El efecto de la posición de partida en la salida de espalda en natación

Las salidas en natación suponen, cada vez más, un componente muy importante del tiempo final de prueba. Los problemas que plantea la investigación de la salida de espalda, debido a que parte del movimiento sucede dentro del agua y parte fuera, ha hecho que no aparezcan estudios previos que aporten luz a las dudas que plantean los entrenadores y los libros de texto sobre el tema. Uno de estos interrogantes es saber si la posición de partida de las piernas debe ser más o menos abierta (ángulos de la rodilla de 15±5º ó 90±5º). Para ello cuatro nadadores experimentados (21.5 ± 0.5 años, 59.3 ± 1.4 seg en 100m espalda y 27.2 ± 0.5 seg en 50m) fueron entrenados durante cuatro semanas en ambas salidas y efectuaron un total de tres salidas de cada, para posteriormente ser elegidas las mejores de cada uno, para cada condición del estudio. Se realizo un test de Wilcoxon para comparación de muestras relacionadas no paramétricas. En contra de lo que podía ser esperado no se encontraron diferencias significativas entre los tiempos a 5, 10 y 15 metros en ninguna de ellas (p=1, p=0.8 y p=0.6), así como en velocidades del centro de gravedad en salida y entrada (p=0.095 y p= 0.145), altura del centro de gravedad (p= 0.5), o longitud del vuelo (p=0.214) entre otras. Las similitudes del movimiento con el de un salto vertical sin contramovimiento, salvando la diferencia de la gravedad, nos hacen pensar que otras variables no controladas como el ángulo de la cadera o factores coordinativos relacionados con la acción de los músculos biarticulares puedan tener una influencia mayor que la variable estudiada. No obstante, los datos no paramétricos nos hacen ser prudentes y esperar a los resultados del análisis del resto de sujetos. Por último, decir que los nadadores usaban una de las dos variables normalmente, encontrándose más cómodos con ella. Esto nos lleva a sugerir a nivel técnico el trabajo de ambas en edades tempranas para posteriormente ver cual produce los mejores resultados.Peer Reviewe

Efecto del ciclismo sobre el rendimiento de la carrera en triatletas jóvenes.

El coste metabólico (CM) de la carrera durante la segunda transición del triatlón ha sido estudiado en numerosas ocasiones, pero aún no se ha explorado este aspecto en triatletas jóvenes. Este estudio evalúa el efecto del ciclismo sobre el CM durante la simulación de una transición ciclismo-carrera de triatlón en deportistas jóvenes de élite. Seis sujetos realizaron dos pruebas en orden aleatorio: 1) Transición (T), consistente en 30 min de ciclismo a una carga correspondiente a 3,5 W·kg-1 seguidos de 3000 m de carrera a la máxima intensidad posible en una pista de 400 m (7,5 vueltas). 2) Carrera de control (C), consistente en 3000 m de carrera a la máxima intensidad posible. No se observaron diferencias (p < 0,05) entre C y T en el CM (250,46 ± 21,47 vs. 256,22 ± 17,82 mL O2·kg-1·km-1, respectivamente) ni en el consumo de oxígeno (VO2) (4238 ± 451 vs. 4220 ± 604 mL·min-1, respectivamente). Sin embargo, la marca conseguida fue significativamente mayor (p < 0,05) en T (669,2 ± 23,8 vs. 646,0 ± 15,8 s, respectivamente). Únicamente, en la primera vuelta de cada 3000 m se observaron diferencias significativas (p < 0,05) entre T y C para el CM y el VO2. Por tanto, concluimos que la prefatiga tiene un efecto negativo sobre el rendimiento de la carrera durante la segunda transición del triatlón sin afectar al CM

Efecte del ciclisme sobre el rendiment de la cursa en triatletes joves.

El cost metabòlic (CM) de la cursa durant la segona transició del triatló ha estat estudiat en nombroses ocasions, però aquest aspecte encara no s’ha explorat en triatletes joves. Aquest estudi avalua l’efecte del ciclisme sobre el CM durant la simulació d’una transició ciclisme-cursa de triatló en esportistes joves d’elit. Sis subjectes van realitzar dues proves en ordre aleatori: 1) Transició (T), consistent en 30 min de ciclisme a una càrrega corresponent a 3,5 W·kg-1 seguits de 3.000 m de cursa a la màxima intensitat possible en una pista de 400 m (7,5 voltes). 2) Cursa de control (C), consistent en 3.000 m de cursa a la màxima intensitat possible. No es van observar diferències (p < 0,05) entre C i T en el CM (250,46 ± 21,47 vs. 256,22 ± 17,82 mL O2·kg-1 · km-1, respectivament) ni en el consum d’oxigen (VO2) (4.238 ± 451 vs. 4.220 ± 604 mL·min-1, respectivament). Tanmateix, la marca aconseguida va ser significativament superior (p < 0,05) en T (669,2 ± 23,8 vs. 646,0 ± 15,8 segons, respectivament). Únicament, en la primera volta de cada 3.000 m es van observar diferències significatives (p < 0,05) entre T i C per al CM i el VO2. Per tant, concloem que la prefatiga té un efecte negatiu sobre el rendiment de la cursa durant la segona transició del triatló sense afectar el CM

Heart rate profile in highly trained triathletes

Nueve triatletas hombres (68,0 ± 2,0 mL·kg-1·min-1, 25 ± 1,9 años, 68,3 ± 2,2 kg y 1,77 ± 0,22 m), realizaron un test incremental en cicloergómetro en tres ocasiones correspondientes con el inicio de la temporada, periodo precompetitivo y periodo competitivo. El consumo de oxígeno máximo y los umbrales ventilatorios (aeróbico y anaeróbico respectivamente) fueron medidos en cada visita. A pesar de los cambios en la distribución del entrenamiento entre disciplinas, tiempo total de entrenamiento, tiempo de entrenamiento por semana, e intensidad del entrenamiento, potencia máxima, consumo de oxígeno máximo, frecuencia cardiaca submáxima, y concentración de lactato permanecieron estables a lo largo de la temporada. Dada la estabilidad mostrada con la relación entre la frecuencia cardiaca y los umbrales ventilatorios en nuestra muestra, concluimos que un único test de laboratorio al comienzo de la temporada podría ser suficiente para prescribir intensidades de entrenamiento (al menos en ciclismo) basándose en zonas de frecuencia cardiaca en triatletas altamente entrenados. Estos resultados deberán ser comprobados además con muestras mayores para poder ser generalizados.Nine male triathletes (68.0 ± 2.0 mL·kg-1·min-1, 25 ± 1.9 years, 68.3 ± 2.2 kg, 177.4 ± 2.2 cm), performed an incremental maximal cycle exercise test on three separate occasions corresponding to the start of the season, pre-competitive period, and competitive period. Maximal oxygen uptake and ventilatory thresholds (aerobic and anaerobic respectively) were assessed in each visit. Despite changes in the distribution of training among disciplines, total training time, training time per week, and intensity of the training, maximal power output, maximal oxygen uptake, submaximal heart rate, and lactate concentration remained stable throughout the season. Due to the stability displayed by the heart rate ventilatory thresholds relationship in our sample, we conclude that a single laboratory testing at the start of the season could be enough to prescribe training intensities (at least for cycling) based on heart rate zones in highly trained triathletes. These results should be compared in future studies with longer samples in order to be generalised.Este estudio ha sido parcialmente financiado por la Universidad Politécnica de Madrid mediante una beca de doctorado a Zapico, AG. Así como el Programa Marier Curie – COFUND (contract UNITE 246565) a becado a Díaz, V., y el Ministerio de Ciencia e Innovación a Ruiz, J. (RYC-2010-05957)

Novel AKT1-GLI3-VMP1 pathway mediates KRAS oncogene-induced autophagy in cancer cells

Autophagy is an evolutionarily conserved degradation process of cytoplasmic cellular constituents. It has been suggested that autophagy plays a role in tumor promotion and progression downstream oncogenic pathways; however, the molecular mechanisms underlying this phenomenon have not been elucidated. Here, we provide both in vitro and in vivo evidence of a novel signaling pathway whereby the oncogene KRAS induces the expression of VMP1, a molecule needed for the formation of the authophagosome and capable of inducing autophagy, even under nutrient-replete conditions. RNAi experiments demonstrated that KRAS requires VMP1 to induce autophagy. Analysis of the mechanisms identified GLI3, a transcription factor regulated by the Hedgehog pathway, as an effector of KRAS signaling. GLI3 regulates autophagy as well as the expression and promoter activity of VMP1 in a Hedgehog-independent manner. Chromatin immunoprecipitation assays demonstrated that GLI3 binds to the VMP1 promoter and complexes with the histone acetyltransferase p300 to regulate promoter activity. Knockdown of p300 impaired KRAS- and GLI3-induced activation of this promoter. Finally, we identified the PI3K-AKT1 pathway as the signaling pathway mediating the expression and promoter activity ofVMP1upstream of the GLI3-p300 complex. Together, these data provide evidence of a new regulatory mechanism involved in autophagy that integrates this cellular process into the molecular network of events regulating oncogene-induced autophagy.Fil: Lo Ré, Andrea Emilia. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; ArgentinaFil: Fernández Barrena, Maite G.. No especifíca;Fil: Almada, Luciana L.. No especifíca;Fil: Mills, Lisa D.. No especifíca;Fil: Elsawa, Sherine F.. No especifíca;Fil: Lund, George. No especifíca;Fil: Ropolo, Alejandro Javier. Universidad de Buenos Aires; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Molejon, Maria Ines. Universidad de Buenos Aires; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Vaccaro, Maria Ines. Universidad de Buenos Aires; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Fernandez Zapico, Martin Ernesto. No especifíca

Programa Escolar de Salud Cardiovascular (PESCA): de la teoría a la práctica

III Congreso de Alimentación, Nutrición y Dietética. Combinar la nutrición comunitaria y personalizada: nuevos retos

Combined body mass index and waist-to-height ratio and its association with lifestyle and health factors among Spanish children: the PASOS study

Background and Aims: The World Health Organization recommended simultaneous measurement of body mass index (BMI) and waist circumference (WC) and suggested joint use to predict disease risks. The aim of this study was to assess the prevalence of BMI and waist-to-height ratio (WHtR) categories among Spanish children and adolescents, as well as their associations with several lifestyle factors. Methods: Cross-sectional analysis of 8–16-year-old children and adolescents (n = 3772) were included in the PASOS nationwide representative study. Children/adolescents and their mothers/female caregivers answered a questionnaire on lifestyle and health factors. Child/adolescent anthropometrics were measured. Four combined BMI-WHtR disease risk categories were built. Results: A third of participants showed combined BMI-WHtR categories with high disease risk (12.3% ‘increased risk’, 9.7% ‘high risk’, 14.3% ‘very high risk’). Participants in the ‘very high risk’ group were less likely to be females (odds ratio 0.63; 95% CI: 0.52–0.76) and adolescents (0.60; 95% CI: 0.49–0.72), to practice ≥60 min/day of moderate-vigorous physical activity (MVPA) (0.73; 95% CI: 0.57–0.93), and to watch <120 min/day of total screen time on weekdays (0.61; 95% CI: 0.49–0.76). Mothers of participants in the ‘very high risk’ group were less likely to have a high educational level, be in the overweight or normal range, have never smoked or were former smokers, and watch <120 min/day of total screen time on weekends. Participants in the ‘increased’ and ‘high risk’ categories had mothers with normal weight and ≥60 min/day of MVPA. Participants in the ’high risk’ group did not achieve ≥60 min/day of MVPA and showed lower adherence to the mediterranean diet. Conclusions: Adherence to a healthy lifestyle in children and adolescents, but also in their mothers/female caregivers during offspring’s childhood and adolescence, is associated with low BMI-WHtR disease risk.The PASOS study was funded by Fundación PROBITAS and the Gasol Foundation. Additional funds were received from the Barça Foundation, Banco Santander, IFA, Vienna and the Fundación Deporte Joven (no references are applicable). J.A.T., C.B., M.M.G., and M.d.M.B. were funded by CIBEROBN (CB12/03/30038) of the Institute of Health Carlos III (ISCIII), and co-funded by the European Regional Development Fund

A Multiple-Choice Maze-like Spatial Navigation Task for Humans Implemented in a Real-Space, Multipurpose Circular Arena

Spatial navigation is a key aspect of human behavior and it is still not completely understood. A number of experimental approaches exist, although most of the published data in the last decades have relied on virtual maze on-screen simulation or not-completely freely moving 3D devices. Some interesting recent developments, such as circular mazes, have contributed to analyze critical aspects of freely moving human spatial navigation in real space, although dedicated protocols only allow for simple approaches. Here, we have developed both specifically designed and home-assembled hardware equipment, and a customized protocol for spatial navigation evaluation in freely moving humans in a real space circular arena. The spatial navigation protocol poses an imitation of a real-space multiple-choice path maze with cul-de-sac and instances of non-linear movement. We have compared the results of this system to those of a number of validated, both virtual and real, spatial navigation tests in a group of participants. The system composed by hardware, the test protocol, and dedicated measure analysis designed in our laboratory allows us to evaluate human spatial navigation in a complex maze with a small and portable structure, yielding a highly flexible, adaptable, and versatile access to information about the subjects’ spatial navigation abilities

Nuclear Factor of Activated T Cells-dependent Down-regulation of the Transcription Factor Glioma-associated Protein 1 (GLI1) Underlies the Growth Inhibitory Properties of Arachidonic Acid

Numerous reports have demonstrated a tumor inhibitory effect of polyunsaturated fatty acids (PUFAs). However, the molecular mechanisms modulating this phenomenon are in part poorly understood. Here, we provide evidence of a novel antitumoral mechanism of the PUFA arachidonic acid (AA). In vivo and in vitro experiments showed that AA treatment decreased tumor growth and metastasis, and increased apoptosis. Molecular analysis of this effect showed significantly reduced expression of a subset of antiapoptotic proteins, including BCL2, BFL1/A1 and 4-1BB, in AA-treated cells. We demonstrated that downregulation of the transcription factor GLI1 in AA-treated cells is the underlying mechanism controlling BCL2, BFL1/A1 and 4-1BB expression. Using luciferase reporters, chromatin immunoprecipitation, and expression studies, we found that GLI1 binds to the promoter of these antiapoptotic molecules, and regulates their expression and promoter activity. We provide evidence that AA-induced apoptosis and downregulation of antiapoptotic genes can be inhibited by overexpressing GLI1 in AA-sensitive cells. Conversely, inhibition of GLI1 mimics AA treatments, leading to decreased tumor growth, cell viability and expression of antiapoptotic molecules. Further characterization showed that AA represses GLI1 expression by stimulating NFATc1 nuclear translocation, which then binds the GLI1 promoter and represses its transcription. AA was shown to increase reactive oxygen species. Treatment with antioxidants reduced the AA-induced apoptosis, downregulation of GLI1 and NFATc1 activation, indicating that NFATc1 activation and GLI1 repression require the generation of reactive oxygen species. Collectively, these results define a novel mechanism underlying AA antitumoral functions that may serve as a foundation for the future PUFA-based therapeutic approaches

The Transcription Factor GLI1 Mediates TGFb1 Driven EMT in Hepatocellular Carcinoma via a SNAI1-Dependent Mechanism

The role of the epithelial-to-mesenchymal transition (EMT) during hepatocellular carcinoma (HCC) progression is well established, however the regulatory mechanisms modulating this phenomenon remain unclear. Here, we demonstrate that transcription factor glioma-associated oncogene 1 (GLI1) modulates EMT through direct up-regulation of SNAI1 and serves as a downstream effector of the transforming growth factor-b1 (TGFb1) pathway, a well-known regulator of EMT in cancer cells. Overexpression of GLI1 increased proliferation, viability, migration, invasion, and colony formation by HCC cells. Conversely, GLI1 knockdown led to a decrease in all the above-mentioned cancer-associated phenotypes in HCC cells. Further analysis of GLI1 regulated cellular functions showed that this transcription factor is able to induce EMT and identified SNAI1 as a transcriptional target of GLI1 mediating this cellular effect in HCC cells. Moreover, we demonstrated that an intact GLI1-SNAI1 axis is required by TGFb1 to induce EMT in these cells. Together, these findings define a novel cellular mechanism regulated by GLI1, which controls the growth and EMT phenotype in HCC.National Institutes of Health Grants CA100882 and CA128633 (to LRR) and CA165076; the Mayo Clinic Center for Cell Signaling in Gastroenterology (NIDDK P30DK084567) (to MEFZ); the Mayo Clinic Cancer Center (CA15083), the Mayo Clinic Center for Translational Science Activities (NIH/NCRR CTSA Grant Number KL2 RR024151), and an American Gastroenterological Association Foundation for Digestive Health and Nutrition Bridging Grant (to LRR)