Ausdauersport und kardiale Adaptation (Sportherz)

Abstract

One essential function of the cardiovascular system is to provide an adequate blood supply to all organs, including the skeletal muscles at rest and during exercise. Adaptation to chronic exercise proceeds mainly via the autonomic nervous system. On the one hand, peripheral muscles influence the autonomic reactions through "feedback" control via ergoreceptors, in particular, mechano- and chemoreceptors. On the other hand, there is central control in the sense of a "feed forward" regulation, e. g., the reaction of an athlete before competition. Along with other influential factors, such as circulatory presso-, chemo-, and volume receptors, the incoming impulses are processed in vegetative centers.A cardiovascular reaction, then, is the result of nerval and humoral sympathetic and parasympathetic activity. At rest, the parasympathetic tone dominates. It reduces heart frequency and conduction velocity. The high vagal tone is initially reduced with increasing physical exertion and switches at higher intensity to increasingly sympathetic activation. This mechanism of reaction to exercise is supported by inverse central and peripheral transmissions.Chronic endurance training leads to an improved local aerobic capacity of the exercised musculature. At rest, it augments parasympathetic activity when the muscle mass is sufficiently large, i. e., 20-30% of the skeletal musculature. The extent of the adaptation depends on individual factors, such as scope, intensity of training, and type of muscle fiber. A higher vagal tone delays the increase in the sympathetic tone during physical exertion. The regulatory range of heart rate, contractility, diastolic function, and blood pressure is increased. In addition, adaptation results in functional and structural changes in the vascular system. Cardiocirculatory work is economized, and maximum performance and oxygen uptake are improved. Endurance training exceeding an individual limit causes harmonic enlargement and hypertrophy of the heart. The thickness of both, the septum and posterior wall increases to the same extent as the interior volume. The mass/volume ratio, and therefore the maximum systolic wall stress, remains constant in contrast to pathologic forms of hypertrophy. Adaptations, including function and size of the heart, show a regression in healthy inactive persons without any structural heart disease.

Cardiac Findings in Amyotrophic Lateral Sclerosis: A Magnetic Resonance Imaging Study

“…The function and the size of the heart show a regression in healthy inactive persons even without any structural heart disease ( 29 ). Therefore, we assume that significantly reduced heart mass and ejection volumes are a consequence of more sedentary/inactive behavior in ALS patients if compared to healthy adults.…”

Impact of specific training and competition on myocardial structure and function in different age ranges of male handball players

“…The quantitative assessment of cardiac structure and function in “juniors” players compared to “schools” shows an enlarging of chamber size, increasing of muscle mass and improvement of LV performance by the increase of the left ventricular ejection time LVET, which directly varies with SV obtained by the increase of LV cavity size translating the progressive adaptation of players to increased training and competition. Furthermore the greater reliance on aerobic metabolism in young athletes must be exploited to increase cardiac size, imposing primarily a volume load on the LV, which is fundamental to improve cardiac performance particularly the SV [ 40 – 42 ], because it is easier to hypertrophy a dilated heart than to dilate a hypertrophied one, then continue progressively by introducing dynamic glycolytic and static exercises generating a pressure load for better forceful heart contractions to sustain a high CO during high-intensity repeated bouts [ 43 , 44 ]. The data got close results to the ones obtained in other team sports as in teenage soccer players [ 30 , 42 ], basketball players [ 10 ] and other disciplines [ 15 , 31 – 33 ].…”

Echokardiografische Gewebedoppleranalyse der Mitralringgeschwindigkeiten bei Patienten mit hypertropher Kardiomyopathie und bei Hochleistungssportlern

“…Im Gegensatz zu o. g. Herzerkrankungen, insbesondere im Gegensatz zur HCM, wird das "Sportherz" als eine physiologische Anpassung des Herzens auf eine sportliche Betätigung angesehen, die zu einer Hypertrophie des Herzens führt [31,33,34]. In Abhängigkeit der Art der sportlichen Belastung, d. h. Ausdauersport (dynamisch) und/oder Kraftsport (statisch), der individuellen genetischen Veranlagung und der Häufigkeit und der Intensität des Trainings finden sich bei Leistungssportlern unterschiedliche Ausprägungen der sportadaptiven Veränderungen und des "Sportherzens" [31].…”

“…In Abhängigkeit der Art der sportlichen Belastung, d. h. Ausdauersport (dynamisch) und/oder Kraftsport (statisch), der individuellen genetischen Veranlagung und der Häufigkeit und der Intensität des Trainings finden sich bei Leistungssportlern unterschiedliche Ausprägungen der sportadaptiven Veränderungen und des "Sportherzens" [31]. Sportadaptive Veränderungen ("Sportherz") sind definitionsgemäß bei Leistungs- sportlern mit entsprechendem intensivem Training durch folgende Merkmale charakterisiert: eine normale linksventrikuläre Geometrie, eine exzentrische Hypertrophie, eine global und regional normale systolische linksventrikuläre Funktion, eine mittels Analyse des transmitralen Einstromprofils nachgewiesene normale diastolische Funktion, sowie eine enddiastolische Septumdicke < 13 mm und ein enddiastolischer LV-Diameterindex (LVEDD index ) von < 30 mm/m 2 [5,31,33,35]. Bei diesen Grenzwerten sollten sowohl die jeweiligen anthropometrischen Daten des jeweiligen Athleten als auch die jeweilige Sportart Berücksichtigung finden und bevorzugt die auf die Körperfläche bezogenen Parameter verwendet werden.…”

“…B. Kernspintomografie mit Gadolinum-Kontrast) und ggf. eine 3-monatige Trainingspause ("De-Training") zur Beurteilung der Regredienz der linksventrikulären Hypertrophie erfolgen [2,5,31,33,40,41].…”