It appears that weekly exercise caloric expenditures that meet or exceed the higher end of this range are more likely to produce the desired lipid changes. Regarding hyperlipidemic disorders, the primary means for intervention is pharmacologic, whereas diet modification, weight loss, and exercise, although important, are viewed as adjunctive therapies. Because much is known about the exercise training-induced plasma lipid and lipoprotein modifications as well as the mechanisms responsible for these changes, rehabilitation professionals can better develop a comprehensive medical management plan that optimizes pharmacologic, reduced dietary fat intake, weight loss, and exercise interventions.
After adjustment for race, body mass index (BMI), and hormone replacement status, a graded reduction in the Framingham risk score was observed across low (5.8%), moderate (4.0%), and high (3.6%) fitness levels (P for trend = 0.009). Women in both the moderate and high fitness categories had a lower (P < 0.01) risk score compared with their low fit counterparts. Significant differences in risk were not seen among low (3.9%), moderate (4.9%), and high (4.4%) physical activity groups. The lack of association between the risk score by physical activity may have been due to the homogeneity of activity levels among participants. Our findings reinforce existing data that show enhanced levels of fitness are associated with lower risk for CHD.
Lipoprotein(a) (Lp(a)) is bound to apolipoprotein B-100 by disulfide linkage and is associated in the upper density range of low density lipoprotein cholesterol. Persons with elevated concentrations of Lp(a) are regarded as having an increased risk for premature coronary artery disease. Although many studies exist evaluating the effects of a single session of exercise on lipids and lipoproteins, little information is available concerning the effects of exercise on Lp(a). Therefore, the purpose of this study was to determine the effects of a single exercise session on plasma Lp(a). Twelve physically active men completed two 30-min submaximal treadmill exercise sessions: low intensity (LI, 50% VO2max) and high intensity (HI, 80% VO2max). Blood samples were obtained immediately before and after exercise. Total cholesterol (LI: before 4.22 +/- 0.26, after 4.24 +/- 0.28; HI: before 4.24 +/- 0.31, after 4.11 +/- 0.28 mmol.l-1, mean +/- SE) and triglyceride (LI: before 1.14 +/- 0.16, after 1.06 +/- 0.16; HI: before 1.12 +/- 0.19, after 1.21 +/- 0.19 mmol.l-1) concentrations did not differ immediately after either exercise session, nor did Lp(a) concentrations differ immediately after either exercise session (LI: before 4.1 +/- 2.2, after 4.0 +/- 2.1: HI: before 3.9 +/- 2.2, after 3.7 +/- 2.0 mg.dl-1). These results suggest that neither a low nor a high intensity exercise session lasting 30 min in duration has an immediate effect on plasma Lp(a).
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