Changes in anthropometry and performance, and their inter-relationships, across three seasons in elite youth rugby league players

This is a non-final version of an article published in final form in Journal of Strength and Conditioning Research, 2014, 28(11), pp. 3128-3136.This study investigated changes in anthropometry and performance, and their inter-relationships, across three consecutive seasons (under-15 to under-17 age group) in elite youth rugby league players. Each player took part in annual anthropometrical and performance assessments, comprising measurements of stature; body mass; limb lengths and circumference; skinfolds, predicted muscle cross-sectional area (CSA); 20 m speed, counter-movement jump height, vertical power and aerobic power. Lean body mass % changed (P < 0.05) between the under-15 (70.9 ± 5.9 %), under-16 (72.0 ± 5.8 %) and the under-17 age groups (74.1 ± 5.7 %). Likewise, predicted quadriceps muscle cross-sectional area (CSA) also changed (P < 0.05) between each age group (under-15 = 120.9 ± 37.8 cm2; under-16 = 133.2 ± 36.0 cm2; under-17 = 154.8 ± 28.3 cm2). Concomitant changes between the under-15 and under-16 group were found for 20 m speed (3.5 ± 0.1 cf. 3.4 ± 0.2 s; P = 0.008) and predicted jumping power (3611.3 ± 327.3 W cf. 4081.5 ± 453.9 W; P = 0.003). Both lean body mass and quadriceps muscle CSA consistently, related to both 20 m sprint time and jumping power, with r-values ranging between -0.39 to –0.63 (20 m sprint time) and 0.55 to 0.75 (jumping power). Our findings demonstrate the importance of gains in lean body mass across later-adolescence that support the ability to generate horizontal speed and predicted vertical power. This information should inform the expectations and subsequent training programs of elite rugby league practitioners

Cushing's Syndrome and Fetal Features Resurgence in Adrenal Cortex–Specific Prkar1a Knockout Mice

Carney complex (CNC) is an inherited neoplasia syndrome with endocrine overactivity. Its most frequent endocrine manifestation is primary pigmented nodular adrenocortical disease (PPNAD), a bilateral adrenocortical hyperplasia causing pituitary-independent Cushing's syndrome. Inactivating mutations in PRKAR1A, a gene encoding the type 1 α-regulatory subunit (R1α) of the cAMP–dependent protein kinase (PKA) have been found in 80% of CNC patients with Cushing's syndrome. To demonstrate the implication of R1α loss in the initiation and development of PPNAD, we generated mice lacking Prkar1a specifically in the adrenal cortex (AdKO). AdKO mice develop pituitary-independent Cushing's syndrome with increased PKA activity. This leads to autonomous steroidogenic genes expression and deregulated adreno-cortical cells differentiation, increased proliferation and resistance to apoptosis. Unexpectedly, R1α loss results in improper maintenance and centrifugal expansion of cortisol-producing fetal adrenocortical cells with concomitant regression of adult cortex. Our data provide the first in vivo evidence that loss of R1α is sufficient to induce autonomous adrenal hyper-activity and bilateral hyperplasia, both observed in human PPNAD. Furthermore, this model demonstrates that deregulated PKA activity favors the emergence of a new cell population potentially arising from the fetal adrenal, giving new insight into the mechanisms leading to PPNAD

Rupture of Abdominal Aortic Aneurysms in Patients Under Screening Age and Elective Repair Threshold

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