The aim of the study was to compare vertical jumping performances in boys and girls during growth. The maximum heights attained in a countermovement jump (CMJ) and squat jump (SJ) were measured using an Ergojump Bosco System. Average power output (PO) was recorded, and percentage of fast-twitch (%FT) muscle fiber distribution was estimated during the rebound jump. Differences in the maximum CMJ and SJ (CMJ-SJ) heights were calculated. Regressions between PO and age, lean body mass (LBM), and leg muscle volume (LMV), respectively, were computed for 240 boys and 239 girls (aged 11-16 years). Height, LMV, and body mass values were larger in boys than girls aged 14 years. Both groups had a similar body mass index independently of age. The CMJ, SJ, PO, and %FT were larger in boys than in girls between 12 and 16 years of age. Strong correlations were found between PO and age in the population as a whole, and between PO and LBM, PO and LMV in each group. The CMJ-SJ decreased with increasing age in both groups without significant differences. Conclusion Jumping performance increases during growth, with gender differences manifesting from 14 years onwards due to the much greater increase in leg length and LMV in boys than in girls.

The aim of this study was to test the hypothesis that venous blood lactate concentrations ([La-]) would vary from the beginning of brief exercise. Maximal vertical jumping was used as a model of brief intense exercise. Eleven healthy male volleyball players, aged [mean (SE)] 18.5 (0.7) years, performed three exercise tests with different protocols, each separated by quiet seated recovery periods of 45 min. After the first test, consisting of a single maximal jump [lasting approximately equals 0.6 s for the pushing phase, and in which the subjects jumped 64 (2.2) cm], forearm venous [La-] increased significantly with respect to rest at 1 min (t1), 3 min (t3), and 5 min (t5) of recovery. The second test, comprising six maximal jumps, each separated by 20-s recovery periods, resulted in an unchanged [La-] with respect to the baseline value. After the third test [i.e., six consecutive maximal jumps that lasted a total of 7.36 (0.33) s], [La-] increased significantly at t3 and t5 with respect to the pre-test value (F= 10.3, P < 0.001). We conclude that a significant venous [La-] increase occurs after vertical jumping. This result may be explained by the activation of lactic anaerobic metabolism at the very onset of exercise, which participates in energy production and/or in the resynthesis of the phosphocreatine that was used during such brief exercise.

Muscular and cardiorespiratory dysfunction contributes to exercise intolerance. Therefore, the aim of the present study was to characterize the cardiopulmonary response andrespiratory muscle oxygenation of children with congenital heart diseases (CHD) when compared with those of healthy children. Twelve children with CHD in New York Heart Association (NYHA) class II or III, and 14 healthy children participated in the study. All subjects performed conventional spirographic measurements and a cardiopulmonary exercise test on a cycle ergometer. Oxygen uptake (VO(2)), carbon dioxide production (VCO(2)), minute ventilation (VE), heart rate (HR), and power output were measured. Oxygenation of respiratory muscles was assessed by near-infrared spectroscopy (NIRS) during exercise and recovery. Pulmonary function was normal and no significant difference was found between groups. At rest, CHD patients had cardiorespiratory variables comparable with those of the healthy group. At submaximal intensity (ventilatory threshold) and at peak exercise, power output, HR, VO(2), VCO(2), and VE were significantly reduced (p < 0.01) in CHD patients. Respiratory muscles deoxygenated during exercise in both groups. However, deoxygenation was more pronounced in the CHD group than in the healthy children from an intensity of 40% up to exhaustion. Likewise, children with CHD showed a slower recovery of oxygenation than healthy children (113.4 +/- 17.5 vs. 74.6 +/- 13.0 s; p < 0.001). Compared with healthy children, these results demonstrated that children with CHD have reduced performance and present a defected exercise capacity. Children with CHD showed a more pronounced decrease of respiratory muscle oxygenation and slower recovery of oxygen kinetics.

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