975 resultados para peak height velocity


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Peak adolescent fracture incidence at the distal end of the radius coincides with a decline in size-corrected BMD in both boys and girls. Peak gains in bone area preceded peak gains in BMC in a longitudinal sample of boys and girls, supporting the theory that the dissociation between skeletal expansion and skeletal mineralization results in a period of relative bone weakness. Introduction: The high incidence of fracture in adolescence may be related to a period of relative skeletal fragility resulting from dissociation between bone expansion and bone mineralization during the growing years. The aim of this study was to examine the relationship between changes in size-corrected BMD (BMDsc) and peak distal radius fracture incidence in boys and girls. Materials and Methods: Subjects were 41 boys and 46 girls measured annually (DXA; Hologic 2000) over the adolescent growth period and again in young adulthood. Ages of peak height velocity (PHV), peak BMC velocity (PBMCV), and peak bone area (BA) velocity (PBAV) were determined for each child. To control for maturational differences, subjects were aligned on PHV. BMDsc was calculated by first regressing the natural logarithms of BMC and BA. The power coefficient (pc) values from this analysis were used as follows: BMDsc = BMC/BA(pc). Results: BMDsc decreased significantly before the age of PHV and then increased until 4 years after PHV. The peak rates in radial fractures (reported from previous work) in both boys and girls coincided with the age of negative velocity in BMDsc; the age of peak BA velocity (PBAV) preceded the age of peak BMC velocity (PBMCV) by 0.5 years in both boys and girls. Conclusions: There is a clear dissociation between PBMCV and PBAV in boys and girls. BMDsc declines before age of PHV before rebounding after PHV. The timing of these events coincides directly with reported fracture rates of the distal end of the radius. Thus, the results support the theory that there is a period of relative skeletal weakness during the adolescent growth period caused, in part, by a draw on cortical bone to meet the mineral demands of the expanding skeleton resulting in a temporary increased fracture risk.

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In the general population, the timing of puberty is normally distributed. This variation is determined by genetic and environmental factors, but the exact mechanisms underlying these influences remain elusive. The purpose of this study was to gain insight into genetic regulation of pubertal timing. Contributions of genetic versus environmental factors to the normal variation of pubertal timing were explored in twins. Familial occurrence and inheritance patterns of constitutional delay of growth and puberty, CDGP (a variant of normal pubertal timing), were studied in pedigrees of patients with this condition. To ultimately detect genes involved in the regulation of pubertal timing, genetic loci conferring susceptibility to CDGP were mapped by linkage analysis in the same family cohort. To subdivide the overall phenotypic variance of pubertal timing into genetic and environmental components, genetic modeling based on monozygous twins sharing 100% and dizygous twins sharing 50% of their genes was used in 2309 girls and 1828 boys from the FinnTwin 12-17 study. The timing of puberty was estimated from height growth, i.e. change in the relative height between the age when pubertal growth velocity peaks in the general population and adulthood. This reflects the percentage of adult height achieved at the average peak height velocity age, and thus, pubertal timing. Boys and girls diagnosed with CDGP were gathered through medical records from six pediatric clinics in Finland. First-degree relatives of the probands were invited to participate by letter; altogether, 286 families were recruited. When possible, families were extended to include also second-, third-, or fourth-degree relatives. The timing of puberty in all family members was primarily assessed from longitudinal growth data. Delayed puberty was defined by onset of pubertal growth spurt or peak height velocity taking place 1.5 (relaxed criterion) or 2 SD (strict criterion) beyond the mean. If growth data were unavailable, pubertal timing was based on interviews. In this case, CDGP criteria were set as having undergone pubertal development more than 2 (strict criterion) or 1.5 years (relaxed criterion) later than their peers, or menarche after 15 (strict criterion) or 14 years (relaxed criterion). Familial occurrence of strict CDGP was explored in families of 124 patients (95 males and 29 females) from two clinics in Southern Finland. In linkage analysis, we used relaxed CDGP criteria; 52 families with solely growth data-based CDGP diagnoses were selected from all clinics. Based on twin data, genetic factors explain 86% and 82% of the variance of pubertal timing in girls and boys, respectively. In families, 80% of male and 76% of female probands had affected first-degree relatives, in whom CDGP was 15 times more common than the expected (2.5%). In 74% (17 of 23) of the extended families with only one affected parent, familial patterns were consistent with autosomal dominant inheritance. By using 383 multiallelic markers and subsequently fine-mapping with 25 additional markers, significant linkage for CDGP was detected to the pericentromeric region of chromosome 2, to 2p13-2q13 (multipoint HLOD 4.44, α 0.41). The findings of the large twin study imply that the vast majority of the normal variation of pubertal timing is attributed to genetic effects. Moreover, the high frequency of dominant inheritance patterns and the large number of affected relatives of CDGP patients suggest that genetic factors also markedly contribute to constitutional delay of puberty. Detection of the locus 2p13-2q13 in the pericentromeric region of chromosome 2 associating with CDGP is one step towards unraveling the genes that determine pubertal timing.

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314 p.

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Adolescence is a unique period in human development encompassing sexual maturation (puberty) and the physical and psychological transition into adulthood. It is a crucial time for healthy development and any adverse environmental conditions, poor nutrition, or chronic infection can alter the timing of these physical changes; delaying menarche in girls or the age of peak height velocity in boys. This study explores the impact of chronic illness on the tempo of puberty in 607 adolescent skeletons from medieval England (AD 900-1550). A total of 135 (22.2%) adolescents showed some delay in their pubertal development, and this lag increased with age. Of those with a chronic condition, 40.0% (n=24/60) showed delay compared to only 20.3% (n=111/547) of the non-pathology group. This difference was statistically significant. A binary logistic regression model demonstrated a significant association between increasing delay in pubertal stage attainment with age in the pathology group. This is the first time that chronic conditions have been directly associated with a delay in maturation in the osteological record, using a new method to assess stages of puberty in skeletal remains.

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Purpose: To investigate whether growth was adversely affected in 137 young competitive female artistic gymnasts involved in different training volumes.

Methods: This was a 2-yr prospective cohort study in which height, sitting height, leg length, weight, skinfolds, and pubertal status were measured in competitive advanced (20–27 h·wk-1) and intermediate (7.5–22 h·wk-1) training level female gymnasts every 6–12 months. Biological parameters of the adolescent growth curve were estimated using the Preece–Baines growth model. Growth rates were estimated for both groups from the mixed-longitudinal data.

Results: Estimated ages at peak height velocity (PHV) (13–13.5 yr) and mean PHV (6.2–6.4 cm·yr-1) for the advanced- and intermediate-level gymnasts suggest that these gymnasts were later maturing and experienced a blunting of the growth spurt relative to reference values for U.S. youth. Comparison of growth velocities by pubertal status revealed that height velocity was lower in the advanced- versus the intermediate-level peripubertal gymnasts, which was due to a significant reduction in sitting height velocity (2.3 vs 3.1 cm·yr-1, P. < 0.05). No marked acceleration in height or sitting height velocity was detected in the advanced-level gymnasts from pre- to peripuberty. Inspection of individual growth rates revealed that over 35% of the pre- and peripubertal gymnasts experienced growth faltering (height velocity less than 4.5 cm·yr-1) during follow-up.

Conclusion: Advanced–and intermediate–training level competitive female gymnasts tend to exhibit an adolescent growth spurt that is similar in timing and tempo to short, normal, slowly maturing girls, but the high frequency of growth faltering suggests that training may alter the tempo of growth and maturation in some, but not all, female gymnasts.

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This study aimed at demonstrating the asymmetry in volume between the dominant and nondominant upper limbs in tennis players, controlled for maturity status. Upper limb volumes on both sides were calculated in 72 tennis players and 84 control subjects, using the truncated cone method. The participants’ maturity status was determined using the predicted age at peak height velocity (PHV). The results showed significant larger side-to-side asymmetry in volume in tennis groups than
in control groups. These findings suggested that, even before PHV, specific-sport adaptations occurred in the dominant upper limb in tennis players.

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Biological maturation may attenuate hypothesized sex differences in children’s physical activity but overall the evidence for this is equivocal. In this study, we investigated how the selection of different physical activity assessment instruments affects the detected relationship between biological maturation and late primary school children’s physical activity. Altogether, 175 children (97 girls, 78 boys) aged 10.690.3 years completed the PAQ-C self-report questionnaire and wore ActiGraph GT1M accelerometers for 5 consecutive days. Maturity status was predicted by estimating attainment of age at peak height velocity. Following initial exploration of sex differences in PAQ-C (t-test) and multiple ActiGraph outcome variables (MANOVA), the influence of maturity status was controlled using ANCOVA and MANCOVA. Unadjusted analyses revealed that boys were significantly more active than girls according to the PAQ-C (PB0.0001, d0.52) and ActiGraph (PB0.0001, d0.360.72). After controlling for maturity status, the differences in PAQ-C scores increased (P0.001, d0.64), but the significant differences disappeared for the ActiGraph data (P0.36, d0.170.33). The detected relationship between maturity status and late primary school children’s physical activity is dependent on the physical activity assessment tool employed, reflecting the different aspects of physical activity captured by the respective measures.

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Short stature and later maturation of youth artistic gymnasts are often attributed to the effects of intensive training from a young age. Given limitations of available data, inadequate specification of training, failure to consider other factors affecting growth and maturation, and failure to address epidemiological criteria for causality, it has not been possible thus far to establish cause–effect relationships between training and the growth and maturation of young artistic gymnasts. In response to this ongoing debate, the Scientific Commission of the International Gymnastics Federation (FIG) convened a committee to review the current literature and address four questions: (1) Is there a negative effect of training on attained adult stature? (2) Is there a negative effect of training on growth of body segments? (3) Does training attenuate pubertal growth and maturation, specifically, the rate of growth and/or the timing and tempo of maturation? (4) Does training negatively influence the endocrine system, specifically hormones related to growth and pubertal maturation? The basic information for the review was derived from the active involvement of committee members in research on normal variation and clinical aspects of growth and maturation, and on the growth and maturation of artistic gymnasts and other youth athletes. The committee was thus thoroughly familiar with the literature on growth and maturation in general and of gymnasts and young athletes. Relevant data were more available for females than males. Youth who persisted in the sport were a highly select sample, who tended to be shorter for chronological age but who had appropriate weight-for-height. Data for secondary sex characteristics, skeletal age and age at peak height velocity indicated later maturation, but the maturity status of gymnasts overlapped the normal range of variability observed in the general population. Gymnasts as a group demonstrated a pattern of growth and maturation similar to that observed among short-, normal-, late-maturing individuals who were not athletes. Evidence for endocrine changes in gymnasts was inadequate for inferences relative to potential training effects. Allowing for noted limitations, the following conclusions were deemed acceptable: (1) Adult height or near adult height of female and male artistic gymnasts is not compromised by intensive gymnastics training. (2) Gymnastics training does not appear to attenuate growth of upper (sitting height) or lower (legs) body segment lengths. (3) Gymnastics training does not appear to attenuate pubertal growth and maturation, neither rate of growth nor the timing and tempo of the growth spurt. (4) Available data are inadequate to address the issue of intensive gymnastics training and alterations within the endocrine system.

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Growth is the opportune time to modify bone accrual. While bone adaptation is known to be dependent on local loading and consequent deformations (strain) of bone, little is known about the effects of sex, and bone-specific physical activity on location-specific cross-sectional bone geometry during growth. To provide more insight we examined bone traits at different locations around tibial cross sections, and along the tibia between individuals who vary in terms of physical activity exposure, sex, and pubertal status. Data from 304 individuals aged 5-29 years (172 male, 132 female) were examined. Peripheral quantitative computed tomography (pQCT) was applied at 4%, 14%, 38%, and 66% of tibial length. Maturity was established by estimating age at peak height velocity (APHV). Loading history was quantified with the bone-specific physical activity questionnaire (BPAQ). Comparisons, adjusted for height, weight and age were made between sex, maturity, and BPAQ tertile groups. Few to no differences were observed between sexes or BPAQ tertiles prior to APHV, whereas marked sexual dimorphism and differences between BPAQ tertiles were observed after APHV. Cross-sectional location-specific differences between BPAQ tertiles were not evident prior to APHV, whereas clear location-specificity was observed after APHV. In conclusion, the skeletal benefits of physical activity are location-specific in the tibia. The present results indicate that the peri- or post-pubertal period is likely a more favourable window of opportunity for enhancing cross-sectional bone geometry than pre puberty. Increased loading during the peri-pubertal period may enhance the bone of both sexes.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)