Musculoskeletal injuries are commonly associated with muscle atrophy as a function of immobilization or change of normal function. For example, injuries to the anterior cruciate ligament (ACL) which may involve ligament reconstruction, results in the "quadriceps avoidance" gait which leads to atrophy of the knee extensormuscles. In these situations it is not clear whether or not the atrophy is associated with loss of specific muscle fibre types with accompanying functional deficits. Such knowledge would be helpful in implementing exercise regimes designed to compensate for loss of particular fibre types. It is believed that isokinetic exercise performed at speeds below 180° per second strengthens type I muscle fibres, and type II fibres at fast speeds. However, there is no evidence to indicate the specific muscle fibre response to different rates of muscle contraction. Identification of muscle fibre type is most directly determined by biopsy technique but is too invasive for a routine measurement. Electromyography median frequency has been used as a non-invasive measure to infer muscle fibre composition in various studies. However, the reliability and accuracy of this technique has been questioned and improvement is necessary. This research was designed to provide a more accurate and reliable protocol for the determination of EMG median frequency which may be used, after validation against more direct biopsy techniques, as a routine method for inferring muscle fibre composition. The investigation also explored the muscular response as measured by EMG median frequency to varying speeds of muscle contraction, fatiguing exercise and atrophy following ACL reconstruction. The ultimate aim of this research was to improve the reliability of the determination of EMG median frequency to enhance its application as a predictor of muscle fibre composition. This provides information which may improve ACL rehabilitation programs designed to restore and prevent specific muscle fibre types loss that have not previously been targeted by current rehabilitation programs. This research was conducted in three studies. Study one determined the stability of the EMG median frequency bilaterally for the quadriceps and hamstrings muscles and identified the mode of contraction associated with the greatest reliability. The strength and EMG median frequency of the vastus lateralis, medial hamstrings and vastus medialis of 55 subjects was determined across 5 speeds from 0° to 240° per second using a Kin-Com isokinetic dynamometer and an EMG data acquisition system. Isometric contraction was found to have the least bilateral discrepancy (4.01% ±3.06) and between trials standard deviation (4.50) in the vastus lateralis, medial hamstrings and vastus medialis. Study two investigated the EMG median frequency changes in the vastus lateralis which occur immediately following different speeds of isokinetic exercise to the point of fatigue in normal subjects. Thirty-four subjects participated in the study, and performed a 90-second period of isokinetic exercise to activate the knee extensors at either 30° or 300° per second. EMG median frequency of the vastus lateralis was determined before, immediately after and 7 minutes after the fatiguing exercise. The percentage drop in EMG median frequency of the vastus medialis was gnificantly (p<0.05) greater after slow speed (27.9%) than fast speed (20.25%) exercise, while no significant difference was found for the percentage drop in extension torque. Full recovery was found 7 minutes after the fatiguing exercise. By reference to previous research showing a relationship between EMG median frequency and muscle fibre type, an increase in activation of type I muscle fibres with slow speed exercise and an increase in type II muscle fibres with fast speed exercise was observed. Study three identified the changes in EMG median frequency following ACL reconstruction and evaluated the bilateral differences in EMG median frequency of the knee muscles. The relationships between EMG median frequency and the measures of knee functional ability, knee muscle strength, age and time since surgery were also investigated. Twelve subjects who had undergone ACL reconstruction using a semitendinosus and gracilis graft 6 to 12 months earlier, participated in the study. EMG median frequency was determined from an 8-second isometric contraction and knee functional ability was assessed using the Cincinnati Rating Scale. Bilateral EMG median frequency shifts were inconsistent among subjects. On the basis of previous research which indicated a relationship between EMG median frequency and fibre type, no consistent pattern of muscular fibre type atrophy subsequent to ACL reconstruction occurred within 6 to 12 months (ranged from -43 to 57 Hz). Additionally, no significant correlations were found between the EMG median frequency and the knee functional score and knee extension and flexion torques, age, time since operation and the bilateral differences in EMG median frequency. The results of this investigation will serve to improve the reliability of EMG median frequency across a range of conditions in which it has been evaluated. Further research is needed to confirm the relationship between EMG median frequency and direct observations of muscle fibre composition to improve the predictive value of this measure. Following this validation it will be possible to evaluate the bilateral EMG median frequency shift to infer the type of muscle fibre atrophy, and use this measure in determining the efficacy of specific rehabilitation programs. In conclusion * An 8-second isometric contraction is recommended for determining EMG median frequency. * EMG median frequency of a muscle decreases significantly more after slow fatiguing exercise than after fast speed fatiguing exercise. * There was no generalised bilateral EMG median frequency shift found in a group of subjects 6 to 12 months following semitendinosus and gracilis graft ACL reconstruction. * The results of this study will serve to improve the reliability of procedures used to determine EMG median frequency under a range of different contractile conditions. The EMG median frequency changes in response to these conditions require further validations with muscle biopsy in future.

La chair de poisson et de mammifères marins constitue une source importante de protéines et de bons nutriments, tels que le sélénium (Se), la vitamine E et les acides gras polyinsaturés à longues chaînes. Cependant, la chair de ces animaux peut aussi bioaccumuler la forme organique de mercure (Hg), le méthylmercure (MeHg). Ce contaminant a fait l’objet de plusieurs études épidémiologiques, notamment en raison de sa neurotoxicité résultant d’une exposition in utero, étroitement reliée à l’ingestion de poissons fortement contaminés en MeHg. En réponse à ce risque toxicologique, les autorités sanitaires ont émis des lignes directrices quant à la consommation de poissons dans le but de protéger la population. Cependant, ces recommandations présentent certaines limites qui sont liées aux prémisses et aux omissions de l’équation déterministe utilisée pour évaluer l’exposition au MeHg par Santé Canada: (1) elles considèrent que 100% du Hg présent dans la chair de poisson est sous forme de MeHg, (2) elles supposent que le MeHg est distribué de façon homogène à l’intérieur de la chair de poisson, (3) elles prennent pour acquis que 100% du MeHg sera absorbé par le consommateur et (4) par l’utilisation d’une approche déterministe, elles omettent la potentielle incertitude et variabilité intra-populationnelle au niveau des données. L’objectif de cette thèse visait à explorer ces limites, afin de mieux comprendre l’exposition du consommateur au MeHg. Nous avons tout d’abord évalué la distribution du MeHg, du Se (antagoniste du MeHg) et de l’arsenic (As : antagoniste du Se) à l’intérieur de l’appareil musculaire d’un même poisson, en fonction de sa composition en biomolécules (protéines et lipides). Nos résultats démontrent que la présence concomitante de muscles rouges et blancs induit un gradient important de biomolécules à l’intérieur de l’appareil musculaire d’un même individu, provoquant par le fait même une variation moyenne de 2.2 fois quant à la distribution des métal(loide)s, qui se distribuent en fonction de leurs affinités biochimiques. Ces résultats confirment que le MeHg peut se distribuer de façon hétérogène à l’intérieur du muscle de poisson, ce qui pourrait mener à une sous- ou surestimation de l’exposition au MeHg pour le consommateur, en fonction de la partie du poisson qui est consommée. Par la suite, nous nous sommes attardés à l’hypothèse stipulant que 100% du MeHg est absorbé par le consommateur. Une des méthodes utilisées pour estimer la fraction de MeHg qui serait disponible à être absorbée par la paroi intestinale consiste à mesurer la bioaccessibilité, c’est-à-dire la fraction soluble de MeHg, à l’aide d’un modèle de digestion in vitro. Plusieurs études ayant utilisé cette approche observent que la cuisson de la chair de poisson diminue significativement la bioaccessibilité du MeHg, ce qui diminuerait sa potentielle absorption intestinale. Nous avons donc conduit une expérience in vivo en utilisant un modèle porcin et en parallèle, nous avons utilisé un modèle de digestion in vitro. Selon les profils sanguins porcins, la biodisponibilité orale du MeHg provenant de la chair de thon cuite n’est pas moins élevée que celle mesurée avec la chair de thon crue. En contraste, nous avons obtenu une bioaccessibilité de MeHg moins élevée avec la chair de thon cuite. Nos résultats démontrent que les modèles de digestion in vitro actuels ne sont pas suffisamment optimisés pour être utilisés directement dans les calculs d’exposition au MeHg, tels que proposés récemment dans la littérature. Finalement, nous avons testé l’impact d’ajout de variables supplémentaires dans l’équation déterministe actuellement utilisée par Santé Canada pour évaluer l’exposition du consommateur au MeHg, en conduisant une évaluation probabiliste du risque. Notamment, nous avons considéré (1) la proportion de Hg méthylée par rapport à la quantité de Hg, (2) la bioaccessibilité et (3) l’augmentation de la concentration du MeHg suite à la cuisson de la chair de poisson, créée par la perte d’humidité. Nos résultats sont clairs : chaque ajout de variable indépendante augmente ou diminue significativement l’exposition calculée, soulignant la sensibilité de l’équation utilisée pour évaluer l’exposition au MeHg. Ceci suggère que de plus amples recherches devront être conduites avant d’effectuer une quelconque modification dans l’équation de l’exposition au MeHg, par souci de ne pas sous-estimer celle-ci. Cette thèse illustre que les recommandations sont difficilement généralisables puisque la chair de poisson et de mammifères présente des propriétés différentes, en fonction de l’espèce animale considérée. Cette thèse démontre que l’équation déterministe utilisée par Santé Canada dans l’évaluation de l’exposition au MeHg devrait être mieux approfondie par la sphère scientifique, particulièrement dans le cas des mammifères marins. / Fish flesh and marine mammals is an important source of proteins and nutrients, such as selenium (Se), vitamin E and long chain polyunsaturated fatty acids. However, flesh of those animals may bioaccumulate the organic form of mercury (Hg), methylmercury (MeHg). This contaminant has been the subject of various epidemiological studies, namely because of its neurotoxicity through in utero exposure, closely related to highly MeHg contaminated fish consumption. In response to this toxicological risk, health authorities have set fish consumption guidelines in order to protect the population. Still, those guidelines present limits that are related to premises and omissions of the determinist equation used by Health Canada in order to assess the exposure to MeHg: (1) it considers that 100% of Hg in fish flesh is MeHg, (2) it supposes that MeHg is homogeneously distributed within fish flesh, (3) it takes for granted that 100% of MeHg will be absorbed by the consumer and (4) by using a determinist approach, they omit the potential uncertainty and intra-population variability in the data. The aim of this thesis was to address these limits, in order to better understand the exposure of MeHg for consumers. We first assessed the distribution of MeHg, Se (MeHg antagonist) and arsenic (As, Se antagonist) within fish musculature, as a function of its biomolecule composition (proteins and lipids). Our results demonstrated that the concomitant presence of white and red muscle induces a large gradient of protein and lipid within the muscular apparatus of the same individual. This in turn causes on average a variation by 2.2-fold regarding MeHg, Se and As bioaccumulation, which are distributed according to their biochemical affinity. Those results confirmed that MeHg can distribute heterogeneously within fish muscle, which could lead to an under- or overestimation of MeHg exposure for consumers, as function of the part of the fish consumed. Subsequently, we focused on the hypothesis stipulating that 100% of MeHg is absorbed by the consumer. A method used to assess the fraction of MeHg that would be available to be further absorbed by the gut wall consists of measuring the bioaccessibility, i.e. the soluble fraction of MeHg, using an in vitro digestion model. Several studies that assessed the bioaccessibility of cooked fish flesh observed a decreased of MeHg solubility, that would potentially diminish its intestinal absorption. However, those results have not been yet validated in vivo. To that end, we conducted an in vivo experience using the pig model and, in parallel, we used an in vitro digestion model. According to the pig’s blood profile, the oral bioavailability of MeHg from cooked tuna flesh is not less bioavailable than the MeHg from the raw tuna. Contrasting results have been found with the in vitro model, with a decrease of MeHg bioaccessibility observed when fish flesh is cooked. Our results demonstrated that in vitro digestion models are not optimized to be directly used in MeHg exposure calculus as recently proposed in the literature. Finally, we tested the impact of adding variables to the deterministic equation currently used by Health Canada to assess consumer exposure to MeHg, by conducting a probabilistic risk assessment. We considered (1) the proportion of Hg that is MeHg, (2) the MeHg bioaccessibility and (3) the increased of MeHg level after the cooking of fish flesh due to moisture loss. Our results showed that each individual variable significantly increases or decreases the calculated exposure. Thereby, it highlights the sensitivity of the equation used to assess the exposure of MeHg. It strongly suggests that more research is needed to improve Hg exposure calculation to avoid underestimating the potential health risks of MeHg exposure. This thesis presents important results regarding the exposure of MeHg through fish and marine mammals’ consumption. This thesis shows that the recommendations are difficult to generalize since the flesh of fish and mammals has different properties, depending on the animal species considered. The conclusions of this thesis demonstrate that the premises and omissions of the deterministic equation used by Health Canada in the assessment of exposure to Hg should be better investigated by the scientific sphere, especially in the case of marine mammals.