PubMed Health⌕ Search

Biomedical subjects

H H Dickhuth

Publications and source records attributed to H H Dickhuth.

At least 73 records · Page 4Linked to original sources
PubMed1989

[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↗
PubMed1989

[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↗
PubMed1988

[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↗
PubMed1987

[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↗
PubMed1987

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↗
PubMed1987

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↗
PubMed1985

[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↗
PubMed1985

[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↗
PubMed1984

Plasma catecholamines, beta-adrenergic receptors, and isoproterenol sensitivity in endurance trained and non-endurance trained volunteers.

Six male non-endurance trained subjects (S) and six marathon runners (M) underwent graded treadmill exercise (T) and isoproterenol stimulation (I; 2 and 4 microgram X min-1). beta-adrenergic receptor density was additionally determined as the amount of 3H-Dihydroalprenolol (DHA) specifically bound on intact polymorphonuclear leucocytes. Heart rate, VO2 uptake, lactate, plasma noradrenaline, and adrenaline were estimated during T. Heart rate, stroke volume, cardiac output, as well as lactate, glucose, free fatty acids (FFA), and glycerol levels in the blood were determined during I. M showed the known training-dependent responses during T, such as lower heart rates, lactate levels, and plasma catecholamines at identical work loads, as well as higher VO2 max than S. I-induced cardiac output increase was quite similar in both groups. Stroke volume, however, increased significantly in M and stayed constant in S. Lactate decreased (S), glucose increased significantly (M), glycerol increased similarly in both groups, FFA rise was less marked in S. I-induced stroke volume response (I) may be indicative of a more economic regulation of heart work in M than S. Lactate decrease and less marked FFA increase, as observed in S, may be the result of a somewhat higher cardiac energy demand, dependent on less economic heart work. Higher DHA-binding as observed in M, as well as stroke volume response and glucose increase, may be indicators of a training-dependent rise in sensitivity to catecholamines. The unsolved question is, however, to what extent beta-receptor responses in intact blood cells are significant for receptor behavior in other organs.

Adult↗
PubMed1983

Two-dimensional echocardiographic measurements of left ventricular volume and stroke volume of endurance-trained athletes and untrained subjects.

The left ventricular volume (EDV), the left ventricular total volume (TDV), and the stroke volume (SV) of 40 male untrained subjects and 68 endurance athletes were determined using one-dimensional echocardiography, two-dimensional echocardiography, and a combined method. The accuracy of the volume and stroke volume measurements was checked by comparing them to ergometrically determined maximum oxygen pulse (max O2-P) and to radiographic heart volume (HV). There was clear improvement in the EDV, TDV, and SV measurements when using two-dimensional echocardiography and the combined method in comparison to one-dimensional echocardiography. The best correlation to the max-O2-P was reached by TDV2 (combined method, r = 0.8738). This method includes the myocardium of the left ventricle similar to heart volume measurements. The relationship is as close as between HV and max O2-P (r = 0.8665). The method suggested here is sufficiently accurate to be used in performance diagnosis to determine the size of the left ventricular volume and to classify pathological size changes or those due to training.

Adolescent↗
PubMed1983

[Two-dimensional stress echocardiography and plasma catecholamine measurements in the evaluation of the physiologically hypertrophied heart].

Two-dimensional stress echocardiography was performed in 8 untrained subjects, 8 long-distance runners, and 8 cyclists. The ergometric investigation was performed with subjects in supine position on a bicycle ergometer with increasing work loads of 50 Watts. At each working level, lactate, norepinephrine, and epinephrine were measured. The long-distance runners and the cyclists had an equal maximum oxygen uptake when tested with treadmill or bicycle ergometer. Absolute and relative heart volumes also showed the same amount of hypertrophy. In spite of this, lactate, catecholamines, and heart rate of the long-distance runners rose earlier during the supine ergometer test. End-diastolic volume and stroke volume in the cyclists increased significantly more (delta EDV = 15%, delta SV = 32%) than in the long-distance runners (delta EDV = 1%, delta SV = 13%) and untrained subjects (delta EDV = 5%, delta SV = 9%). It is assumed that this difference in heart function is caused by diminished sympathetic activity, which is dependent on the aerobic capacity of the working muscles.

Adolescent↗
PubMed1983

[Simultaneous determination of hemodynamics and plasma catecholamines in trained and untrained subjects and patients with contraction disorders of the heart during rest and physical activity].

6 trained (TS) and 7 untrained (US) subjects and 16 patients (P) with left ventricular dysfunction were investigated by means of a Swan-Ganz floating catheter during graded bicycle ergometry in a supine position. 9 P suffered from a myocardial infarction and 10 were known to be hypertensive; 10 suffered from acute coronary insufficiency during exercise. Hemodynamic values, free plasma catecholamines, and heart volume at rest were determined in all cases. The relative heart volume was increased training-dependent in the TS as compared with US and P. In TS stroke volume increased more than in US, whereas in P a heart-rate-dependent adaptation of cardiac output was observed during exercise. In P cardiac output was slightly reduced during exercise and the arteriovenous oxygen difference augmented. Systolic and diastolic pulmonary artery pressure, pulmonary wedge pressure, and peripheral diastolic arterial pressure rose more in P during exercise than in TS and US. TS showed reduced, whereas P showed increased levels of circulating free plasma catecholamines (norepinephrine and epinephrine). Training-dependent changes in hemodynamic values and catecholamine levels were seen as an economic adaptation of the heart to physical stress, and the results in the patients were interpreted as indicating an uneconomic stress adaptation. In patients with disturbed left ventricular function, extracardiac compensatory mechanisms such as enhanced sympathetic activity and increased arteriovenous oxygen difference are necessary for the adaptation to physical stress.

Arrhythmias, Cardiac↗
PubMed1983

[Ventricle function in low-dose digitoxin in patients with chronic heart failure (stage II/III)].

Using one- and two-dimensional echocardiographic parameters, left ventricular function and dimensions were investigated in 11 patients with chronic heart failure (NYHA stages II-III) and in 10 normal subjects after administration of low-dose digitoxin (0.07 mg). Tests were performed before the begin of therapy, on the 3rd day following rapid saturation, and on the 15th day under maintenance therapy. There was no significant decrease either of heart volume as assessed by X-ray or of enddiastolic volume measured echocardiographically. However--predominantly in patients--a marked decrease in endsystolic diameter (p less than 0.01) and an increase in posterior wall motion amplitude (p less than 0.05) was observed resulting in increased stroke volume, shortening fraction (p less than 0.001). Early diastolic left ventricular filling speed also increased significantly in both groups (p less than 0.01). Changes in these parameters were more pronounced in patients than in normal subjects. In both groups the effects were achieved soon after rapid saturation, increasing slightly during the period of chronic administration of low-dose digitoxin. Parallel to the changes in echocardiographic parameters, a noticeable clinical improvement occurred among patients. No side effects were observed as serum digitoxin levels were in the therapeutic range. It may be concluded that low-dose digitoxin can be employed to increase cardiac contractility in patients with heart failure.

Adult↗