Körperliche Aktivität in der Prävention kardiovaskulärer Erkrankungen

Zusammenfassung

Lebensstiländerungen mit Verbesserung der Ernährungsgewohnheiten und körperlichen Aktivität tragen wesentlich zur Lebensverlängerung bei. Epidemiologische Daten untermauern die Bedeutung der körperlichen Aktivität bei der Prävention von kardiovaskulären Erkrankungen, insbesondere der koronaren Herzerkrankung (KHK). Das Gesamtbzw. kardiovaskuläre Mortalitätsrisiko kann durch körperliche Aktivität primär um 35% reduziert werden. Im Bereich der sekundären Prävention führt die Intensivierung der körperlichen Aktivität zu einer Reduktion der Gesamtmortalität von 27% bzw. der KHK-gebundenen Mortalität von 31%.

Ursachen hierfür sind Verbesserungen des kardiovaskulären Risikoprofils, des arteriellen Blutdrucks, Lipidprofils, Diabetes mellitus Typ 2 oder der Adipositas als sekundäre Effekte. Bedeutende primäre Effekte sind die Verbesserung der Endothelfunktion, Reduktion der Thrombozytenreaktivität, eine mögliche Regression oder verminderte Progression der Koronarsklerose, eine mögliche Kollateralbildung bzw. die Verbesserung der Gefäßreparatur mit Hilfe von zirkulierenden endothelialen Vorläuferzellen durch die Therapie ˶körperliche Aktivität bzw. Ausdauersport“. Dieses ˶Medikament“ ist – bei korrekter und indikationsgerechter Anwendung – nahezu ohne unerwünschte Nebenwirkung sowie kostengünstig für fast jeden Menschen zugänglich. Aufgabe für die Zukunft wird es sein, eine individuellere Dosierung hinsichtlich Art, Umfang, Intensität und Häufigkeit der körperlichen Aktivität zu erreichen.

Summary

Life expectancy can be increased by life style changes such as improvement of nutrition habits and by physical activities. The relevance of physical activity for the prevention of cardiovascular diseases, especially coronary artery disease, is supported by several epidemiological studies. These data show a clear reduction by 35% in total as well as in cardiovascular- related mortality risk, due to primary prevention by physical activity. Within the secondary prevention, additional physical exercise leads to a marked decrease by 27% in the total, and by 31% in the cardiovascular-related mortality.

This is due to improvement of the cardiovascular risk profile, including arterial blood pressure, lipid profile, type 2 diabetes, obesity as secondary effects. However, of particular importance are primary effects, such as restoration of the endothelial function, decrease of platelets reactivity, regression or a reduced progression of coronary sclerosis, and possible collateral formation as well as improvement of vascular repair by circulated endothelial progenitor cells. These beneficial effects can all be induced by the therapy called ˶physical activity or endurance sports”. Provided this ˶medicament” is used correctly and individually adapted, it will be a low cost therapy and nearly without any adverse side effects for everyone. In order to maximise the outcome of individual health programs, an individually adjusted dosage of the type, intensity, duration, and frequency of physical activity is required.

Schlüsselwörter

Endothelzellfunktion - körperliche Aktivität - koronare Herzerkrankung - Arteriosklerose

Keywords

Endothelial cell function - exercise - atherosclerosis - arteriosclerosis

• References

• 1 Lee IM, Skerrett PJ. Physical activity and all-cause mortality: what is the dose-response relation?. Med Sci Sports Exerc 2001; 33 (Suppl. 06) S459-S471 S93-S94.
• 2 Blair SN, Kohl 3rd HW, Barlow CE. et al. Changes in physical fitness and all-cause mortality. A prospective study of healthy and unhealthy men. JAMA 1995; 273: 1093-1098.
• 3 Sarna S, Sahi T, Koskenvuo M. et al. Increased life expectancy of world class male athletes. Med Sci Sports Exerc 1993; 25: 237-244.
• 4 Berlin JA, Colditz GA. A meta-analysis of physical activity in the prevention of coronary heart disease. Am J Epidemiol 1990; 132: 612-628.
• 5 Löllgen H. Primary prevention of cardiovascular diseases. Deutsches Ärzteblatt 2003; 100: A987-A996.
• 6 Sesso HD, Paffenbarger Jr RS, Lee IM. Physical activity and coronary heart disease in men: The Harvard Alumni Health Study. Circulation 2000; 102: 975-980.
• 7 Haapanen N, Miilunpalo S, Vuori I. et al. Characteristics of leisure time physical activity associated with decreased risk of premature all-cause and cardiovascular disease mortality in middle-aged men. Am J Epidemiol 1996; 143: 870-880.
• 8 Haennel RG, Lemire F. Physical activity to prevent cardiovascular disease. How much is enough? Can Fam Physician 2002; 48: 65-71.
• 9 Lee IM, Sesso HD, Oguma Y. et al. Relative intensity of physical activity and risk of coronary heart disease. Circulation 2003; 107: 1110-1116.
• 10 Haskell WL, Lee IM, Pate RR. et al. Physical activity and public health: updated recommendation for adults from the American College of Sports Medicine and the American Heart Association. Circulation 2007; 116: 1081-1093.
• 11 Nelson ME, Rejeski WJ, Blair SN. et al. Physical activity and public health in older adults: recommendation from the American College of Sports Medicine and the American Heart Association. Med Sci Sports Exerc 2007; 39: 1435-1445.
• 12 Tuzcu EM, Kapadia SR, Tutar E. et al. High prevalence of coronary atherosclerosis in asymptomatic teenagers and young adults: evidence from intravascular ultrasound. Circulation 2001; 103: 2705-2710.
• 13 Strong WB, Malina RM, Blimkie CJ. et al. Evidence based physical activity for school-age youth. J Pediatr 2005; 146: 732-737.
• 14 Jolliffe JA, Rees K, Taylor RS. et al. Exercise-based rehabilitation for coronary heart disease. Cochrane Database Syst Rev 2001; CD001800.
• 15 Halle M, Berg A, Hasenfuss G. Physical exercise and secondary prevention of coronary heart disease. Deutsches Ärzteblatt 2003; 100: A2650-A2656.
• 16 Dickinson HO, Mason JM, Nicolson DJ. et al. Lifestyle interventions to reduce raised blood pressure: a systematic review of randomized controlled trials. J Hypertens 2006; 24: 215-233.
• 17 Durstine JL, Grandjean PW, Davis PG. et al. Blood lipid and lipoprotein adaptations to exercise: a quantitative analysis. Sports Med 2001; 31: 1033-1062.
• 18 Shephard RJ, Balady GJ. Exercise as cardiovascular therapy. Circulation 1999; 99: 963-972.
• 19 Yetik-Anacak G, Catravas JD. Nitric oxide and the endothelium: history and impact on cardiovascular disease. Vascul Pharmacol 2006; 45: 268-276.
• 20 Bauersachs J, Schafer A. Tetrahydrobiopterin and eNOS dimer/monomer ratio – a clue to eNOS uncoupling in diabetes?. Cardiovasc Res 2005; 65: 768-769.
• 21 Linke A, Mobius-Winkler S, Hambrecht R. Exercise training in the treatment of coronary artery disease and obesity. Herz 2006; 31: 224-233.
• 22 Vallance P, Chan N. Endothelial function and nitric oxide: clinical relevance. Heart 2001; 85: 342-350.
• 23 Xiao Z, Zhang Z, Ranjan V. et al. Shear stress induction of the endothelial nitric oxide synthase gene is calcium-dependent but not calcium-activated. J Cell Physiol 1997; 171: 205-211.
• 24 Poppa V, Miyashiro JK, Corson MA. et al. Endothelial NO synthase is increased in regenerating endothelium after denuding injury of the rat aorta. Arterioscler Thromb Vasc Biol 1998; 18: 1312-1321.
• 25 Kojda G, Cheng YC, Burchfield J. et al. Dysfunctional regulation of endothelial nitric oxide synthase (eNOS) expression in response to exercise in mice lacking one eNOS gene. Circulation 2001; 103: 2839-2844.
• 26 Laughlin MH, Pollock JS, Amann JF. et al. Training induces nonuniform increases in eNOS content along the coronary arterial tree. J Appl Physiol 2001; 90: 501-510.
• 27 Hambrecht R, Adams V, Erbs S. et al. Regular physical activity improves endothelial function in patients with coronary artery disease by increasing phosphorylation of endothelial nitric oxide synthase. Circulation 2003; 107: 3152-3158.
• 28 Kojda G, Hambrecht R. Molecular mechanisms of vascular adaptations to exercise. Physical activity as an effective antioxidant therapy? Cardiovasc Res 2005; 67: 187-197.
• 29 Linke A, Erbs S, Hambrecht R. Exercise and the coronary circulation-alterations and adaptations in coronary artery disease. Prog Cardiovasc Dis 2006; 48: 270-284.
• 30 Chen ZP, Mitchelhill KI, Michell BJ. et al. AMPactivated protein kinase phosphorylation of endothelial NO synthase. FEBS Lett 1999; 443: 285-289.
• 31 Haram PM, Adams V, Kemi OJ. et al. Time-course of endothelial adaptation following acute and regular exercise. Eur J Cardiovasc Prev Rehabil 2006; 13: 585-591.
• 32 Hambrecht R, Walther C, Mobius-Winkler S. et al. Percutaneous coronary angioplasty compared with exercise training in patients with stable coronary artery disease: a randomized trial. Circulation 2004; 109: 1371-1378.
• 33 Siegel-Axel D, Langer H, Lindemann S. et al. Role of platelets in atherosclerosis and inflammation. Med Klin (Munich) 2006; 101: 467-475.
• 34 Lindemann S, Tolley ND, Dixon DA. et al. Activated platelets mediate inflammatory signaling by regulated interleukin 1beta synthesis. J Cell Biol 2001; 154: 485-490.
• 35 Gawaz M, Brand K, Dickfeld T. et al. Platelets induce alterations of chemotactic and adhesive properties of endothelial cells mediated through an interleukin- 1-dependent mechanism. Implications for atherogenesis. Atherosclerosis 2000; 148: 75-85.
• 36 Hilberg T, Schmidt V, Losche W. et al. Platelet activity and sensitivity to agonists after exhaustive treadmill exercise. J Sports Sci & Med 2003; 2: 15-22.
• 37 Hilberg T, Gla D, Schmidt V. et al. Short-term exercise and platelet activity, sensitivity to agonist, and platelet-leukocyte conjugate formation. Platelets 2003; 14: 67-74.
• 38 Hilberg T, Schmidt V, Glaser D. et al. Platelet activity, sensitivity to agonist, and platelet – leukocyte conjugate formation after long-term exercise. Platelets 2002; 13: 273-277.
• 39 Wang JS, Jen CJ, Chen HI. Effects of exercise training and deconditioning on platelet function in men. Arterioscler Thromb Vasc Biol 1995; 15: 1668-1674.
• 40 Ornish D, Brown SE, Scherwitz LW. et al. Lifestyle changes and heart disease. Lancet 1990; 336: 741-742.
• 41 Haskell WL, Alderman EL, Fair JM. et al. Effects of intensive multiple risk factor reduction on coronary atherosclerosis and clinical cardiac events in men and women with coronary artery disease. The Stanford Coronary Risk Intervention Project (SCRIP). Circulation 1994; 89: 975-990.
• 42 Schuler G, Hambrecht R, Schlierf G. et al. Regular physical exercise and low-fat diet. Effects on progression of coronary artery disease. Circulation 1992; 86: 1-11.
• 43 Niebauer J, Hambrecht R, Velich T. et al. Attenuated progression of coronary artery disease after 6 years of multifactorial risk intervention: role of physical exercise. Circulation 1997; 96: 2534-2541.
• 44 Walther C, Hambrecht R. Endothelial dysfunction in cardiovascular diseases – the influence of exercise training. Deutsche Zeitschrift für Sportmedizin 2001; 52: 215-221.
• 45 White FC, Bloor CM, McKirnan MD. et al. Exercise training in swine promotes growth of arteriolar bed and capillary angiogenesis in heart. J Appl Physiol 1998; 85: 1160-1168.
• 46 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.
• 47 Shantsila E, Watson T, Lip GY. Endothelial progenitor cells in cardiovascular disorders. J Am Coll Cardiol 2007; 49: 741-752.
• 48 Laufs U, Werner N, Link A. et al. Physical training increases endothelial progenitor cells, inhibits neointima formation, and enhances angiogenesis. Circulation 2004; 109: 220-226.
• 49 Adams V, Lenk K, Linke A. et al. Increase of circulating endothelial progenitor cells in patients with coronary artery disease after exercise-induced ischemia. Arterioscler Thromb Vasc Biol 2004; 24: 684-90.