No abstract

Weight loss, induced by increased energy expenditure and reduced energy intake, occurs regularly during prolonged exposure to altitude above 5000 m. Loss of fat accounts for up to 74% of this weight loss. 1 Furthermore, loss of appetite is one of the most frequent symptoms of acute mountain sickness (AMS). 2 As leptin is a key mediator in the neuroendocrine regulation of energy homeostasis and appetite, 3 we investigated the effect of hypobaric hypoxia at high altitude on serum leptin levels in men, using a highly sensitive and speci®c method for leptin quanti®cation. 4 Mean serum leptin levels in 20 male mountaineers after active ascent to 4559 m (age: 19 ± 42 y) increased from 1.22 AE 0.19 ngaml (120 m, all values mean AE s.e.m. 9:00 a.m.) to 2.06 AE 0.34 ngaml (mean pO 2 : 43.2 mmHg, 9:00 a.m., 22 h after ascent, P 0.0003). This effect was not reversible after 1 h of treatment with 33% oxygenenriched air and appeared to be more pronounced in subjects with loss of appetite (78% increase, n 11), than in those without loss of appetite (52% increase, n 9). Loss of appetite was documented by the Environmental Symptom Questionnaire. 1 However, physical strain during the active ascent and single measurements of leptin, which is secreted in a pulsatile manner by adipocytes were identi®ed as possible confounding factors in this study. Therefore, in a second study serum leptin levels were measured in 18 volunteers (age: 20 ± 41 y) at 490 m (after 1, 4, 12 and 20 h) and at 4559 m (1, 4, 12, 20 (and 32) h after transportation by helicopter). In individuals with loss of appetite mean serum leptin levels increased from 3.19 AE 0.89 ngaml (490 m, 6:00 a.m.) to 4.89 AE 1.18 ngaml (4559 m, 6:00 a.m., P 0.02, n 12), but no signi®cant increase was found in individuals without loss of appetite (2.17 ngaml vs 2.55 ngaml, n 6, 6:00 a.m., P 0.35). An increase in integrated serum leptin levels (mean area under the curve) from 53.8 AE 13.8 ngaml h to 66.3 AE 16.2 ngaml h was found in individuals with loss of appetite (1 ± 20 h, P 0.008), but not in volunteers without loss of appetite (38.7 AE 6.4 ngaml h (490 m), 6.00 a.m. 40.8AE 13.2 ngaml h (4559 m, P 0.35). As loss of appetite is a frequent symptom of AMS 2 it is not surprising that at 4559 m a signi®cant increase in serum leptin levels was also found in those volunteers with AMS, compared to levels at 490 m. AMS was de®ned as a functional Lake Louise Score b1 (n 10, P 0.028). 5 Statistics were performed by non-parametric testing (Mann ± Whitney test and Wilcoxon test). Effects due to change in plasma volume have been excluded. Individuals with loss of appetite showed a tendency to higher leptin levels baseline than those without loss of appetite (P 0.1), but mean body mass indices were not signi®cantly different between the analysed subgroups. In summary, in two independent studies, elevated leptin levels at high altitude were demonstrated, and found to be associated with loss of appetite. Thus, leptin may be a player in the altered neuroendocrine regulation of energy homeostasis...

Summary:To determine whether adjustment of myocardial blood flow (MBF) , myocardial oxygen consumption (MVOl) and myocardial substrate uptake (MSU) to acute arterial hypoxia is influenced by training effects on the heart, 7 trained and 7 untrained healthy individuals were investigated. MBF (argon method), MV'Ol and MSU of glucose, lactate and free fatty acids were measured at rest during normoxia and two different stages of acute arterial hypoxia: a) 12.82 vol% Ol; b) 8.74 vol% Ol. Measurements were carried out during hemodynamic and respiratory steady state conditions.Myocardial flow and metabolism of athletes were significantly (p

ZusammenfassungBei einer Häufigkeit von 5-10% im Kindesalter stellt ein über einen längeren Zeitraum persistierender Zehenspitzengang immer wieder Anlass zur Vorstellung beim Pädiater dar. Mit über 90% ist die häufigste Ursache der idiopathische oder habituelle Zehenspitzengang. Seltener sind das angeborene Syndrom der kurzen Achillessehne, Zehenspitzengang bei Spastik (meist bei infantiler Zerebralparese), neuromuskuläre und neurodegenerative Erkrankungen.Diagnostisch stehen Anamnese und klinische Untersuchung im Vordergrund. Seitendifferenzen ohne ausreichende klinische Erklärung sollten immer Anlass zur bildgebenden ZNS-Diagnostik geben. Die Elektromyographie ist nur bei begründetem klinischem Verdacht auf eine neuromuskuläre Erkrankung sinnvoll. Auch beim idiopathischen Zehenspitzengang kann es zu einer zunehmenden Verkürzung der Achillessehne kommen. Der therapeutische Schwerpunkt liegt entsprechend auf der Vermeidung einer fortschreitenden Achillessehnenverkürzung und deren Sekundärfolgen, insbesondere Haltungsschäden im Bereich der Hüfte und der Wirbelsäule. An erster Stelle stehen Physiotherapie und Dehnungsübungen. Orthesen beeinflussen die Langzeitprognose nur gering positiv, sodass die Achillessehnen-Verlängerungsoperation beim Auftreten von Sekundärfolgen frühzeitig in Erwägung gezogen werden sollte. Neben der Spastik bietet Botulinumtoxin (Botox®) möglicherweise künftig eine auch Erfolg versprechende Therapieoption beim idiopathischen Zehenspitzengang.

The raising prevalence of obesity in childhood appears to preceed the development of atherosclerosis and the increased incidence of cardiovascular diseases in adulthood. This might be related to the fact that already in children, obesity is associated with classical risk factors for coronary disease, like hypertension, hyperlipidemia, or diabetes. Therefore, aim of the present study was to evaluate, whether obese children (compared to lean controls) are characterized by vascular damages and altered regenerative capacity of circulating endothelial progenitor cells (CPCs) as an early indicator of developing atherosclerosis. Methods: In 30 obese (11±3 years of age, BMI 28.1±1.3) and 30 lean control children (12±3 years of age, BMI 17.5±0.4) insulin sensitivity was evaluated by oral glucose tolerance testing (OGT). Peripheral flow-mediated dilatation (FMD) and intima media thickness (IMT) of the carotid artery were assessed as measures of vascular integrity. The number of CD34/KDR+ CPCs was quantified using FACS analysis and the functional capacity of CPCs was determined by migration assay. Results: Obesity in early childhood is associated with peripheral insulin resistance as an early manifestation of diabetes (serum insulin in OGT after 120 min: 543±102 pmol/L in obese vs. 275±39 pmol/L in lean, p<0.05). FMD was significantly impaired in obese compared to lean children (reactive hyperemia index 1.25±0.05 vs. 1.55±0.08, p<0.05). Already in childhood, obesity was accompanied by a gain in IMT (0.40±0.01 mm vs. 0.30±0.01 mm in lean, p<0.05). Obese children had significantly reduced numbers of circulating CPCs compared to lean children (70±7 vs. 119±13 cells/mL blood, p<0.05). There was an inverse correlation between the number of CPCs and the extent of obesity as determined by BMI-SDS (r=−0.27, p<0.05). Additionally, functional capacity of CPCs was significantly reduced in obese children (migration following a SDF-1 gradient: 170±31 CPCs/1000 plated CPCs in obese vs. 258±37 CPCs/1000 plated CPCs in lean, p<0.05). Conclusion: Already in childhood, obesity is associated with an impaired endogenous regenerative capacity, which might result in generalized vascular damage as an early stage of atherosclerosis.