We investigated the effect of a fatty meal on plasma concentrations of lipids, apolipoproteins, and the cholesterol component of lipoproteins. Sixteen nonobese, healthy, asymptomatic males, 22-34 years of age, served as subjects for this study. None smoked, consumed more than two alcoholic drinks per day, or took any medication known to alter plasma lipids. After a 12 h fast, baseline plasma samples were obtained just before subjects consumed a high fat meal. The meal, standardized to a 70 kg individual, contained approximately 70 g fat, 580 mg cholesterol, and 1100cal, with 56% of the calories coming from fat. During the 8 h following consumption of the meal, subjects rested quietly and consumed no food or beverages except water. Blood specimens were obtained hourly. There was a significant increase in plasma triglyceride (150% from baseline at 3 h, P < 0•0005). Very low density lipoprotein cholesterol (VLDL-C) concentrations increased 150% at 3 h (P < 0,0005) while low density lipoprotein cholesterol (LDL-C) concentration decreased 37% at 3 h (P < 0'005) when estimated by Friedewald's formula. No statistically significant differences were observed between fasting total cholesterol, high density lipoprotein cholesterol (HDL-C), HDL2-C, and HDU-C, apolipoprotein AI (apo AI, All), and B-IOO concentrations and non-fasting samples. We conclude that plasma triglyceride concentration is significantly affected in the post-prandial state. As a result, VLDL-C and LDL-C when assessed by the Friedewald formula are also altered. A minimum of 8 h fasting is required to assess these concentrations accurately in this population. The concentrations of total cholesterol, HDL-C, HDL2-C, HDU-C, apo AI, apo All, and apo B-lOO can be determined adequately using a non-fasting specimen.

To test the hypothesis that endurance training Is associated with a decreased llpemla after a high fat meal, 16 young men [22 to 34 years old, nine of whom were trained (T) and seven of whom were untrained (UT)] were recruited. T ran >30 or blked >100 miles a week, while UT had been sedentary for at least the preceding 3 months. Dally caloric Intake and dally caloric expenditure during exercise were 35% and 704% greater, respectively, In T than In UT. V O i^ was 31% greater, while percent body fat was 36% lower In T than In UT. Dietary composition and body height and weight were similar. After a fasting blood sample was taken, the men ate a high fat meal (approximately 56% of total calories as fat In 1100 kcal adjusted to body weight), and additional blood samples were taken hourly for 8 hours. Fasting llplds were similar. Postprandial peak trtglyceride (TGw), percent TG Increase (%TGI), and total llpemlc response (TLR, the area under the llpemla curve In excess of fasting TG) were 42%, 54%, and 75% greater, respectively, In UT vs. T. Stepwlse regression analysis showed that the same three-variable model (training status, fasting TG, and VOJ™,) described the variation In T G^ (/7'=0.97), %TGI (ft'=0.75), and TLR (ft 2 =0.92). Furthermore, this same analysis showed that after adjustment for fasting TG and VOftn.,, the UT group had a significantly greater postprandial llpemla whether expressed as T G^ (/X0.0001), %TGI (p=0.0002), or TLR (p=0.0002). Thus, endurance training appears to be associated with a diminished llpemla after a high fat meal in young adult men. (Arteriosclerosis 9:217-223, March/April 1989) A therosclerosis is the major underlying cause of death and disability in Western society.1 Most research dealing with the etiology of atherosclerotic vascular disease has linked elevated postabsorptive blood cholesterol and low density lipoproteins with an increased risk of developing the disease. In contrast, little attention has been paid to fat tolerance, which may be defined as the plasma triglyceride (TG) response to a fatty meal.2 However, the magnitude of the triglyceridemic response to a standard fatty meal (postprandial lipemia) differs substantially among apparently healthy individuals who are considered normolipidemic on the basis of fasting blood lipid values.3 Even among apparently normolipidemic individuals, the variability in postprandial lipemia may be pathophysiological, since a significant lipemia may persist throughout most of the day in normal adults consuming fatty foods over three meals. 4 In fact, recent work by Zilversmit 3 suggests that postprandial metabolism of TGrich lipoproteins may constitute an atherogenic process in individuals who chronically eat a diet rich in fat and cholesterol. Furthermore, Engelberg 6 has recently reviewed some older literature, which suggests that tissue hypoxia Received January 4,1988; revision accepted October 24,1988. can also result from this postprandial lipemia and that this hypoxia may also be atherogenic. Thus, if the rate of atherogenesis ...

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