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Effects of Short-Term Detraining on Postprandial Metabolism, Endothelial Function, and Inflammation in Endurance-Trained Men: Dissociation between Changes in Triglyceride Metabolism and Endothelial Function

Departments of Pathological Biochemistry (J.M.R.G., M.J.C., C.J.P.) and Medicine (W.R.F.), Glasgow Royal Infirmary, Glasgow, Scotland G31 2ER, United Kingdom; and Department of Human Nutrition (C.M., F.T., D.M.), University of Glasgow, Glasgow, Scotland G12 8QQ, United Kingdom

Address all correspondence and requests for reprints to: Dr. Jason M. R. Gill, Division of Neuroscience and Biomedical Systems, Institute of Biomedical and Life Sciences, West Medical Building, University of Glasgow, Glasgow, G12 8QQ, United Kingdom. E-mail: j.gill{at}bio.gla.ac.uk.

Endurance-trained athletes experience a low level of postprandial lipaemia, but this rapidly increases with detraining. We sought to determine whether detraining-induced changes to postprandial metabolism influenced endothelial function and inflammation. Eight endurance-trained men each undertook two oral fat tolerance tests [blood taken fasted and for 6 h following a high-fat test meal (80 g fat, 80 g carbohydrate)]: one during a period of their normal training (trained) and one after 1 wk of no exercise (detrained). Endothelial function in the cutaneous microcirculation was assessed using laser Doppler imaging with iontophoresis in the fasted state and 4 h postprandially during each test. Fasting plasma triglyceride (TG) concentrations increased by 35% with detraining (P = 0.002), as did postprandial plasma (by 53%, P = 0.002), chylomicron (by 68%, P = 0.02) and very low-density lipoprotein (by 51%, P = 0.005) TG concentrations. Endothelial function decreased postprandially in both the trained (by 17%, P = 0.03) and detrained (by 22%, P = 0.03) conditions but did not differ significantly between the trained and detrained conditions in either the fasted or the postprandial states. These results suggest that, although fat ingestion induces endothelial dysfunction, interventions that alter postprandial TG metabolism will not necessarily concomitantly influence endothelial function.

Abbreviations: ACh, Acetylcholine; apo B, apolipoprotein B; HDL, high-density lipoprotein; LDL, low-density lipoprotein; NEFA, nonesterified fatty acid; NO, nitric oxide; VLDL, very LDL; SNP, sodium nitroprusside; TG, triglyceride.

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