REDUCED ADIPOSE-TISSUE LIPOPROTEIN-LIPASE RESPONSES, POSTPRANDIAL LIPEMIA, AND LOW HIGH-DENSITY LIPOPROTEIN-2 SUBSPECIES LEVELS IN OLDER ATHLETES WITH SILENT-MYOCARDIAL-ISCHEMIA

Healthy older (64 ± 1 years, mean ± SEM) athletic (maximal oxygen consumption [VOmax] > 40 mL/kg/min) normocholesterolemic men with no prior history of coronary artery disease (CAD) were recruited for cardiovascular and metabolic studies. Thirty-three percent had asymptomatic exercise-induced ST segment depression on their exercise electrocardiogram (ECG), consistent with silent myocardial ischemia (SI). We hypothesized that abnormalities in high-density lipoprotein (HDL) and postprandial triglyceride (TG) metabolism may increase their risk for CAD. Compared with 12 nonischemic controls of comparable age, percent body fat, and VOmax, the 13 men with SI had decreased fasting HDL cholesterol ([HDL-C] 41 ± 2 v 50 ± 2 mg/dL, P < .001) and %HDL2b subspecies levels as measured by gradient gel electrophoresis (22 ± 2 v 34 ± 3, P < .001). Fasting plasma TG and low-density lipoprotein cholesterol (LDL-C) levels were the same in both groups. Although plasma glucose levels during an oral glucose tolerance test (OGTT) were similar in both groups, the total insulin area was higher in men with SI (P < .05). After consumption of a standard high-fat maal (680 kcal/m2 body surface area of a formula in which 86% of the calories were derived from fat), postprandial plasma TG, chylomicron-TG, and very-low-density lipoprotein (VLDL)-TG levels and postprandial areas were higher in men with SI (P < .001). In stepwise multiple regression, the only independent predictors of postprandial TG areas were fasting TG levels (R2 = .76, P < .001) and log10 insulin area (R2 = .06, P < .02), which accounted for 82% of the variance in TG area. Therefore, after covarying for fasting plasma TG levels and total plasma insulin areas (ANCOVA), the difference in postprandial TG area between groups was no longer significant. The men with SI had higher postheparin hepatic lipase (HL) activity (P < .02), but had postheparin lipoprotein lipase (LPL) activity comparable to that of the control subjects. Fasting abdominal adipose tissue (AT) LPL activity was higher in the men with SI than in the control subjects (P < .05), but it did not change with feeding (0% ± 12%). In contrast, abdominal AT-LPL activity increased by 57% ± 19% at 4 hours (P < .05) in the control subjects. Postprandial TG areas were positively correlated with both the percent change in abdominal AT-LPL activity (r = -.41, P < .05) and postheparin HL activity (r = .58, P < .005). Thus, older normocholesterolemic nondiabetic athletic men with SI have increased insulin resistance, increased postheparin HL activity, and a reduced postprandial response of abdominal AT-LPL activity to feeding, which are associated with low HDL2 subspecies levels and increased postprandial lipemia. These abnormalities in HDL and postprandial TG metabolism may increase their risk for CAD. © 1994.