Tout au long de leur vie, les espèces animales vont transformer de l'énergie apportée par l'alimentation en énergie utilisable par la cellule. Cependant, dans l'environnement naturel, l'accès à la ressource alimentaire est souvent limité et dépendant des conditions climatiques. Cette contrainte oblige les espèces sauvages à mettre en place des compromis d'allocation d'énergie permettant de favoriser la survie, la croissance ou la reproduction. Les espèces aviaires représentent de bons modèles pour étudier les adaptations aux contraintes environnementales puisqu'elles ont colonisé la quasi-totalité du globe et notamment les niches écologiques les plus « extrêmes ». Parmi les oiseaux sauvages vivant en conditions défavorables, notre intérêt s'est porté sur le manchot royal (Adptenodytes patagonicus) et plus particulièrement sur son poussin qui, au cours la 1ère année de vie va subir un jeûne hivernal de 4 à 5 mois au cours duquel les nourrissages sont peu fréquents et aléatoires. Ainsi, cette espèce est naturellement adaptée à des conditions thermiques défavorables pouvant être associées à des phases de jeûne alimentaire. Plusieurs travaux ont montré que malgré l'exposition prolongée au froid, la dépense énergétique diminue au cours des phases de jeûne, permettant ainsi d'économiser les réserves énergétiques et de préserver les protéines nécessaires aux fonctions cellulaires. La forte proportion que représente le muscle squelettique lui confère une part importante de la dépense énergétique. Des études ont montré que malgré son implication dans la thermogenèse, l'activité oxydative (consommation d'oxygène) mitochondriale est diminuée au cours du jeûne hivernal. Cependant, ces travaux ont porté uniquement sur l'étude de la capacité oxydative et non sur le couplage entre les oxydations et les phosphorylations (synthèse d'ATP). Ce couplage représente l'efficacité avec laquelle les mitochondries vont produire de l'énergie (ATP) en consommant de l'oxygène. C'est donc un paramètre important dans la gestion des réserves énergétiques. Mes travaux de thèse ont reposé sur l'hypothèse selon laquelle, la plasticité de l'efficacité mitochondriale du muscle squelettique expliquerait en partie les capacités de survie des oiseaux en conditions défavorables, aussi bien lorsque ces derniers sont exposés à une contrainte thermique importante que lorsqu'ils sont soumis à un jeûne prolongé / Throughout their life, wild species face periods of food-deprivation that induce energy tradeoffs between survival, growth and reproduction. These fasting periods occur either when food availability is lacking due to adverse climatic conditions or because individuals are engaged in biological processes that prevent food access. This later reason is particularly well illustrated in the king penguin (Aptenodytes patagonicus), a sea bird that has to moult and reproduce on shore whereas he feed exclusively at sea. Moreover king penguin chicks exhibit exceptional survival capacities during their first year of life when they experience a long period of fast in winter. Thus, this species that lives in sub-Antarctic latitudes, is exposed to environmental and physiological energy constraints during food shortage periods. Since king penguins are endotherms, they need to maintain their body temperature at high level despite variations of ambient temperature. Thus thermoregulation is one of the most expensive process and skeletal muscles account for the greater part of heat production in birds. Several studies showed that despite long term cold exposure, energy expenditure of fasting birds decreases allowing energy savings and especially protein sparing. Since skeletal muscles have high implications in energy expenditure and heat production the question of their implication in energy saving mechanisms arises. During my PhD project I studied skeletal muscle metabolism through mitochondrial efficiency. These sub-cellular organelles are the last effectors of energy transduction from nutrient into ATP, an usable energy for cells. Our hypothesis is based on the flexibility of mitochondrial efficiency as a regulator of energy sparing mechanisms which would explain long term resistance to starvation. My studies were conducted in a wild species, the king penguin chicks, that are naturally acclimated to cold environment and experienced long term fasting stage. To further investigate mitochondrial plasticity in response to energy constraints, I developed several experimental procedures in controlled conditions on a laboratory model (Muscovy ducklings)

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Physiological cross sectional area (PCSA) is used to compare force-producing capabilities of skeletal muscles. PCSA has been defined as the summation of the cross sectional area of the fiber bundles composing the muscle. As PCSA cannot be measured directly from a specimen, a formula requiring averaged muscle architectural parameters has traditionally been used. The purpose of this study was to develop a finite element method (FEM) to calculate PCSA of extensor carpi radialis longus (ECRL) and brevis (ECRB) directly from digitized fiber bundle data obtained throughout the volume of the muscle and to compare the PCSAs calculated using the FEM and formula methods. Differences were found between the FEM and formula method for both muscles. The FEM provides an approach that takes into account architectural variances while minimizing the need for averaged architectural parameters.

Physiological cross sectional area (PCSA) is used to compare force-producing capabilities of skeletal muscles. PCSA has been defined as the summation of the cross sectional area of the fiber bundles composing the muscle. As PCSA cannot be measured directly from a specimen, a formula requiring averaged muscle architectural parameters has traditionally been used. The purpose of this study was to develop a finite element method (FEM) to calculate PCSA of extensor carpi radialis longus (ECRL) and brevis (ECRB) directly from digitized fiber bundle data obtained throughout the volume of the muscle and to compare the PCSAs calculated using the FEM and formula methods. Differences were found between the FEM and formula method for both muscles. The FEM provides an approach that takes into account architectural variances while minimizing the need for averaged architectural parameters.

No description available.

Understanding and characterising the diffusive transport of capillary oxygen and nutrients in striated muscles is key to assessing angiogenesis and investigating the efficacy of experimental and therapeutic interventions for numerous pathological conditions, such as chronic ischaemia. In articular, the influence of both muscle tissue and microvascular heterogeneities on capillary oxygen supply is poorly understood. The objective of this thesis is to develop mathematical and computational modelling frameworks for the purpose of extending and generalising the current use of histology in estimating the regions of tissue supplied by individual capillaries to facilitate the exploration of functional capillary oxygen supply in striated muscles. In particular, we aim to investigate the balance between local capillary supply of oxygen and oxygen demand in the presence of various anatomical and functional heterogeneities, by capturing tissue details from histological imaging and estimating or predicting regions of capillary supply. Our computational method throughout is based on a finite element framework that captures the anatomical details of tissue cross sections. In Chapter 1 we introduce the problem. In Chapter 2 we develop a theoretical model to describe oxygen transport from capillaries to uniform muscle tissues (e.g. cardiac muscle). Transport is then explored in terms of oxygen levels and capillary supply regions. In Chapter 3 we extend this modelling framework to explore the influence of the surrounding tissue by accounting for the spatial anisotropies of fibre oxygen demand and diffusivity and the heterogeneity in fibre size and shape, as exemplified by mixed muscle tissues (e.g. skeletal muscle). We additionally explore the effects of diffusion through the interstitium, facilitated--diffusion by myoglobin, and Michaelis--Menten kinetics of tissue oxygen consumption. In Chapter 4, a further extension is pursued to account for intracellular heterogeneities in mitochondrial distribution and diffusive parameters. As a demonstration of the potential of the models derived in Chapters 2--4, in Chapter 5 we simulate oxygen transport in myocardial tissue biopsies from rats with either impaired angiogenesis or impaired arteriolar perfusion. Quantitative predictions are made to help explain and support experimental measurements of cardiac performance and metabolism. In the final chapter we summarize the main results and indicate directions for further work.