The effects of physical exercise on plasma prebeta-1 high-density lipoprotein.
The impact of physical exercise on high-density lipoprotein (HDL) metabolism is recognized as a major mechanism of coronary artery disease (CAD) risk reduction. Prebeta-1 HDL subparticle species play a pivotal role in initiating reverse cholesterol transport (RCT). We examined the effect of acute physical exercise on plasma prebeta-1 HDL levels. Nineteen nonsmoking, healthy men (n = 11) and women (n = 8) not receiving lipid-altering medications completed dietary surveys, and had percent body fat determinations, and fasting blood drawn for measurements of plasma lipids, lipoproteins, apolipoprotein A-I (Apo A-I), and absolute and percent prebeta-1 HDL. Each subject completed cardiopulmonary exercise stress testing to Vo(2max) followed by a 4-km course of run-jogging. Laboratory measurements were repeated from blood drawn immediately after exercise. Mean +/- SD values were determined for age, percent body fat, dietary calories, dietary cholesterol, dietary fat, and plasma lipids, lipoproteins, Apo A-I, and absolute and percent prebeta-1 HDL using 1-way analysis of variance (ANOVA). One-way ANOVA comparisons were made for measurements of plasma lipids, lipoproteins, Apo A-I, and absolute and percent prebeta HDL measurements taken before and after exercise for all subjects combined. Entry characteristics showed the following (mean +/-SD): age, 24 +/- 5.8 years; body mass index (BMI), 22.4 +/- 2.6; percent body fat, 13 +/- 5.7; and Vo(2max), 49.1 +/- 7.9 mL O(2)/kg/min. Exercise significantly increased absolute plasma prebeta HDL (0.10 +/- 0.05 to 0.130 +/- 0.07 microg/mL, P =.039) and decreased plasma HDL-triglycerides (23.3 +/- 10.8 to 12.5 +/- 5.6 mg/dL, P =.012). Our findings indicate that prebeta-1 HDL and HDL-triglyceride metabolism are significant components of the effect of acute exercise on RCT. These findings have important relevance for studies pertaining to exercise-related effects on HDL metabolism as pertains to CAD risk reduction.
Jafari
Mahtab
M
Department of Medicine, University of California, Irvine, USA.
Leaf
David Alexander
DA
Macrae
Holden
H
Kasem
Julie
J
O'conner
Patricia
P
Pullinger
Clive
C
Malloy
Marry
M
Kane
John P
JP
D000328:Adult; D000375:Aging / Q000502:physiology; D016632:Apolipoprotein A-I / Q000097:blood; D001053:Apolipoproteins / Q000097:blood; D001823:Body Composition / Q000502:physiology; D015992:Body Mass Index; D002791:Cholesterol, Dietary / Q000494:pharmacology; D004041:Dietary Fats / Q000494:pharmacology; D002149:Energy Intake; D015444:Exercise / Q000502:physiology*; D005260:Female; D053442:High-Density Lipoproteins, Pre-beta; D006801:Humans; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D008075:Lipoproteins, HDL / Q000097:blood*; D008297:Male
D016632:Apolipoprotein A-I; D001053:Apolipoproteins; D002791:Cholesterol, Dietary; D004041:Dietary Fats; D053442:High-Density Lipoproteins, Pre-beta; D008055:Lipids; D008074:Lipoproteins; D008075:Lipoproteins, HDL