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Lipid Profile Disorders Induced by Long-Term Cessation of Physical Activity in Previously Highly Endurance-Trained Subjects

University of Bordeaux 2; Institut National de la Santé et de la Recherche Médicale, Unité 577, Bio-Organic Chemistry Group (C.P., G.D.); and Faculty of Sport Sciences and Physical Education (C.P.); Department of Medicinal Biochemistry and Molecular Biology, Laboratory of Biochemistry (A.C.), and Department of Nutrition-Diabetology, Hospital of Haut-Levèque (H.G.); Bordeaux Centre Hospitalier Universitaire, 33076 Bordeaux, France

Address all correspondence and requests for reprints to: Dr. Cyril Petibois, Université Victor Segalen Bordeaux 2, Institut National de la Santé et de la Recherche Médicale, Unité 577, Groupe de Chimie Bio-Organique, 146 rue Léo Saignat, 33076 Bordeaux, France. E-mail: cyril.petibois{at}bioorga.u-bordeaux2.fr.

The objective of this study was to describe long-term detraining effects on lipid profile in previously highly endurance-trained athletes. The study design was longitudinal, with a 2-yr follow-up study of changes in lipid profile during hard training and detraining. Ten subjects trained for 2 yr (22 h/wk; two 47-wk training periods with a 5-wk recovery period), and the 10 others stopped training after wk 47. Main blood lipid profile parameters, energy intake, and body composition were measured at baseline (wk 1) and at wk 24, 47, 52, 76, and 99. Although food caloric intake was reduced (2411 ± 256 vs. 5697 ± 455 kcal/d, detraining vs. training), detraining induced a decrease in high density lipoprotein cholesterol and increases in fat mass (by 6.5 ± 1.1 kg), body mass index, leptin, low density lipoprotein cholesterol, low density lipoprotein/high density lipoprotein ratio, and apolipoprotein B, although insulin resistance (determined by homeostasis model assessment) stabilization had previously occurred. Further disorders appeared in triglycerides (TG) metabolism during detraining, with a persistent increase in TG (from 1.0 ± 0.3 to 1.4 ± 0.3 mmol/liter), whereas glycerol decreased (from 88 ± 9 to 73 ± 8 µmol/liter), and very low density lipoprotein-TG, chylomicrons, and apolipoprotein C₃ remained stable. Plasma lipoprotein lipase activity decreased whereas hepatic lipase activity remained stable. As well as a rapid loss of endurance-training benefits for the cholesterolemic profile, detraining also induced disorders in TG metabolism, possibly as a result of the elevated TG turnover acquired with long-term hard training.

Abbreviations: Apo, Apolipoprotein; BMI, body mass index; HDL-C, high density lipoprotein cholesterol; HL, hepatic lipase; LDL-C, low density lipoprotein cholesterol; LPL, lipoprotein lipase; Pl-LPL, plasma lipoprotein lipase; RER, respective respiratory exchange ratio; TC, total cholesterol; TG, triglycerides; VLDL, very low density lipoprotein; VCO₂, CO₂ volume; VO₂max, maximal oxygen consumption.

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