title: Structural and functional adaptations of the cardiovascular system by training.
abstract: Muscular training induces structural and functional adaptations within the cardiovascular system which vary according to type, intensity and duration of muscular exertion. Dynamic muscular training for more than 5 h a week involving more than 1/6th of the skeletal muscle mass causes an increase in parasympathetic tone and an eccentric myocardial hypertrophy. The dimensions of all cardiac chambers enlarge up to 20% and the cardiac muscle mass may increase by 70%-80%. Static muscular training does not induce any change in the parasympathetic heart regulation, nor does it lead to any disproportional increase in cardiac muscle mass relative to skeletal muscle mass. However, a tendency towards a concentric myocardial hypertrophy can be observed. The effects of regular muscular training on the arteries are the subject of current scientific investigation. To explain the acute and chronic adaptations of the arterial vasculature to exercise, a "shear stress" hypothesis has been proposed. During dynamic muscular exercise the regional arterial blood flow is enhanced. This leads to an acute increase in intraluminal shear forces, which stimulates the vascular endothelium with a reactive flow-dependent regional vasodilation mediated by endothelial-derived relaxing factors (EDRF, EDNO). Chronic enhancement of shear forces induces endothelial cell-mediated alterations in gene expression (endothelin, growth factors, regulators of fibrinolysis) and chronic structural adaptations of the vascular wall (cytoskeletal redistribution, cell shape change). Recent duplex sonographic studies in humans have revealed a significant lumen increase of muscular type arteries induced by dynamic, predominantly aerobic muscular training, but not by static muscular training. These structural adaptations are confined to those arteries supplying exercising muscle groups, whereas functional adaptations with an improvement of regional compliance are found in all arteries.
authors.affiliation: Department of Rehabilitation, Prevention and Sports Medicine, Freiburg University Hospital, Germany.
authors.forename: M
authors.initials: M
authors.lastname: Huonker
authors.forename: M
authors.initials: M
authors.lastname: Halle
authors.forename: J
authors.initials: J
authors.lastname: Keul
mesh_terms: D000222:Adaptation, Physiological; D000328:Adult; D000818:Animals; D001158:Arteries / Q000033:anatomy & histology / Q000502:physiology; D001808:Blood Vessels / Q000033:anatomy & histology* / Q000502:physiology; D003599:Cytoskeleton / Q000648:ultrastructure; D016232:Endothelins / Q000235:genetics; D004730:Endothelium, Vascular / Q000502:physiology; D005786:Gene Expression Regulation; D006133:Growth Substances / Q000235:genetics; D006321:Heart / Q000033:anatomy & histology* / Q000502:physiology; D018056:Hemorheology; D006801:Humans; D018482:Muscle, Skeletal / Q000033:anatomy & histology / Q000098:blood supply / Q000502:physiology; D009569:Nitric Oxide / Q000502:physiology; D010275:Parasympathetic Nervous System / Q000033:anatomy & histology / Q000502:physiology; D012039:Regional Blood Flow; D013177:Sports / Q000193:education / Q000502:physiology*; D013314:Stress, Mechanical; D018616:Ultrasonography, Doppler, Duplex; D014664:Vasodilation
chemical_list: D016232:Endothelins; D006133:Growth Substances; D009569:Nitric Oxide