Physical activity is known to have an anabolic effect on bone tissue. It has been shown to increase the bone mineral density (BMD) in young adults, as well as in teenagers. But there is little information about the effect of intensive physical activity in childhood, particularly at the prepubertal stage. To examine the influence of an early intensive physical training on BMD, we have studied a group of elite prepubertal girls, at the starting phase of their peak bone mass acquisition. Subjects were engaged either in sport requiring significant impact loading on the skeleton, or in sport without impact loading. Forty-one healthy prepubertal girls took part in this study. The sport group consisted of 10 swimmers (10.5 +/- 1.4 years old) and 18 gymnasts (10.4 +/- 1.3 years old), who had performed 3 years of high-level sport training (8-12 h per week for swimmers, 10-15 h per week for gymnasts). Thirteen girls (10.7 +/- 1 years old) doing less than 3 h per week of physical activity served as a control group. BMD measurements were done using dual-energy X-ray absorptiometry. There was no statistical significant difference between groups as regards age, body height and weight, and body composition. There was no statistical significant difference between swimmers and controls for all the BMD measurements. Mean BMD in gymnasts was statistically higher than in the control group for mid-radius (+15.5%, p < 0.001), distal radius (+33%, p < 0.001), L2-4 vertebrae (+11%, p < 0.05), femoral neck (+15%, p < 0.001) and Ward's triangle (+15%, p < 0.01). Moreover, in gymnasts, BMD at radius, trochanter and femoral neck was above normative values. We conclude that physical activity in childhood could be an important factor in bone mineral acquisition in prepubertal girls, but only if the sport can induce bone strains during a long-term program: gymnastics has such characteristics, unlike swimming. Such acquisition could provide protection against risks of osteoporosis in later life, but this remains debatable.

Chronic CO exposure promotes a pathological phenotype of cardiomyocytes in the absence of underlying cardiomyopathy. The less severe phenotype in vivo suggests a role for compensatory mechanisms. Arrhythmia propensity may derive from intracellular Ca(2+) overload.

The aim of the present study was to analyse the effect of 1 year of intensive swimming training on lung volumes, airway resistance and on the flow-volume relationship in prepubertal girls. Five girls [9.3 (0.5) years old] performing vigorous swimming training for 12 h a week were compared with a control group of 11 girls [9.3 (0.5) years old] who participated in various sport activities for 2 h per week. Static lung volumes, maximal expiratory flows (MEF) at 75, 50 and 25% of vital capacity, 1-s forced expiratory volume (FEV1.0) and airway resistance (R(aw)) were measured by means of conventional body plethysmograph techniques. Prior to the training period there were no significant differences between the two groups for any of the parameters studied. Moreover, for both groups, all parameters were within the normal range for children of the corresponding age. After 1 year of training, vital capacity (VC), total lung capacity (TLC) and functional residual capacity (FRC) were larger (P < 0.05) in the girl swimmers than in the control group, while physical development in terms of height and weight was similar. FEV1.0 (P < 0.01), MEF25, MEF50 (P < 0.05) and MEF75 as well as the ratio MEF50/TLC (P < 0.05) had increased in the girl swimmers but were unchanged in the control group. R(aw) tended to be lower in the girl swimmers and higher in the control group. The results indicate that intensive swimming training prepuberty enhances static and dynamic lung volumes and improves the conductive properties of both the large and the small airways. As to the causative mechanism, it can be speculated that at prepuberty intensive swimming training promotes isotropic lung growth by harmonizing the development of the airways and of alveolar lung spaces.

Myostatin up-regulation is associated with the skeletal muscle response to hypoxic stimuli, Molecular and Cellular Endocrinology (2010), doi:10.1016/j.mce.2010 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Version postprintComment citer ce document : Hayot, M., Rodriguez, J., Vernus, B., Carnac, G., Jean, E., Allen, D., Goret, L., Obert, P., Candau, R., A c c e p t e d M a n u s c r i p t 2 ABSTRACTMyostatin and hypoxia signalling pathways are able to induce skeletal muscle atrophy, but whether a relationship between these two pathways exists is currently unknown. Here, we tested the hypothesis that a potential mechanism for hypoxia effect on skeletal muscle may be through regulation of myostatin. We reported an induction of myostatin expression in muscles of rats exposed to chronic hypoxia. Interestingly, we also demonstrated increased skeletal muscle myostatin protein expression in skeletal muscle of hypoxemic patients with severe Keywords : hypoxic stimulus, myostatin, skeletal muscle atrophy, COPD, myotubes Version postprintComment citer ce document : Hayot, M., Rodriguez, J., Vernus, B., Carnac, G., Jean, E., Allen, D., Goret, L., Obert, P., Candau, R., Bonnieu, A. (2011). Myostatin up-regulation is associated with the skeletal muscle response to hypoxic stimuli.

In children, the fact that cardiac anatomy and function, particularly during the diastolic phase, can adapt to endurance training is still uncertain. Therefore, this study was undertaken to evaluate the effect of a long-term intensive endurance swimming program on the cardiac structure and function of 10-11 year old children. The population consisted of 9 children who belonged to a local youth swimming team (S) and 11 recruited from a primary school to serve as a control group (C). The swimmers had been training on average 10 to 12 h x wk(-1) for at least 2 years. All the subjects were examined by M-mode, 2-dimensional and pulsed-wave Doppler analyses according to standard procedures recommended by the American Society of Echocardiography. Investigations were carried out at rest with the subjects in a supine position. The results showed that highly trained children exhibited significantly higher left ventricular (LV) internal diameter (S: 41.6+/-1.6, C: 39.0+/-2.2 mm/m(1/3) surface area, p<0.01) and LV mass (S: 68+/-7, C: 59+/-5 g/m2 SA, p<0.01). There were, however, no differences between S and C for chamber wall thickness (posterior wall S: 5.2+/-0.6, C: 5.3+/-0.6 mm/m(1/3) SA; septum S: 5.8+/-0.3, C: 5.8+/-0.4 mm/m(1/3) SA), LV systolic function parameters (ejection fraction S: 77.1+/-0.3, C: 77.7+/-0.4%; shortening fraction S: 38.9+/-3.0, C: 39.7+/-4.1%) and the diastolic function parameters, estimated from LV inflow velocitometry (E wave S: 1.04+/-0.12, C: 1.07+/-0.16 m/s; A wave S: 0.45+/-0.10, C: 0.55+/-0.11 m/s). Finally, transaortic Doppler examinations demonstrated similar resting cardiac output (Qc) between both groups (S: 3.76+/-0.81, C: 3.90+/-0.67 l x min(-1)). However, Qc were obtained with significantly lower heart rates (S: 69+/-7, C: 83+/-14 beat x min(-1), P<0.01) and higher stroke volumes (S: 55.2+/-8.0, C: 47.5+/-8.5 ml, P<0.05) in S when compared to C. Thus, these findings strongly suggest that, as has been shown before in adults, several cardiac adaptations (including resting bradycardia, increased stroke volume and enlarged left ventricular internal dimensions) can occur in prepubertal children as a result of intensive endurance training. However, our results did not demonstrate any effects of such training during prepuberty on both diastolic and systolic functions parameters.