The purpose of this investigation was to examine the acute hormonal response to a bout of kettlebell swing exercise. Ten healthy men (19-30 y, 23.6 ± 3.5 y, 174.6 ± 5.7 cm, 78.7 ± 9.9 kg) who were engaged in resistance training at least twice per week but were inexperienced with kettlebell swings participated in this study. Participants were familiarized with the kettlebell swing exercise during an initial visit. During the subsequent experimental protocol visit, participants performed 12 rounds of 30 seconds of 16-kg kettlebell swings alternated with 30 seconds of rest. Heart rate (HR) and rating of perceived exertion (RPE) were measured at the end of every round of swings. Fasted blood samples were collected pre-exercise (PRE), immediately post (IP), 15 minutes post (P15), and 30 minutes post exercise (P30) and analyzed for total testosterone (T), growth hormone (GH), cortisol, and lactate concentrations. Participants completed a total of 227 ± 23 swings (average swings per round: 19 ± 2). HR and RPE increased significantly (P < 0.05) throughout the exercise protocol. Lactate concentrations were significantly increased at all post exercise time points compared to PRE. T was significantly increased at IP compared to PRE. GH was significantly increased at IP, P15, and P30 compared to PRE. Cortisol was significantly increased at IP and P15 compared to PRE. 12 rounds of 30 seconds of kettlebell swing exercise induced an acute increase in T, GH, and cortisol concentrations in resistance trained men. Additionally, this exercise protocol induced a large increase in HR and lactate concentration. Thus, the kettlebell swing exercise might provide an effective method for simultaneous endurance and resistance training.

Puberty is a critical period of development that is characterized by significant remodeling and reorganization of neuronal connections. Additionally, this period is marked by the transition to a fertile state and the development of secondary sex characteristics driven by a surge in gonadal steroid hormones. Puberty is also vulnerable to stress exposure, as pubertal stress during this period results in negative enduring changes to the brain and behavior. Treatment with the bacterial endotoxin lipopolysaccharide (LPS) results in enduring dysfunction of the hypothalamic-pituitary-gonadal (HPG) axis in male and female mice. However, the mechanism underlying this dysfunction was unclear. Thus, this thesis was designed to investigate possible mechanisms through which pubertal stress could alter HPG axis functioning. This work first examined the acute effects of LPS treatment on various components of the HPG axis, such as kisspeptin (Kiss1) and kisspeptin receptor (Kiss1R) expressions in the brain, and luteinizing (LH) and follicle stimulating hormone (FSH) concentrations in the blood (Study 1). The next study examined the enduring effects of LPS treatment on inflammation as well as on Kiss1 and Kiss1R expressions in the brain, and LH and FSH concentrations in the blood (Study 2). The findings showed that Kiss1 and Kiss1R were downregulated in an acute and enduring manner following LPS treatment and are likely responsible for HPG axis downregulation. The final study amalgamates the novel discoveries of the previous findings and hypothesizes that pharmaceutical Kiss1 treatment will prevent adult sexual behavior dysfunction after pubertal LPS treatment. Findings from this study will inform us whether the enduring HPG axis downregulation following pubertal LPS treatment is reversible in adulthood and could provide a viable prospective intervention for fertility complications across species.

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Tableau d'honneur de la Faculté des études supérieures et postdoctorales, 2006-2007 / Les agents antipsychotiques sont, depuis plus de 50 ans, les médicaments utilisés pour traiter les symptômes reliés à la schizophrénie. Malheureusement, ces drogues sont reconnues pour provoquer des effets secondaires divers importants et ont une efficacité mitigée. Même si ces médicaments font l'objet d'études intensives depuis plusieurs années, les mécanismes cellulaires et moléculaires impliqués dans les effets thérapeutiques et la production d'effets secondaires indésirables sont encore mal connus. Récemment, un facteur de transcription membre de la grande famille des récepteurs nucléaires, nommé Nur77, a été identifié comme un candidat potentiellement impliqué à la fois dans les effets antipsychotiques ainsi que dans la production des effets secondaires. Cette hypothèse provient principalement de trois prémices : 1) les agents antipsychotiques induisent fortement Nur77 dans des structures cérébrales associées à l'effet antipsychotique et aux effets secondaires, 2) certains effets indésirables des antipsychotiques (e.g catalepsie) sont altérés dans les souris déficientes en Nur77 et 3) les souris déficientes en Nur77 montrent des signes suggérant une atteinte des voies cérébrales associées au développement des psychoses. À ce jour, les cascades signalétiques qui mènent à l'induction de Nur77 suite à un traitement aux antipsychotiques sont encore inexplorées. Le but de cette étude est de 1) caractériser le patron d'induction de Nur77, Nor-1 et Nurrl (récepteurs nucléaires de la famille des Nurs) suite à un traitement aux antipsychotiques typiques et atypiques et 2) identifier les sous-types de récepteurs membranaires impliqués dans l'induction de Nur77 après un traitement aux antipsychotiques. Nos travaux indiquent d'une part que les antipsychotiques typiques et atypiques modulent différemment l'expression de Nur77 dépendamment de leur affinité pour les récepteurs D2 et 5-HT2A- D'autre part, l'induction de Nur77 par les antipsychotiques semble être dépendante des récepteurs NMDA indiquant que cette induction pourrait être indirecte et ne se ferait pas par l'intermédiaire des récepteurs D2 post-synaptiques des neurones épineux moyens. Une meilleure compréhension de l'implication des Nurs dans les effets des antipsychotiques est indispensable pour éclaircir le mécanisme d'action encore inexploré de ces drogues. La caractérisation des voies signalétiques menant à l'induction de Nur77 pourrait éventuellement mener à la découverte de meilleures cibles pharmacologiques pour traiter les symptômes de la schizophrénie et améliorer la qualité de vie des patients schizophrènes. / Antipsychotic drugs have been extensively used in the treatment of schizophrenia symptoms. Unfortunately, these drugs are known to produce important side effects and their clinical efficacy is still a matter of debate. Recently, a transcription factor member of the nuclear receptors superfamily, namely Nur77, has been implicated in antipsychotic drugs action. To this day, intracellular signaling events that lead to Nur77 induction after antipsychotic drugs administration are still unexplored. The aim of the present study is to understand the implication of Nurs (Nurrl, Nur77 and Nor-1) in the action of antipsychotic drugs and to characterize signaling pathways involved in the induction of Nur77 following treatment with antipsychotic drugs. A better understanding of the molecular and cellular events leading to Nur77 induction after antipsychotic drug treatment might shed light on new pharmacological targets to treat schizophrenia symptoms.