Increased reverse cholesterol transport in athletes.

Proposed mechanisms for the cardioprotective benefits of exercise include decreased lipid deposition and increased reverse cholesterol transport (RCT). RCT involves the efflux of tissue free cholesterol into high-density lipoprotein (HDL) particles, esterification by lecithin:cholesterol acyltransferase (LCAT), transfer to other lipoproteins by cholesterol ester transfer proteins (CETP), and liver excretion. We tested the hypothesis that RCT is enhanced in athletes and that this can occur without large increases in plasma HDL cholesterol (HDL-C) mass levels. Fasting venous blood was drawn from 13 sedentary men and 11 athletes exercising at the rate of 5,185 +/- 501 kcal/wk. Compared with controls, athletes had similar age, body mass index (BMI), HDL-C (P > .1) and apolipoprotein (apo) A-1 (P > .5) levels, and lower low-density lipoprotein cholesterol (LDL-C) (P < .05) and apo B (P < .03) levels. The net mass of free cholesterol transported (NMCT) out of cultured human fibroblasts into the athletes' serum was greater than that for controls (25.5 +/- 8.0 v 7.1 +/- 2.6 micrograms/mL/h, P = .048). The efflux component of this transport correlated with HDL-C and apo A-1 levels and was similar between groups (P = .24), suggesting that athletes' antiatherogenic NMCT findings were due to decreased cholesterol influx into the cells. Athletes had increased plasma LCAT (20.3 +/- 2.1 v 13.9 +/- 1.5 micrograms/mL/h, P = .028) and CETP activities (69.7 +/- 4.5 v 21.5 +/- 4.8%/mL/h, P < .001). The NMCT positively correlated with CETP and LCAT activities and inversely with apo B levels and the cardiac risk ratio apo B/A-1.(ABSTRACT TRUNCATED AT 250 WORDS)