title: Endurance training reduces circulating inflammatory markers in persons at risk of coronary events: impact on plaque stabilization?
abstract: Inflammatory pathways are involved in destabilization of atherosclerotic plaques. We assessed the hypothesis that endurance training decreases circulating concentrations of inflammatory markers in persons with coronary artery disease (CAD) and cardiovascular risk factors (CVRFs). Thirty-two subjects with CAD and/or CVRFs joined a 12-week supervised endurance training. We found a significant decrease of the chemokines interleukin (IL)-8 (pre: 3.9+/-0.6, change: -1.2+/-0.4 pg/ml, -21%, p=0.002) and monocyte chemoattractant protein-1 (pre: 213+/-9, change: -20.4+/-8.2 pg/ml, -5%, p=0.03). Diabetes mellitus (DM) significantly influenced changes of IL-8 (p=0.002). IL-8 substantially dropped by 39% in diabetics. Moreover, matrix metalloproteinase-9 (MMP-9) highly significantly decreased in response to training (pre: 750+/-98, change: -278+/-77 ng/ml, -18%, p=0.005). Exercise-induced changes of MMP-9 were influenced by concomitant use of statins (p=0.038). We observed a particularly strong MMP-9 reduction of 44% in patients treated with statins. Acute phase reactants IL-6 (pre: 1.7+/-0.3, change: +0.25+/-0.7 pg/ml, +4%, p=0.58) and high sensitivity C-reactive protein (pre: 2.1+/-0.5, change: -0.25+/-0.4 mg/l, -9%, p=0.54) did not change in response to training. In conclusion, endurance training decreased circulating chemokines and MMP-9, which may in part explain its beneficial effect on coronary risk. Patients with DM or treated with statins because of hypercholesterolemia may particularly take advantage.
authors.affiliation: Department of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090 Vienna, Austria. alexander.niessner@meduniwien.ac.at
authors.forename: Alexander
authors.initials: A
authors.lastname: Niessner
authors.forename: Bernhard
authors.initials: B
authors.lastname: Richter
authors.forename: Martina
authors.initials: M
authors.lastname: Penka
authors.forename: Sabine
authors.initials: S
authors.lastname: Steiner
authors.forename: Barbara
authors.initials: B
authors.lastname: Strasser
authors.forename: Sophie
authors.initials: S
authors.lastname: Ziegler
authors.forename: Elke
authors.initials: E
authors.lastname: Heeb-Elze
authors.forename: Gerlinde
authors.initials: G
authors.lastname: Zorn
authors.forename: Angelika
authors.initials: A
authors.lastname: Leitner-Heinschink
authors.forename: Christina
authors.initials: C
authors.lastname: Niessner
authors.forename: Johann
authors.initials: J
authors.lastname: Wojta
authors.forename: Kurt
authors.initials: K
authors.lastname: Huber
mesh_terms: D018932:Chemokine CCL2 / Q000097:blood*; D003324:Coronary Artery Disease / Q000097:blood / Q000517:prevention & control*; D004797:Enzyme-Linked Immunosorbent Assay; D005081:Exercise Therapy / Q000379:methods*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007249:Inflammation / Q000097:blood; D016209:Interleukin-8 / Q000097:blood*; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000097:blood*; D008875:Middle Aged; D010807:Physical Endurance / Q000502:physiology*; D011379:Prognosis; D011446:Prospective Studies; D012307:Risk Factors; D012720:Severity of Illness Index
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D016209:Interleukin-8; D020780:Matrix Metalloproteinase 9