Deviations from maximum weight predict high-density lipoprotein cholesterol levels in runners: the National Runners' Health Study

Abstract

Objective: The inverse relationship between adiposity and high-density lipoprotein (HDL) cholesterol is well established, however, we believe that its usual representation lacks an important dimension. The purpose of this study is to test whether the relationship depends upon past weight history in addition to current weight.

Design: Physician-supplied medical data were compared to questionnaires from a national cross-sectional survey.

Subjects: 6847 men who ran between zero and 171 km per week.

Measurements: Self-reported current weight, greatest lifetime weight and body circumferences were compared to physician-supplied data for plasma concentrations of HDL cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides.

Results: Current HDL-cholesterol levels were greatest in those runners with the greatest weight loss since their maximum lifetime weight and the greatest reductions in circumference of their waist, hip, and chest since their maximum weight. Plasma levels of triglycerides, LDL-cholesterol, and total cholesterol/HDL-cholesterol were also significantly lower for runners showing the greatest decreases in total and regional adiposity since their maximum weight. The results remained significant when adjusted for current body mass index and running mileage.

Conclusion: These results suggest that the lipoprotein concentrations of runners are in part dependent upon whether the current weight is relatively high or low within the historical range of weights experienced by the individual.

Figures

Figure 1

Mean plasma concentrations of HDL-cholesterol, triglycerides and the ratio of total cholesterol to HDL-cholesterol (vertical axis) in men divided into groups according to their changes in body mass index and waist circumference since greatest weight. Significant group differences (P < 0.05) by changes in body mass index are coded: * different from > − 2.0 kg/m2; † different from − 2 to − 4 kg/m2; § different from − 4 to − 6 kg/m2. Significant group differences (P < 0.05) by changes in waist circumference are coded: * different from > − 3 cm; † different from − 3 to − 6 cm; § different from − 6 to − 9 cm.

Figure 2

High lipoprotein lipase activity may increase HDL-cholesterol in previously overweight runners by reducing the pool of triglyceride-rich lipoproteins (for example chylomicrons, VLDL) thereby favoring the pathway of low cholesteryl ester triglyceride exchange [20,21]. Specifically, cholesteryl ester, formed from free cholesterol by L:CAT (lecithin:cholesterol acyltransferase); (A), is incorporated into the HDL core (B). This process is continued (F,G,H,I) leading to the formation of HDL2. Under the alternative pathway of high cholesteryl ester triglyceride exchange, HDL forms a ternary complex with cholesteryl ester transfer protein and either chylomicron or VLDL particles (C). When this occurs, the cholesteryl ester transfer protein may mediate the net transfer of cholesteryl ester from HDL to the chylomicron or VLDL particle (C). In exchange for the cholesteryl ester, triglyceride is transferred to HDL (D), which may then be hydrolyzed by hepatic lipase (E), so that HDL-cholesteryl ester does not accumulate.