Effect of adaptation to physical loads on the contractile function and mass of the left ventricle of the heart]

Echocardiography was used to examine 20 highly trained athletes and 12 untrained persons at rest and during increasing physical load. It was established that in untrained persons the stroke volume in moderate and large physical loads increases mainly due to an increase in the diastolic output with the systolic output unchanged. In highly trained athletes the stroke volume with an equal load increases due both to growth in the diastolic output and to considerable decrease in the systolic output, i.e., due to the more complete ejection of blood from the cavity of the ventricle. As a result in trained patients a sufficient minute output in physical exertion is attained with less external work of the left ventricle and myocardial tension.     

Effects of adaptation to high altitude hypoxia on the contractile function and adrenoreactivity of the heart

Summary Effects of adaptation to mountain altitude of 3200 m on the contractile function and adrenoreactivity of the heart in rats have been investigated. It was shown that adaptation to altitude increased the contractile force and contraction and relaxation velocities of the left ventricle as compared to the controls. Simultaneously, a significant increase in cardiac response to noradrenaline developed in the course of adaptation. The increased response was accompanied by its more rapid disappearance. These changes may be explained by the increase in the activity of myocardial adenylate cyclase and phosphodiesterase. It was also shown that the decrease in cardiac function produced by cardiac denervation was less pronounced in adapted rats. This fact may be explained by increased effectiveness of cardiac autoregulatory mechanism. The comparison of these results with the data of other investigators suggests that in well adapted animals the strength of interaction between the levels of the regulatory hierarchy of the whole organism changes, i. e., the capacity of autoregulatory cell mechanisms and their reactivity to neurohumoral stimuli increase. As a result, control of the organism's reactions by higher levels of the regulatory system is more economical in adapted animals.

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Auswirkungen einer Adaptation an hypoxische Bedingungen unter Höhenexposition auf kontraktile Funktion und Noradrenalin-Empfindlichkeit

Zusammenfassung An Ratten wurden die Auswirkungen einer Höhenanpassung (3200 m) auf die kontraktile Funktion des Herzens und dessen Ansprechbarkeit für adrenerge Substanzen untersucht. Es wurde gezeigt, daß die Höhenanpassung mit einer Zunahme der Kontraktionskraft und der Geschwindigkeit von Kontraktion und Erschlaffung des linken Ventrikels, verglichen mit den Kontrolltieren, einherging. Gleichzeitig entwickelte sich im Laufe der Anpassung eine signifikante Steigerung der Ansprechbarkeit auf Noradrenalin. Diese Veränderungen könnten durch einen Anstieg der Aktivität der myokardialen Adenylatcyclase und Phosphodiesterase erklärt werden. Es wurde weiterhin gezeigt, daß die Beeinträchtigung der Herzfunktion als Folge einer Denervierung des Organs bei den adaptierten Ratten weniger ausgeprägt war. Diese Tatsache, kann durch eine erhöhte Wirksamkeit der autoregulativen Mechanismen erklärt werden. Der Vergleich dieser Ergebnisse mit den Daten anderer Untersuchter läßt vermuten, daß die Kapazität autoregulativer Mechanismen und ihre Ansprechbarkeit für neurohumorale Stimuli bei gut angepaßten Tieren zunimmt. Dies führt dazu, daß bei angepaßten Tieren die Kontrolle der Reaktionen des Organismus bei höherer Beanspruchung des regulatorischen Systems ökonomischer erfolgt.

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With 2 figures and 3 tables     

Effect of emotional stress on the contractile function of human heart (according to the echocardiographic data)]

Cardiac function was studied by echocardiography in 12 healthy sixth-year students at mid-semester, immediately before taking an exam and 30 minutes after it. It was found that the emotional stress experienced prior to the exam is attended with an increase in cardiac output by one and a half times and external work by two. This increase of the pump cardiac function is ensured without any essential increase in the diastolic dimensions of the left cardiac ventricle at the expense of fuller blood ejection from the left ventricle and decrease of its residual systolic volume. Since the students had taken more than 50 exams in the past and were adapted to the pre-examination situation, the circulatory changes revealed may be regarded as adaptive providing for the rich flow of blood to the brain.     

Comparative evaluation of the effect of preliminary adaptation of the body to moderate physical loading and brief stress exposures on heart contractile function disorders in long-term stress

The effect of repeated emotional-painful stress stimuli and repeated moderate exercise (swimming) on cardiac resistance to long-term emotional-painful stress (EPS) was studied in Wistar rats. Adaptation to repeated exercises was found to significantly increase tension developed by the myocardium of an isolated auricle and myocardial resistance to hypoxia and excessive calcium, but it could not prevent the EPS-induced depression of contractility. Adaptation to short-term stress on the contrary, did not significantly affect myocardial tension and cardiac resistance to hypoxia and excessive calcium, but it completely prevented the long-term EPS-induced depression and considerably reduced the stress-potentiating effect on the development of calcium and hypoxic contractures. Therefore, adaptation to stressful effects proper, rather than moderate exercise, can build up heart resistance to damaging stress effects.     

Effect of preliminary adaptation to moderate and intensive physical loads on cardiac electrical stability and contractile function in experimental myocardial infarct

Preliminary adaptation of animals to a moderate swimming exercise prevented the fall of ventricular fibrillation electrical threshold and limited drastically the heart ectopic activity in acute myocardial infarction. Adaptation to intense stress, i.e. prolonged swimming with a load, had less preventive effect. The rationing of preventive exercise, to be used for the prophylaxis of myocardial infarction, is discussed.     

Formation and reversal development of the local mechanisms of heart protection during adaptation to continuous stress

Experiments with isolated rat hearts demonstrated that in the course of adaptation to continuous immobilized stress of moderate intensity (1, 5, and 15 days), the heart gradually (at day 15) formed the defense mechanism previously described, that is the adaptive structural stabilization phenomenon (ASSP). ASSP defends cardiac contractile function and has a powerful antiarrhythmic and cytoprotective effect in total ischemia, reperfusion, and under the action of toxic concentrations of calcium and catecholamines. The protective ASSP effect formed over 15 days of continuous stress proved to be steady-state, remaining for 15 days of adaptation cessation. Thus, during adaptation to continuous stress higher regulatory mechanisms determine the gradual development of a highly effective defense mechanism in the heart at the cellular level.     

Effect of compensatory myocardial hypertrophy on the electric stability of the heart

Dog heart was shown to be more prone to ventricular fibrillation at the stage of completed right-ventricular hypertrophy about 5 months after pulmonary arterial trunk was stenosed by 2/3 of the original lumen, as compared to normal heart. Electrical instability of the heart with completed right-ventricular hypertrophy increases in proportion to the magnitude of hypertrophy.     

Prevention of disorders of myocardial contractile function under stress by the preliminary adaptation of animals to physical load

Rats adapted to exercise (daily swimming for one hour over 30 days) and control animals were subjected to emotional-painful stress (EPS) according to the pattern of anxiety neurosis. It has been established that EPS decreases the amplitude as well as the rate of contractions and relaxations of the isolated papillary muscles of animals by 2-3 times and also reduces the resistance of the contractile function of the myocardium to the excess of Na+ and H+ ions, ousting Ca2+ from the sites of its binding in the sarcolemma. Adaptation to exercise exerts an opposite effect. The preliminary adaptation of animals prior to EPS prevents or limits the stress-related depression of the contractility of the myocardium and the diminution of its resistance to the factors replacing Ca2+. The preliminary adaptation to exercise may be used for preventing stress-related disorders of cardiac contractility.     

Prevention of arrhythmogenic and contractile effects of excessive Ca2+ on the heart through adaptation to stress by increasing the activity of sarcoplasmic reticulum

The experiments with rat isolated hearts and papillary muscles showed that adaptation to short-term stresses increased myocardial resistance to arrhythmogenic and contractile effects of excessive Ca2+. Adaptation caused a three- and fivefold reduction in the contracture and premature beats, respectively, while Ca2+ levels were increased from 1.36 to 10 mM. In the experiments with papillary muscles, the adaptation showed a 6.5-fold decrease in the contracture and significantly limited resting potential depression resulted from lower Na+ concentrations (up to 9 mM) in the perfusion solution. The adaptation to stresses was found to restrict depression of cardiomyocyte electrophysiological parameters that was due to high Ca2+ levels and high heart rate. With the factors, the resting potential in adaptation proved to be significantly higher than in controls and the time of action potential was twice as such as in controls. Biochemical studies demonstrated that Ca2+ transport rates in the sarcoplasmic reticulum, cardiomyocytes of adapted animals were increased by more than 30% whereas the sarcoplasmic reticulum of the heart was more resistant to the effects of endogenous factors of degradation. The authors also discuss a possible mechanism of the cardioprotective effects of adaptation to stress undamaging exposures, which is associated with limited depression of electrophysiological parameters on pathological exposures and with increased Ca2+-transporting capacity of the sarcoplasmic reticulum.     

Effect of verapamil on contractile function of the isolated perfused rat heart during postnatal ontogeny

Summary The negative inotropic effect of the calcium antagonist, verapamil, was compared in isolated hearts from 15-, 30-, 45-, 60-, and 90-day-old rats. Electrically paced hearts were perfused in vitro according to Langendorff, either under constant pressure or under constant flow conditions. An intraventricular-pressure curve was measured isovolumetrically and analyzed on-line using a microcomputer. Changes in pressure amplitude and maximum rate of pressure development were evaluated during a stepwise increase of the verapamil concentration in the perfusion solution (10^–9–3.3×10^–7 mol·l^–1). It was found that the sensitivity of cardiac contractile function to verapamil declines gradually in the course of postnatal ontogeny. The higher sensitivity of the developing heart to calcium channel blockade is probably a consequence of a higher functional dependence of the immature myocardium on trans-sarcolemmal calcium influx.     

Effect of vitamins A and E on the contractile function of the heart in experimental myocardial infarction

An experimental study in rabbits demonstrated that the animals treated with vitamins A and E (400 IU/kg and 0.4 mg/kg, respectively) in the presence of experimental myocardial infarction induced through ligation of the anterior descending coronary artery, showed a much more pronounced reduction of cardiac contractility as compared to the untreated animals with induced infarction or those treated with much higher doses (10000 IU/kg and 10 mg/kg, respectively). Vitamins A and E administered in small doses to intact animals and rabbits with experimental myocardial infarction produced marked damage of lysosome membranes, whereas high doses of vitamins had no similar effect in either intact or experimental-infarction animals.