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Biomedical subjects

W Kemmler

Publications and source records attributed to W Kemmler.

At least 19 recordsLinked to original sources
PubMed2006

Effect of exercise, body composition, and nutritional intake on bone parameters in male elite rock climbers.

A low body mass index is considered essential for high performance in rock climbing; however its effect on bone may be negative. In this study we compared the BMD of competitive male rock climbers (n = 20) and age- and BMI-matched non-training controls (n = 11). Subjects with any medication or illness affecting bone metabolism or a family history of osteoporosis were not included in the analysis. Total body BMD was measured by dual-energy X-ray absorptiometry. Quantitative computed tomographic scans were made from the femoral neck and the lumbar spine. Dietary intake was assessed by a 5-day protocol. BMD of the TB-scan was significantly higher in the climbers group for all sub-regions except the skull (p = 0.191) and the lower extremities (p = 0.079). Trabecular and cortical BMD of the LS were significantly higher (p = 0.036 and p = 0.004) in the climbers. The same was true for total (p = 0.005) and cortical (p = 0.002) BMD of the FN. Trabecular BMD (p = 0.054), CSA (p < 0.343) and cortical thickness (p = 0.065) of the FN was non-significantly higher for the climbers. Our study indicates that the effect of climbing on bone parameters PER SE is not detrimental in elite male athletes. Contrarily climbers demonstrated significantly higher BMD values at all loaded regions without "steal effects" at skeletal sites with low mechanical impact. Although we determined a moderately negative effect of low BMI on BMD we could not decide whether a low BMI value should be used as an exclusion criterion in high level climbing competitions as practized by the Austrian Sportclimbing Organization.

Absorptiometry, Photon↗
PubMed2005

Exercise maintains bone density at spine and hip EFOPS: a 3-year longitudinal study in early postmenopausal women.

It is an important aim in the prevention of osteoporosis to stop or decelerate bone loss during the early postmenopausal years. Here we report on results of the 3-year EFOPS exercise trial in osteopenic women. The exercise strategy emphasized low-volume high-resistance strength training and high-impact aerobics. Forty-eight fully compliant women (55.1+/-3.3 years) with no medication or illness affecting bone metabolism participated in the exercise group (EG); 30 women (55.5+/-3.0 years) served as non-training controls (CG). At baseline there were no significant between-group differences with respect to physical fitness, bone mineral density, pain and nutritional status. The training consisted of two group training and two home training sessions per week. The study participants of both groups were individually supplemented with calcium and vitamin D (cholecalciferol). Bone mineral density (BMD) was measured by DXA at the lumbar spine, proximal femur and distal forearm and by QCT at the lumbar spine. Speed of sound and broadband ultrasound attenuation were determined at the calcaneus by quantitative ultrasound (QUS). Pain frequency and intensity at different skeletal sites were assessed via questionnaire. After 38 months, the following within-group changes were measured: DXA lumbar spine, EG: 0.8% n.s.; CG: -3.3% P<0.001; QCT trabecular ROI, EG: 1.1% n.s; CG: -7.7% P<0.001; QCT cortical ROI, EG: 5.3% P<0.001; CG: -2.6% P<0.001; DXA total hip: EG: -0.2% n.s; CG -1.9%, P<0.001; DXA distal forearm, EG: -2.8% P<0.001; CG: -3.8% P<0.001; BUA, EG: -0.3% n.s; CG -5.4% P<0.001; SOS, EG: 0.3% n.s; CG -1.0% P<0.001. At year 3 between-group differences relative to the exercise group were: DXA lumbar spine: 4.1% P<0.001; QCT trabecular ROI: 8.8% P<0.001; QCT cortical ROI: 7.9% P<0.001; DXA total hip: 2.1%, P<0.001; DXA distal forearm: 1.0% n.s.; BUA: 5.8% P<0.05; SOS: 1.3% P<0.001. Pain frequency and intensity in the spine significantly decreased in the exercise group and increased in the control group, while no between-group differences were detected in the main joints. In summary, over a period of 3 years our low-volume/high-intensity exercise program was successful to maintain bone mineral density at the spine, hip and calcaneus, but not at the forearm.

Aging↗
PubMed2005

Power training is more effective than strength training for maintaining bone mineral density in postmenopausal women.

Physical exercise has a favorable impact on bones, but optimum training strategies are still under discussion. In this study, we compared the effect of slow and fast resistance exercises on various osteodensitometric parameters. Fifty-three postmenopausal women were randomly assigned to a strength training (ST) or a power training group (PT). Both groups carried out a progressive resistance training, a gymnastics session, and a home training over a period of 12 mo. During the resistance training, the ST group used slow and the PT group fast movements; otherwise there were no training differences. All subjects were supplemented with Ca and vitamin D. At baseline and after 12 mo, bone mineral density (BMD) was measured at the lumbar spine, proximal femur, and distal forearm by dual-energy X-ray absorptiometry. We also measured anthropometric data and maximum static strength. Frequency and grade of pain were assessed by questionnaire. After 12 mo, significant between-group differences were observed for BMD at the lumbar spine (P < 0.05) and the total hip (P < 0.05). Whereas the PT group maintained BMD at the spine (+0.7 +/- 2.1%, not significant) and the total hip (0.0 +/- 1.7%, not significant), the ST group lost significantly at both sites (spine: -0.9 +/- 1.9%; P < 0.05; total hip: -1.2 +/- 1.5%; P < 0.01). No significant between-group differences were observed for anthropometric data, maximum strength, BMD of the forearm, or frequency and grade of pain. These findings suggest that power training is more effective than strength training in reducing bone loss in postmenopausal women.

Aged↗
PubMed2004

The effect of habitual physical activity, non-athletic exercise, muscle strength, and VO2max on bone mineral density is rather low in early postmenopausal osteopenic women.

CONTEXT: Although the positive effect of well-designed exercise regimes on bone mineral density (BMD) is established the osteo-anabolic relevance of habitual physical activity and non-athletic exercise is still under discussion. OBJECTIVE: To determine the effects of habitual physical activity, non-athletic exercise muscle strength, VO2max and anthropometric parameters on BMD in early post-menopausal women. DESIGN: Cross-sectional study. METHODS: 150 early postmenopausal women (55.5+/-3.4 years), which were free of diseases or medication affecting bone metabolism and had no athletic history were investigated. The influence of weight, body composition, physical activity, isometric strength, VO2max, and nutritional intake on BMD was measured at multiple sites using different techniques. Further bone markers (Osteocalcin, CTX) were determined. Activity and weight-bearing activity were assessed by questionnaire. Maximum strength was measured isometrically. Aerobic capacity was measured with an spirometric system in a stepwise treadmill test and dietary intake was monitored over 5 days. RESULTS: Slight relationships between physical activity, exercise, muscle strength and VO2max with bone parameters were determined by univariate analysis. After adjusting for confounding variables in a stepwise regression analysis, significant relationships with BMD measured at the hip or the spine could no longer be detected for physical activity, exercise, and physical fitness (strength indices, VO2max). The same was true for osteocalcin and CTX. Arm strength explained 4.5% of the variation of forearm BMD (DXA). At the calcaneal site, osteogenic exercise was significantly related to the quantitative ultrasound index (r2 = 0.27). CONCLUSION: The isolated effect of habitual physical activity, unspecific exercise participation, and muscle strength on bone parameters is rather low in (early-) postmenopausal women. CLINICAL RELEVANCE: Women at risk should take specific exercise programs into consideration rather than to increasing the amount of habitual physical activity.

Biomarkers↗
PubMed2003

Acute hormonal responses of a high impact physical exercise session in early postmenopausal women.

The effect of a single bout of exercise on hormones affecting bone metabolism was studied in 25 early postmenopausal women with osteopenia. The complex training session was performed between 8:00 a.m. and 9:05 a.m. Serum concentrations of dehydroepiandrosterone-sulfate (DHEA-S), total testosterone, free testosterone, 17beta-estradiol, cortisol, human growth hormone (hGH), insulin-like growth factor-I (IGF-I), and insulin-like growth factor binding protein-3 (IGFBP-3) were determined. Blood samples were obtained immediately before (baseline) and after exercise, as well as 2 h and 22 h post-exercise. DHEA-S increased by 10% immediately after exercise and remained increased 2 h later. Testosterone showed no increase immediately after exercise but fell by 21% 2 h post-exercise. Free testosterone was increased by almost 20% immediately after exercise and returned to baseline levels after 2 h. Two hours post-exercise a 20% increase in the estradiol level was measured. Cortisol decreased by 36% during exercise and a further 14% during the next 2 h, a loss higher than the normal diurnal decrease. hGH increased by 80% during exercise and fell 30% under baseline values after 2 h. Even though the assessment period was prolonged to 22 h no significant change could be demonstrated for IGF-I. Serum IGFBP-3 showed a biphasic increase. During the exercise session IGFBP-3 increased by 35%, returned to baseline values 2 h post-exercise and increased again by 40% 22 h post-exercise. In summary, this study showed that a single bout of exercise typically used in osteoporosis prevention programs could have an influence on hormones affecting bone metabolism.

Adaptation, Physiological↗
PubMed1984

Extrapancreatic action of the sulphonylurea gliquidone: post-receptor effect on insulin-stimulated glycogen synthesis in rat hepatocytes in primary culture.

The effects of a sulphonylurea, gliquidone, on insulin binding and the insulin induced rate of glycogen synthesis, were studied in rat hepatocytes in primary culture. Hepatocytes were cultured for 48 h. During the second 24 h of this period, the hepatocytes were incubated with or without gliquidone (5 mg/l). The binding of 125I-insulin and the insulin stimulation of glycogen synthesis from 14C-glucose were measured. Gliquidone influenced neither insulin binding nor the basal rate of glycogen synthesis, but it did enhance the effect of insulin on glycogen synthesis. Responsiveness was increased by gliquidone at all insulin concentrations used (10-10,000 mU/l); at 1000 mU/l the drug increased glycogen synthesis from 310 to 430% above the basal rate. Half-maximal stimulation was reached in control cells at an insulin concentration of 95 mU/l and in gliquidone-treated cells at 94 mU/l, which indicates unchanged insulin sensitivity. Based on these experiments with cultured rat hepatocytes it appears that the extrapancreatic action of gliquidone is not mediated by an effect on insulin binding.

Animals↗
PubMed1983

Catecholamine-induced insulin resistance of glucose transport in isolated rat adipocytes.

The effects of pre-incubation with isoprenaline and noradrenaline on insulin binding and insulin stimulation of D-glucose transport in isolated rat adipocytes are reported. (1) Pre-incubation of the cells with isoprenaline (0.1-10 microM) in Krebs-Ringer-Hepes [4-(2-hydroxyethyl)-1-piperazine-ethanesulphonic acid] buffer (30 min, 37 degrees C) at D-glucose concentrations of 16 mM, in which normal ATP levels were maintained, caused a rightward-shift in sensitivity of D-glucose transport to insulin stimulation by 50% and a decrease in maximal responsiveness by 30% (2) [A14-125I]insulin binding was reduced significantly by 35% at insulin concentrations less than 100 mu-units/ml and Scatchard analysis showed that this consisted mainly of a decrease in high-affinity binding. (3) Pre-incubation with catecholamines under the same conditions but at low glucose concentrations (0-5 mM) caused a fall in intracellular ATP levels of 65 and 45% respectively. (4) The fall in ATP additionally lowered insulin binding by 50% at all insulin concentrations and a parallel shift of the binding curves in the Scatchard plot showed that this was due to a decrease in the number of receptors. (5) At low and high ATP concentrations the insulin stimulation of D-glucose transport was inhibited to a similar extent. (6) Pre-incubation with catecholamines thus inhibited insulin stimulation of D-glucose transport in rat adipocytes mainly by a decrease in high-affinity binding of insulin, which was not mediated by low ATP levels. This mechanism may play a role in the pathogenesis of catecholamine-induced insulin resistance in vivo.

Adenosine Triphosphate↗
PubMed1983

Cyclic AMP modulates insulin binding and induces post-receptor insulin resistance of glucose transport in isolated rat adipocytes.

The effect of cAMP on insulin binding and insulin stimulation of glucose transport was investigated in isolated rat adipocytes. Preincubation for 30 min in medium containing 16 mmol/l glucose and either db-cAMP or bromo-cAMP in concentrations of 10(-4)-10(-3) M inhibited high affinity binding of insulin by 15 to 30% and glucose transport by 30 to 50%. Preincubation with IBMX (10(-4)-10(-3) M) reduced insulin binding by 25% and glucose transport by 70%. Closer analysis of these data indicated that preincubation with these compounds caused not only a decrease in insulin binding but also a post-receptor resistance. High intracellular cyclic AMP-levels seem therefore to induce insulin resistance at both receptor and post-receptor levels.

1-Methyl-3-isobutylxanthine↗
PubMed1982

Insulin binding and action in antibody-induced diabetes in the rat.

The influence of antibody-induced insulin deficiency in rats on the insulin binding and insulin sensitivity of adipocytes was studied. Rats were injected intraperitoneally with an insulin antibody preparation; the development of hyperglycaemia was followed and the animals were sacrificed 3 and 5 h after antibody injection. Up to 3 h, no significant change of insulin binding or sensitivity of the adipocytes occurred. At 5 h, cells of antibody-treated rats showed an approximately 40% increased binding capacity compared with untreated rats. The increased binding capacity was accompanied by an approximate two-fold increased sensitivity of the insulin effect on lipogenesis from glucose in these cells.

Adipose Tissue↗
PubMed1982

Relation of insulin receptor occupancy and deactivation of glucose transport.

Kinetics of association and dissociation of 125I-insulin and of activation and deactivation of 3-O-methylglucose transport were determined in isolated rat fat cells. Equilibrium bound insulin (7.5, 25, 100 microunits/ml) dissociated with a t1/2 of 2 min (100 microunits/ml), 4 min (25 microunits/ml), and 16 min (7.5 microunits/ml). Consecutive deactivation of transport is observed only in the presence of glucose (1 mM); the t1/2 of deactivation is approximately 60 min (100 and 25 microunits/ml) and 20 min (7.5 microunits/ml). At 15 degrees C, the t1/2 of dissociation (7.5 microunits/ml) is 25 min, and deactivation is not observed. Addition of dithioerythritol (5 mM) during the association of insulin decreased the binding rapidly; however, a reduced insulin effect was only seen if the binding decreased during the early activation phase of transport. In conclusion, the maintenance of the insulin effect on transport does not require persistent receptor occupancy; dissociation and deactivation are, with respect to kinetics, temperature dependency and requirement of glucose, independent processes. Receptor occupancy probably only controls the activation of transport; deactivation seems to be controlled by postreceptor processes.

3-O-Methylglucose↗
PubMed1981

Coupling of insulin binding and insulin action on glucose transport in fat cells.

The initial lag phase of insulin action on glucose transport in adipocytes reflects an unknown process that couples receptor binding and glucose transport activity. The influence of temperature, cellular ATP, cyclic AMP, and calcium on this process and a possible relation to internalization of insulin were studied. The Arrhenius plot of the coupling shows a break in slope at 30 degrees C; the activation energy below 30 degrees C is 17.5 kcal/mol. Reduction of cellular ATP by 70% prolongs the coupling process; initial binding and final maximal response of the glucose transport remain unaffected. Further reduction of ATP (greater than 90%) before addition of insulin abolishes the coupling completely. Reduction of ATP at different time points after addition of insulin blocks further activation; however, the actual state of activity is preserved. Calcium depletion by EDTA prolongs the coupling and decreases the maximal response. Internalization of insulin as determined in chloroquine-treated cells begins later than transport activation and is in contrast to transport activation not observable at 15 degrees C. In conclusion, the coupling is not related to internalization; it is ATP-dependent, whereas the initial binding and the activated transport system are ATP-independent. Calcium but not cyclic AMP might be second messenger or cofactor in the coupling process.

3-O-Methylglucose↗
PubMed1980

Insulin binding and insulin action in rat fat cells after adrenalectomy.

Insulin binding and the effect of insulin on the transport of 3-O-methylglucose, lipogenesis from glucose, glucose oxidation and lipolysis was studied in fat cells of adrenalectomised rats and of a control group of sham-operated rats. The serum insulin level of the adrenalectomised rats (0.7 ng/ml) was lower than that of the controls (1.6 ng/ml). In adrenalectomised rats as compared to sham-operated rats the insulin concentrations causing half-maximal effect were reduced by 50% in lipogenesis and antilipolysis and by 30% in glucose transport. The increase in sensitivity to submaximal insulin concentrations was not observed in glucose oxidation. The maximal responsiveness was unchanged in all test systems. The increase in sensitivity in three of the four studied insulin effects may be related to the 37% increase in the binding capacity of fat cells from adrenalectomised compared with sham-operated rats. The unchanged sensitivity with respect to glucose oxidation indicates possible post-receptor modulation. When adrenalectomised rats were substituted with either insulin or cortisol serum insulin levels were elevated above normal; however, the changes in the receptor were prevented in the cortisol supplemented rats and only partially in the insulin supplemented rats. The observation suggests, that the insulin receptor is regulated not only by the serum insulin level but also by cortisol.

Adipose Tissue↗
PubMed1979

[Effect on carbohydrate metabolism of a new saluretic, etozolin].

The influence of Etozolin (Elkapin) on the carbohydrate metabolism was studied in 10 healthy volunteers, 6 patients with chemical diabetes and 10 with overt diabetes by blood glucose measurements and oral glucose tolerance tests with determinations of serum insulin levels. The healthy volunteers received 800 mg Etozolin per day during the treatment period of 3 days, the two groups of patients 400 mg Etozolin for 8 days. The laboratory parameters of the treatment period were compared with the corresponding values of the pre- and posttreatment periods and evaluated statistically. There was no statistically significant difference in the carbohydrate metabolism between the 3 test periods in all groups studied. As a result of the induced diuresis body weight, serum electrolytes and urine volume changed significantly during the Etozolin treatment as compared with the pre- and posttreatment values. Other changes of laboratory parameters could not be seen. In diabetic hypertensive patients a significant reduction of blood pressure was observed.

Adult↗
PubMed1979

Free insulin, bound insulin, C-peptide and the metabolic control in juvenile onset diabetics: comparison of C-peptide secretors and non-secretors during 24 hours conventional insulin therapy.

In two groups of juvenile onset diabetics similar in age, weight, diet and daily insulin dosage (eight without C-peptide, group I; eight with C-peptide, group II) the serum levels of free and antibody bound insulin, C-peptide, glucose, lactate, alanine and FFA were determined over 24 h. In addition the affinity and binding capacity of the insulin antibodies were determined in vitro. No correlation was found between free or bound insulin and glucose. This holds true for the individual profiles as well as for the averaged profiles of the two groups. Free insulin and lactate or alanine were positively correlated in the C-peptide secreting group. C-peptide secretion followed the flucturations of the glucose level during 24 h in each individual patient. As a group, C-peptide secretors were better controlled than non-secretors with respect to mean blood glucose, M-value and the lability index and showed higher free insulin levels despite a similar daily insulin dosage. The possible reasons for this fact are discussed. No correlation was found between the affinity characteristics of the insulin antibodies and the degree of metabolic control or the daily insulin dosage.

Adolescent↗