Schneiter P. and Tappy L. and Lecoultre V. Department of Physiology, University of Lausanne, Lausanne, Switzerland. Introduction It is generally accepted that lactate is produced by skeletal muscle during exercise, and is either used in adjacent muscle fibers (lactate shuttle) or recycled to glucose in the liver. We have shown that ingestion of fructose-containing drinks stimulates lactate production and release from the liver during exercise, and that fructose-derived lactate is subsequently used as an energy substrate by muscle. The regulation of this liver to muscle fructose-lactate shuttle remains unknown. In this study, we assessed whether consumption of fructose-containing beverages alters the effects of training on fructose and lactate metabolism. Methods Two groups of eight sedentary male subjects were endurance-trained for three weeks while ingesting 489 mL/h of either a 9.8%-glucose 6.2%-fructose beverage (GLUFRU) or water (C) during exercise training sessions. An incremental test to exhaustion and a metabolic test were performed before and after the interventions to assess training adaptations and substrate use during endurance-type exercise. Indirect calorimetry, [1-13C]lactate and [6,6-2H2]glucose were used to calculate plasma lactate appearance, clearance and oxidation and glucose kinetics. Results Anthropometrics and performance parameters were similar in both groups at baseline. Plasma glucose concentrations (+1±3 vs. +3±3 % vs. baseline values), glucose rate of appearance (+3±7 vs. +2±3 %) and metabolic clearance (+6±8 vs. +1±5 %) remained stable after both GLUFRU and C training (all p=n.s.). Overall, lactate concentrations were decreased after intervention in both GLUFRU and C, but not differently between groups (-10±5 vs. -20±4 %; p<0.01 vs. baseline, p=n.s. between GLUFRU and C), as a result of an increased lactate metabolic clearance (+26.5±11.4 vs. +17.5±10.2 mL·min-1; p=0.01 vs. baseline, p=0.56 between GLUFRU and C). Lactate appearance (+10±6 vs. -4±9 %) and oxidation (+9±6 vs. - 6±9 %) remained unchanged across time and conditions (all p=n.s.). Maximal oxygen consumption (+287±53 vs. +249±104 mL·min-1) and power eliciting lactate threshold (+25±5 vs. +25±8 W) were similarly increased in GLUFRU and C (both p<0.01 vs. baseline, p=n.s. between GLUFRU and C). Discussion These data corroborate our earlier observation that fructose is converted into lactate by the liver and subsequently oxidized during exercise. Endurance training did not alter liver lactate release, but increased lactate metabolic clearance. The effects of endurance training were not differently altered by the consumption of fructose during training sessions, however

Effects of Dietary Protein and Fat Content on Intrahepatocellular and Intramyocellular Lipids during a 6-Day Hypercaloric, High Sucrose Diet: A Randomized Controlled Trial in Normal Weight Healthy Subjects.

Sucrose overfeeding increases intrahepatocellular (IHCL) and intramyocellular (IMCL) lipid concentrations in healthy subjects. We hypothesized that these effects would be modulated by diet protein/fat content. Twelve healthy men and women were studied on two occasions in a randomized, cross-over trial. On each occasion, they received a 3-day 12% protein weight maintenance diet (WM) followed by a 6-day hypercaloric high sucrose diet (150% energy requirements). On one occasion the hypercaloric diet contained 5% protein and 25% fat (low protein-high fat, LP-HF), on the other occasion it contained 20% protein and 10% fat (high protein-low fat, HP-LF). IHCL and IMCL concentrations (magnetic resonance spectroscopy) and energy expenditure (indirect calorimetry) were measured after WM, and again after HP-LF/LP-HF. IHCL increased from 25.0 ± 3.6 after WM to 147.1 ± 26.9 mmol/kg wet weight (ww) after LP-HF and from 30.3 ± 7.7 to 57.8 ± 14.8 after HP-LF (two-way ANOVA with interaction: p < 0.001 overfeeding x protein/fat content). IMCL increased from 7.1 ± 0.6 to 8.8 ± 0.7 mmol/kg ww after LP-HF and from 6.2 ± 0.6 to 6.9 ± 0.6 after HP-LF, (p < 0.002). These results indicate that liver and muscle fat deposition is enhanced when sucrose overfeeding is associated with a low protein, high fat diet compared to a high protein, low fat diet

Measurement of electroweak parameters from hadronic and leptonic decays of the Z 0

We have studied the reactions e + e − →hadrons, e + e − , μ + μ − and τ + τ − , in the energy range 88.2 GeV. A total luminosity of 5.5 pb −1 , corresponding to approximately 115000 hadronic and 10000 leptonic Z 0 decays, has been recorded with the L3 detector. From a simultaneous fit to all of our measured cross section data, we obtain assuming lepton universality:Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47890/1/10052_2005_Article_BF01475788.pd

Effects of fructose-containing caloric sweeteners on resting energy expenditure and energy efficiency: a review of human trials.

Epidemiological studies indicate that the consumption of fructose-containing caloric sweeteners (FCCS: mainly sucrose and high-fructose corn syrup) is associated with obesity. The hypothesis that FCCS plays a causal role in the development of obesity however implies that they would impair energy balance to a larger extent than other nutrients, either by increasing food intake, or by decreasing energy expenditure. We therefore reviewed the literature comparing a) diet-induced thermogenesis (DIT) after ingestion of isocaloric FCCS vs glucose meals, and b) basal metabolic rate (BMR) or c) post-prandial energy expenditure after consuming a high FCCS diet for > 3 days vs basal,weight-maintenance low FCCS diet. Nine studies compared the effects of single isocaloric FCCS and glucose meals on DIT; of them, six studies reported that DIT was significantly higher with FCCS than with glucose, 2 reported a non-significant increase with FCCS, and one reported no difference. The higher DIT with fructose than glucose can be explained by the low energy efficiency associated with fructose metabolism. Five studies compared BMR after consumption of a high FCCS vs a low FCCS diet for > 3 days. Four studies reported no change after 4-7 day on a high FCCS diet, and only one study reported a 7% decrease after 12 week on a high FCCS diet. Three studies compared post-prandial EE after consumption of a high FCCS vs a low FCCS diet for > 3 days, and did not report any significant difference. One study compared 24-EE in subjects fed a weight-maintenance diet and hypercaloric diets with 50% excess energy as fructose, sucrose and glucose during 4 days: 24-EE was increased with all 3 hypercaloric diets, but there was no difference between fructose, sucrose and glucose. We conclude that fructose has lower energy efficiency than glucose. Based on available studies, there is presently no hint that dietary FCCS may decrease EE. Larger, well controlled studies are however needed to assess the longer term effects of FCCS on EE