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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)
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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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Literatur
- 1 Morris J, Heady JA, Raffle PAB et al. Coronary artery disease and physical activity of work. Lancet 1953; 265: 1053-1057
- 2 Lee DC, Artero EG, Sui X et al. Mortality trends in the general population: the importance of cardiorespiratory fitness. J Psychopharmacol 2010; 24 (4 Suppl.) 27-35
- 3 Balligand JL, Feron O, Dessy C. eNOS activation by physical forces: from short-term regulation of contraction to chronic remodeling of cardiovascular tissues. Physiol Rev 2009; 89: 481-534
- 4 Lüscher TF, Landmesser U, von Eckardstein A et al. High-density lipoprotein: vascular protective effects, dysfunction, and potential as therapeutic target. Circ Res 2014; 114: 171-182
- 5 Adams V, Besler C, Fischer T et al. Exercise training in patients with chronic heart failure promotes restoration of HDL functional properties. Circ Res 2013; 113: 1345-1355
- 6 Laufs U, Werner N, Link A et al. Physical training increases endothelial progenitor cells, inhibition of neointima formation, and enhances angiogenesis. Circulation 2004; 109: 220-226
- 7 Tanaka H, Dinenno FA, Monahan KD et al. Aging, habitual exercise, and dynamic arterial compliance. Circulation 2000; 102: 1270-1275
- 8 Steppan J, Sikka G, Jandu S et al. Exercise, vascular stiffness, and tissue transglutaminase. J Am Heart Assoc 2014; 3: e000599
- 9 Marin T, Gongol B, Chen Z et al. Mechanosensitive microRNAs-role in endothelial responses to shear stress and redox state. Free Radic Biol Med 2013; 64: 61-68
- 10 Loyer X, Potteaux S, Vion AC et al. Inhibition of microRNA-92a prevents endothelial dysfunction and atherosclerosis in mice. Circ Res 2014; 114: 434-443
- 11 Weber M, Baker MB, Moore JP et al. MiR-21 is induced in endothelial cells by shear stress and modulates apoptosis and eNOS activity. Biochem Biophys Res Commun 2010; 393: 643-648
- 12 Lin J, Wu H, Tarr PT et al. Transcriptional co-activator PGC-1 alpha drives the formation of slow-twitch muscle fibres. Nature 2002; 418: 797-801
- 13 Krämer DK, Ahlsen M, Norrbom J et al. Human skeletal muscle fibre type variations correlate with PPAR alpha, PPAR delta and PGC-1 alpha mRNA. Acta Physiol 2006; 188: 207-216
- 14 Rosca MG, Hoppel CL. Mitochondrial dysfunction in heart failure. Heart Fail Rev 2013; 18: 607-622
- 15 Golbidi S, Laher I. Molecular mechanisms in exercise-induced cardioprotection. Cardiol Res Pract 2011; 2011: 972807
- 16 Yamashita N, Hoshida S, Otsu K et al. Exercise provides direct biphasic cardioprotection via manganese superoxide dismutase activation. J Exp Med 1999; 189: 1699-1706
- 17 Zbinden R, Zbinden S, Meier P et al. Coronary collateral flow in response to endurance exercise training. Eur J Cardiovasc Prev Rehabil 2007; 14: 250-257
- 18 Uhlemann M, Adams V, Lenk K et al. Impact of different exercise training modalities on the coronary collateral circulation and plaque composition in patients with significant coronary artery disease (EXCITE trial): study protocol for a randomized controlled trial. Trials 2012; 13: 167