title: [Value of training-induced effects on arterial vascular system and skeletal muscles in therapy of NYHA II/III heart failure].
abstract: Dynamic muscular exercise performed by healthy subjects leads to a rise in the left ventricular blood ejection with an acute increase in the local wall shear stress on the endothelium of the arterial vessels. These hemodynamic changes results in a release of endothelium-dependent relaxing factors, one of them concerns nitric oxide (NO). Therefore an arterial vasodilatation with an acute increase in the blood flow volume to the exercising muscle groups occurs. If more than 1/6 of the skeletal musculature is involved in exercise and if training duration exceeds 3-5 hours a week the chronically increased blood flow volume in the cardiovascular system triggers structural and functional changes of the heart and the arterial vessels. It develops a functional intact excentric hypertrophy of the myocardium; within the arterial vessels an increase in the diameter of the muscular arteries supplying the trained muscle groups occurs. These training-induced adaptations of the cardiovascular system are adjusted to improve the aerobic skeletal muscle metabolism. In congestive heart failure a pathological excentric myocardial hypertrophy is found. In this case the systolic myocardial function is impaired and the left ventricular ejection fraction is reduced already in early stages, so that the cardiac output can not be sufficiently increased during exercise. In addition a dysfunction of the endothelium of the arterial vessels occurs. As a consequence the endothelium-dependent arterial vasodilation is reduced, so that the peripheral arteries could not supply the muscle groups involved in exercise with enough blood flow volume. Therefore, the acute delivery of the working musculature with oxygen and energy substrates is insufficient, so that premature muscular fatigue occurs. The reduced exercise resistance of the patients leads chronically to a generalized skeletal muscle atrophy. Ultrastructural analysis revealed a decrease of oxidative type 1 muscle fibers with a relative increase of more glycolytic type 2 fibers. In addition, the volume density and the surface area of the cristae of mitochondria are reduced. All these changes results in a decrease of aerobic skeletal muscle metabolism independent of the blood flow volume, so that the physical fitness of the patients progressively decline. On the basis of the training-induced physiological adaptations of the cardiovascular system, a special exercise therapy supervised by a physician was developed for patients with congestive heart failure NYHA II/III. It have been shown that various exercise programs, which are adjusted to the degree of cardiac function impairment are suitable to restore the endothelial dysfunction of the arterial vessels as well as to cure the disturbed skeletal muscle metabolism in these patients independent of an improvement of cardiac function. Therefore in patients with congestive heart failure NYHA II/III who underwent regularly such an exercise therapy, the secondary impaired physical fitness could be rebuild without an excessive risk for an acute exercise-induced cardiovascular emergency.
authors.affiliation: Medizin. Univ.-Klinik Freiburg Abt. Prävention, Rehabilitation & SportMedizin Hugstetter Strasse 55 79106 Freiburg/Br., Germany. honki@msm1.ukl.uni-freiburg.de
authors.forename: M
authors.initials: M
authors.lastname: Huonker
authors.forename: J
authors.initials: J
authors.lastname: Keul
mesh_terms: D002302:Cardiac Output / Q000502:physiology; D004730:Endothelium, Vascular / Q000503:physiopathology*; D015444:Exercise / Q000502:physiology*; D006333:Heart Failure / Q000503:physiopathology / Q000534:rehabilitation*; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D018482:Muscle, Skeletal / Q000503:physiopathology*; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology*; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology / Q000534:rehabilitation
vernacular_title: Stellenwert von trainingsbedingten Rückwirkungen am arteriellen Gefässystem und der Skelettmuskulatur in der Therapie der Herzinsuffizienz NYHA II/III.