Chronic exercise leads to antiaggregant, antioxidant and anti-inflammatory effects in heart failure patients.

Autor:	de Meirelles LR; State University of Rio de Janeiro, Rio de Janeiro, Brazil., Matsuura C; State University of Rio de Janeiro, Rio de Janeiro, Brazil., Resende Ade C; State University of Rio de Janeiro, Rio de Janeiro, Brazil., Salgado AA; State University of Rio de Janeiro, Rio de Janeiro, Brazil., Pereira NR; State University of Rio de Janeiro, Rio de Janeiro, Brazil., Coscarelli PG; State University of Rio de Janeiro, Rio de Janeiro, Brazil., Mendes-Ribeiro AC; State University of Rio de Janeiro, Rio de Janeiro, Brazil Federal University of the State of Rio de Janeiro, Rio de Janeiro, Brazil., Brunini TM; State University of Rio de Janeiro, Rio de Janeiro, Brazil tbrunini@uerj.br.
Jazyk:	angličtina
Zdroj:	European journal of preventive cardiology [Eur J Prev Cardiol] 2014 Oct; Vol. 21 (10), pp. 1225-32. Date of Electronic Publication: 2013 May 21.
DOI:	10.1177/2047487313491662
Abstrakt:	Background: Heart failure (HF) patients are at an increased risk of thrombotic events. Here, we investigated the effects of exercise training on platelet function and factors involved in its modulation in HF. Design and Methods: Thirty HF patients were randomized to 6 months of supervised exercise training or to a control group that remained sedentary. Exercise training consisted of 30 min of moderate-intensity treadmill exercise, followed by resistance and stretching exercises, performed three times a week. Blood was collected before and after the intervention for platelet and plasma obtainment. Results: Peak VO2 increased after exercise training (18.0 ± 2.2 vs. 23.8 ± 0.5 mlO2/kg/min; p < 0.05). Exercise training reduced platelet aggregation induced by both collagen and ADP (approximately -6%; p < 0.05), as well as platelet nitric oxide synthase activity (0.318 ± 0.030 vs. 0.250 ± 0.016 pmol/10(8) cells; p < 0.05). No difference in the above-mentioned variables were observed in the control group. No significant difference was observed in intraplatelet cyclic guanosine monophosphate levels among groups. There was a significant increase in the activity of the antioxidant enzymes superoxide dismutase and catalase in plasma and platelets, resulting in a decrease in both lipid and protein oxidative damage. Systemic levels of the inflammatory markers C-reactive protein, fibrinogen, and tumour necrosis factor α were also reduced in HF after training. Conclusions: Our results suggest that regular exercise training is a valuable adjunct to optimal medical management of HF, reducing platelet aggregation via antioxidant and anti-inflammatory effects, and, therefore, reducing the risk of future thrombotic events. (© The Author(s) 2013 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.)
Databáze:	MEDLINE
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