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
Authors: Gill, J.M.R., Caslake, M.J., McAllister, C., Tsofliou, F., Ferrell, W.R., Packard, C.J. and Malkova, D.
Journal: Journal of Clinical Endocrinology and Metabolism
Volume: 88
Issue: 9
Pages: 4328-4335
ISSN: 0021-972X
DOI: 10.1210/jc.2003-030226
Abstract:Endurance-trained athletes experience a low level of post-prandial 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.
Source: Scopus
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. j.gill@bio.gla.ac.uk.
Authors: Gill, J.M.R., Caslake, M.J., McAllister, C., Tsofliou, F., Ferrell, W.R., Packard, C.J. and Malkova, D.
Journal: J Clin Endocrinol Metab
Volume: 88
Issue: 9
Pages: 4328-4335
ISSN: 0021-972X
DOI: 10.1210/jc.2003-030226
Abstract: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.
Source: PubMed
Preferred by: Fotini Tsofliou
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
Authors: Gill, J.M.R., Caslake, M.J., McAllister, C., Tsofliou, F., Ferrell, W.R., Packard, C.J. and Malkova, D.
Journal: JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
Volume: 88
Issue: 9
Pages: 4328-4335
ISSN: 0021-972X
DOI: 10.1210/jc.2003-030226
Source: Web of Science (Lite)
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. j.gill@bio.gla.ac.uk.
Authors: Gill, J.M.R., Caslake, M.J., McAllister, C., Tsofliou, F., Ferrell, W.R., Packard, C.J. and Malkova, D.
Journal: The Journal of clinical endocrinology and metabolism
Volume: 88
Issue: 9
Pages: 4328-4335
eISSN: 1945-7197
ISSN: 0021-972X
DOI: 10.1210/jc.2003-030226
Abstract: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.
Source: Europe PubMed Central