The primary purpose of this investigation was to examine the physiological profile of a National Hockey League (NHL) team over a period of 26 years. All measurements were made at a similar time of year (pre-season) in 703 male (mean age +/- SD = 24 +/- 4 y) hockey players. The data were analyzed across years, between positions (defensemen, forwards, and goaltenders), and between what were deemed successful and non-successful years using a combination of points acquired during the season and play-off success. Most anthropometric (height, mass, and BMI) and physiological parameters (absolute and relative VO2 peak, relative peak 5 s power output, abdominal endurance, and combined grip strength) showed a gradual increase over the 26 year period. Defensemen were taller and heavier, had higher absolute VO2 peak, and had greater combined grip strength than forwards and goaltenders. Forwards were younger and had higher values for relative VO2 peak. Goaltenders were shorter, had less body mass, a higher sum of skinfolds, lower VO2 peak, and better flexibility. The overall pre-season fitness profile was not related to team success. In conclusion, this study revealed that the fitness profile for a professional NHL ice-hockey team exhibited increases in player size and anaerobic and aerobic fitness parameters over a 26 year period that differed by position. However, this evolution of physiological profile did not necessarily translate into team success in this particular NHL franchise.
504 overweight children admitted to hospital between 1921 and 1947 were followed up for 40 years by questionnaires at 10 year intervals. The mean weight for height (W/H) standard deviation score (SDS) reached a maximum in puberty (+3.5). The SDS fell to about +1 in adulthood. 47% patients were still obese (SDS greater than +1) in adulthood; 84.6% of these had SDS more than +2 in childhood. The degree of obesity in the family (parents and grandparents) and the degree of overweight in puberty were the most important factors for weight level in adulthood. Even when their food intake was in accordance with recommended levels, obese children had higher than normal weight as adults. Excessive overweight in puberty (SDS greater than +3) was associated with higher than expected morbidity and mortality in adult life. Weight-reducing measures should be started early in life to improve the unfavourable long-term prognosis for very obese children.
Over a 10-year period, from 1984-1995, in the Norwegian county of Vest-Agder, five patients in a paediatric clinic were diagnosed as having chromosome constitution 47,XYY. There are 1,250 males born a year in Vest-Agder. The patients were identified with bias, and not in a routine or prospective screening programme. All patients except one, a child who was diagnosed by chance at the age of one week; were admitted because of moderate conduct disorders or problems at school and striking tallness of stature. The half-brother of one of the 47,XYY boys had Klinefelter's syndrome 47,XYY. We conclude that identification of 47,XYY syndrome and information about it were of significance and help in counselling the patients and their families.
To construct new Danish growth charts for 0- to 20-year-olds and to compare them with Danish references from 1982 and with World Health Organization (WHO) standards for children aged 0-5 years from 2006, by applying similar inclusion and exclusion criteria.
Anthropometric data from three contemporary Danish population-based studies were combined. References for height were based on healthy Caucasian children born at term. A total of 12,671 height measurements (8055 in boys and 4616 in girls) were included. Reference charts were developed using the generalised additive models for location, scale and shape.
From prepubertal ages, a secular increase in height was observed for both genders. The differences were most pronounced in puberty, and final heights were increased by 1.4 cm in boys and 2.9 cm in girls compared to 1982 references. In boys, but not girls an upward shift in body mass index (BMI) above median levels was found. Reference curves for height were superimposable with standard curves based on the selective WHO criteria. Danish children were longer/taller and heavier and they had larger head circumferences than those reported in the recent multiethnic WHO standards.
We recommend national implementation of these contemporary 2014 Danish references for anthropometric measurements.
The first Danish case of Aarskog syndrome is reported. The child had attended several specialized out-patient clinics before the diagnosis was suggested. This underlines the need for dysmorphology in paediatrics.
We present a 9.1-year-old girl of Calabrian (Italy) ancestry, with clinical features (cranio-facial dysmorphism, short stature with delayed bone age and speech delay) suggesting the diagnosis of Floating-Harbor syndrome (FHS). Physical examination showed: height 113.9 cm (-2.9 SD), with a parent's target of 156.2 cm (+1.0 SD), weight 20.7 kg, BMI 16.0 (-0.04 SD), and many phenotypic abnormalities: long eyelashes, large bulbous nose with broad nasal bridge, short philtrum, moderately broad mouth, tooth folding and malocclusion, posteriorly rotated ears, low posterior hair line, short neck, clinodactyly of the 5th finger and hyperextensible finger joints. Diffused hyperpigmentation and hypertrichosis with sporadic pubic terminal hairs, but neither clitoromegaly nor other signs of hyperandrogenism and/or precocious puberty, were observed (T1, P1). Carpal bone evaluation showed a delayed bone age (TW2: 5-5/10, - 3.6 yr) and the statural age/bone age ratio was 1.1. Other dysmorphic syndromes were excluded on the basis of clinical evidence, also evaluated by a computer-assisted search (P.O.S.S.U.M. version 3.5, 1992). Analysis of chromosome 22 by the FISH method, using specific probes Cos29 and Tuple1, excluded microdeletions in the region 22q11.2, typical of Velo-cardio-facial syndrome. In this case, we report the impairment of serum GH responsiveness (GH baseline values: 0.2-1.9 ng/ml) to the administration of oral 150 microg clonidine [peak 4.7 ng/ml, normal values (nv)>10 ng/ml] and oral 4 mg dexamethasone (8.1 ng/ml, nv>10 ng/ml). Moreover, the evaluation of spontaneous 24-h GH secretion (Carmeda AB, Stockholm, Sweden) showed low mean GH levels (1.75 ng/ml, nv>3.0 ng/ml), with a maximum sleep-related peak of 2.8 ng/ml. Serum IGF-1 values were in the low-normal range (80-176 ng/ml, nv 133-626 ng/ml). While in FHS the cranio-facial features minimize with advancement of age, the impairment of growth velocity is permanent and results in severe dwarfism. In our case, treatment with recombinant GH (0.10 U/kg/day), administered by a needle-free device, induced a dramatic increase of growth velocity, increasing the height from -2.8 to -1.9 SD after 18 months, thus indirectly confirming a role of GH deficiency in the pathogenesis of FHS dwarfism.