WorldCat Identities

Favret, Fabrice

Overview
Works: 13 works in 14 publications in 2 languages and 22 library holdings
Roles: Thesis advisor, Author, Opponent, Other
Publication Timeline
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Most widely held works by Fabrice Favret
Adaptations cérébrales chez un modèle de souris déficientes en érythropoiétine acclimatées à l'hypoxie by Raja El Hasnaoui( Book )

2 editions published in 2008 in French and held by 3 WorldCat member libraries worldwide

L'augmentation de la ventilaton et la polyglobulie sont considérées comme des facteurs majeurs d'acclimatation à l'hypoxie. Cependant des souris transgéniques déficientes en érythropoiètine (Epo-Tagh) survivent en hypoxie chronique de 14 jours à 4200 m, malgré leur anémie sévére, en partie grâce à une hyperventilation normoxique et hypoxique. La question est de savoir quels sont les mécanismes permettant un apport adéquat d'oxygène, en particulier au cerveau. Une augmentations des facteurs centraux impliqués dans le contrôle de la ventilation, du flux cérébral sanguin ainsi qu'une angiogenèse cérébrale pourrait intervenir en normoxie et seraient accentués en hypoxie chronique.Nous avons montré, au cours de nos différents travaux, que l'acclimation ventilatoire à l'hypoxie est médiée par une voie bulbaire faisant intervenir les récepteurs NMDA, la NOS neuronale et le NO qui peut réguler directement la ventilation. Chez les souris anémiques, l'hyperventilation normoxique serait en partie médiée par les récepteurs NMDA bulbaire, mais probablement ausi par les récepteurs à l'Epo et la voie Jak2/STAT-5 favoriseraient les processus de neuroprotection mais aussi d'angiogenèse. En hypoxie chronique, alors que les souris sauvages s'acclimatent grâce à une polyglobulie et une angiogenèse cérébrale, chez les souris Epo-Tagh, en revanche, seuls les métabolites du NO étaient très augmentés, suggérant, soit un flux cérébral sanguin amélioré, soit une cytotoxicité du NO pouvant conduire à des lésions cérébrales. En conclusion, une plasticité cérébrale induite par l'anémie et l'hypoxie chroniques se met en place pour maintenir ou augmenter l'apport en oxygène au cerveau. Par ailleurs, l'exploration ds facteurs moléculaires, biochimiques et morphologiques du tissu cérébral soumis à l'anémie et l'hypoxie s'avère intéressant pour la compréhension de la physiopathologie du déficit d'apporrt en oxygène au cerveau. De plus, la comparaison des résultats dans le cerveau avec les mécanismes d'apport en oxygène vers le coeur mais aussi vers les muscles permettrait d'approfondir les mécanismes d'acclimatation à l'hypoxie en absence d'Epo
Determinants of maximal oxygen uptake in moderate acute hypoxia in endurance athletes by Pascal Mollard( )

1 edition published in 2007 in English and held by 2 WorldCat member libraries worldwide

Fatigue neuromusculaire induite par répétition de sprints : Etiologie et impact de l'hypoxie by Arthur Peyrard( )

1 edition published in 2019 in French and held by 2 WorldCat member libraries worldwide

The ability to repeat short maximal sprints is considered as a good performance index in a variety of intermittent sports (e.g. team or racket sports). This work focused on the neuromuscular fatigue induced by repeated sprint exercise and the impact of hypoxia on its development. In normoxic condition, it is rather established that fatigue mainly originates from the muscle itself (i.e. peripheral) during the early stage of the task whereas central fatigue (i.e. the incapacity of the central nervous system to fully activate the muscles) arise during the latter stage of exercise. When performed under hypoxic condition, central fatigue is exacerbated due to two potential mechanisms. The first one implies a direct brain hypoxic effect that would reduce the brain activity and therefore the motor drive to the exercising muscles. The second one would be through a decrease in oxygen delivery to the muscle, decreasing the energy furnished by the aerobic pathway, increasing the reliance on anaerobic metabolism and leading to the production of more metabolites. Those are known to increase the firing rate of muscle afferents inhibiting the central drive. One of the objectives of this thesis was to isolate those mechanisms thanks to the use of localized muscle hypoxia obtain through blood flow restriction and to determine if exercising in that condition would increase the development of central fatigue. The present results suggest that systemic and localized hypoxia impaired similarly sprint performance but with distinct mechanisms. Systemic hypoxia exacerbates the development of central fatigue through a direct brain hypoxic effect whereas blood flow restriction increased peripheral fatigue due to the accumulation of metabolites. However, the methodology used for this study and classically in the literature involves a delay between the end of the repeated sprint exercise and the fatigue measurement. This is problematic as fatigue is known to recover quickly and at different rates depending on its origin, thus leading to a probable underestimation and misinterpretation of fatigue etiology. Furthermore, it prevents the possibility of having kinetics of fatigue development allowing to determine more precisely the apparition and the evolution of central and peripheral fatigue. Therefore, following the first study, the aim was to propose a new methodological approach to allow several measures of fatigue during the exercise without any delay. This work presents the development and the validation of a new ergometer making possible to assess neuromuscular function during repeated sprint cycling exercise
Skeletal muscle mitochondrial dysfunction precedes right ventricular impairment in experimental pulmonary hypertension by Irina Enache( )

1 edition published in 2012 in English and held by 2 WorldCat member libraries worldwide

Effects of nifedipine-induced pulmonary vasodilatation on cardiac receptors and protein kinase C isoforms in the chronically hypoxic rat by Olivier-Eric Morel( )

1 edition published in 2003 in English and held by 2 WorldCat member libraries worldwide

Adaptations cérébrales chez un modèle de souris déficientes en érythropoiétine acclimatée à l'hypoxie by Raja El Hasnaoui( )

1 edition published in 2008 in French and held by 2 WorldCat member libraries worldwide

Polycythemia and the increase in ventilation are considered as the major factors of acclimatization to hypoxia. However, erythropoietin deficient mice (Epo-TAgh) survive to 14 days at 4200 m despite severe anemia probably through the increase in their ventilation in normoxia as well as in hypoxia. The mechanisms underlying the oxygen delivery, particularly in the brain of thèse mince were questionned in our works. We hypothesized that the factors implied in the central control of the ventilation, in the cerebral blood flow and the cerebral angiogenesis could be increased in normoxia and that they would be overexpressed after chronic hypoxia. We should that ventilatory aclimatization in hypoxia, in control mice is mediated through medullary NMDA receptors and neuronal NOS leading to NO production which could regulate ventilation. In anemic mice, noroxic hyperventilation could be partially mediated through NMDA receptors and probably through Epo receptors, while the mechanisms of their ventilatory acclimatization in hypoxia remained to be determined. In addition, anemic mice in normoxia compensate Epo deficiency by an increase in the cerebral cortical angiogenesis mediated by HIF-1/VEGF signalisation, while Epo receptors and Jak2/STAT-5 pathway could mediate neuroprotection as well as angiogenesis. In chronic hypoxia, wild type mice acclilmatize through polycythemia and cerebral ngiogenesis, while in Epo-TAgh mice, only NO metabolites were greatly increased, suggesting either a higher cerebral blood flow, or NO cytotoxicity which could lead to cerebral lesions. In conclusion, cerebral plasticity occurs following chronic anemia as well as chronic hypoxia to maintain or increase the oxygen delivery. I addition, molecular, biochemical and morphological studies in the anemic and hypoxic brain could be of interest to understand the physiopathology of the lack of oxygen delivery to the brain. Furthermore, the comparison of results obtained in the brain with the mechanims underlying oxygen delivery to the heart but also to the muscles could enhance the knowledge of the mechanisms of acclimatization to hypoxia in the lack of Epo
Modifications du transport de l'oxygène et des récepteurs adrénergiques et muscarines cardiaques au cours de l'acclimatation à l'hypoxie : influence de l'entrainement by Fabrice Favret( Book )

1 edition published in 2001 in French and held by 2 WorldCat member libraries worldwide

L'exposition chronique à l'hypoxie induit une hyperactivité sympathique conduisant à la down-régulation des récepteurs ß[béta]-adrénergiques cardiaques. La densité des récepteurs muscariniques cardiaques est augmentée. Ces modifications du système nerveux autonome antraîne une réduction de la fréquence cardiaque maximale (Fc[max]) après acclimatation, ce qui explique, en partie, que la consommation maximale d'oxygène (Vo[2max]) n'augmente pas après acclimatation malgré la hausse du contenu artériel en oxygène due à la polyglobulie. L'entraînement physique induit une diminution de l'activité sympathique et une augmentation du tonus parsympathyque. Fc, pour un exercice de même intensité, est donc réduite chez les rats entraînés. Parce que l'acclimatation à l'altitude et l'entraînement physique semblent avoir des effets opposés sur l'activité sympathique, nous pensons que l'entraînement physique peut influencer la régulation des récepteurs adrénergiques et muscariniques cardiaques en hypoxie. Ces éventuelles modifications peuvent également jouer un rôle sur le transport de l'oxygène et Vo[2max]. Notre première étude nous a permis nous de montrer l'étroite corrélation entre l'évolution de la Fc[max] et des récepteurs ß-adrégéniques et muscariniques cardiaques au cours du temps d'acclimatation à l'hypoxie. Nous avons donc démontré le rôle important joué par le système nerveux autonome dans la limitation de Vo[2max]. Nous avons ensuite montré que l'entraînement physique permettait d'atténuer l'internalisation des récepteurs ß-adrégéniques cardiaques et de modérer l'hypertrohpie du ventricule droit lors d'une exposition à 2300 mètres. [...]
Cardiac adaptation to high altitude in the plateau pika (Ochotona curzoniae)( )

1 edition published in 2013 in English and held by 1 WorldCat member library worldwide

Etude du rôle de l'Erythropoïétine et des systèmes de neurotransmission dans la mise en place des réponses ventilatoires à l'hypoxie et à l'hypercapnie by Florine Jeton( )

1 edition published in 2016 in French and held by 1 WorldCat member library worldwide

When PO2 and PCO2 are modified, various mechanisms are being established to maintaintissue oxygenation, such as ventilation and metabolism adaptations. In case of hypoxia orhypercapnia stimulation, we observed a ventilatory response, characterized by an increase in minuteventilation. Among the factors involved in the hypoxic response, Epo plays a key role. In addition toits role in erythropoiesis, Epo has other functions, especially in the central nervous system. Thisthesis presents the study of Epo involvement in the ventilatory responses to hypoxia (HVR) andhypercapnia (HcVR).We demonstrate the involvement of NO, glutamate and serotonin in the HVR and in acclimatizationto sustained hypoxia (VAH) in Epo deficient mice (Epo-TAgh) and in an animal adapted to highaltitude, the plateau Pika. Then we studied the impact of Epo-deficiency on HcVR and confirmed thatEpo is not mandatory to obtained HcVR but we demonstrate that Epo can modulate the ventilatorypattern and central nervous system structures involvement in this response. During this study, wealso demonstrate that in female mice, estrous cycle is not involved in HVR or HcVR but it seems thatthere is an interaction between Epo and female sexual hormones in these responses. Finally, someexperiments in collaboration with different countries (Chile, Canada) allowed us to study the effectsof Epo on peripheral and central chemoreceptors during HVR and HcVR.In fine, these experiments allows us to specify the factors involved in ventilatory responses tohypoxia and hypercapnia, which could be helpful to better understand respiratory pathologies suchas anemia or pathologies associated with high altitude
Effets de l'entraînement à haute intensité associé au renforcement musculaire sur les capacités physiques et la qualité de vie chez les patients atteints de sclérose en plaques by Pierre Zaenker( )

1 edition published in 2017 in French and held by 1 WorldCat member library worldwide

After being contraindicated, physical activity take an increasingly important place in the management of multiple sclerosis (MS). The training at mild to moderate intensity is widely documented, contrary to the high intensity training. This work has focused on the effects of high intensity interval training combined with resistance training during 12 weeks in 26 MS patients. Our results show that peak oxygen consumption, maximum tolerated power, isokinetic muscle strength in both quadriceps and hamstrings and quality of life are improved. Women show more important and more numerous improvements than men, however, the disability level does not seem to limit improvements. Our work has demonstrated that high intensity interval training combined with resistance training is well tolerated and allows physical capacities and quality of life improvements
Optimisation de la performance en trail : étude des réponses cardiorespiratoires et des facteurs de la performance en course en montée vs descente by Marcel Lemire( )

1 edition published in 2019 in French and held by 1 WorldCat member library worldwide

It is admitted that uphill running mostly elicits concentric muscle actions whereas downhill running requires braking muscle actions inducing preferentially eccentric muscle action. Consequently, high running speed can be achieved in downhill (i.e., a high level of mechanical stress), despite low metabolic demands (i.e., low metabolic power). Using 3 experimental studies, this doctoral thesis explores the specific physiology of downhill vs uphill running as well as its physiological determinants. Our first study shows lower magnitude of the cardiorespiratory responses, a more superficial ventilation pattern and inverse V̇O2 and HR slow components in submaximal constant and same downhill vs uphill running velocity (8,5 km·h-1, 15% slope). During maximal incremental downhill vs uphill and level running, our study 2 part A demonstrates that well-trained endurance athletes, accustomed to downhill running, can reach maximal heart rate but not V̇O2max in downhill running. When downhill and uphill running are performed at similar metabolic demand (70% V̇O2max), our study 2 part B demonstrates that downhill running (19 km·h-1, -15% slope) elicits greater cardiorespiratory responses (HR and V̇E), a significant V̇O2 slow component and exacerbates muscle fatigue compared to uphill running (6 km·h-1, +15% slope). Finally, a field study (study 3) shows that 5-km downhill vs uphill running performances share some physiological predictors (V̇O2max, lower limb muscle strength) although in different proportions. In addition, this study also demonstrates that both time-trial performances are also determined by specific physiological predictors (i.e., musculotendinous stiffness for downhill and body mass index for uphill running). All in all, our results further our understanding of the specific physiology of downhill vs uphill running and open the way to training applications in trail runners with the ultimate goal to optimize trail running performance
Catalyzing role of erythropoietin on the nitric oxide central pathway during the ventilatory responses to hypoxia( )

1 edition published in 2014 in English and held by 1 WorldCat member library worldwide

Abstract The N-Methyl-d-Aspartate (NMDA) receptors - neuronal nitric oxide synthase (nNOS) pathway is involved in the ventilatory response to hypoxia. The objective was to assess the possible effect of erythropoietin deficiency and chronic exposure to hypoxia on this pathway during ventilatory response to acute hypoxia. Wild-type (WT) and erythropoietin-deficient (Epo-TAgh) male mice were exposed (14days) either to hypobaric hypoxia (Pb=435mmHg) or to normoxia. The ventilation was measured at 21% or 8% O2 after injection of vehicle (NaCl), nNOS inhibitor (SMTC) or NMDA receptor antagonist (MK-801). Nitric oxide production and the expression of NMDA receptor and nNOS were assessed by real-time RT-PCR and Western blot analyses in the medulla. At rest, Epo-TAgh mice displayed normal ventilatory parameters at 21% O2 but did not respond to acute hypoxia despite a larger expression of NMDA receptors and nNOS in the medulla. Ventilatory acclimatization to hypoxia was observed in WT but was absent in Epo-TAgh mice. nNOS inhibition blunted the hypoxic ventilatory acclimatization of WT mice without any effect in Epo-TAgh mice. Acute hypoxic ventilatory response (HVR) was increased after chronic hypoxia in WT but remained unchanged in Epo-TAgh mice. Ventilatory response to acute hypoxia was modified by MK-801 injection in WT and Epo-TAgh mice. The results confirm that adequate erythropoietin level is necessary to obtain an appropriate HVR and a significant ventilatory acclimatization to hypoxia. Furthermore, erythropoietin plays a potential catalyzing role in the NMDA-NO central pathway during the ventilatory response and acclimatization to hypoxia
 
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