© 2005 European Society of Cardiology
Exercise training in chronic heart failure: effects on pro-inflammatory markers
a Cardiac Medicine, Royal Brompton Hospital and NHLI London, UK
b Herzzentrum der Universität Leipzig Leipzig, Germany
c Cardiac Medicine, University of Hull UK
d University of Sydney Australia
* Corresponding author. Herzzentrum der Universität Leipzig, Innere Medizin/Kardiologie, Strümpellstr. 39, 04289 Leipzig. Tel.: +49 341 865 0; fax: +49 341 865 1461. E-mail address: j.niebauer{at}medizin.uni-leipzig.de
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Abstract |
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Background: Acute bouts of exercise have been shown to induce inflammatory cytokine activation and peripheral hypoxia in patients with chronic heart failure (CHF). In this study, we set out to investigate the impact of chronic exercise training on pro-inflammatory cytokines and markers of endothelial damage.
Methods and results: We measured tumor necrosis factor 
(TNF), its soluble TNF-receptors 1 and 2, interleukin 6 (IL-6), soluble e-selectin, soluble intracellular adhesion molecule-1 (sICAM) and sCD14 in 18 patients with CHF and 9 age-matched controls in a randomized cross-over study of 8 weeks of exercise training (5 days/week, submaximal bicycle ergometer training, 30 min/day; calisthenics 9 min/day) versus 8 weeks of rest. At baseline, patients had a lower peak VO2 (p=0.009) and a trend for higher levels of e-selectin (p=0.08) and sCD14 (p=0.06), in addition to significantly elevated levels of sICAM (p=0.02), TNF (p=0.02) and TNF-R2 (p=0.002); TNF-R1 and IL-6 were not elevated. Although exercise training was effective and led to an increase in peak VO2 in CHF (p<0.003), there was no activation of any of the above variables observed, neither in patients nor controls.
Conclusions: Chronic heart failure is associated with increased levels of TNF and markers of endothelial damage. Whereas acute bouts of exercise have been reported to lead to an increase in pro-inflammatory cytokines and markers of endothelial damage, these effects are not seen when exercise is performed chronically.
Key Words: Heart failure • Endothelial damage • Tumor necrosis factor • Exercise
Received March 22, 2004; Revised June 3, 2004; Accepted July 21, 2004
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