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The most recent version of this article was published on 1 February 2008

Br J Sports Med. Published Online First: 23 July 2007. doi:10.1136/bjsm.2007.035188
Copyright © 2007 BMJ Publishing Group Ltd & British Association of Sport and Exercise Medicine.

Paper

Longterm Endurance Exercise decreases the Antiangiogenic Endostatin Signaling in adipose men aged between 50-60 years

Klara Brixius 1*, Sybile Schoenberger 1, Dennis Ladage 2, Helge Knigge 3, Gisa Falkowski 3, Martin Hellmich 4, Christine Graf 3, Jo Latsch 3, Georgina Montiel 3, Georg Predel 3 and Wilhelm Bloch 1

1 Department of Molecular and Cellular Sport Medicine, German Sport University Cologne, Germany
2 Lab. for Muscle Research and Molecular Cardiology, Dept. III of Internal Med., University of Cologne, Germany
3 Department of Cardiology and Sports Medicine, German Sport University Cologne, Germany
4 Institute of Medical Statistics, Informatics and Epidemiol. Univ. of Cologne, Germany

* To whom correspondence should be addressed. E-mail: brixius{at}dshs-koeln.de.

Accepted 25 June 2007


Abstract

Endurance training may decrease the risk for coronary artery disease. It has been speculated that these effects may be due to an exercise-induced stimulation of angiogenesis. The underlying mechanisms are not yet clear. Therefore, we investigated the plasma concentration of the vascular endothelial growth factor (VEGF, angiogenic factor) and of endostatin (antiangiogenic factor) in a group of untrained men aged between 50-60 years with obesity using the ELISA technique. All men were randomized into a ‘running’ group (RUN, training 3 times a week, 60 min each, n=7), a ‘cycling’ group (CYCLE, training 3 times a week, 90 min each, n=7) and a sedentary control group (CON, n=7). Both training groups worked at moderate intensity (2-4 mM lactate). The intervention had a duration of 6 months. Before and after this period, blood samples were taken from the participants at rest and they underwent a medical investigation. Body-mass index (BMI), systolic und diastolic blood pressure, as well as VEGF- and endostatin plasma concentration were comparable in all three groups. Endurance training significantly reduced body mass index in both exercise groups (before vs. after (kg/m²): RUN: 29.7±0.7 vs. 29.1±0.6; CYCLE: 31.1±0.7 vs. 30.1±0.9) but not in CON (before vs. after (kg/m²): 30.0±1.0 vs. 30.2±0.8). Endurance training did not influence VEGF plasma concentration (before vs. after (ng/ml), RUN: 1.3±0.4 vs. 1.5±0.2; CYCLE: 1.6±0.3 vs. 1.5 ± 0.2; CON: 2.5±0.6 vs. 2.1±0.7). Plasma concentration of endostatin was significantly reduced in RUN (before vs. after (ng/ml): 20.9±1.6 vs. 17.5±1.0) and CYCLE (before vs. after: 21.3±1.4 vs. 18.0±1.6) but not in CON (19.7±1.3 vs. 17.7±1.1 ng/ml). Conclusions: Endurance training seems to reduce the antiangiogenic mechanisms in men aged between 50-60 years and may thereby decrease the risk for cardiovascular diseases.

Key Words: Antiangiogenic, Cardiovascular Disease, Endostatin, Exercise, VEGF


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Commentary on "Long-term endurance exercise decreases antiangiogenic endostatin signalling in overweight men aged 50–60 years"
Robert H G Schwinger
Br. J. Sports Med. 2008 42: 129. [Extract] [Full Text] [PDF]

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