Inactivity, exercise training and detraining, and plasma lipoproteins. STRRIDE: a randomized, controlled study of exercise intensity and amount

2007 ◽  
Vol 103 (2) ◽  
pp. 432-442 ◽  
Author(s):  
Cris A. Slentz ◽  
Joseph A. Houmard ◽  
Johanna L. Johnson ◽  
Lori A. Bateman ◽  
Charles J. Tanner ◽  
...  
Keyword(s):  
Exercise Training ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Lipoproteins ◽  
Moderate Intensity ◽  
Controlled Study ◽  
Low Density ◽  
Moderate Intensity Exercise ◽  
Beneficial Effects ◽  
Vigorous Intensity

Exercise has beneficial effects on lipoproteins. Little is known about how long the effects persist with detraining or whether the duration of benefit is effected by training intensity or amount. Sedentary, overweight subjects ( n = 240) were randomized to 6-mo control or one of three exercise groups: 1) high-amount/vigorous-intensity exercise; 2) low-amount/vigorous-intensity exercise; or 3) low-amount/moderate-intensity exercise. Training consisted of a gradual increase in amount of exercise followed by 6 mo of exercise at the prescribed level. Exercise included treadmill, elliptical trainer, and stationary bicycle. The number of minutes necessary to expend the prescribed kilocalories per week (14 kcal·kg body wt−1·wk−1for both low-amount groups; 23 kcal·kg body wt−1·wk−1for high-amount group) was calculated for each subject. Average adherence was 83–92% for the three groups; minutes per week were 207, 125, and 203 and sessions per week were 3.6, 2.9, and 3.5 for high-amount/vigorous-intensity, low-amount/vigorous intensity, and low-amount/moderate-intensity groups, respectively. Plasma was obtained at baseline, 24 h, 5 days, and 15 days after exercise cessation. Continued inactivity resulted in significant increases in low-density lipoprotein (LDL) particle number, small dense LDL, and LDL-cholesterol. A modest amount of exercise training prevented this deterioration. Moderate-intensity but not vigorous-intensity exercise resulted in a sustained reduction in very-low-density lipoprotein (VLDL)-triglycerides over 15 days of detraining ( P < 0.05). The high-amount group had significant improvements in high-density lipoprotein (HDL)-cholesterol, HDL particle size, and large HDL levels that were sustained for 15 days after exercise stopped. In conclusion, physical inactivity has profound negative effects on lipoprotein metabolism. Modest exercise prevented this. Moderate-intensity but not vigorous-intensity exercise resulted in sustained VLDL-triglyceride lowering. Thirty minutes per day of vigorous exercise, like jogging, has sustained beneficial effects on HDL metabolism.

scholarly journals Effectiveness of Low to Moderate Physical Exercise Training on the Level of Low-Density Lipoproteins: A Systematic Review

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Ali M. Albarrati ◽  
Mansour Saleh M. Alghamdi ◽  
Rakan I. Nazer ◽  
Maarab M. Alkorashy ◽  
Nora Alshowier ◽  
...  
Keyword(s):  
Exercise Training ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density Lipoproteins ◽  
Moderate Intensity ◽  
Current Evidence ◽  
Low Density ◽  
Moderate Intensity Exercise ◽  
Randomized Controlled ◽  
Increased Risk

Background. Regular exercise reduces risk factors associated with cardiovascular disease (CVD). Elevated low-density lipoprotein (LDL) contributes to atherosclerosis formation, which is associated with an increased risk of CVD. The relationship between exercise therapy and lipid levels has been widely studied, but it is established that high-intensity exercise improves lipid profile. However, the effectiveness of low- to moderate-intensity exercise in altering LDL levels is controversial. This review aims to identify the current evidence and existing gaps in literature in this area. Methods. We searched and reviewed various randomized controlled clinical trials in the electronic databases EMBASE, CINAHL, the Web of Science, Cochrane, Pedro, Medline (PubMed), and Google Scholar using the keywords “low and moderate aerobic training,” “exercise”, “low-density lipoproteins,” “cholesterol,” “atherosclerosis,” and “coronary artery diseases markers.” We included studies that involved low- and/or moderate-intensity exercise training in apparently healthy adults over a period of 8 weeks and its effect on LDL levels. We selected a total of 11 studies from 469; nine were randomized controlled trials and two were systematic reviews. Results. Aerobic exercise of both low and moderate intensity resulted in a significant reduction of total cholesterol. Effects on low-density lipoprotein levels were significant, and most of the studies showed changes in the level without significant relation to the type of exercise. At the same time, exercise improved the health status and physical fitness of all the participants in the included studies. Conclusion. This study found that low- and moderate-intensity exercise and low-density lipoprotein levels were not proven to be significantly related, except in a few studies that were limited to dyslipidemia population.

Oxidized Low-Density Lipoprotein and Cell Adhesion Molecules Following Exercise Training

2017 ◽  
Vol 39 (02) ◽  
pp. 83-88 ◽  
Author(s):  
Yunsuk Koh ◽  
Jin Park ◽  
Rick Carter
Keyword(s):  
Cell Adhesion ◽  
Exercise Training ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Serum Lipids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Moderate Intensity ◽  
Oxidized Low Density Lipoprotein ◽  
Moderate Intensity Exercise

AbstractElevated oxidized low-density lipoprotein (ox-LDL) and cell adhesion molecules are associated with inflammation and atherosclerosis. The role of exercise in circulating ox-LDL, enzyme mediators, and cell adhesion molecules are not clearly understood in obesity. As a randomized controlled design, 27 obese (BMI>30 kg/m2) sedentary men (N=13) and women (N=14) were randomly assigned to either an exercise (N=15) or a control (N=12) group. The exercise group performed a 60-min supervised treadmill exercise at moderate intensity (70% of HRmax) for 3 days per week for 4 weeks, while the control group did not exercise. Overnight fasting blood samples were collected before and after the study period to analyze serum lipids, lipoprotein-cholesterol, ox-LDL, 12- and 15-lipoxygenases, myeloperoxidase (MPO), and soluble vascular cell adhesion molecules-1 and intercellular adhesion molecule-1. Moderate-intensity exercise training lowered both ox-LDL (from 44.76±1.99 to 38.51±1.99 U/L, p=0.032) and MPO (from 31.48±2.20 to 23.09±2.20 ng/mL, p=0.010), without significantly altering body weight, other parameters of serum lipids and lipoproteins, or soluble cell adhesion molecules. Moderate intensity exercise training reduced the levels of ox-LDL and MPO, indicating a reduced risk for developing CVD and additional protection to the possible metabolic complications associated with obesity.

Studies on the Thromboplastic Effect of Human Plasma Lipoproteins

1976 ◽  
Vol 35 (01) ◽  
pp. 178-185 ◽  
Author(s):  
Helena Sandberg ◽  
Lars-Olov Andersson
Keyword(s):  
High Density Lipoprotein ◽  
Human Plasma ◽  
Platelet Rich Plasma ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Lipoproteins ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Free Plasma ◽  
Good Agreement

SummaryHuman plasma lipoprotein fractions were prepared by flotation in the ultracentrifuge. Addition of these fractions to platelet-rich, platelet-poor and platelet-free plasma affected the partial thromboplastin and Stypven clotting times to various degrees. Addition of high density lipoprotein (HDL) to platelet-poor and platelet-free plasma shortened both the partial thromboplastin and the Stypven time, whereas addition of low density lipoprotein and very low density lipoprotein (LDL + VLDL) fractions only shortened the Stypven time. The additions had little or no effect in platelet-rich plasma.Experiments involving the addition of anti-HDL antibodies to plasmas with different platelet contents and measuring of clotting times produced results that were in good agreement with those noted when lipoprotein was added. The relation between structure and the clot-promoting activity of various phospholipid components is discussed.

scholarly journals Rabbit and rat C-reactive proteins bind apolipoprotein B-containing lipoproteins.

1984 ◽  
Vol 159 (2) ◽  
pp. 604-616 ◽  
Author(s):  
I F Rowe ◽  
A K Soutar ◽  
I M Trayner ◽  
M L Baltz ◽  
F C de Beer ◽  
...  
Keyword(s):  
Acute Phase ◽  
Apolipoprotein B ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Lipoproteins ◽  
Free Form ◽  
Low Density ◽  
Serum Samples ◽  
Acute Phase Serum

Immobilized rabbit and rat C-reactive protein (CRP) were found to selectively bind apolipoprotein B (apoB)-containing lipoproteins (low density lipoprotein, LDL and very low density lipoprotein, VLDL) from whole serum in a manner similar to that previously reported with human CRP. In acute phase human serum the CRP is in a free form, not complexed with lipoprotein or any other macromolecular ligand, and in acute phase serum from most rabbits fed on a normal diet the rabbit CRP was also free. However, in acute phase serum or heparinized plasma from hypercholesterolemic rabbits part or all of the CRP was found by gel filtration and immunoelectrophoretic techniques to be complexed with beta-VLDL, an abnormal apoB-containing plasma lipoprotein present in these animals. The presence of extent in different serum samples of CRP complexed with lipoprotein correlated closely with the serum apoB concentration. The formation of complexes between native, unaggregated rabbit CRP in solution and apoB-containing lipoproteins was readily demonstrable experimentally both with the isolated proteins and in whole serum. In all cases these interactions were calcium-dependent and inhibitable by free phosphoryl choline. The present findings extend earlier work in man and the rabbit and indicate that among the C-reactive proteins from different species, which are structurally highly conserved, the capacity for selective binding to apoB-containing plasma lipoproteins is also a constant feature. These interactions may therefore be related to the in vivo function of CRP in all species and this function may in turn be relevant to pathological conditions, such as atherosclerosis, in which lipoproteins are important.

scholarly journals An essential role for lysophosphatidylcholine in the inhibition of platelet aggregation by secretory phospholipase A2

Blood ◽  
1995 ◽  
Vol 86 (11) ◽  
pp. 4166-4174 ◽  
Author(s):  
Y Yuan ◽  
SP Jackson ◽  
HH Newnham ◽  
CA Mitchell ◽  
HH Salem
Keyword(s):  
Platelet Aggregation ◽  
Phospholipase A2 ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Lipoproteins ◽  
Ionophore A23187 ◽  
Low Density ◽  
Secretory Phospholipase A2 ◽  
Secretory Phospholipase ◽  
Inhibition Of Platelet Aggregation

The release of secretory phospholipase A2 (sPLA2) into the mammalian circulation may contribute to the development of hemorrhagic and inflammatory diseases. sPLA2 has previously been shown to alter the behavior of platelets, leukocytes, and endothelial cells, although the molecular basis for these cellular effects has not been established. Our studies indicate that the inhibition of platelet aggregation by snake, bee venom, and pancreatic sPLA2 is dependent on a plasma cofactor. This cofactor resides within the lipoprotein fraction of plasma, with 54%, 31%, and 11% of the activity present in the high- density lipoprotein (HDL), low-density lipoprotein (LDL), and very low density lipoprotein (VLDL) fractions, respectively. Delipidation of HDL and LDL was associated with the complete loss of platelet-inhibitory activity. Incubation of purified sPLA2 with the HDL fraction of plasma resulted in the time-dependent generation of lysophosphatidylcholine (lysoPC). The formation of lysoPC correlated with the inhibition of platelet aggregation. Purified lysoPC (10 to 100 micrograms/mL) inhibited platelet aggregation and dense granule release induced by thrombin (0.05 U/mL), collagen (1 micrograms/mL), ionophore A23187 (2 mumol/L), ADP (12.5 mumol/L), and adrenaline (3.2 mumol/L). The inhibition of platelet aggregation by lysoPC was dose-dependent and correlated with decreased fibrinogen binding to glycoprotein IIb-IIIa. Our studies indicate that the enzymatic generation of lysoPC from plasma lipoproteins is essential for the sPLA2-mediated inhibition of platelet activation in the presence of albumin. These results raise the possibility that the toxic effects of circulating sPLA2 may be due in part to the generation of the bioactive lysophospholipid, lysoPC.

scholarly journals Physicochemical transfer of [3H]cholesterol from plasma lipoproteins to cultured human fibroblasts

1985 ◽  
Vol 228 (1) ◽  
pp. 219-225 ◽  
Author(s):  
B B Lundberg ◽  
L A Suominen
Keyword(s):  
Free Cholesterol ◽  
Water Solubility ◽  
Low Density Lipoprotein ◽  
Human Fibroblasts ◽  
Density Lipoprotein ◽  
Plasma Lipoproteins ◽  
Lung Fibroblasts ◽  
Cell Protein ◽  
Low Density ◽  
Free System

The transfer of free cholesterol from [3H]cholesterol-labelled plasma lipoproteins to cultured human lung fibroblasts was studied in a serum-free medium. The uptake of [3H]cholesterol depended upon time of incubation, concentration of lipoprotein in the medium, and temperature. Modified (reduced and methylated) low-density lipoprotein (LDL), which did not enter the cells by the receptor pathway, gave a somewhat lower transfer rate than unmodified LDL, but if the transfer values for native LDL were corrected for the receptor-mediated uptake of cholesterol the difference was eliminated. The initial rates of transfer of [3H]cholesterol from LDL and high-density lipoprotein (HDL) were of the same order of magnitude (0.67 +/- 0.05 and 0.75 +/- 0.06 nmol of cholesterol/h per mg of cell protein, respectively) while that from very-low-density lipoprotein (VLDL) was much lower (0.23 +/- 0.02 nmol of cholesterol/h per mg) (means +/- S.D., n = 5). The activation energy for transfer of cholesterol from reduced, methylated LDL to fibroblasts was determined to be 57.5 kJ/mol. If albumin was added to the incubation medium the transfer of [3H]cholesterol was enhanced, while that of [14C]dipalmitoyl phosphatidylcholine was decreased compared with the protein-free system. The results demonstrate that, in spite of its low water solubility, free cholesterol can move from lipoproteins to cellular membranes, probably by aqueous diffusion. We propose that physicochemical transfer of free cholesterol may be a significant mechanism for net uptake of the sterol into the artery during atherogenesis.

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