[Sports and prevention of cardiovascular diseases].
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Cardiovascular Diseases↗
Biomedical subjects
H H Dickhuth
Publications and source records attributed to H H Dickhuth.
[Fitness for swimming after myocardial infarct].
Standardized telemetry during swimming and blood pressure monitoring were performed on 25 consecutive patients (22 men and 3 women: mean age 59 +/- 7 years) after myocardial infarction, sustained on average 28 +/- 26 months ago. Mean exercise tolerance, as judged by symptoms during bicycle ergometry, was 1.31 +/- 0.5 W/kg (pulse limit 117 +/- 21 beats/min). The swimming test had to be discontinued in six patients because of severe arrhythmias, in two because of severe angina. Seven patients completed the full swimming distance, but were also considered unsuitable for swimming because of moderate angina and dyspnoea. Ten patients proved to be fit for swimming. Their average ergometrically determined exercise tolerance (1.27 +/- 0.51 W/kg, pulse limit 114 +/- 16 beats/min) was not different from that of unfit patients (1.34 +/- 0.50 W/kg; 119 +/- 24 beats/min). During swimming the unfit patients had a significantly higher heart rate and blood pressure rise than the fit ones. Only in the unfit patients the exercise tolerance limit determined by bicycle ergometry was exceeded during swimming. This indicates that postinfarction patients should undergo swimming telemetry before declared fit for swimming.
Angina Pectoris↗
Training-overtraining. A prospective, experimental study with experienced middle- and long-distance runners.
Overtraining may be one frequent cause of stagnation or decrease in performance capacity of athletes. Israel (19) differentiates between addisonoid (parasympathetic) and basedowoid (sympathetic) overtraining, characterized by inhibition or excitation. We tried to induce an overtraining syndrome in 8 experienced middle- and long-distance runners, based on an increase in training volume from an average 85.9 km (week 1) to 115.1 km (week 2) and 143.1 km (week 3) to 174.6 km per week (week 4). The influence of this training on cardiovascular, metabolic and hormonal parameters was examined with special respect to plasma and urinary catecholamines. Laboratory testing including graded treadmill running was performed on the days 0, 14 and 28. Training was held six days each week, with nearly 30 km per day in the fourth week. A stagnation in endurance performance capacity (running velocity at the aerobic-anaerobic transition range) and a decrease in maximum working capacity were observed in 6 and a stagnation in 2 of the 8 sportsmen, indicated by a decrease in total running distance from 4719 + 912 m to 4361 + 788 m during incremental treadmill ergometry. The sportsmen could neither improve nor could they even approximately reach their personal records during the subsequent competitive season. Subjective complaints, classified on a four-point scale, increased from 1.2 (week 1) to 3.2 in week 4. Glucose, lactate, ammonia, glycerol, free fatty acids, albumin, LDL, VLDL cholesterol, hemoglobin level (transient), leukocytes, and heart rate (before and during exercise) decreased significantly. Urea, creatinine, uric acid, GOT, GPT, gamma-GT, serum electrolytes (except phosphate and calcium) remained constant at the measuring times, CPK was elevated.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
The relationship between heart rate and QT interval during atrial stimulation.
The relationship between heart rate and QT interval was investigated during atrial stimulation (intrinsic effect of heart rate) in ten healthy male volunteers prior to and after administration of sotalol. The QT interval in the ECG (paper speed 200 mm/s) was determined at rates of 70, 85, 100, 115, 130, 145, and 160 beats/min and at pacing periods of 180 s each at 30, 60, 120, and 180 s. After a 15-minute period, 2.0 mg sotalol/kg body weight were administered iv and the stimulation protocol was repeated. The analysis of QT interval behavior reveals contradictions to the mathematical implications of Bazett's equation QT = QTc square root of 60/HR, so that the relationship between heart rate and QT interval is not adequately described under the given conditions. After examination of approaches reported in the literature and our own approaches, the expression QT = a e-b (HR-60) is used as a possibility differentially to describe the data by nonlinear regression. The parameters a and b may be interpreted as QT reference value and shortening parameter. The QT reference value a, a parameter in reference to heart rate of 60 beats/min, has a comparable significance to the expression QTc in the Bazett equation. A reduction in the shortening parameter b indicates whether substances influencing the QT interval additionally produce overproportional shortening of the QT interval with increasing heart rate. After administration of sotalol, an increase can be observed in both the QT reference value and also in the shortening parameter. The suggested approach is an attempt to provide a more precise assessment of the QT interval under different conditions.
Adult↗
[Effect of beta blockade on hemodynamics in physical exertion].
Beta-receptor blocking agents are known for more than 20 years. They are of definite use in the therapy of arterial hypertension and coronary heart disease. Beta-blockers lower the sympathoadrenergic discharge to the heart and circulation, particularly if the former is increased. Beta-blockers induce a negative chronotropic and inotropic effect and inhibit beta 2-mediated vasodilation. Thus beta-sympathicolysis during physical activity results in damping of heart rate increase and of elevation of cardiac contractility. Systolic blood pressure does not increase much, and usually there is no decline in diastolic blood pressure, due to elevated peripheral resistance. With adequate dosage, there may even be a slight increase in diastolic pressure, an effect eventually vaning in chronic therapy. Pulmonary capillary wedge pressure is elevated to above normal via inhibition of contractility and relaxation of the heart. Stroke volume, cardiac output and the double-product decrease, the arteriovenous oxygen difference under exercise increases clearly and the maximum aerobic performance capacity decrease in healthy individuals. In coronary patients, this may protect against cardiac overload and increase symptom-free physical work capacity, due to a relative decrease in the myocardial O2 requirement and improved coronary perfusion resulting from prolonged diastole. With verified indication (hypertensive-hyperkinetic impairments of cardiovascular function, coronary heart disease), the goal is an overlapping, endurance-oriented training to reduce the overall sympathetic activation, in order to minimize medication in the long run.
Adrenergic beta-Antagonists↗
[Current aspects of modern ergometry].
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Energy Metabolism↗
[Doping--also a problem in general practice?].
In 1986, the Medical Commission of the IOC defined doping as the use of pharmacological substances belonging to disallowed groups of active substances (stimulants, narcotics, anabolic steroids, beta-blockers, diuretics). With certain restrictions, this applies also to alcohol, local anesthetics and corticosteroids. The use of disallowed methods (blood doping, manipulation of a urine sample) is also forbidden. These days the greatest importance is attached to anabolic steroids (including testosterone), since these substances--discontinued in good time--cannot be detected on the day of competition but still have a promoting effect on performance. Competitive sports prepared the way here for the use of anabolic steroids in general athletics and in particular usually non-olympic sports (such as bodybuilding). Against this background, effects, adverse effects and the risks of anabolic steroid use are discussed. The aim must be to prevent the use of doping, especially in uncontrollable general sports, by promoting proper awareness.
Anabolic Agents↗
The long-term involution of physiological cardiomegaly and cardiac hypertrophy.
The long-term involution of physiological cardiomegaly and cardiac hypertrophy. Med. Sci. Sports Exerc., Vol. 21, No. 3, pp. 244-249, 1989. Forty-five former athletes in endurance disciplines, primarily Olympic medalists and World Cup, European Cup, and German champions, for whom results of an exercise ECG and radiological heart volume measurement were available from their active competitive phase, were examined. The study protocol included clinical examination, laboratory controls, resting and exercise ECG, determination of cardiac volume, and one- and two-dimensional echocardiographic examination. Of the 45 former athletes contacted, 38 appeared for examination. Of these, four presented with heart disease (two with infarction, one with aortic stenosis, and one with arrhythmia). The remaining 34 were divided into groups of still active (more than 300 kcal.wk-1) and inactive (less than 300 kcal.wk-1) athletes. The interval between the first and second examination averaged 23 yr. The active former athletes showed a weight increase of 5.2% (P less than 0.01) and a reduction of 14% in ergometric performance (P less than 0.02). The inactive group had a marked weight increase of 17.4% (P less than 0.001); the ergometric performance was lowered by 20% (P less than 0.001). The absolute heart size had decreased in the active group by 6.1% (NS) and the relative heart size by 10.7% (P less than 0.005); the corresponding values in the inactive group were 4.5% (NS) and 18% (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Adaptation, Physiological↗
[Form, size and function of the sports heart--differentiation from pathological findings].
Dependent on the nature, intensity and scope of muscular exercise, regular athletic training can result in changes in the size and form of the heart, which can be recorded by radiologic and echocardiographic techniques. Brief anaerobic exercise and purely static forms of training (sprint, strength sports) do not produce substantial increases in the size of the heart, but a rotund heart shape with rounding of the cardiac tip and in some cases a discrete increase in the wall thickness of the ventricular myocardium is frequently observed. Dependent on the scope of the training and the intensity, aerobic, endurance-oriented training (endurance sports) can induce considerable enlargement of all cardiac chambers with a change in the cardiac configuration, which is most nearly comparable to combination mitral vitium. Comparison of physiological hypertrophy of the athletic heart with pathological forms of cardiac hypertrophy (such as cardiomyopathies) is in many cases not unequivocally possible with plain X-ray films, but it is usually successful with echocardiographic examination methods.
Adult↗
[Hypertension, the heart and physical activity (sports)].
Cross-sectional analyses show a lower incidence of hypertension among endurance athletes compared to the general population, but not among strength athletes or high-performance swimmers. The favorable influence of increased physical activity of the endurance type on cardiovascular regulation is based on peripheral adaptation processes with a reduction in sympathetic tone and elevation of parasympathetic tone. The results are a reduction in catecholamine release, in heart rate, and in mean arterial pressure at the same exercise level. Following chronic strength training there is also a slight reduction in catecholamine levels at the same time the vagal activity decreases, so that no reduction in heart rate and pressure, and thus no economization of cardiac work results. Thus, endurance training is suited for prevention and also for the reduction of blood pressure in primary hypertension and for cardiac relief, while strength training is not. In the case of hypertension, physical activity may only be engaged in when the cardiac functional status and other organ impairments are known. The stages of cardiac adaptation and damage, particularly the differentiation between concentric and eccentric hypertrophy, are particularly important. Exercise ECG and echocardiography are therefore obligatory measures prior to initiating physical activity and for continuous monitoring of hypertension. In primary hypertension Stage I (70-80% according to WHO), in which no cardiac hypertrophy is present, endurance training may be started without drug therapy if diastolic pressure is not greater than 104 mmHg and systolic pressure up to 170 mmHg (mild hypertension). Additional drug therapy does not show any convincing advantages. Higher pressures require adjuvant drug therapy. In concentric cardiac hypertrophy (Stage II), there is clear indication for the use of hypotensive drugs. An endurance sport is to be recommended additionally after normalization of blood pressure; the regression of cardiac hypertrophy should be examined within one year. In eccentric hypertrophy (damage stage), "training" is not indicated in addition to drug therapy, but rather physical therapy according to defined exercise capacity. The selection of medications for reducing blood pressure in sportsmen must take into consideration that they have varying performance limiting effects, which may be an essential factor in compliance.
Blood Pressure↗
[Differential diagnosis: physiologic-pathologic hypertrophy of the heart. A case report].
We report on a 52-year-old asymptomatic patient, whom we have examined regularly since 1981. The principal finding is a marked terminal negativity of the T-wave in the extremities and left precordial chest leads in the electrocardiogram with regression at high exercise levels. The patient engages intensively in sports (running, cross-country skiing, gymnastics). His performance capacity is above normal at 4.5 (1981) and 3.8 watts/kg body weight (1988). The echographically determined left ventricular muscle mass (LVM) increased from 2.1-2.3 g/kg body weight to 2.9 g/kg, the end-diastolic thickness of the septum from 9 to 13, and the posterior wall from 8 to 12 mm. In physiological cardiac hypertrophy (athlete's heart), a LVM of 2.9 g/kg is not unusual, whereby the end-diastolic wall thickness does not, exceed 10 to 11 mm and the mass-volume ratio (LVM/end-diastolic ventricular volume) remains constant (about 1.2 g/ml) in contrast to the 1.75 g/ml in our patient. Thermodilution catheter examination of the heart showed a pathological increase in mean pulmonary capillary pressure (26 mm Hg) under exercise as an indication of impaired left-ventricular function. Normal myocardial scintigraphy (resting and exercise) and a lack of symptoms permit the exclusion of relevant coronary heart disease. We diagnosed non-obstructive hypertrophic cardiomyopathy. The problems of differentiating between physiological and pathological cardiac hypertrophies are discussed.
Cardiac Volume↗
[Determination of wall thickness (by echocardiography and autopsy) in the diagnosis of heart hypertrophy].
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Cardiac Volume↗
[Effect of vitamins and iron on performance and recovery in humans and in sports anemia].
In sports, vitamins along with minerals, particularly iron, and the energy nutrients such as carbohydrates, are considered especially important. Frequently single or multiple vitamins in combination with other active substances such as iron, other minerals or carbohydrates are administered. In sports, vitamins are added to carbohydrate mixtures or electrolytes enriched with vitamins are offered and frequently used. There is no doubt that due to the numerous effects of vitamins, a connection must exist between the vitamin status and athletic performance capability. It can be concluded that vitamin deficiencies have a negative effect on physical and mental performance. The release of energy can only attain its maximum output when the organism has the required substances at its disposal. Iron is of central importance among these active substances, since its presence in haemoglobin is essential for the transport of oxygen and carbon dioxide, makes it possible for myoglobin to function as an oxygen supply depot and guarantees the functioning of internal respiration in the respiratory chain and various key enzymes. Muscle training increases not only the respiratory chain but also several other iron-rich enzymes. This makes even more astonishing the fact that a variety of recently published articles report on iron deficiency among athletes. The effect of the iron deficiency with anaemia (sports anaemia) is manifest in a reduction of aerobic capacity with an increase in lactate acidosis, greater fatigue, loss of appetite, muscular cramps and vasomotor disturbances.
Anemia, Hypochromic↗
Sensitivity of the physiologically hypertrophied heart to isoproterenol.
Cardiovascular reactions to isoproterenol stimulation (2 and 4 micrograms/min for 12 min each) were evaluated in seven endurance-trained athletes (marathon runners, VO2 max 66.0 +/- 3.7 ml/kg) and seven untrained subjects (VO2 max 54.4 +/- 3.6 ml/kg). At rest and during stimulation, the heart rate, blood pressure as well as one-dimensional (end-diastolic and end-systolic dimensions, shortening fraction) and two-dimensional (end-diastolic and end-systolic volumes, ejection fraction, stroke volume, cardiac output) echocardiographic parameters were determined. The increase in the heart rate of the endurance-trained athletes (28%; 2 micrograms/min) (58%; 4 micrograms/min) was less than in the untrained controls (34%/76%). The blood pressure behaved similarly in both groups. The stroke volume of the endurance-trained subjects rose during stimulation (14%, 4 micrograms/min); the end-diastolic volume remained nearly constant as the end-systolic emptying increased. The stroke volume of the untrained subjects tended to decrease as the end-diastolic and end-systolic volumes were reduced. In absolute terms, the shortening fraction and ejection fraction were identical. Referring to the heart rate, however, they were elevated in the endurance-trained subjects. Hence, under isoproterenol the rise in heart rate was weaker and the increase in ventricular performance seemed to be stronger in the trained subjects compared to the untrained controls. The causes appear to be different regulative effects of the autonomic nervous system on the sinus node and the ventricular myocardium; intrinsic cardiac mechanisms remain to be discussed.
Adult↗
Physical training, vegetative regulation, and cardiac hypertrophy.
Dynamic physical training leads to functional and structural adaptations in the cardiovascular system. Functional changes, such as bradycardia, occur after only relatively little training and in advance of structural changes. They are the result of elevated parasympathetic tone at rest and reduced sympathetic activity in the submaximal range. Sympathetic activity cannot be correlated only with the plasma catecholamine level because the affinity and density of the beta-receptors and alpha receptors are influenced by training. In humans, endurance training appears to result in an elevation in beta 2-receptors and a decrease in alpha 2 receptors; the results of animal experiments are discrepant. Conformant, however, is the increased responsiveness of the myocardium to isoproterenol with respect to the mechanical response. Independent of this, other changes at the membrane level must be discussed since the intrinsic heart frequency is reduced in athletic individuals following autonomic blockade, even before hypertrophy can be observed. The functional changes remain intact or intensify when cardiac hypertrophy is induced by increased training. The maximum values for training-induced hypertrophy [left ventricular muscle mass (LVM) = 3.5 g/kg] are about 70-80% of the baseline weights (LVM = 2.1 g/kg). The left ventricle is enlarged during end diastole and end systole, the ejection fraction is normal, and the stroke volume is increased. The mass/volume ratio remains constant (LV = 1.2 g/ml), as does the maximum systolic wall stress (196 x 10 dyn/cm). Compared with pathological forms of hypertrophy and to the normal heart, the trained heart is capable of increasing the stroke volume considerably with exercise and maintaining the increase to a high-frequency range.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiomegaly↗
[Cardiocirculatory regulation in heart hypertrophy].
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Cardiomegaly↗
[Estimation of heart size--x-ray versus 2-dimensional echocardiography].
Radiologic heart volume measurement (HV) and two dimensional echocardiographic estimation of left ventricular volume and ejection fraction (EF) were carried out in 108 healthy subjects and 68 patients with hypertony, dilatative cardiomyopathy and hypertrophic-obstructive cardiomyopathy (HOCM). Healthy subjects show a close relationship between echocardiographic determined volume and absolute heart volume (HV), in patients with hypertony, dilatative cardiomyopathy and HOCM there is also a significant correlation. However, no correlation exists between EF and HV and HV/kg in patients with hypertony and HOCM, whereas patients with dilatative cardiomyopathy show a high significant inverse relationship. It is concluded that these results are caused by great differences in muscle mass. The clinical value of radiologic heart volume as a parameter of left ventricular systolic function seems to be low and depends on cause of the heart enlargement.
Cardiac Volume↗
[Capacity for regression of the athletic heart].
Dynamic exercise leads to an increase in heart size and to hypertrophy depending on the intensity and extent of training. The maximum of left ventricular muscle mass is reached at 3.5 g/kg, which is 70-80% higher compared to untrained subjects. The mass/volume ratio remains constant (left ventricle 1.0-1.2 g/ml). Systolic wall stress and ejection fraction of the enlarged left ventricle do not change. No heart hypertrophy can be found in athletes carrying out maximum static exercise. Heart size and heart hypertrophy regress when training stops completely. The velocity of regression is not exactly known, a maximum regression of 10-15% within three weeks is probable. Investigations of former athletes show a decrease of heart size and heart hypertrophy, especially when related to body weight. The degree of regression depends on the actual physical activity; another factor may be the duration of the competition activity. It is supposed that only a small degree of training prevents the decrease of heart enlargement, heart hypertrophy and higher performance ability. Damage to the cardiovascular system caused by maximum exercise training cannot be found.
Cardiac Output↗