High, but not moderate frequency and duration of exercise training induces downregulation of the expression of inflammatory and atherogenic adhesion molecules.
BACKGROUND
Lifestyle changes which include daily exercise training have been shown to slow the progression of coronary artery disease. We designed a study to examine the effects of a multifactorial intervention on atherogenic adhesion molecules on the surface of monocytes in patients with coronary artery disease.


METHODS
We randomized 39 patients with coronary artery disease to (i) an intervention program which consisted of 4 weeks of daily 6x15 min ergometer training at submaximal intensity in addition to a 1 h/week group exercise session, followed by 5 months of home-based ergometer training of 30 min/day again in addition to a 1 h/week group exercise session or (ii) conventional therapy. All patients received a statin. Monocyte-bound cellular adhesion molecules LFA-1 (CD11a), MAC-1 (CD11b), VLA-4 (CD49d) and L-selectin (CD62L) were assessed by fluorescence activated cell sorting analysis.


RESULTS
After 4 weeks the multifactorial intervention led to a significant improvement of maximal work capacity, lipid profile, body mass index, blood pressure, fasting glucose and hemoglobin A1c. This was associated with a reduced expression of MAC-1 and VLA-4. After 5 months of a home-based intervention the beneficial effects of the cardiovascular risk profile were still apparent, whereas the effects on the expression of adhesion molecules were blunted.


CONCLUSIONS
In patients treated with statins, 4 weeks of high frequency and long duration exercise training led to a diminished expression of atherogenic adhesion molecules MAC-1 und VLA-4. After 5 months of home-based exercise training of moderate frequency and duration, these effects were blunted. Our data suggest that our patients in cardiac rehabilitation programs might further benefit from the antiatherogenic effects of an even higher amount of exercise training.
Peschel
Thomas
T
Department of Internal Medicine/Cardiology, University of Leipzig, Heart Center, Austria.
Sixt
Sebastian
S
Beitz
Frido
F
Sonnabend
Melanie
M
Muth
Gerhard
G
Thiele
Holger
H
Tarnok
Attila
A
Schuler
Gerhard
G
Niebauer
Josef
J
D000368:Aged; D050197:Atherosclerosis / Q000150:complications / Q000276:immunology / Q000628:therapy; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D003131:Combined Modality Therapy; D003324:Coronary Artery Disease / Q000097:blood / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology / Q000628:therapy*; D015536:Down-Regulation; D005081:Exercise Therapy; D017079:Exercise Tolerance; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D007249:Inflammation / Q000150:complications / Q000276:immunology / Q000628:therapy; D039041:Integrin alpha4beta1 / Q000378:metabolism*; D008055:Lipids / Q000097:blood; D016177:Macrophage-1 Antigen / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000276:immunology*; D013997:Time Factors; D016896:Treatment Outcome
D001786:Blood Glucose; D006442:Glycated Hemoglobin; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D039041:Integrin alpha4beta1; D008055:Lipids; D016177:Macrophage-1 Antigen; C517652:hemoglobin A1c protein, human