Article

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. 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 alpha 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.
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Langue : ANGLAIS