[Irrespective of their educational status, patients with insulin-dependent type 2 diabetes mellitus benefit from patient-centered medical behavioral training].
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Biomedical subjects
Publications and source records attributed to U Tegtbur.
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Exercise exerts heterogeneous effects on TSH secretion. Whereas TSH is rapidly stimulated by physical exercise within minutes, and these effects are well supported by careful experiments, the results of studies concerning intermediate and long-term response of TSH release to exercise remain unclear, and the underlying mechanism for both is still open to speculation.
BACKGROUND: Quality of life in lung transplant recipients (LTR) is reported to be comparable with that of the general population. However, previous studies have shown that exercise capacity was reduced to 30 - 40 % of normal values. The purpose of this study was to investigate the gap between good self-reported quality of life and reduced exercise capacity in LTR, to describe possible correlations and to compare the results with those of a control group (CG). METHODS: 27 LTR 208 +/- 67 days after bilateral lund transplantation (16 male, 11 female; age: 46 +/- 10 years; body mass index: 24 +/- 3 kg x m (- 2), FEV (1) % 75 +/- 27 %) and 30 controls (17 male 13 female; age 47 +/- 15 years; BMI: 26 +/- 4 kg x m (- 2), FEV (1) % 103 +/- 15 %) performed cardiopulmonary exercise testing and were interviewed with the standardized German "Quality of life profile for chronic disease" self-rating questionnaire. RESULTS: Significant differences were shown in objective exercise related variables (peak oxygen consumption: LTR 15.1 +/- 1.8, CG 34.5 +/- 9.1 ml x min (- 1) x kg (- 1); p < 0,01); peak workload: LTR 1.0 +/- 0.2; CG 2.4 +/- 1.0 W. kg (- 1); p < 0.01); percentage of predicted workload: LTR 44 +/- 12, CG 115 +/- 33 %; p < 0.01). The rating of subjective quality of life in physical, psychological and social domains of LTR did not differ from values of the CG or of the general population (n = 1143). The quality of life in the physical domain correlated significantly with peak exercise capacity (LTR r = 0.44, p < 0.05; CG r = 0.37; p < 0.05). CONCLUSION: Patients 7 months after lung transplantation described their physical, social and psychological quality of life as equally good as the healthy control group. However, peak exercise capacity and oxygen consumption were markedly reduced. To improve physical capacity in the range of daily activities, an exercise training program should be offered to patients after lung transplantation.
BACKGROUND: Quality of life late after heart transplantation is reported to be comparable with that of the general population. However, peak exercise capacity remained approximately 60% of what was normal between 1 and 10 years after transplantation. The gap between patients' good quality of life and their impaired exercise tolerance is not yet explained. The purpose of our study was to examine the relation between quality of life and exercise- related variables in heart transplant recipients (HTR). Then, the results of these examinations were compared with those of patients having congestive heart failure (CHF), with the use of controls (C), respectively. METHODS: (Mean values+/-SD) 29 HTR 4.4 +/- 2.1 years after transplantation, 29 CHF (NYHA II n = 22, III n = 7) and 29 C (age 54 +/- 9, 61 +/- 10, 56 +/- 10 years, body mass index 28 +/- 3, 29 +/- 5, 28 +/- 4 kg x m(-2), body fat 25 +/- 4, 27 +/- 6, 26 +/- 5%, respectively) performed cardiopulmonary exercise testing and were interviewed with the standardized German "Quality of life profile for chronic diseases" questionnaire. RESULTS: Peak oxygen consumption was impaired in HTR and in CHF compared with C (19.0 +/- 4.5, 18.6 +/- 4.3, and 30.2 +/- 6.6 ml x min x kg(-1), respectively; p < 0.01 vs. C each). HTR and CHF patients' quality of life in the physical scores were both impaired (p < 0.05 or p < 0.01 vs. C, respectively), but HTRs have reported better scores than CHF (p < 0.05). In the psychological role, CHF was impaired against C (p < 0.05), and HTR scores were comparable with C. In social functioning HTR and CHF patients both showed reduced quality of life dimensions. The Pearson correlation analysis showed that quality of life in physical functioning was related to peak oxygen consumption (p < 0.001) and percentage of predicted workload (p < 0.001). Quality of life in the social and psychological domains showed no association to exercise-related values. CONCLUSIONS: In HTR and in CHF, exercise testing variables were dominant predictors among the physical scales in quality of life, but not among social or psychological scales. Therefore, even late after heart transplantation, improving physical capacity should be a therapeutic goal with the intention of further increasing the quality of life.
INTRODUCTION: Longterm treatment after heart transplantation (HTX) improves survival, although the quality of life and exercise tolerance decreased continuously between one and ten years after transplantation. The role of physical exercise and psychological support in longterm treatment after HTX has not been determined. We analyzed the effects of a one year outpatient rehabilitation program in combination with a home based, computer assisted training program on exercise capacity, coronary risk factors and quality of life. METHODS: 20 heart transplant recipients in an intervention group and 12 patients after HTX in a control group participated in the study (IG (CG); 5.1+/-2.2 (4.5+/-2.3) years after HTX; age: 55+/-7 (54+/-8) years; body mass index: 28.3+/-1.0 (28.7+/-0.9) kg.m(-2)). Before and after the intervention, maximum and constant load exercise capacity, and self-reported quality of life were evaluated. The 12 month intervention period included 10 days of exercise testing as well as medical and psychological support. Furthermore, the IG group performed a computer-assisted and controlled home ergometer training every second day. RESULTS: After one year with 114+/-18 exercise training sessions, maximum oxygen consumption increased in the IG from 18.8+/-4.2 to 20.1+/-4.2 ml.min(-1).kg(-1) (p<0.05; CG 19.3+/- 4.5 to 18.5+/-2.8 ml.min(- 1).kg(-1); p<0.01 IG vs CG). In the IG, lower back pain, body fat, and blood pressure were all reduced, while the self-reported quality of life, endurance exercise capacity and HDL cholesterol were increased. No significant changes occurred in the control group. CONCLUSIONS: When initiated years after heart transplantation, longterm rehabilitation reduced coronary risk factors and significantly improved both the subjects' quality of life, as well as a near to normal capacity for physical work.
Exercise training for patients with coronary artery disease (CAD) is recommended in a wide range between 40-85% of maximum functional capacity (MFC) or 55-90% of maximum heart rate (HR). During exercise, high levels of catecholamines and metabolic acidosis could induce arrhythmia and ischemia. But catecholamines have never been determined in CAD during constant load exercise in the upper range of recommended intensities. In 11 CAD patients (age 58+/-8 years, BMI 26.1+/-4.0 kg x m(-2), NYHA I n=7, II n=4) we tested the maximum functional capacity (MFC), norepinephrine (NE), epinephrine (E) and blood lactate ([Lac(-)](B)) in a symptom-limited incremental ergometer test. Related to the exercise recommendation, the kinetics of NE, E and [Lac(-)](B) were determined in two 30 min constant load tests in randomized order: one was performed at the anaerobic lactate threshold (CTAT), a second was performed 10% above the individual threshold intensity (CT+10%). In the incremental tests maximum workload and VO(2) were 141+/-54 W and 1766+/-532 ml x min(-1), respectively (85+/-22% of normal; [Lac(-)](B) 5.7+/-1.9 mmol x l(-1), HR 138+/-28 b x min(-1), NE 11.7+/-5.1, E 1.6+/-1.4 nmol x l(-1)). In CTAT the anaerobic threshold (63+/-7% of MFC) represented the mean range of recommended exercise intensity for CAD (40-85%) and could be validated as steady-state intensity because catecholamines and [Lac(-)](B) concentrations remained constant after the initial increase (workload 88+/-35 W, [Lac(-)](B) 3.3+/-1.4 mmol x l(-1), HR 117+/- 23 b x min(-1), NE 8.3+/-3.5, E 0.8+/- 0.7 nmol x l(-1)). In all patients CT+10% (71+/-7% of MFC) led to a continuous rise in [Lac(-)](B), to a NE overload and to earlier exhaustion, although the intensities were in the recommended training range (workload 100+/-38 W, [Lac(-)](B) 5.8+/- 1.9 mmol x l(-1), HR 129+/- 29 b x min(-1), NE 13.9+/-6.9, E 1.5+/- 1.7 nmol x l(-1); p<0.01 against CTAT for all except E). Conclusions In the upper range of recommended training intensity for CAD patients, norepinephrine and lactate were higher during endurance exercise than at MFC in incremental tests. Endurance exercise with intensities >70% of MFC could overload the cardiac patient and increase the risk of arryhthmia and ischemia. Therefore, endurance exercise should be performed below 70% of MFC or below 85% of maximum HR, respectively, whereas higher intensities should apply to interval exercise.
Intensive physical exercise improves cardiac perfusion, skeletal muscle function and risk factors in patients with coronary artery disease (CAD). Otherwise, overdosed intensity can induce training adaptation as well as cardiac events. Therefore, we tested whether exercise intensity corresponding to an equilibrium between lactate production and elimination from the blood during incremental exercise tests represented the blood lactate [Lac-]B steady-state intensity during constant physical training. Randomized into two groups with 30 CAD patients each (T1: 25 male, 5 female; 59 +/- 7 years; T2: 26 male, 4 female; 60 +/- 9 years), the patients initially performed two successive incremental exercise tests. In the first test, workload was increased stepwise until exhaustion or symptom limitation (maximal workload: T1 142 +/- 48 watts, T2 145 +/- 45 watts) with the corresponding [Lac-]B accumulation of up to 6.7 +/- 2.6 (T1) or 6.5 +/- 2.0 (T2) mmol/l, respectively. After a seven minute active rest the second test began with 25 watts, increased with 5 (maximum workload in first test < 100 watts) or 10 watts per minute, respectively. During lower intensities in the second test, [Lac-]B initially decreased to an individual lactate minimum intensity (workload at LMI 83 +/- 32 in T1 or 86 +/- 29 in T2 watts, respectively; [Lac-]B at LMI 4.6 +/- 2.2 and 4.9 +/- 1.8 mmol/l, respectively) and then increased again. To check if the individual LMI represented the [Lac-]B steady-state workload in constant workload exercise, the patients performed 30 min constant load tests with the LMI (CT1) or a 30 min constant load test with an intensity 10% above the LMI (CT2), respectively. The workload in CT1 was 83 +/- 32 watts with a mean exercise time of 29.0 +/- 1.7 min. After 10 min of exercise the [Lac-]B steady state was reached at 3.3 +/- 1.4 mmol/l with no further increase in the last 20 min. The mean workload in CT2 was 95 +/- 31 watts with an exercise time of 23.3 +/- 8.3 min (p < 0.01). [Lac-]B increased from 4.4 +/- 1.7 mmol/l after 10 min to 4.7 +/- 2.0 mmol/l at the end (p < 0.01). Fifty percent of patients stopped CT2 before the 30 minute end. The results indicates that the LMI, estimated during lactic acidosis in two successive incremental tests, represented the individual lactate steady-state intensity also during constant load exercise. Therefore, training regimens for CAD patients could be deduced from LMI.
After acute hospital therapy of myocardial infarction or bypass surgery the patient in Germany will be treated using an inpatient rehabilitation programme for 3-4 weeks. One year later only 10% of them are still active in outpatients groups. In our study 61 cardiac patients performed an one-year outpatient rehabilitation (instead of 4 weeks inpatient) programme with intense supervised exercise and behaviour therapy. The money input per patient was the same for the usual care 4 weeks inpatient (6000 DM) as for 1 year outpatient rehabilitation (5800 DM). The exercise capacity per heart rate-blood pressure-product was increased by 43% (p > 0.01) after 12 months. The maximum exercise capacity was reached in the 57th week. Without increased medical treatment, cholesterol and LDL-cholesterol were reduced after 12 months by 3.9% down to 195 +/- 25 mg/dl or by 6.6% down to 122 +/- 21 mg/dl, respectively (n.s.). HDL-cholesterol increased by 2.8% to 48 +/- 8 mg/dl (n.s.). This study shows results similar to outpatient rehabilitation programmes in the United States or in Sweden. The long intervention time and the intensity are main factors for the success of cardiac rehabilitation and patient health. Financial resources should primarily be concentrated on long-term outpatient rehabilitation programmes.
In Germany cardiac rehabilitation contains a comprehensive 3 to 4 week inpatient program. The aim of our study was to perform an outpatient long-term rehabilitation including intense exercise and behavior therapy. In this setting the health benefits could be increased over the first 6 months. Hundred and twelve patients (94 men and 18 women, age 55 +/- 11 years) after myocardial infarction (52%), bypass-surgery (37%), PTCA (23%), and others (15%) were included in the ongoing study. Cholesterol and LDL-cholesterol diminished significantly. HDL-cholesterol was increased significantly after 6 months. The endurance exercise capacity per rate-pressure-product was increased by 46% during the 6 months period. The intake of cholesterol could significantly be diminished from 307 +/- 25 to 258 +/- 19 mg per day. Five of 16 patients became free from smoking. The first results from the long-term outpatient program show that the time of intervention and also the intensity of the medical, exercise and the behavior therapy are important factors for a successful rehabilitation.
During an incremental exercise test after a preceding bout of maximum exercise, blood lactate initially decreases to an individual minimum and then increases again. To determine whether this minimum represents an individual equilibrium between lactate production and catabolism during constant load exercise, the following field tests were performed: in 25 runners and five basketball players (series 1) the speed corresponding to the individual lactate minimum (LM) was measured in test 1 (incremental test after exercise induced lactic acidosis). On two occasions, two constant speed runs over 8 km were performed, one using the LM speed (LMS) (test 2), and another at a running speed of 0.2 m.s-1 above the LMS (test 3). Results of runners/basketball players: blood lactate concentration ([Lac-]B) in test 2 changed from 3.6/4.9 mmol.l-1 to 4.0/4.9 mmol.l-1 during the last 4.8 km, in test 3 from 4.6/4.6 mmol.l-1 to 6.5/6.9 mmol.l-1. These results indicate: 1) the LM speed in test 1 corresponds to a maximum lactate steady state speed during constant load exercise; 2) only a slight speed increase above the LM speed results in continuous marked [Lac-]B increase and earlier exhaustion. Variation of the increment duration in 13 males (series 2) shows no change of the LMS using 800-m and 1200-m increments (4.49 and 4.44 m.s-1) but a marked shift to higher speed using 400-m increments (4.96 m.s-1). Effects of low muscle glycogen stores on the LMS were determined in 10 males (series 3).(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of this study was to investigate middle-term influences of a marathon race on plasma volume (PV) and red cell production. We performed the following measurements in the blood of 15 male athletes: haemoglobin ([Hb]), haematocrit (Hct), plasma protein concentration ([Prot]), plasma osmolality, sodium concentration ([Na+]), potassium concentration ([K+]), aldosterone concentration ([Aldo]), haptoglobin concentration ([Hpto]), and the reticulocyte count, as well as the calculation of relative changes in PV, 3 days before and on 3-consecutive days after a marathon race. By the 2nd day of recovery PV had increased by 16%. Plasma osmolality and [K+] remained constant, whereas [Na+] had decreased slightly 2 days after the competition and [Aldo] tended to be elevated 1 day after the competition. [Hpto] was low before and 1 day after the competition and increased on the following days. Reticulocyte count was unaffected 1 day after the race, but increased by 106% on the 2nd day and was still elevated after 3 days. The causes for higher post-marathon plasma volumes and reticulocyte counts could be in the complex variations in hormonal regulation, which have not yet been sufficiently investigated.