Lipid metabolism response to a single, prolonged bout of endurance exercise in healthy young men

1 Washington University School of Medicine, St. Louis, Missouri; and 2 Department of Nutrition and Dietetics, Harokopio University, Athens, Greece Submitted 9 June 2005 ; accepted in final form 29 September 2005 To discover the alterations in lipid metabolism linked to postexercise hypotriglyceridemia, we measured lipid kinetics, lipoprotein subclass distribution and lipid transfer enzymes in seven healthy, lean, young men the day after 2 h of cycling and rest. Compared with rest, exercise increased fatty acid rate of appearance and whole body fatty acid oxidation by 65 and 40%, respectively ( P < 0.05); exercise had no effect on VLDL-triglyceride (TG) secretion rate, increased VLDL-TG plasma clearance rate by 40 ± 8%, and reduced VLDL-TG mean residence time by 40 min and VLDL-apolipoprotein B-100 (apoB-100) secretion rate by 24 ± 8% (all P < 0.05). Exercise also reduced the number of VLDL but almost doubled the number of IDL particles in plasma ( P < 0.05). Muscle lipoprotein lipase content was not different after exercise and rest, but plasma lipoprotein lipase concentration increased by 20% after exercise ( P < 0.05). Plasma hepatic lipase and lecithin:cholesterol acyltransferase concentrations were not affected by exercise, whereas cholesterol ester transfer protein concentration was 10% lower after exercise than after rest ( P = 0.052). We conclude that 1 ) greater fatty acid availability after exercise does not stimulate VLDL-TG secretion, probably because of the increase in fatty acid oxidation and possibly also fatty acid use for restoration of tissue TG stores; 2 ) reduced secretion of VLDL-apoB-100 lowers plasma VLDL particle concentration; and 3 ) increased VLDL-TG plasma clearance maintains low plasma TG concentration but is not accompanied by similar increases in subsequent steps of the delipidation cascade. Acutely, therefore, the cardioprotective lowering of plasma TG and VLDL concentrations by exercise is counteracted by a proatherogenic increase in IDL concentration. lipoprotein; fatty acid; stable isotope; metabolism Address for reprint requests and other correspondence: B. Mittendorfer, Washington Univ. School of Medicine, Div. of Geriatrics and Nutritional Sciences, 660 South Euclid Ave., Campus Box 8031, St. Louis, MO 63110 (e-mail: mittendb{at}wustl.edu )