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DOI: 10.1055/s-0034-1383337
Wirkmechanismus von Sport in der Prävention von kardiovaskulären Erkrankungen
Mechanisms of Exercise in Prevention of Cardiovascular DiseasesPublication History
Publication Date:
08 December 2014 (online)
Zusammenfassung
Molekularbiologische Analysen haben dazu beigetragen, die präventiven Mechanismen von Sport bei Patienten mit kardiovaskulären Erkrankungen zu verstehen. Am Myokard bewirkt Sport hauptsächlich eine gesteigerte Expression von Stressproteinen (Schutzfaktoren) sowie von antioxidativen Enzymen, die für eine verringerte Last an reaktiven Sauerstoffspezies (ROS) verantwortlich sind. Ob Sport auch zu einem myokardialen Kollateralwachstum führt, wird noch kontrovers diskutiert. Betrachtet man das vaskuläre System und im Speziellen das Endothel, ist eine Modulation des bioverfügbaren Stickstoffmonoxids (NO) durch gesteigerte körperliche Aktivität der zentrale Faktor. Ferner wird die Gefäßsteifigkeit reduziert, und endotheliale Vorläuferzellen sorgen für eine verbesserte Reparatur von Endothelschäden. Im peripheren Skelettmuskel bewirkt eine gesteigerte sportliche Aktivität hauptsächlich eine Veränderung der Faserzusammensetzung der Muskulatur sowie einen reduzierten Proteinkatabolismus. Dies ist wahrscheinlich durch eine Modulation der Inflammation und durch reaktive Sauerstoffspezies vermittelt.
Abstract
Molecular biology contributed to our current understanding of the beneficial mechanisms elicited by increased physical activity in patients with cardiovascular diseases. With respect to the myocardium an increased physical activity leads mainly to an increased expression of heat shock proteins and a decreased load of reactive oxygen species (ROS) due to an increased activity of ROS scavenger enzymes. The impact of collateral growth is still unclear. In the cardiovascular system a modulation of the nitric oxide bioavailability by exercise training (ET) is the central effect. In addition the endogenous repair of the endothelial cell layer by progenitor cells is discussed. Last but not least in the skeletal muscle ET results in a shift of fibre type composition and a reduced protein catabolism, probably modulated by ROS.
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