The relative contributions of anthropometric variables to vertical jumping ability and leg power in Tunisian children.

The purpose of this study was to examine the relative contributions of anthropometric variables to vertical jumping ability and leg power and to establish reference values of vertical jumping parameters in athletic Tunisian children aged 7-13 years in both sexes. Three hundred and ninety-one athletic Tunisian children (208 boys and 183 girls) aged 7-13 years were randomly selected to participate in our study. They were asked to perform squat jumps and countermovement jumps. Jump heights and leg power were simultaneously provided by the optojump device. Full and stepwise regression models were calculated to identify which anthropometric parameters significantly contributed to performance variables. The multiple regressions showed that age, weight, standing height and fat-free mass were the predictors of jumping performance. The results may help in verifying the effectiveness of a specific training program and detecting highly talented athletes.

Effects of nifedipine-induced pulmonary vasodilatation on cardiac receptors and protein kinase C isoforms in the chronically hypoxic rat.

In chronic hypoxia, pulmonary hypertension induces a right ventricular (RV) hypertrophy (RVH) and the catecholamine-activated adrenergic system modulates cardiovascular responses through alpha- and beta-adrenergic pathways. The alpha(1)-adrenergic receptor (alpha(1)-AR) and protein kinase C (PKC) may play an important role in the signaling pathway leading to RVH. The aim of this study was to examine the relationship between nifedipine-induced pulmonary vasodilatation, the blunting of RVH and the modifications in the density of alpha(1)-AR, PKC activity and expression of PKC isoforms. In rats exposed to 15 days of hypoxia (380 torr, 50.66 kPa), RV pressure increased and RVH developed. Nifedipine, a calcium antagonist, given through gastric administration, partially decreased RV pressure and RVH. In both ventricles, hypoxia decreased alpha(1)-AR and beta-AR density and increased muscarinic acetylcholine receptor density. Nifedipine decreased alpha(1)-AR density only in normoxia. Expression of epsilon, delta and zeta PKC isoforms increased with RVH and normalized with nifedipine treatment. In conclusion, in this in vivo model of hypoxic rat, no relation was found between a RVH decrease and cardiac receptor densities. However, the development and regression of pulmonary hypertension and RVH were related to the expression of some PKC isoforms suggesting that pathways other than alpha(1)-AR might be involved in hypoxia-induced ventricular hypertrophy.