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indexation en cours; Chemosensory anxiety signals effectively prime motor responses related to withdrawal behavior, such as the startle reflex, in adult humans. As the reproductive status strongly affects the response to social chemosignals, the current study examined whether chemosensory anxiety signals would augment the startle response in prepubertal children as it does in adults. Using cotton pads, axillary sweat was collected from 28 men while waiting for an important oral examination (anxiety condition), and during ergometer training (sport control condition). Using a constant-flow olfactometer, sweat samples and pure cotton samples (cotton control) were presented to 10 prepubertal girls aged 9-13years (M=11.25, SD=1.25) for 3000ms during inhalation. White noise bursts of 102dB(A) served as startle probes, and startle responses were recorded via electromyography of the orbicularis oculi muscle. The girls showed larger startle amplitudes to probes presented in the context of chemosensory anxiety signals as compared to a context of sport control sweat (p

Purpose:This study examined the effects of a five-week intervention combining vigorous interval training (VIT) with diet among twenty-four obese adolescents. Fourteen girls and ten boys (aged 14–15) schooled in a pediatric rehabilitation center participated. Methods:The VIT intensity was targeted and remained above 80% of maximal heart rate (HR) and over six kilocalories per minute. Pre- and postintervention measures were body composition (BMI, weight, body fat percentage), physical self-perceptions (PSP), physical fitness (6-min walking distance and work) and its associated physiological responses (HRpeak and blood lactate concentration). A series of two-way analyses of variance or covariance controlling for weight loss were used to examine the changes. Results:Significant improvements were found in body composition, physical fitness and PSP (endurance, activity level, sport competence, global physical self-concept and appearance). In addition, boys presented higher levels of perceived strength and global physical self-concept than girls. Finally, there was a significant increase in perceived endurance, sport competence, and global physical self-concept in girls only. Conclusion:This five-week VIT program combined with diet represents an effective means for improving body composition, physical fitness, and PSP in obese adolescents, the effects on PSP being larger among girls.

Claude Bernard, and his master François Magendie, by the constitution of physiological science, has brought the establishment of a unifying representation system in the field of medicine. According to these representations, the diseases and the therapeutics would be considered by medical doctors as following the same laws of physiology. Physiology would be the condition of a real scientific medicine. How this positioning may be applied to psychiatry? To answer this question, this article proposes first of all to summarize the principal concepts structuring clinical physiology since Claude Bernard. These concepts are those of the "milieu intérieur", its stability and its regulation. The principles of this regulation system introduced by Claude Bernard lead us to consider him as the first modern systemic physiologist. Moreover these principles of regulation offer the possibility to understanding in an original way the processes of adaptation and acclimatization of an organism. This article then to analyze how these physiological concepts can be applied to psychiatry, including a discussion on the distinction of normal and pathological (by underlining that the difficulty in defining the disease is not specific to mental disorders), by providing a physiological perspective of the notion of syndrome for linking together in a practical way, the requirements of scientific medicine to that of rigorous clinical medicine., Claude Bernard, et son maitre François Magendie, ont permis, par la constitution de la science physiologique, la mise en place d'un système de représentation unificatrice dans le champ de la médecine où la pathologie et la thérapeutique seraient considérées par les médecins comme suivant les mêmes lois de la physiologie. La physiologie serait ainsi la condition d'une véritable médecine scientifique. Comment ce positionnement peut il s'appliquer à la psychiatrie ? Afin de répondre à cette question, cet article se propose, tout d'abord de rappeler les concepts essentiels structurant la physiologie clinique depuis Claude Bernard. Ces concepts sont ceux de milieu intérieur, de sa constance et de sa régulation. Les principes de ce système de régulation introduis par Claude Bernard font de lui un précurseur de la physiologie systémique moderne et permettent de comprendre de manière originale les processus d'adaptation et d'acclimatation d'un organisme. Cet article se propose ensuite d'analyser comment ces concepts peuvent s'appliquer à la psychiatrie et notamment à la distinction du normal et du pathologique (et de souligner que la difficulté dans la définition de la maladie n'est pas propre aux troubles mentaux), en offrant une perspective physiologique à la notion de syndrome, concept permettant de lier ensemble, et de manière pratique, les exigences d'une médecine scientifique à celle d'une médecine clinique rigoureuse.

International audience; Cognitive abilities are largely dependent on activation of cerebral tropomyosin-related kinase B receptors (TrkB) by brain-derived neurotrophic factor (BDNF) that is secreted under a bioactive form by both neurons and endothelial cells. In addition, there is mounting evidence for a link between endothelial function and cognition even though the underlying mechanisms are not well known. Therefore, we investigated the cerebral BDNF pathway, either neuronal or endothelial, in rheumatoid arthritis (RA) that combines both endothelial dysfunction (ED) and impaired cognition. Adjuvant-induced arthritis (AIA) in rats was used as a model of RA. Clinical inflammatory symptoms were evaluated from an arthritis score and brains were collected at day 31 ± 2 post-immunization. Neuronal expression of BDNF and TrkB phosphorylated at tyrosine 816 (p-TrkB) was examined in brain slices. Endothelial BDNF and p-TrkB expression was examined on both brain slices (hippocampal arterioles) and isolated cerebral microvessels-enriched fractions (vessels downstream to arterioles). The connection between endothelial nitric oxide (NO) and BDNF production was explored on the cerebrovascular fractions using endothelial NO synthase (eNOS) levels as a marker of NO production, Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) as a NOS inhibitor and glyceryl-trinitrate as a slow releasing NO donor. Brain slices displayed lower BDNF and p-TrkB staining in both neurons and arteriolar endothelial cells in AIA than in control rats. For endothelial cells but not neurons, a strong correlation was observed between BDNF and p-TrkB staining. Of note, a strong correlation was also observed between neuronal p-TrkB and endothelial BDNF staining. In cerebral microvessels-enriched fractions, AIA led to decreased BDNF and eNOS levels with a positive association between the 2 parameters. These effects coincided with decreased BDNF and p-TrkB staining in endothelial cells. The exposure of AIA cerebrovascular fractions to GTN increased BDNF levels while the exposure of control fractions to L-NAME decreased BDNF levels. Changes in the cerebral BDNF pathway were not associated with arthritis score. The present study reveals that AIA impairs the endothelial and neuronal BDNF/TrkB pathway, irrespective of the severity of inflammatory symptoms but dependent on endothelial NO production. These results open new perspectives for the understanding of the link between ED and impaired cognition.

Myocardial infarction is one of the leading causes of global mortality and improved management and reperfusion techniques have improved patient survival. Cardioprotection methods have been developed to limit the infarct size after ischemia reperfusion episode in order to limit the deleterious effects of myocardial infarction, such as ventricular remodeling and heart failure.In our study, we focused particularly on the major role of mitochondria in cell death phenomena associated with ischemia reperfusion. Within the mitochondria, our main target was sirtuin 3 (SIRT3), whose associated post-translational modifications have been shown to have a potential role in modulating ischemia-related reperfusion cell death. Thus, in the first part of our work, we were able to highlight (1) the need for SIRT3 in cardioprotection mechanisms in young mice and (2) the importance of SIRT3 deacetylation of cyclophilin D (CypD) in the success of cardioprotection.Recently, numerous preclinical studies have highlighted new techniques of effective cardioprotection in different animal models, which have not yet proved their worth after transposition in clinical study. In a second part of our work, we have endeavored to understand one of the reasons for these different clinical failures, based on the simple observation that preclinical studies are carried out on young animals, while myocardial infarction is a pathology of senescent people. We studied the impact of aging on various cardioprotection methods used in the laboratory, and demonstrated (3) mitochondrial changes impacting the deacetylation of CypD in response to cardioprotection techniques in aged mice. This study allowed us to raise a major problem of preclinical studies, namely the age of animal models used in relation to the pathology studied.This work has thus made it possible to determine the crucial role of deacetylation of CypD and SIRT3 in cardioprotection, but also to raise the question of the age of animal models before possible transfer of therapeutic advances in human clinical practice, L'infarctus du myocarde est une des première cause de mortalité mondiale et l'amélioration de la prise en charge et des techniques de reperfusion ont permis une amélioration de la survie des patients. Les méthodes de cardioprotection se sont développées afin de limiter la taille d'infarctus après l'épisode d'ischémie reperfusion dans le but de limiter les effets délétères de l'infarctus du myocarde, tels que le remodelage ventriculaire et l'insuffisance cardiaque.Dans notre étude, nous nous sommes particulièrement focalisés sur le rôle majeur de la mitochondrie dans les phénomènes de mort cellulaire associés à l'ischémie reperfusion. Au sein de la mitochondrie, notre cible principale était la sirtuine 3 (SIRT3), dont les modifications post-traductionnelles associées ont été montrées comme ayant un rôle potentiel dans la modulation de la mort cellulaire liée à l'ischémie reperfusion. Ainsi, dans la première partie de notre travail, nous avons pu mettre en évidence (1) la nécessité de la SIRT3 dans les mécanismes de cardioprotection chez les souris jeunes et (2) l'importance de la déacétylation par la SIRT3 de la cyclophiline D (CypD) dans la réussite de la cardioprotection.Récemment, de nombreuses études précliniques ont mis en avant de nouvelles techniques de cardioprotection efficace chez différents modèles animaux, qui n'ont pourtant pas fait leur preuve lors de la transposition en étude clinique. Dans une seconde partie de notre travail, nous nous sommes attachés à comprendre une des raisons de ces différents échec cliniques, en nous appuyant sur le simple constat que les études précliniques sont réalisées sur des animaux jeunes, alors que l'infarctus du myocarde est une pathologie des personnes sénescentes. Nous avons ainsi étudié l'impact du vieillissement sur différentes méthodes de cardioprotection utilisées au laboratoire, et avons mis en évidence (3) des modifications mitochondriales impactant la déacétylation de la CypD en réponse aux techniques de cardioprotection chez les souris âgées. Cette étude nous a permis de soulever un problème majeur des études précliniques, à savoir l'âge des modèles animaux utilisés par rapport à la pathologie étudiée.Ce travail a donc permis de déterminer le rôle crucial de la déacétylation de la CypD et de la SIRT3 dans la cardioprotection, mais aussi de soulever la question de l'âge des modèles animaux avant de possibles transferts des avancées thérapeutiques en clinique humaine

In 2015, Nature published the largest pangenomic association study to date linking genetic variants to body mass index. This study highlighted the role of the central nervous system in vulnerability to obesity and supports an original concept that cerebral plasticity plays an important role in the control of energy balance. Thus, reduced cerebral plasticity capacities could lead to inadequate dietary behaviors, which would increase the risk of weight gain under caloric pressure. The anorectic neurons POMC and the orexigenic neurons AgRP of the melanocortin system, which control the energy balance, actually show synaptic plasticity properties in the adult brain. These phenomena are shown in response to intense hormonal fluctuations induced by drastic genetic, surgical or nutritional manipulations. However, the physiological role of this synaptic plasticity within the melanocortin system has not been demonstrated yet. This study shows that cerebral plasticity phenomena are recapitulated at the meal scale in mice, depending on the prandial state, in response to moderate metabolic and hormonal changes. Indeed, 1 h standard diet exposure increases the electrical activity of the POMC neurons, which is correlated with a retraction of the astrocytic coverage around the POMC somas, with no change in synaptic configuration compared to the preprandial state. In contrast, 1 hour of high fat diet exposure does not modify the electrical activity of the POMC neurons and does not involve retraction of the astrocytic coverage. In addition, by pharmacological blockade of postprandial hyperglycemia, we showed that glucose is required for postprandial glial retraction. Finally, by a pharmacogenetic approach, we have shown that the inactivation of astrocytes modifies the feeding behavior and decreases the astrocytic coverage around the POMC neurons. These results suggest i)that astrocytes would play an inhibitory role on the electrical activity of POMC neurons ii) and that the post-prandial astrocytic retraction around POMC somas might remove inhibition of POMC neurons and might promote the sensation of satiety. This mode of regulation would not be activated during a high-fat meal, which would explain the low satietogenic properties of this type of meal., En 2015, la revue Nature a publié la plus grande étude d’association pangénomique à ce jour reliant des variants génétiques à l’indice de masse corporelle. Cette étude a mis en avant le rôle du système nerveux central dans la vulnérabilité à l’obésité, et soutient un concept original selon lequel la plasticité cérébrale jouerait un rôle important dans le contrôle de la balance énergétique. Ainsi, des capacités de plasticité cérébrale réduites pourraient favoriser des comportements alimentaires inadaptés, ce qui augmenterait le risque de prise de poids sous pression calorique. Les neurones anorexigènes POMC et les neurones orexigènes AgRP qui composent le système à mélanocortine et qui contrôlent la balance énergétique, conservent effectivement des propriétés de plasticité synaptique dans le cerveau adulte. Celles-ci se manifestent en réponse à des fluctuations hormonales intenses, induites par des manipulations génétiques, chirurgicales ou nutritionnelles drastiques. Cependant le rôle physiologique de cette plasticité synaptique au sein du système à mélanocortine n’a pas encore été démontré. Nos résultats montrent que des phénomènes de plasticité cérébrale sont récapitulés à l’échelle des repas chez la souris, en fonction de l’état prandial, en réponse à des changements métaboliques et hormonaux modérés. En effet, une exposition à 1h de régime standard augmente l’activité électrique des neurones POMC, ce qui est corrélé à une rétractation de la couverture astrocytaire autour des somas POMC, sans changement de configuration synaptique par rapport à l’état préprandial. A l’opposé, une exposition à 1h de régime riche en lipides ne modifie pas l’activité électrique des neurones POMC et n’entraine pas de rétractation de la couverture astrocytaire. De plus, par blocage pharmacologique de l’hyperglycémie post-prandiale, nous avons montré que le glucose était nécessaire pour initier la rétractation gliale post-prandiale. Enfin, par une approche pharmacogénétique, nous avons montré que l’inactivation des astrocytes modifie le comportement alimentaire et diminue la couverture astrocytaire autour des neurones POMC. Ces résultats suggèrent que l’astrocyte jouerait un rôle inhibiteur sur l’activité électrique des neurones POMC et que la rétractation astrocytaire post-prandiale, autour des somas POMC lèverait l’inhibition des neurones POMC et favoriserait la sensation de satiété. Ce mode de régulation ne serait pas déclenché lors d’un repas riche en graisses, ce qui expliquerait le faible pouvoir satiétogène de ce type de repas.

VEGF is a validated target for treatment of metastatic colorectal cancer (mCRC) with bevacizumab (avastin) and aflibercept (zaltrap) being approved for first and second line treatment, respectively. Despite intense efforts, no predictive biomarkers are available to identify patients likely to respond, or not, to VEGF-targeted therapies. Recently, different subtypes of CRC have been identified based on gene expression analysis including CMS4, a molecular subgroup with a mesenchymal phenotype, prominent angiogenesis and poor prognosis. We here wish to establish if the mesenchymal phenotype is predictive for the response to VEGF-targeted agents. CRC cell lines were examined for expression of epithelial (E-cadherin, gamma-catenin, cytokeratin 18) and mesenchymal (vimentin, N-cadherin, fibronectin) markers in vitro and in vivo by qRT-PCR and Western blot analysis and for the cellular distribution of E-cadherin and beta-catenin by ICC. Five CRC models were selected ranging from pronounced epithelial (HT-29, DLD-1), intermediate (HCT-116) to mesenchymal (HCT-116/5-FU, LS174T) and the tumor growth inhibitory activity of bevacizumab and aflibercept was established. VEGF-secretion was determined by ELISA and the microvascular density was characterized by quantitative IHC analysis. The mesenchymal phenotype was associated with higher microvascular density, but not with the expression of VEGF ligands. Two CRC xenograft models (DLD-1, HCT-116/5-FU) were sensitive to both bevacizumab and aflibercept, two models were more sensitive to aflibercept, compared to bevacizumab (HT-29, HCT-116), and one model (LS174T) was resistant to both agents. Aflibercept was more potent than bevacizumab in all CRC models. The mesenchymal phenotype was not predictive for the response to VEGF-targeted agents, neither positively nor negatively., Le VEGF est une cible validée pour le traitement du cancer colorectal métastatique avec le bevacizumab (Avastin) et l’aflibercept (Zaltrap) qui sont approuvés en première ligne et seconde ligne de traitement. Malgré les efforts intenses, il n’existe pas de biomarqueurs prédictifs pour identifier les patients qui pourraient répondre ou non aux therapies anti-VEGF. Récemment, différents sous-groupes de cancers colorectaux ont été identifies se basant sur l’expression de genes, incluant le groupe CMS4, un sous-groupe de phénotype mésenchymateux, angiogénique et de mauvais prognostic. Nous voulons établir si le phenotype mésenchymateux est prédictif pour la réponse aux agents anti-VEGF. Les cellules de cancer colorectal ont été étudiées in vitro et in vivo pour l’expression des marqueurs épithéliaux (E-cadherine, gamma-catenine, cytokeratine 18) et mésenchymateux (vimentine, N-cadherine, fibronectine) par qRT-PCR and western-blot et leur distribution par E-cadherine et beta-catenine pour immunocytochimie. Cinq modèles de cancer colorectal ont été rangés selon un phénotype épithélial prononcé (HT-29 et DLD-1), intermédiaire (HCT-116) à mésenchymateux (HCT-116/5-FU, LS174T) et les capacités d’inhibition de la croissance par le bevacizumab et l’aflibercept ont été établi. La sécrétion de VEGF a été déterminé par ELISA et la densité microvasculaire a été caractérisé par immunohistochimie quantitative. Le phénotype mésenchymateux est associé à une grande densité vasculaire mais pas aux ligands VEGF. Deux modèles de xénogreffes (DLD-1, HCT-116/5-FU) sont sensibles au bevacizumab et à l’aflibercept, deux modèles sont plus sensibles à l’aflibercept qu’au bevacizumab et un modèle est résistant aux deux molécules. L’aflibercept est plus efficace que le bevacizumab sur l’ensemble des modèles. Le phénotype mésenchymateux n’est pas prédictif pour la réponse aux agents ciblant le VEGF, ni positivement, ni négativement.

PPARγ-deficient mice die at E9.5 due to placental abnormalities. The mechanism by which this occurs is unknown. We demonstrated that the new endocrine factor EG-VEGF controls the same processes as those described for PPARγ, suggesting potential regulation of EG-VEGF by PPARγ. EG-VEGF exerts its functions via prokineticin receptor 1 (PROKR1) and 2 (PROKR2). This study sought to investigate whether EG-VEGF mediates part of PPARγ effects on placental development. Three approaches were used: 1) in vitro, using human primary isolated cytotrophoblasts and the extravillous trophoblast cell line (HTR-8/SVneo); 2) ex vivo, using human placental explants ( n = 46 placentas); and 3) in vivo, using gravid wild-type PPARγ+/− and PPARγ−/− mice. Major processes of placental development that are known to be controlled by PPARγ, such as trophoblast proliferation, migration, and invasion, were assessed in the absence or presence of PROKR1 and PROKR2 antagonists. In both human trophoblast cell and placental explants, we demonstrated that rosiglitazone, a PPARγ agonist, 1) increased EG-VEGF secretion, 2) increased EG-VEGF and its receptors mRNA and protein expression, 3) increased placental vascularization via PROKR1 and PROKR2, and 4) inhibited trophoblast migration and invasion via PROKR2. In the PPARγ−/− mouse placentas, EG-VEGF levels were significantly decreased, supporting an in vivo control of EG-VEGF/PROKRs system during pregnancy. The present data reveal EG-VEGF as a new mediator of PPARγ effects during pregnancy and bring new insights into the fine mechanism of trophoblast invasion.

Aim Neuromuscular electrical stimulation (NMES) causes early onset of neuromuscular fatigue. Peripheral electrophysiological explorations suggest that supra-spinal alterations are involved through sensitive afferent pathways. As sensory input is projected over the primary somatosensory cortex (S1), S1 area involvement in inhibiting the central motor drive can be hypothesized. This study assessed cortical activity under a fatiguing NMES protocol at low frequency. Methods Twenty healthy males performed five NMES sequences of 17 trains over the plantar flexors (30 Hz, 4 s on/6 s off). Before and after each sequence, neuromuscular tests composed of maximal voluntary contractions (MVCs) were carried out. Cortical activity was assessed during MVCs with functional near-infrared spectroscopy over S1 and primary motor (M1) areas, through oxy- [HbO] and deoxy-haemoglobin [HbR] variation. Electrophysiological data (H-reflex during MVC, EMG activity and level of voluntary activation) were also recorded. Results MVC torque significantly decreased after the first 17 NMES trains (P

The increase in blood pressure observed during physical activities is exaggerated in patients with hypertension, exposing them to a higher cardiovascular risk.Neural signals from the skeletal muscles appear to be overactive, resulting in this abnormal response in hypertensive patients.In the present study, we tested whether the attenuation of these neural signals in hypertensive patients could normalize their abnormal increase in blood pressure during physical activity.Attenuation of the neural signals from the leg muscles with intrathecal fentanyl injection reduced the blood pressure of hypertensive men during cycling exercise to a level comparable to that of normotensive men.Skeletal muscle afferent overactivity causes the abnormal cardiovascular response to exercise and was reverted in this experimental model, appearing as potential target for treatment.

Successful endurance performance requires the integration of multiple physiological and psychological systems, working together to regulate exercise intensity in a way that will reduce time taken or increase work done. The systems that ultimately limit performance of the task are hotly contested, and may depend on a variety of factors including the type of task, the environment, external influences, training status of the individual and a host of psychological constructs. These factors can be studied in isolation, or inclusively as a whole-body or integrative system. A reductionist approach has traditionally been favoured, leading to a greater understanding and emphasis on muscle and cardiovascular physiology, but the role of the brain and how this integrates multiple systems is gaining momentum. However, these differing approaches may have led to false dichotomy, and now with better understanding of both fields, there is a need to bring these perspectives together.

International audience

Previous studies suggest that, while both medical students and professional anatomists recognize the importance of gender issues and do not wish to associate with sexism, most are unaware of the possible negative aspects of sexism within anatomy (Morgan et al. 2014, J. Anat. 224:352–365; 2016, Clin. Anat. 29:892–910). To further investigate this issue, we provided second year medical students at Cardiff University (n = 293) and at the University of Paris Descartes, Sorbonne Paris Cité (n = 142) and professional anatomists (n = 208) with a questionnaire inviting them to address the possibility that gender factors within anatomical imagery (both historical and contemporary) hinder the dispassionate representation of anatomy. Ethical approval for the survey was obtained from the universities at both Cardiff and Paris. In the light of previous findings, the hypothesis tested was that medical students and professional anatomists do not perceive a gender bias when reflected in imagery that is based on anatomical iconography. Our survey results support this hypothesis and suggest that most students and anatomists are unaware of the possible negative aspects of sexism within the culture of anatomy. We consequently recommend that teachers of anatomy and authors of anatomical textbooks should be aware of the possibility of adverse effects on professional matters relating to equality and diversity issues when using imagery. Clin. Anat. 30:711–732, 2017. © 2017Wiley Periodicals, Inc.

International audience; BACKGROUND: Age-related declines in sport performance are characteristic of all endurance and sprinting disciplines. However, it is not known if the mode of locomotion (i.e. swimming, cycling or running) influences the age-related decline in sport performance in sprinting and endurance events.METHODS: To examine the age-related decline in three different modes of locomotion (i.e. swimming, cycling and running) for endurance and sprint events, the world best performances achieved for males in the age-groups 18-39 years, 40-44 years, 45-49 years, 50-54 years, 55-59 years, 60-64 years, 65-69 years, 70-74 years, 75-79 years and 80-84 years, were compared in swimming (1500-m and 50-m), cycling (1-h and 200-m) and running (10-km and 100-m). Each performance was considered as an average speed (throughout the distance) and the age-related decline in performance was expressed as a percentage of the world record (regardless of age group) for that discipline.RESULTS: The results showed that the age-related decline in 1-h track cycling is less pronounced compared to 1500-m swimming and 10-km running after 60 years. In contrast, the age-related decline was similar among the three locomotion modes for the sprinting events.CONCLUSION: Our data show that the maintenance of high performance in cycling persists longer into old age than for running or swimming.

BACKGROUND: During myocardial infarction, alteration of calcium homeostasis between sarcoplasmic reticulum (SR), mitochondria and cytosol occurs in cardiomyocytes (CM) and leads to cell death. Calcium leak channels are thought to be key regulators of the reticular calcium homeostasis. Translocon (TLC), a major component of the translation machinery, is a major reticular calcium leak channel.METHODS: By the mean of photonics, we first assessed the spatial organization and the function of TLC in the SR of adult mouse CM. In a second time, we questioned if and how the pharmacological TLC modulation could reduce ischemia/reperfusion (I/R)-mediated heart injury in a model of mouse myocardial infarction.RESULTS: Our data show that TLC is specifically located in the longitudinal SR in adult mouse CM. We demonstrate that puromycin induces a partial reduction of calcium stores in the longitudinal SR, while we observe no alteration in the ryanodine receptor-dependent calcium stores in the junctional SR. Puromycin preconditioning of mouse subjected to myocardial infarction significantly decreases the infarct area by near 30.9±6.3%. This is correlated with a decrease in the activation of mitochondrial pro-apoptotic proteins and an increase of a pro-survival mechanism: autophagy. We further demonstrated that puromycin preconditioning decreases the rate of calcium increase in the cytosol of adult CM during the ischemia duration in correlation with the decreased activation of calcium-dependent calpains.CONCLUSIONS: In this study, we characterized TLC as a leak channel specifically located in the longitudinal SR compartment of adult mouse CM. We found that the pharmacological activation of TLC before myocardial infarction exerts a preconditioning effect on myocardium without altering the ryanodine-dependent calcium stores. Altogether, these findings emphasize the present knowledge on the duality between junctional and longitudinal SR in CM and open up new therapeutic perspectives; CONTEXTE: Au cours de l'infarctus du myocarde, l'homéostasie du calcium entre leréticulum sarcoplasmique (SR), les mitochondries et le cytosol est altérée chez lescardiomyocytes (CM) et conduit à la mort cellulaire. Les canaux de fuite de calcium sontconsidérés comme des régulateurs clés de l'homéostasie calcique réticulaire. Le translocon(TLC), un composant majeur de la machine de la traduction protéique, est un important canalde fuite calcique réticulaire.METHODES: Par des moyens optiques, nous avons d'abord évalué l'organisation spatiale etla fonction du TLC dans le SR de souris adultes CM. Dans un second temps, nous avonsinterrogé si et comment la modulation pharmacologique TLC pourrait réduire les lésionsd'ischémie/reperfusion (I/R) cardiaque dans un modèle d'infarctus du myocarde de souris.RÉSULTATS: Nos données montrent que le TLC est spécifiquement localisée dans le SRlongitudinale des CM chez la souris adulte. Nous démontrons que la puromycine (activateurpharmacologique du TLC) induit une réduction partielle des réserves de calcium dans le SRlongitudinale, alors que nous n'observons aucune altération des réserves de calcium dépendantdu récepteur ryanodine dans le SR jonctionnelle. Le préconditionnement de la souris par lapuromycine, soumis à un infarctus du myocarde, diminue significativement la zone d'infarctusde près de 30,9±6,3%. Ceci est corrélé à une diminution de l'activation des protéines proapoptotiquesmitochondriales et à une augmentation d'un mécanisme de pro-survie:l'autophagie. Nous avons également démontré que le préconditionnement de la puromycinediminue la vitesse d'augmentation du calcium dans le cytosol du CM adulte pendant la duréede l'ischémie en corrélation avec la diminution de l'activation des calpains calciques.CONCLUSIONS: Dans cette étude, nous avons caractérisé le TLC comme un canal de fuitespécifiquement situé dans le compartiment longitudinale du SR dans les CM de souris adultes.Nous avons constaté que l'activation pharmacologique de la TLC avant l'infarctus dumyocarde exerce un effet de préconditionnement sur le myocarde sans altérer les réserves de calcium dépendant de la ryanodine. Dans l'ensemble, ces résultats mettent l'accent sur les connaissances actuelles sur la dualité entre le SR jonctionnelle et le SR longitudinale et ouvrent de nouvelles perspectives thérapeutiques

International audience; The aim of this study was to compare cardiovascular hemodynamics and cerebral oxygenation/perfusion (COP) during and after maximal incremental exercise in obese individuals according to their aerobic fitness versus age-matched healthy controls (AMHC). Fifty-four middle-aged obese (OB) and 16 AMHC were recruited. Maximal cardiopulmonary function (gas exchange analysis), cardiac hemodynamics (impedance cardiography), and left frontal COP (near-infrared spectroscopy: NIRS) were measured continuously during a maximal incremental ergocycle test. During recovery, reoxygenation/perfusion rate (ROPR: oxyhemoglobin: Delta O(2)Hb, deoxyhemoglobin: Delta HHb and total hemoglobin: Delta tHb; with NIRS) was also measured. Obese participants (OB, n = 54) were divided into two groups according to the median VO2 peak: the low-fit obese (LF-OB, n = 27) and the high-fit obese (HF-OB, n = 27). During exercise, end tidal pressure of CO2 (PETCO2), and COP (Delta O(2)Hb, Delta HHb and Delta tHb) did not differ between groups (OB, LF-OB, HF-OB, AMHC). During recovery, PETCO2 and ROPR (Delta O(2)Hb, Delta HHb and DtHb) were similar between the groups (OB, LF-OB, HF-OB, AMHC). During exercise and recovery, cardiac index was lower (P < 0.05) in LF-OB versus the other two groups (HF-OB, AMHC). As well, systolic blood pressure was higher during exercise in the OB, LF-OB and HF-OB groups versus AMHC (P < 0.05). When compared to AMHC, obese individuals (OB, LF-OB, HF-OB) have a similar cerebral vasoreactivity by CO2 and cerebral hemodynamics during exercise and recovery, but a higher systolic blood pressure during exercise. Higher fitness in obese subjects (HF-OB) seems to preserve their cardiopulmonary and cardiac function during exercise and recovery.

International audience; Periodontitis is based on a complex inflammatory over-response combined with possible genetic predisposition factors. The RANKL/RANK/OPG signaling pathway is implicated in bone resorption through its key function in osteoclast differentiation and activation, as well as in the inflammatory response. This central element of osteo-immunology has been suggested to be perturbed in several diseases, including periodontitis, as it is a predisposing factor for this disease. The aim of the present study was to validate this hypothesis using a transgenic mouse line, which over-expresses RANK (R Tg) and develops a periodontitis-like phenotype at 5 months of age. R Tg mice exhibited severe alveolar bone loss, an increased number of TRAP positive cells, and disorganization of periodontal ligaments. This phenotype was more pronounced in females. We also observed dental root resorption lacunas. Hyperplasia of the gingival epithelium, including Malassez epithelial rests, was visible as early as 25 days, preceding any other symptoms. These results demonstrate that perturbations of the RANKL/RANK/OPG system constitute a core element of periodontitis, and more globally, osteo-immune diseases.

International audience; Claudins are a family of proteins that forms paracellular barriers and pores determining tight junctions (TJ) permeability. Claudin-16 and-19 are pore forming TJ proteins allowing calcium and magnesium reabsorption in the thick ascending limb of Henle's loop (TAL). Loss-of-function mutations in the encoding genes, initially identified to cause Familial Hypomagnesemia with Hypercalciuria and Nephrocalcinosis (FHHNC), were recently shown to be also involved in Amelogenesis Imperfecta (AI). In addition, both claudins were expressed in the murine tooth germ and Claudin-16 knockout (KO) mice displayed abnormal enamel formation. Claudin-3, an ubiquitous claudin expressed in epithelia including kidney, acts as a barrier-forming tight junction protein. We determined that, similarly to claudin-16 and claudin-19, claudin-3 was expressed in the tooth germ, more precisely in the TJ located at the apical end of secretory ameloblasts. The observation of Claudin-3 KO teeth revealed enamel defects associated to impaired TJ structure at the secretory ends of ameloblasts and accumulation of matrix proteins in the forming enamel. Thus, claudin-3 protein loss-of-function disturbs amelogenesis similarly to claudin-16 loss-of-function, highlighting the importance of claudin proteins for the TJ structure. These findings unravel that loss-of-function of either pore or barrier-forming TJ proteins leads to enamel defects. Hence, the major structural function of claudin proteins appears essential for amelogenesis.

IF 4.134; International audience; The sense of taste is responsible for the detection and ingestion of food to cover energetic requirements in health and disease. The change in taste perception might lead to malnutrition that is usually one of the frequent causes of morbidity and mortality in patients with cancer. In this review, we summarize the mechanisms of taste perception and how they are altered in cancer. We also address the question of the implication of inflammation, responsible for the alterations in taste modalities. We highlight the role of radio- and chemotherapy in the modulation of taste physiology. Other several factors like damage to taste progenitor cells and disruption of gut microbiota are also dealt with relation to taste perception in cancer. We further shed light on how to restore taste acuity, by using different preventive methods, dietary modifications and pharmacotherapy in subjects with advanced cancer state.

Background The alarming progression of pediatric obesity is associated with the development of sleep-disordered breathing (SDB), and both exhibit similar adverse cardiometabolic health outcomes. Physical activity level (PAL) may counteract sleep and metabolic disturbances. The present study investigates i) the association between the metabolic syndrome in childhood obesity and SDB, ii) the impact of SDB severity on cardiometabolic risk scores and PAL in children with obesity. Methods Maturation status (Tanner stages), anthropometric (height, weight, body mass index, waist circumference, body adiposity index) and cardiometabolic characteristics (systolic and diastolic blood pressure, lipid and glycemic profiles) were assessed in 83 obese children (mean ± SD, age: 10.7 ± 2.7 years). PAL and SDB were investigated with a step test and interviews, and an overnight sleep monitor, respectively. The presence or absence of metabolic syndrome (MS) was established and continuous cardiometabolic risk scores were calculated (MetScoreBMI and MetScoreWC). Results Obese children with (61.4%) and without (38.6%) MS present similar SDB. SDB severity is associated with increased insulin concentrations, MetScoreBMI and MetScoreWC (p Conclusions In a context where no consensus exists for SDB diagnosis in children, our results suggest the influence of SDB severity on cardiometabolic risk factors. Further studies are needed to explore the association between PAL and both metabolic and sleep alterations in obese children.

International audience; This study aims to examine the repeated effects of three sessions of vigorous interval training (VIT) in basketball, running-biking, and boxing on the physical self-perceptions (PSP) of obese adolescents participating in a dietary program. A sample of 24 obese adolescents performed the consecutive VIT sessions every week for 5 weeks. PSP were measured immediately after each training session. Analyses of covariance were used to examine changes in PSP. The results showed rapid and constant increases in PSP with significant differences according to sex, time, type of VIT, and an interaction of sex by time by type of VIT, mainly for basketball.

The aim of this investigation was to evaluate the effect of a 6-day food restriction period on the physiological responses and performance of 11 high-level weightlifters. After a period of weight maintenance (T2), they were assigned into two groups depending on whether they lost (Diet group, n = 6) or maintained their body weight (Control group, n = 5) during the course of those 6 days. An evaluation of performance and the measurement of salivary cortisol concentrations and salivary α-amylase (sAA) activity were performed during a simulated weightlifting competition which took place at T2, after a 6-day period of food restriction (T3). Dietary data were collected using a 6-day diet record. We noted a 41.8% decrease in mean energy intake during the dietary restriction period, leading to a 4.34% weight loss for the Diet group. Dietary restriction did not modify absolute performance levels, whilst a significant improvement was noted for the Control group. Furthermore, we noted a response of decreased...

This study examined the age-related decline in endurance running performance of one of the greatest master runners ever, Ed Whitlock, who died recently. His running performances from 1500 m to marathon were analyzed for 5 periods of 5 years from 65–69 years to 85–89 years. Despite exceptional running performances for his advanced age, the rate of decline in his performances increased after 80 years and was drastically amplified after 85 years.

International audience; High-intensity exercise may pose a risk to patients with postconcussion syndrome (PCS) when symptomatic during exertion. The case of a paralympic athlete with PCS who experienced a succession of convulsion-awakening periods and reported a marked increase in postconcussion symptoms after undergoing a graded symptom-limited aerobic exercise protocol is presented. Potential mechanisms of cerebrovascular function failure are then discussed.

Grain legume pulse crops are of great interest to allow a production of seeds high nutritional value without any contribution of nitrate fertilizer. The nitrogen nutrition of legumes depends indeed mainly on the fixation in nodules of atmospheric dinitrogen through the plant-rhizobium symbiosis, and to a lesser extent, absorption by roots of soil mineral nitrogen.A better understanding has been obtained on the genetic control of the development of roots and nodules and on their impact on nitrogen nutrition. High genetic variability of these characters has been detected, and the existence of genetic correlations between them demonstrated. A quantitative genetic approach has identified several genomic regions that may be involved in their variations. The two different ways to improve nitrogen nutrition were also studied: the improvement of nitrogen acquisition by roots through a detailed study of a root architecture mutant, and the improvement of symbiosis via the study of the ability of peas to promote symbiotic associations with the most effective rhizobia.The results provide interesting bases for the design of a pea nitrogen-nutrition ‘ideotype’. Beyond the essential complementarity between the two pathways of nitrogen acquisition, it is necessary to optimize the interaction between the two symbiotic partners, which is a complex mechanism involving nodules formation and functioning in connection with complex signaling and trophic interactions between the partners and intra-plant., La culture de Légumineuses présente le double intérêt de permettre une production de graines à haute valeur nutritionnelle sans nécessité d’un apport d’engrais azoté. La nutrition azotée des légumineuses dépend en effet majoritairement de la fixation symbiotique de l’azote atmosphérique réalisée par des bactéries du sol, les rhizobia, au sein des nodosités, et dans une moindre mesure, de l’assimilation de l’azote minéral du sol par les racines.Une meilleure compréhension a été acquise sur le contrôle génétique de la mise en place des racines et des nodosités et sur leur impact sur la nutrition azotée. Une grande variabilité génétique pour ces caractères a été mise en évidence, ainsi que l’existence de corrélations génétiques entre eux. Une approche de génétique quantitative a permis d’identifier des régions génomiques pouvant être impliquées dans leurs variations. Deux pistes d’amélioration de la nutrition azotée ont aussi été étudiées : l’amélioration de l’acquisition d’azote par les racines à partir d’une étude détaillée d’un mutant de développement racinaire, et l’amélioration de la symbiose via l’étude de la capacité des pois à favoriser les associations symbiotiques avec les rhizobia les plus performants.Les résultats obtenus apportent des bases de réflexion concernant la conception d’un idéotype de nutrition azotée. Au-delà de la complémentarité indispensable entre les deux voies d’acquisition d’azote, il convient d’optimiser l’interaction entre les deux partenaires symbiotiques, mécanisme complexe mettant en jeu la formation et le fonctionnement des nodosités, en lien avec une signalétique et des interactions trophiques entre partenaires et intra-plante.

Stroke is the leading cause of disabilities worldwide and is mainly caused by atherosclerosis. But this is not the only risk for patients. Indeed, as this pathology is due to a lack of circulating cholesterol management and could lead to more pernicious outcomes such as cerebrovascular units disorganization whom, when combined with systemic and local inflammation can result in serious brain aftermath.Aged murine and non-human primate (NHP) animal models under high cholesterol diet were used to be closest to the human pathology. A translational approach with longitudinal follow-up of circulating and imaging biomarkers combined with a tissular characterization of inflammation was performed in order to elucidate the specificities of the inflammatory response in vascular wall of large vessels and brain tissue.We showed that in old ApoE-/- mice exercise can counterbalance deleterious effects of high fat diet when caloric intake is controlled but no longer when food is given ad libitum. The leakage of blood-brain barrier might explain the neuroinflammation observed in vivo and confirmed by tissular analysis. The study on NHP showed the interest of combine multimodal imaging with blood dosage for cardiovascular risk stratification and the importance of associating metabolic, inflammatory but also anti-inflammatory markers.We highlighted the importance of controlling calories intake in order to benefit of protective effects of exercise on atherosclerosis and the relevance of having an overview of the patient’s status for an accurate individual stratification of cardio and cerebrovascular risk, Les accidents vasculaires cérébraux sont la première cause mondiale d'handicap et l'athérosclérose en est le principal facteur. Cette pathologie, liée à une mauvaise prise en charge du cholestérol pourra avoir des conséquences plus pernicieuses comme la fragilisation des unités cérébrovasculaires qui, combinée à une inflammation systémique et locale, peut entraîner d'importantes répercussions cérébrales.Pour être au plus proche de l'humain nous avons utilisé des modèles animaux murins et primate non-humain (PNH) âgés sous régime gras. Une approche translationnelle avec suivi longitudinal de biomarqueurs sanguins et d'imagerie combinée à la caractérisation tissulaire de l'inflammation a été effectuée pour tenter d'élucider les spécificités de la réponse inflammatoire dans la paroi vasculaire des grosses artères et le tissu cérébral.Nous avons montré que chez des souris ApoE-/- âgées l'exercice physique peut contrecarrer les effets délétères d'un régime gras lorsque l'apport calorique est contrôlé mais plus lorsqu'il ne l'est pas. La dégradation de la barrière hémato-encéphalique pourrait expliquer l'inflammation observée in vivo et confirmée par l'analyse tissulaire. L'étude des PNH a montré l'intérêt d'associer imagerie multimodale et dosages sanguins dans la stratification du risque cardiovasculaire ainsi que l'importance d'associer des marqueurs métaboliques, inflammatoires et anti-inflammatoires.Nous avons montré l'intérêt de contrôler les apports caloriques pour bénéficier des effets protecteurs de l'exercice sur l'athérosclérose et l'importance d'avoir une vue globale du patient pour une stratification individuelle précise du risque cardio et cérébrovasculaire

International audience; Endurance performance involves the prolonged maintenance of constant or self-regulated power/velocity or torque/force. While the impact of numerous determinants of endurance performance has been previously reviewed, the impact of fatigue on subsequent endurance performance still needs to be documented. This review aims to present the impact of fatigue induced by physical or mental exertion on subsequent endurance performance. For the purpose of this review, endurance performance refers to performance during whole-body or single-joint endurance exercise soliciting mainly the aerobic energy system. First, the impact of physical and mental exertion on force production capacity is presented, with specific emphasize on the fact that solely physical exertion and not mental exertion induces a decrease in force production capacity of the working muscles. Then, the negative impact of fatigue induced by physical exertion and mental exertion on subsequent endurance performance is highlighted based on experimental data. Perception of effort being identified as the variable altered by both prior physical exertion and mental exertion, future studies should investigate the underlying mechanisms increasing perception of effort overtime and in presence of fatigue during endurance exercise. Perception of effort should be considered not only as marker of exercise intensity, but also as a factor limiting endurance performance. Therefore, using a psychophysiological approach to explain the regulation of endurance performance would allow a better understanding of the interaction between physiological and psychological phenomena known to impact endurance performance.

IF 2.388; International audience; Pyrethroid insecticides are extensively used in agriculture and in household activities. During pregnancy, they might affect maternal metabolic status and there after fetal development. In this work, we studied metabolic and redox effects of low dose alpha-cypermethrin exposure in pregnant rats and their offspring. The diet containing alpha cypermethrin at 0.02 mg/kg/day was consumed during the entire gestation. Plasma biochemical parameters as well as liver lipid and oxidative stress markers were determined. Our results showed that alpha-cypermethrin induced an increase in body weight and in plasma glucose and lipid levels, as well as in plasma aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase activities in pregnant rats and their newborns. Pregnant rats showed cellular oxidative stress and altered oxidant antioxidant status when treated by the insecticide and these disturbances were also seen in their newborns. In conclusion, low dose alpha-cypermethrin exposure induced several metabolic and redox alterations leading to maternal physiological impairments and to fetal metabolic changes. Alpha-cypermethrin should be used with caution especially during pregnancy. (C) 2016 Elsevier Inc. All rights reserved.

En 2013, on estime que 40 à 50% des accidents corporels seraient dus à des défauts d'attention de la part du conducteur. Des études récentes ont mis en évidence la possibilité de détecter des états attentionnels dégradés afin de pouvoir mieux assister le conducteur ; ce thème de recherche représente donc un nouveau gisement de sécurité routière. Cette étude se concentre sur la détection de l'effort cognitif fournit par les conducteurs et cherche, par l'étude de la variation du rythme cardiaque, à identifier un indicateur d'effort sensible sur de courtes fenêtres temporelles.Chacun des 18 participants a passé 8 conditions expérimentales sur simulateur de conduite : la moitié où seule une tâche de comptage était demandée et l'autre moitié en réalisant une tâche supplémentaire de conduite sur simulateur. Il a été demandé aux participants soit d'effectuer la tâche cognitive soit de se relaxer et de ne pas prêter attention aux stimuli présentés (Effort Vs. Relaxation). Afin de réaliser la tâche de comptage, deux types de stimuli auditifs ont été présentés aux participants. Les participants ont effectué les conditions expérimentales dans des ordres partiellement contrebalancés. Le rythme cardiaque et la respiration ont été collectés.Les résultats de différents auteurs ont été répliqués y compris en conduite automobile. Dans les secondes qui suivent un effort cognitif, une légère décélération du rythme cardiaque puis une forte accélération ont été mises en évidence. A l'inverse, en condition de relaxation, une simple décélération cardiaque a été observée. Au terme de notre étude, il s'avère qu'il est possible de distinguer des patterns cardiaques d'effort et de relaxation sur de courtes fenêtre temporelle en observant la variation du rythme cardiaque moyenné sur un nombre conséquent d'épisodes. Toutefois, dans l'objectif de développer des systèmes capables de détecter en temps réel un effort cognitif important, ces dispositifs devront être capables de visualiser l'effort sur un unique évènement. Une piste intéressante consisterait à explorer la faisabilité de la suppression de l'influence de la respiration sur la variation du rythme cardiaque. Si cela s'avère efficace, des assistances pourraient ainsi permettre d'alerter le conducteur ou de pallier ses erreurs lorsque celui-ci ne peut plus assurer la tâche de conduite en raison d'un effort cognitif important.

IF 4.066; International audience

IF 4.066; International audience

IF 4.066; International audience

IF 4.066; International audience

IF 4.066; International audience

IF 4.066; International audience

International audience; The purpose of this study was to test the hypothesis that fat oral-intensity perception may be associated with level of physical activity, food preferences and consumption of fat-rich foods. METHODS: 52 top athletes from different discipline (weightlifting, kayaking, athletics…) of both sexes (27 male, 25 female) underwent anthropometric measurement, assessment of body composition, and completed a 4-day diet record and physical activity diary. In addition, they were screened for oral sensitivity to oleic acid (0.375 mM, 0.75mM, 1.5mM, 3mM, 6mM, 12mM) using triplicate sensory evaluations for each concentration. According to the threshold of fat perception, subjects were allocated to three groups G1 (0.375mM-3mM), G2 (6mM-12mM), G3> (12mM). Further, food habits and behaviors (food habits and behaviors questionnaire) were also established. RESULTS: Male athletes; BMI, 25,3±4,4kg/m², age, 18,88±1,53 years, BF%, 12,52±9,2, TEE, 3763,1±460 kcal . Female athletes; BMI, 24,17±4,54 kg/m², age, 16,11±1,93 years, BF% 21,70±7,4, TEE, 3106±310,05 cal. 85%. (n = 44) of subjects were classified as hyposensitive and nonsensitive (G2, G3). These subjects differed from those who were classified as hypersensitive (G1). Hyposensitive and nonsensitive subjects have a higher training volume, and total energy expenditure. They consumed significantly more energy, fat, saturated fat, fatty foods, , compared to hypersensitive subjects (all P < 0.05). CONCLUSION: An inability to perceive low concentrations of fatty acids in foods was associated with higher training volume and greater consumption of fatty foods. Our results suggest the probability of criminalization of physical activity in the regulation of orosensory fat taste perception and therefore fat intake.

IF 4.066; International audience

International audience

International audience

The neural networks underlying the liking and wanting responses to food odors are modified in bulimia nervosa. 25. Congress of the european chemoreception research organisation (ECRO)

ClC-K2 is present on the basolateral membrane of kidney epithelial cells, but little is known about its single channel properties. Pinelli et al. record unitary ClC-K2 currents from intercalated cells of mouse connecting tubules and investigate their regulation by voltage, pH, Cl−, and Ca2+., ClC-K2, a member of the ClC family of Cl− channels and transporters, forms the major basolateral Cl− conductance in distal nephron epithelial cells and therefore plays a central role in renal Cl− absorption. However, its regulation remains largely unknown because of the fact that recombinant ClC-K2 has not yet been studied at the single-channel level. In the present study, we investigate the effects of voltage, pH, Cl−, and Ca2+ on native ClC-K2 in the basolateral membrane of intercalated cells from the mouse connecting tubule. The ∼10-pS channel shows a steep voltage dependence such that channel activity increases with membrane depolarization. Intracellular pH (pHi) and extracellular pH (pHo) differentially modulate the voltage dependence curve: alkaline pHi flattens the curve by causing an increase in activity at negative voltages, whereas alkaline pHo shifts the curve toward negative voltages. In addition, pHi, pHo, and extracellular Ca2+ strongly increase activity, mainly because of an increase in the number of active channels with a comparatively minor effect on channel open probability. Furthermore, voltage alters both the number of active channels and their open probability, whereas intracellular Cl− has little influence. We propose that changes in the number of active channels correspond to them entering or leaving an inactivated state, whereas modulation of open probability corresponds to common gating by these channels. We suggest that pH, through the combined effects of pHi and pHo on ClC-K2, might be a key regulator of NaCl absorption and Cl−/HCO3− exchange in type B intercalated cells.

International audience; The aim of the study was to determine whether stretching durations influence acute changes of mechanical and neurophysiological properties of plantar flexor muscles. Plantar flexors of 10 active males were stretched in passive conditions on an isokinetic dynamometer. Different durations of static stretching were tested in 5 randomly ordered experimental trials (1, 2, 3, 4 and 10×30-s). Fascicle stiffness index, evoked contractile properties and spinal excitability (Hmax/Mmax) were examined before (PRE), immediately after (POST0) and 5 min after (POST5) stretching. No stretch duration effect was recorded for any variable. Moreover, whatever the stretching duration, stiffness index, peak twitch torque and rate of force development were significantly lower at POST0 and POST5 as compared to PRE (P

International audience; This study compared knee extensors' neuromuscular fatigue in response to two 30-minute stimulation patterns: constant frequency train (CFT) and doublet frequency train (DFT). Fifteen men underwent two separate sessions corresponding to each pattern. Measurements included torque evoked by each contraction and maximal voluntary contractions (MVC) measured before and immediately after the stimulation sessions. In addition, activation level and torque evoked during doublets (Pd) and tetanic contractions at 80-Hz (P80) and 20-Hz (P20) were determined in six subjects. Results indicated greater mean torque during the DFT stimulation session as compared with CFT. But, no difference was obtained between the two stimulation patterns for MVC and evoked torque decreases. Measurements conducted in the subgroup depicted a significant reduction of Pd, P20 and P80. Statistical analyses also revealed bigger P20 immediate reductions after CFT than after DFT. We concluded that DFT could be a useful stimulation pattern to produce and maintain greater force with quite similar fatigue than CFT.

Background: Psychological stress and recovery monitoring is a key issue for increasing athletes' health, well-being, and performance. This multi-study report examined changes and the dose–response relationships between recovery–stress psychological states, training load (TL), heart rate (HR), heart rate recovery (HRR), and heart rate variability (HRV) while providing evidence for the factorial validity of a short French version of the Recovery–Stress Questionnaire for Athletes (RESTQ-36-R-Sport). Methods: Four hundred and seventy-three university athletes (Study 1), 72 full expert swimmers (Study 2), and 11 national to international swimmers (Study 3) participated in the study. Data were analyzed through confirmatory factor analyses (Study 1), repeated ANOVAs and correlational analyses (Study 2), t tests and correlational analyses (Study 3). Results: Multiple-group confirmatory factor analyses showed that the RESTQ-36-R-Sport scores were partially invariant across gender, type of sport, and practice level (Study 1). A dose–response relationship was performed between TL and RESTQ-36-R-Sport scores during an ecological training program (Study 2). Finally, relationships were found between physiological (HRR) and psychological (RESTQ-36-R-Sport) states during an ecological tapering period leading to a national championship (Study 3). Conclusion: As a whole, these findings provided evidence for the usefulness of the short version of the RESTQ-36-R-Sport for regular monitoring to prevent potential maladaptation due to intensive competitive sport practice. Keywords: Adaptation, Confirmatory factor analysis, Heart rate variability, Monitoring, Recovery, Stress

International audience; An attraction for palatable foods rich in lipids is shared by rodents and humans. Over the last decade, the mechanisms responsible for this specific eating behavior have been actively studied, and compelling evidence implicates a taste component in the orosensory detection of dietary lipids [i.e., long-chain fatty acids (LCFA)], in addition to textural, olfactory, and postingestive cues. The interactions between LCFA and specific receptors in taste bud cells (TBC) elicit physiological changes that affect both food intake and digestive functions. After a short overview of the gustatory pathway, this review brings together the key findings consistent with the existence of a sixth taste modality devoted to the perception of lipids. The main steps leading to this new paradigm (i.e., chemoreception of LCFA in TBC, cell signaling cascade, transfer of lipid signals throughout the gustatory nervous pathway, and their physiological consequences) will be critically analyzed. The limitations to this concept will also be discussed in the light of our current knowledge of the sense of taste. Finally, we will analyze the recent literature on obesity-related dysfunctions in the orosensory detection of lipids ("fatty" taste?), in relation to the overconsumption of fat-rich foods and the associated health risks.

International audience; Among the running field tests that measure aerobic fitness indirectly , the 20-m shuttle run test is the one most commonly used among obese youth. However, this back and forth running test induces premature cessation of exercise in this population. The present study aimed to examine the psycho-physiological responses of obese adolescents to an intermittent (15-15) progressive and maximal run test as compared with a continuous shuttle run test. Eleven obese adolescents (age: 14-15 years; BMI = 34.01 ± 5.30 kg • m-2) performed both tests. A two-way ANOVA examined the main effects of the running test, participant's sex, and their interaction on maximal aerobic performance (net exercise duration and final velocity), physiological values (heart rate, pulmonary oxygen uptake, respiratory exchange ratio and blood lactate concentration) and psychological responses (rating of perceived exertion, and physical self-perceptions). Oxygen uptake and heart-rate values at 9 km • h-1 were also compared. Compared with a 20-m shuttle run, the 15-15 test induced lower pulmonary oxygen uptake values at 9 km/h (28.3 ± 2.7 vs. 35.4 ± 2.7 ml • min-1 • kg-1) and finished with higher maximal velocity and net exercise duration (566 ± 156 vs. 346 ± 156 s, p < 0.001), with no inter-test physiological difference. The 15-15 test also resulted in higher ratings of perceived exertion (16.0 ± 1.2 vs. 12.7 ± 1.6, p < 0.001) and improved perceived physical condition compared with the 20-m shuttle run (+1.4 ± 1.4 vs. +0.2 ± 1.0, p < 0.05). Both tests induced a maximal aerobic power of obese adolescents, but the 15-15 test provided a more progressive speed increment and longer exercise duration. The 15-15 test also elicited a significant improvement of perceived physical condition. In conclusion the 15-15 test can be considered a relevant field test for assessing the aerobic fitness of obese adolescents.

IF 4.066; International audience

IF 4.066; International audience

IF 4.066; International audience

International audience; This study examined the changes in the individual contribution of each discipline to the overall performance of Olympic and Ironman distance triathlons among males and females. Between 1989 and 2013, overall performances and their component disciplines (swim, cycle, run) were analyzed from the top 50 overall male and female finishers. Regression analyses determined that for the Olympic distance, the split times in swimming and running decreased over the years (r = 0.25 - 0.43, p < 0.05), while the cycle split and total time remained unchanged (p > 0.05), for both sexes. For the Ironman distance, the cycling and running splits, and total time decreased (r = 0.19 - 0.88, p < 0.05) while swimming time remained stable, for both males and females. The average contribution of the swim stage (∼18%) was smaller than the cycle and run stages (p < 0.05), for both distances and both sexes. Running (∼47%) and then cycling (∼36%) had the greatest contribution to overall performance for the Olympic distance (∼47%), while for the Ironman distance, cycling and running presented similar contributions (∼40%, p > 0.05). Across the years, in the Olympic distance, swimming contribution significantly decreased for females and males (r = 0.51 and 0.68, p < 0.001, respectively), while running increased for males (r = 0.33, p = 0.014). In the Ironman distance, swim and cycle contributions changed in an undulating fashion, being inverse between the two segments, for both sexes (p < 0.01), while running contribution decreased for males only (r = 0.61, p = 0.001). These findings highlight that strategies to improve running performance should be the main focus on the preparation to compete in the Olympic distance. Whereas in the Ironman both cycling and running are decisive and should be well developed.