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Exercise performed immediately after fructose ingestion enhances fructose oxidation and suppresses fructose storage

Egli, Léonie ; Lecoultre, Virgile ; Cros, Jérémy ; Rosset, Robin ; Marques, Anne-Sophie ; Schneiter, Philippe ; Hodson, Leanne ; Gabert, Laure ; Laville, Martine ; Tappy, Luc

In: The American Journal of Clinical Nutrition, 2016, vol. 103, no. 2, p. 348-355

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    Title
    • Exercise performed immediately after fructose ingestion enhances fructose oxidation and suppresses fructose storage
    Author
    • Egli, Léonie. Department of Physiology, University of Lausanne, Lausanne, Switzerland
    • Lecoultre, Virgile. Department of Physiology, University of Lausanne, Lausanne, Switzerland
    • Cros, Jérémy. Department of Physiology, University of Lausanne, Lausanne, Switzerland
    • Rosset, Robin. Department of Physiology, University of Lausanne, Lausanne, Switzerland
    • Marques, Anne-Sophie. Department of Physiology, University of Lausanne, Lausanne, Switzerland
    • Schneiter, Philippe. Department of Physiology, University of Lausanne, Lausanne, Switzerland
    • Hodson, Leanne. Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, United Kingdom
    • Gabert, Laure. Centre for Research in Human Nutrition Rhône-Alpes
    • Laville, Martine. Centre for Research in Human Nutrition Rhône-Alpes
    • Tappy, Luc. Department of Physiology, University of Lausanne, Lausanne, Switzerland
    Document Type
    • Postprint
    Language
    • English
    Published in
    • The American Journal of Clinical Nutrition, 2016, vol. 103, no. 2, p. 348-355. Oxford University Press
    Other Version
    OAI-PMH Identifier
    • oai:doc.rero.ch:331976
    Summary
    Background: Exercise prevents the adverse effects of a high-fructose diet through mechanisms that remain unknown. Objective: We assessed the hypothesis that exercise prevents fructose-induced increases in very-low-density lipoprotein (VLDL) triglycerides by decreasing the fructose conversion into glucose and VLDL-triglyceride and fructose carbon storage into hepatic glycogen and lipids. Design: Eight healthy men were studied on 3 occasions after 4 d consuming a weight-maintenance, high-fructose diet. On the fifth day, the men ingested an oral 13C-labeled fructose load (0.75 g/kg), and their total fructose oxidation (13CO2 production), fructose storage (fructose ingestion minus 13C-fructose oxidation), fructose conversion into blood 13C glucose (gluconeogenesis from fructose), blood VLDL-13C palmitate (a marker of hepatic de novo lipogenesis), and lactate concentrations were monitored over 7 postprandial h. On one occasion, participants remained lying down throughout the experiment [fructose treatment alone with no exercise condition (NoEx)], and on the other 2 occasions, they performed a 60-min exercise either 75 min before fructose ingestion [exercise, then fructose condition (ExFru)] or 90 min after fructose ingestion [fructose, then exercise condition (FruEx)]. Results: Fructose oxidation was significantly (P < 0.001) higher in the FruEx (80% ± 3% of ingested fructose) than in the ExFru (46% ± 1%) and NoEx (49% ± 1%). Consequently, fructose storage was lower in the FruEx than in the other 2 conditions (P < 0.001). Fructose conversion into blood 13C glucose, VLDL-13C palmitate, and postprandial plasma lactate concentrations was not significantly different between conditions. Conclusions: Compared with sedentary conditions, exercise performed immediately after fructose ingestion increases fructose oxidation and decreases fructose storage. In contrast, exercise performed before fructose ingestion does not significantly alter fructose oxidation and storage. In both conditions, exercise did not abolish fructose conversion into glucose or its incorporation into VLDL triglycerides. This trial was registered at clinicaltrials.gov as NCT01866215.