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Biomedical subjects

H Heck

Publications and source records attributed to H Heck.

At least 19 recordsLinked to original sources
PubMed2002

[Influence of a resistance training on pulmonary function and performance measures of patients with COPD].

BACKGROUND: Training therapy with its manifold effects should be part of a modern and multi modular treatment of the COPD. Because of the specific symptoms (e. g. muscle atrophy, dyspnea, low testosterone levels) and the deconditioning of these patients, a resistance training might meet the demands of a COPD-exercise-therapy rather than an endurance training. The aim of this research project was to evaluate the efficiency of a hypertrophic maximal strength training on various COPD relevant parameters. METHODS: 28 patients with moderate to severe COPD (m12/f16) were randomized and divided in a treatment and a control group. The patients in the treatment group underwent a resistance training (hypertrophic maximal strength training) for 12 weeks, initially two times, then three times a week. RESULTS: Considering the results of the daily Peak-Flow-Measurement, there was no significant change in both groups, but a trend towards an improvement could be found in the treatment group. There was no difference in the change of FEV 1. The performance on the ergo cycle showed a highly significant improvement (p < 0.001) in the treatment group of 18.7 % (21.9 Watt). The results of the SGRQ showed a significant improvement (p < 0.05) of the HRQL in the treatment group. A change of the HRQL in the control group was not found. CONCLUSIONS: These data support the hypotheses that a short term high intensity strength training programme is suitable to improve performance measures of patients with moderate to severe COPD and it might also improve pulmonary function. The conclusion can be drawn, that this kind of resistance training can be prefered as COPD-specific training therapy and offers new treatment perspectives.

Exercise↗
PubMed1999

In utero exposure to antiandrogens alters the responsiveness of the prostate to p,p'-DDE in adult rats and may induce prostatic inflammation.

DDE is an environmental pollutant with antiandrogenic properties. Following administration to pregnant rats, DDE was shown to cause feminization in the male offspring at the neonatal stages but did not affect the pubertal growth of accessory sex organs. In this study, we examined the potential of in utero exposure to antiandrogens to alter the responsiveness of the male rats to subsequent DDE challenge. Pregnant Long-Evans rats were dosed by gavage from Gestation Day 14 to 18 at 0, 10 (low dose), or 100 (high dose) mg DDE, or 40 mg flutamide/kg body wt (bw)/day (in utero treatment). At approximately 80 days of age, the male offspring from each of the four in utero treatment groups were divided into two groups. One group received the adult treatment of four daily gavage administrations of DDE at 70 mg/kg bw (adult treatment), while the second group served as the adult treatment control (adult control). The in utero treatment resulted in 18, 31, and 53% reductions of ventral prostate weights at approximately 85 days of age compared to the control for the low- and high-dose DDE and flutamide groups, respectively. These results suggest that the in utero antiandrogen treatments produced a latent effect on prostate growth that became pronounced only in the postpubertal stage. The in utero treatment also altered the responsiveness of the prostate to the adult treatment, indicated by a significant reduction in ventral prostate weight that was seen only in the control group of the in utero treatment but not in the other groups. The in utero treatment was also associated with expression of testosterone-repressed prostatic message-2 in the adult ventral prostate. In addition, a few prostates in the high-dose DDE- and flutamide-treated groups of the in utero treatment were found to have chronic suppurative prostatitis. While other types of hormonal manipulations have been shown to incite similar responses in rat prostate, the possible linkage between in utero antiandrogen treatment and prostatic inflammation needs to be further evaluated.

Adipose Tissue↗
PubMed1999

Pharmacodynamics of formaldehyde: applications of a model for the arrest of DNA replication by DNA-protein cross-links.

A variety of evidence suggests that formaldehyde (HCHO)-induced DNA-protein cross-links (DPX) are genotoxic as a result of their ability to arrest DNA replication. Although DPX can be removed and the DNA can be repaired, failure to remove the blockage prior to cell division or excision followed by incomplete repair could cause cell death or a mutation. To characterize the concentration and time dependence of this mechanism, a biologically based model for DNA replication in the presence of DPX was developed based on the assumptions that (1) DPX are formed randomly in the DNA and (2) a replication fork can advance up to but not past a DPX. Using a combination of Poisson and binomial statistics, a quantitative relationship between the amount of newly synthesized DNA and the concentration of DPX was derived, which predicts that the rate of DNA replication should decrease nonlinearly with increasing concentrations of DPX. Because the latter is a nonlinear function of the airborne concentration of HCHO, an inverse sigmoidal relationship is predicted between the rate of DNA replication and the concentration of inhaled formaldehyde. The model was parameterized using data derived from a study of the incorporation of [methyl-(14)C]thymidine monophosphate into the DNA of the nasal respiratory mucosa of Fischer-344 rats exposed to (3)HCHO and H(14)CHO (6 ppm, 6 h). The model was then applied to measurements of DNA replication in the nasal mucosa of experimental animals exposed to wide ranges of H(14)CHO (rats: 0.7, 2, 6, or 15 ppm, 3 h; rhesus monkeys: 0.7, 2, or 6 ppm, 6 h). The results indicate that, at airborne concentrations above 6 ppm in rats, there is a marked decrease (ca. 62% at 15 ppm) in the amount of newly synthesized DNA due to DPX formation during a single 6-h exposure to HCHO. The arrest of DNA replication at high HCHO concentrations could result in cytolethality or genotoxicity, both of which are critical factors in the induction of rat nasal cancer by HCHO. However, at concentrations below 2 ppm in monkeys or 1 ppm in rats, the decrease in the rate of DNA replication is predicted to be <1% after a 6-h exposure. This small decrease is probably undetectable using currently available techniques. The parameterized model suggests that the arrest of DNA replication by DPX is mainly a high-dose phenomenon and that at ambient exposure concentrations it is unlikely to be a major risk factor.

Animals↗
PubMed1999

Modulation of testosterone-metabolizing hepatic cytochrome P-450 enzymes in developing Sprague-Dawley rats following in utero exposure to p,p'-DDE.

1,1-Dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE) causes sexual developmental aberrations in male rats through a likely mechanism of androgen receptor antagonism. DDE is also known to induce liver cytochrome P-450 (CYP). The expression of CYP enzymes is regulated by steroid hormones, which, in turn, are inactivated in the liver by CYP-catalyzed hydroxylations and subsequent conjugations. This study was undertaken to examine the potential of in utero DDE exposure to affect the developmental expression of the hepatic CYP enzymes that are responsible for testosterone hydroxylations. Pregnant Sprague-Dawley rats were dosed daily by gavage with DDE at 0, 10, or 100 mg/kg body weight or with flutamide at 40 mg/kg body weight from gestation day 14 to 18. Additional adult male rats were given seven daily doses of DDE at 100 mg/kg. Liver samples were collected from the offspring of the dosed dams on postnatal days (PND) 10 and 21 and from the adult rats a day after the last dosing. Assays for regioselective and sterospecific testosterone hydroxylase activities were performed using hepatic microsomal preparations. Specific liver CYP proteins were detected by immunoblotting. While the CYP2B1 and 3A1 and their hydroxylated testosterone products were highly elevated by the DDE treatments in both adult and developing rats, the responses of 2C11 and 2A1 were development-dependent. The flutamide treatment had little effect on CYP enzyme expression. This study demonstrated that developing offspring rats are susceptible to the hepatic CYP enzyme-modulating action of DDE following its administration to the pregnant dams.

Age Factors↗
PubMed1997

The validity of the telemetric system CORTEX X1 in the ventilatory and gas exchange measurement during exercise.

With the portable spirograph CORTEX X1 both the oxygen consumption and the carbon dioxide output can be determined. Therefore, the aim of the present study was to determine the accuracy of the CORTEX X1 in measuring F(E)O2, F(E)CO2 and V(E) when attached to a motor-driven mechanical syringe and to validate the CORTEX X1 against a standardized breath-by-breath system during a graded bicycle ergometry. Fifteen subjects (8 male, 7 female; 26.7+/-3.3 years) performed two graded exercise tests on a bicycle ergometer (50 W incline every 3 min) until volitional fatigue in randomized order. During rest and during the last 30 s of each step ventilatory and gas exchange parameters were measured with the CORTEX X1 and the OXYCONgamma. At rest and at each step no significant differences exist for VO2 (F = 0.97) and VCO2 (F = 0.90). The orthogonal regression equation of the VO2-values was VO2(X1) = -75.5 + 1.01 x VO2(Oxy) and the equation of the VCO2-values was VCO2(X1) = 21.7-1.008 x VCO2(Oxy). The VO2-max-values were nearly the same: 3569+/-924 ml/min (Oxy) and 3497+/-993ml/min (X1). Similar findings were made with regard to VCO2max 4117+/-1010 ml/min (Oxy) and 4126+/-1090 ml/ min. (X1). Maximal values for heart rate were 181+/-10 beats/ min (X1) and 180+/-8 beats/min (Oxy) (F=0.21), for maximal power 256+/-64 W (X1) and 257+/-63 (Oxy) (F = 0.0001) and for maximal ventilation 118+/-31 l/min) and 120+/-35 l/min (Oxy) (F = 0.03) with no significant difference. When attached to the motor-driven syringe V(E) was accurately measured up to 288 l/ min. Over a period of 40 min there was no drift observed in F(E)O2 and F(E)CO2. In conclusion, with the CORTEX X1 VO2 and VCO2 can be accurately determined.

Adult↗
PubMed1996

Maximal lactate steady state during the second decade of age.

Maximal lactate steady state (MLSS) presumably corresponds to the highest constant workload that can be performed by oxidative metabolism. The anaerobic and, to a minor extent, the oxidative metabolism have been reported to be affected by age. The second decade of life is the key period in the change in energy metabolism between children and adults. The aim of this study was to evaluate the effects of age on MLSS in 34 male subjects (age: 15.4 +/- 2.8 yr, range: 11-20 yr; height: 171.8 +/- 14.9 cm, range: 134-191 cm; body mass: 59.6 +/- 15.5 kg, range: 27-90 kg) performing an incremental load test to determine maximal workload and several constant load tests for MLSS measurement on a cycle ergometer. MLSS (4.2 +/- 0.7 mmol.l-1, range: 2.8 to 5.5 mmol.l-1) and MLSS intensity related to maximal workload (66.5 +/- 7.7%, range: 50-84%) were independent of age. MLSS heart rate (180.1 +/- 10.1 min-1, range: 156-208 min-1) decreased (P < 0.01) with increasing age, whereas absolute (157.2 +/- 54.8 W, range: 65-240 W) and relative MLSS workload (2.6 +/- 0.5 W.kg-1, range: 1.5 to 4.1 W.kg-1) and absolute (236.9 +/- 79.0 W, range: 100-350 W) and relative maximal workload (3.9 +/- 0.6 W.kg-1, range: 2.7 to 5.5 W.kg-1) increased (P < 0.001) with age. The age independence of MLSS supports the theory that neuromuscular factors may contribute to the frequently observed changes in response to given exercise with physical maturity more than changes in oxidative metabolism and/or glycolysis.

Adolescent↗
PubMed1993

The caloric demand of lactation does not alter spontaneous meal patterns, nutrient intakes, or moods of women.

The regulation of food and fluid intake in lactating women was examined by comparing maternal intake during lactation, 6 weeks postpartum, to intake in two groups of nonpregnant, nonlactating women. All subjects completed a questionnaire and then filled out a food-intake diary for seven consecutive days. Lactating women did not differ from body weight-matched, nonlactating controls in their total daily intakes or their meal patterns. However, they consumed a significantly smaller percentage of the recommended dietary allowances (RDA) per day than did their nonlactating counterparts. Lactating women were also significantly more calm both pre- and postmeal than were either of the control groups. These results indicate that the lactating women, at 6 weeks postpartum, did not increase their intake to compensate for the caloric demands of lactation. This may indicate that the lactating women catabolize weight gained during pregnancy faster than accounted for in the RDA, or that lactating women increase their metabolic efficiency.

Adult↗
PubMed1992

Dichloromethane (methylene chloride): metabolism to formaldehyde and formation of DNA-protein cross-links in B6C3F1 mice and Syrian golden hamsters.

Dichloromethane (DCM) is metabolized via a glutathione transferase (GST)-dependent pathway to formaldehyde (HCHO), a mutagenic compound that could play an important role in the carcinogenic effects of DCM observed in the liver and lungs of B6C3F1 mice at 2000 and 4000 ppm. Syrian hamsters metabolize DCM more slowly than mice via this pathway, and hamsters exposed to 3500 ppm showed no apparent carcinogenic response. The possible formation of DNA-protein cross-links (DPX) from DCM in both species was examined. Male mice and hamsters were pre-exposed for 2 days (6 hr/day) to 4000 ppm of DCM and on the third day were exposed (6 hr) to a decaying concentration (4500 to 2500 ppm) of [14C]DCM. DPX were detected in mouse liver, but not in mouse lung, hamster liver, or hamster lung. The failure to detect DPX in mouse lung does not exclude their possible formation in a subpopulation of lung cells. Metabolic incorporation of 14C derived from [14C]DCM into DNA suggested a higher rate of turnover of some mouse lung cells than of hamster lung cells, but no large difference in the turnover rates of liver cells in the two species under these conditions. These results demonstrate that HCHO derived from DCM can form DNA-protein cross-links in the liver of the B6C3F1 mouse. The formation of DPX is dependent on the activity of the GST pathway, and species such as hamsters and humans having much lower rates of DCM metabolism via this pathway may not generate toxicologically significant concentrations of HCHO and DPX.

Animals↗
PubMed1989

[The behavior of arterial blood pressure in dynamic and static muscle exercise with respect to atrial natriuretic peptide and neurotransmitters].

The development of the first semi-automatic blood pressure measuring instrument including optic and acoustic registration of systolic and diastolic blood pressure has led to a reliable assessment of arterial blood pressure during increasing ergometer exercise. There is a linear connection between workload intensity and systolic pressure. Intraarterially and noninvasively obtained values are identical with regard to systolic behavior. In principle, the intraarterially measured diastolic blood pressure, too, increases in healthy subjects, which, nevertheless, may often not be demonstrated in such a clear way due to artefacts occurring during blood pressure measuring. There are no significant differences between untrained and endurance-trained subjects at a given work load. Persons exhibiting a better performance capacity only reach higher maximal systolic values. The male and female subjects' regression lines significantly differ--the reason possibly being the woman's smaller muscle mass. Age-induced differences, too, are significant. Bodybuilders with extremely developed muscle mass do not show any significant differences with regard to blood pressure behavior during exercise. When establishing a relation to the relative muscle force the bodybuilders show blood pressure values even lower than normal values.

Animals↗
PubMed1987

[Exercise hypertension--significance from the viewpoint of sports].

Exercise hypertension refers to an increase in blood pressure during dynamic exercise in excess of the limits in normotensive persons or those with borderline hypertension at rest as well as a disproportionately excessive increase in pressure in hypertensive persons in whom otherwise the increase in exercise pressure is shifted parallel to that of normotensive persons. There is no consensus for the absolute definition of exercise hypertension but traditionally, in sports medicine, systolic blood pressure values of 200 mmHg and more at a workload of 100 watts are considered abnormal. On the basis of the results of a study we performed in 2972 individuals, norms for exercise arterial blood pressure were constructed and found to be related to workload intensity as well as age. In contrast, there was no relationship between exercise blood pressure and exercise capacity or sex. In this regard, indirectly measured diastolic blood pressure is not reliably indicative of the actual prevailing pressure, particularly at higher workloads; it is, therefore, not considered to be useful in detection of exercise hypertension. In agreement with other studies, we found that up to one-third of all patients with normal blood pressure at rest but exercise hypertension eventually developed hypertension at rest. The incidence tended to increase with increasing age. Accordingly, exercise hypertension may be regarded as a precursor to established hypertension at rest.(ABSTRACT TRUNCATED AT 250 WORDS)

Antihypertensive Agents↗
PubMed1986

Cardiovascular effects of extreme physical training.

After a short historical remark the development of athlete's heart in childhood is described. Within 2 years significant differences were observed between endurance-trained (swimming) and untrained girls and boys determined by X-ray and echocardiographical examinations. The limits of the physiological size in relation to body weight were not exceeded within 10 years of longitudinal studies. A second point deals with athlete's heart from physiological and clinical viewpoints. The largest healthy heart ever found in our examinations of athletes had a size of 1,700 ml. Sixteen years after stopping the active career it was reduced to 950 ml without a pathological finding. Questionable and pathological cases are described. A third chapter covers the blood supply of internal organs during exercise combined with air or oxygen breathing. In this connection liver, kidneys, heart, lungs, and brain have been investigated. The reduced blood supply of the liver and kidneys during intense exercise on the cycle ergometer was not influenced significantly by inspiration of oxygen. A significant blood volume increase of the lungs was noticed during incremental rates of work. Exercise augmented also blood flow of the brain in relation to the work rate (at 100 W a 27% increase in grey matter flow of the right hemisphere). A fourth chapter deals with new hormonal and neurohormonal aspects related to the cardiovascular system. Beta-endorphines remained unchanged at work rates below the anaerobic threshold but increased significantly during maximal rate of work. The opiate antagonist naloxone abolished the rise in body temperature seen during ergometer exercise. The serotonin antagonist ketanserin lowered the blood pressure and the arterial lactic acid level during an incremental exercise test, similar to the results with the dopamine agonist pergolide. The hormone cardiodilatin is produced in the atrial appendages, and it is a potent substance in the regulation of the cardiovascular system. The adaptive reaction of the sympathetic nerve fibres in the myocard revealed different directions: activation, degeneration, and regeneration. These findings correlated highly significantly with the total amount of catecholamines in the heart muscle.

Adult↗
PubMed1985

[Preventive cardiology: lack of exercise and physical training from the epidemiologic and experimental viewpoints].

A survey is given on epidemiological and experimental results of lack of exercise as a risk factor for coronary heart disease. The consequences of endurance training are described. It is evident that endurance sport or training during leisure time can have a greater effect than heavy muscular professional work. The selectively analysed factor "lack of exercise" may be less important as a risk factor than the protective influence of endurance training. Directions are given for carrying out a preventive program of training, with contraindications included.

Adrenergic beta-Antagonists↗