Exercise training alters plasma lipoprotein profiles in a manner compatible with decreased coronary artery disease risk. The aim of this study was to ascertain whether interuption of training (detraining) was associated with potentially undesirable changes in the metabolism of post-prandial lipoproteins and plasma levels of Lp(a). Eight normolipidemic, male runners who ran 30-40 miles/week were studied in the trained state and after 14-22 days of detraining. Two of the subjects were studied in the reverse order to control for any confounding effects of exercise sequence. Detraining resulted in (1) a 12% (P = 0.002) reduction in the subjects' aerobic capacity, (2) a 7.7% (P = 0.007) reduction in fasting concentrations of high density lipoprotein cholesterol (HDL-C), (3) a 21% (P = 0.01) reduction in post-heparin lipoprotein lipase activity. Lp(a) concentrations did not change significantly (mean increase 15%, P = 0.076). Fasting plasma concentrations of total cholesterol (TC), triglycerides (TG) and low density lipoprotein-cholesterol (LDL-C) did not change in the detrained state. There was little fluctuation over 24 h in plasma concentrations of TC, LDL-C and HDL-C in either the trained or detrained states. TG concentrations fluctuated over the 24 h in accord with food intake, but there were no exercise-related changes. Exercise had a dramatic effect on chylomicron and chylomicron remnant metabolism as measured by retinyl palmitate measurements. The mean areas under the concentration vs. time curves (AUC) for chylomicron-retinyl esters increased by 41% (P = 0.013) and for chylomicron remnant-retinyl ester by 37% (P = 0.058) following detraining. Thus, brief intervals of detraining reduced fasting concentrations of HDL-C and decreased the metabolism of chylomicrons. These changes are associated with an increased incidence of atherosclerosis.
|Number of pages||9|
|State||Published - Aug 1992|
Bibliographical noteFunding Information:
We would like to thank Cheryl Doyon for typing the manuscript and the study participants and the nurses at Washington University’s Clinical Research Center for their essential assistance and participation. This investigation was supported by Public Health Service Research Grants GCRC No. RRO0036, ROl HL42460-03, 5POl A605562-07, Kl l-DKO1762-05 and HL-17646-17.
- Hepatic triglyceride lipase
- Lipoprotein lipase
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine