Sleep is well-established to become more superficial and fragmented as we age, with deficits in cognitive processing also commonly observed. While effects have been identified in both humans and mice (used in this thesis), there are important species differences in these findings and importantly, very little is known about the neural dynamics underlying these changes. By integrating several state-of-the-art approaches from putative single unit electrophysiological recordings to behavioural and pharmacological assessments, this thesis aimed to provide novel insights into the neural mechanisms involved in the age-dependent changes in sleep and cognition in mice. Firstly, this thesis investigated the neural activity underpinning the known global sleep changes that occur with ageing. Surprisingly, the majority of neuronal measures quantified in this study were resilient to the effects of ageing. Therefore the global sleep disruptions identified with ageing are unlikely to arise from changes in local cortical activity. Secondly, diazepam injection was found to suppress neural activity, in addition to previously reported effects on electroencephalography (EEG). Subtle differences in the effects of diazepam were identified across age groups, which may account for the variability seen in the efficacy of benzodiazepines in older individuals. Thirdly, ageing and sleep deprivation were found to have only a few effects on performance in a spatial learning task, the Morris water maze (MWM). Suggesting that spatial learning may be fairly resilient to the effects of ageing and sleep deprivation. Finally, this thesis presents preliminary analyses that showed mice were able to perform two novel paradigms of the visual discrimination task, suggesting their suitability in studying the link between ageing, sleep and cognition. Together the studies presented in this thesis provide insights into the differences between global and local mechanisms affected by ageing. Only by understanding local mechanisms will we be able improve on current treatments aimed at helping with the unwanted effects of healthy ageing, such as cognitive decline and sleep disruptions.

A privação do sono é um problema sério nos tempos atuais e pode ter graves conseqüências para a fisiologia humana. De fato, a redução no tempo de sono tem sido associada a um notável aumento na incidência de hipertensão arterial, diabetes mellitus, infarto do miocárdio, acidente vascular cerebral e estresse, porém os mecanismos envolvidos são pobremente compreendidos. Objetivos: Avaliar o impacto da privação parcial do sono na função endotelial venosa e no controle autonômico cardiovascular em homens saudáveis. Métodos: Treze voluntários do sexo masculino, saudáveis e com idade média de 31±2 anos, tiveram o sono monitorado por diário de sono e actigrafia de pulso durante 12 noites consecutivas, nas quais foram divididas em 2 dois períodos. Um período de 5 noites denominado de privação parcial do sono (dormir<5h por noite) e outro de 5 noites denominado de sono controle (dormir>7h por noite). Entre estes períodos, foi interposto por 2 noites de sono irrestrito (com pelo menos de 7 horas de sono por noite). A escolha do período inicial de sono foi randomizada. Ao término de cada período de 5 dias, foi analisada a reatividade vascular venosa (com a técnica da veia do dorso da mão, Dorsal Hand Vein), a sonolência diurna excessiva (através da Escala de Sonolência de Epworth), realizada avaliação hemodinâmica e autonômica (no momento em repouso e mediante o teste de inclinação postural tilt test), exames de sangue e dosagem de norepinefrina plasmática. A freqüência cardíaca e pressão arterial de batimento a batimento na posição supina e com a manobra de \"tilt test\" foi monitorado com intervalo (RR) e variabilidade de pressão arterial. Resultados: Os indivíduos dormiram em média 8.0 h durante o período de sono controle e 4.5 h no período de privação parcial do sono, sendo a diferença significativa entre os mesmos (p<0.01). O período privação de sono não mudou a frequência cardíaca e a pressão arterial basal significativamente, mas promoveu um aumento significante em baixas freqüências cardíacas e variabilidade da pressão arterial, como também na norepinefrina plasmática. O \"tilt test\" promoveu uma queda em PA sistólica depois da privação parcial do sono, que foi significativamente maior depois do período de sono controle (p<0.05). A privação parcial do sono causou uma redução significantiva na venodilatação endotélio-dependente e não mudou venodilatação endotélio-independente. Conclusão: Privação parcial do sono durante só 5 noites já é o suficiente para causar disfunção endotelial venosa, um aumento significantivo na atividade simpática e no prejuízo do controle da pressão arterial / Background: Sleep curtailment is a serious and common problem in western societies and can have significant consequences in the human physiology. In fact epidemiological studies showed that sleep deprivation (reduction in sleeping time) is associated with increased blood pressure, higher incidence of diabetes mellitus, myocardial heart attack, strokes in the brain, and stress, however the mechanisms are poorly understood. Objectives: Evaluate the impact of partial sleep deprivation in the venous endothelial function and the autonomic cardiovascular autonomic control in healthy men. Methods: Thirteen healthy male volunteers (average age: 31±2 years) had their sleep monitored by sleep diary and wrist actigraphy during 12 consecutive nights, these were divided into two periods. The subjects were randomized and crossed over to 5 nights of control sleep (> 7hs) and 5 nights of partial sleep deprivation (<5hs), interposed by 2 nights of unrestricted sleep (at least 7 hours sleep per night). The choice of the initial sleeping period was randomized. At the end of each period of 5 days heart rate and beat-to-beat blood pressure in the supine position and head up tilt test maneuver were monitored with off line determination of RR-interval and blood pressure variability. In addition, serum norepinephrine and venous endothelial functions were measured by dorsal hand vein technique; also we performed the evaluation of excessive day sleepiness (evaluated through the Epworth Sleepiness Scale), hemodynamic and autonomous evaluation (during sleep and through the tilt test). Results: The subjects slept 8.0 and 4.5 hs during control and partial sleep deprivation periods, respectively (p<0.01). Sleep deprivation did not change significantly the resting heart rate and blood pressure but promoted a significant increase in the low frequency bands of heart rate and blood pressure variability as well as serum norepinephrine. Tilt test promoted a significantly greater drop in systolic BP after partial sleep deprivation than after control sleep (p<0.05). Partial sleep deprivation caused a considerable reduction of acetylcholine induced venodilatation (endothelium dependent) and did not change sodium nitroprusside venodilatation (independent from the endothelium). Conclusion: Partial sleep deprivation for only 5 nights is sufficient to cause significant increase in sympathetic activity, impairment of blood pressure control and endothelial dysfunction

Em uma sociedade que lida com pressão diariamente para completar suas tarefas, a privação de sono é uma consequência comum. Como artifício para manter-se apto a trabalhar ou se divertir à noite, algumas pessoas utilizam a cocaína, cujo consumo é estudado há décadas, mas cuja associação com a privação de sono ainda não foi avaliada pela toxicologia. Este estudo utiliza a metabolômica para gerar um mapa de alterações metabólicas associadas a estas condições e sua iteração. Utilizando análise cromatográfica líquida no modo HILIC e espectrometria de massas com um analisador do tipo \"tempo de voo\" (TOF), os cromatogramas e espectros urinários de 60 ratos Wistar machos foram analisados utilizando o pacote XCMS (Bioconductor) na plataforma R. Os tratamentos estatísticos de dados (PCA, OPLS-DA, MANOVA) foram realizados através dos programas SIMCA 11 P+ e IBM SPSS, culminando em atribuições putativas dos metabólitos discriminantes nas condições estudadas (efeito da cocaína, efeito da privação total de sono e seu efeito combinado). Foram então evidenciados cinco marcadores biológicos de dano associados à cocaína, três associados à privação de sono e dois à sua iteração. Estes metabólitos foram identificados putativamente através de busca em banco de dados (Metlin, MassTrix, HMDB, Lipidmaps) e tiveram suas rotas metabólicas associadas através do banco de rotas metabólicas KEGG. Há diferenças metabólicas estatisticamente evidenciáveis e inclusive duradouras nas vias do ciclo da tirosina e do sistema dopaminérgico, além do ciclo do citrato. / In a society that deals daily with pressure to complete its tasks, sleep deprivation is a common consequence. As an excuse to keep oneself fit to work but to have fun at night some people use cocaine, whose consumption is studied for decades, but the association with sleep deprivation had not yet been evaluated by toxicology. This study uses metabolomics to generate a map of metabolic abnormalities associated with these conditions and its iteration. Using liquid chromatographic in HILIC mode and \"time of flight\" mass spectrometry (TOF), mass chromatograms of urine from 60 male Wistar rats were analysed using XCMS package (Bioconductor) running on R platform. Statistical data treatment (PCA, OPLS-DA, MANOVA) were performed using the programs SIMCA P + 11 and IBM SPSS, culminating in putative metabolites assignments that discriminate the conditions in the study (cocaine effect, total sleep deprivation effect and their combined effect). We highlighted five biological markers of damage associated with cocaine, three associated with sleep deprivation and their iteration. These metabolites were putatively identified by public databases (Metlin, MassTrix, HMDB, Lipidmaps) and their associated metabolic pathways were assessed through KEGG database. There are significant differences on metabolic pathways of the tyrosine cycle, the dopaminergic system and the citrate cycle.

Submitted by Jorge Silva (jorgelmsilva@ufrrj.br) on 2016-10-20T18:52:30Z No. of bitstreams: 1 2016 - Joyce Mattos de Oliveira.pdf: 2259979 bytes, checksum: dca983fbb22cab52bfa67209c105ae2f (MD5) / Made available in DSpace on 2016-10-20T18:52:30Z (GMT). No. of bitstreams: 1 2016 - Joyce Mattos de Oliveira.pdf: 2259979 bytes, checksum: dca983fbb22cab52bfa67209c105ae2f (MD5) Previous issue date: 2016-03-31 / CAPES / Modern life has diminished the sleep time for the majority of the population, and the consequences of this reduction have been studied both in humans and animal models. In spite of this, only a few studies elucidate the effect sleep deprivation has on the thyroid function, as well as studies on any role exercise might have in the prevention of such alterations. The objective of this study is to assess the protective effect of the strength exercise on the thyroid function in rats that went through paradoxical sleep deprivation for 24 and 96 hours, as well as a rebound sleep for 24 hours. For this study male and female Wistar rats were used (200-250g), submitted to sleep deprivation using the modified multiple platforms, and the isometric exercise was offered by the inverted box proposed by Lac & Cavalie (1999). The animals were distributed in 6 groups: Control (C, males n=8, females = 13); Trained (T, males n=8; females n=13), Trained, with Sleep Deprivation of the paradoxical sleep for 24 and 96 hours (respectively TPSP24 e TPSP96 males n=10; females n=13); Trained with Sleep Deprivation for 24 and 96 hours, plus a rebound sleep for 24 hours (TPSP24R e TPSP96R males n=10; females n=13). All animals went through and adaptation to the strength exercise for 5 days, enduring 5 series of 30 seconds of strength with rest periods of 25 seconds between each series. After adaptation, an extra weight was added to the animal's tail. All animals were killed on the same day and their blood was collected for analysis of T3 (ng/dL), T4 (ug/dL), e TSH (ng/mL) using the radioimmunoassay technique. Ethics committee approval was granted by number UFRRJ N?003/2015. After the statistical analysis we observed a significant body weight loss, both in females and males, and a relative loss in hypophysis weight in males from group T. On the other hand, the relative weight of the adrenal was reduced in the T group of males, and increased in both the T and TP24 groups of females. In males, seric TSH levels have risen with the exercise, normalizing after the deprivation of 24 and 96 hours, and the rebound in the PS96 group. The PSP was able to induce a raise in the T3 level in the groups TP24 and TP96 in males ? no significant alterations were observed in females. As for the seric T4 in males, there was no alteration, although in females the 24 hours PSP was able to rise those values. This study indicates a protective effect by the isometric exercise, preventing TSH and seric T4 and T3 alterations induced by deprivation of the paradoxical sleep. As such more studies are necessary to clarify the mechanisms involved in such protection / A vida moderna tem diminu?do o tempo de sono da maioria da popula??o e as consequ?ncias dessa redu??o t?m sido estudadas em humanos e modelos animais. J? o papel da tire?ide na priva??o de sono associada com exerc?cios de for?a n?o est? bem estabelecido, pois n?o tem sido estudado. Este estudo, no entanto, tem como objetivo avaliar o efeito protetor do exerc?cio de for?a sobre a fun??o tireoidiana em ratos ap?s a priva??o de sono paradoxal (PSP) por 24 e 96 horas assim como o sono rebote de 24 horas. Para a realiza??o deste trabalho, foram utilizados ratos machos e f?meas Wistar (200-250g) submetidos a priva??o de sono pela metodologia das plataformas m?ltiplas modificadas e o exerc?cio isom?trico foi feito pela metodologia da caixa invertida proposta por Lac & Cavalie (1999). Os animais machos foram distribu?dos em 6 grupos: Controle (C n=8 machos; f?meas, n=13); Treinado (T=8 machos; f?meas, n=13); Treinado com Priva??o de sono paradoxal por 24 horas e 96 horas (TPSP24 e TPSP96 n=10, machos; f?meas, n=13); Treinado com Priva??o de sono paradoxal por 24 horas e 96 horas mais per?odo de sono rebote por 24 horas (TPSP24R e TPSP96R n=10, machos; f?meas, n=13). Os animais foram adaptados ao exerc?cio de for?a por 5 dias, onde era constitu?do por 5 s?ries de 30 segundos de for?a com intervalos de descanso por 25 segundos entre as s?ries. Ap?s a adapta??o, foi adicionado um peso extra na cauda desses animais. Todos os animais foram eutanasiados no mesmo dia, o sangue coletado para an?lise de T3 ng/dL, T4 ?g/dL, e TSH ng/mL pela t?cnica de Radioimunoensaio. Aprova??o pelo comit? de ?tica da UFRRJ N?003/2015. Ap?s an?lise, observamos perda do peso corporal tanto nas f?meas quanto nos machos e uma diminui??o no peso relativo da hip?fise apenas nos machos do grupo T. Por outro lado, o peso relativo da adrenal se manteve reduzido no grupo T dos machos e aumentado no grupo T e TP24 das f?meas. Os n?veis s?ricos de TSH nos machos aumentaram com o exerc?cio nos grupos T, normalizando com a priva??o de 24 horas e retornando ao aumento no grupo TP24R. A PSP foi capaz de provocar um aumento nos n?veis de T3 nos grupos TP24 e TP96 dos machos, e nas f?meas n?o foi observado altera??es significativas. Quanto aos valores de T4 nos machos, n?o foi constatado altera??es significativas e nas f?meas a PSP foi capaz de elevar tais valores. Sugerimos que o exerc?cio de for?a esteja contribuindo para a prote??o dos impactos agressivos causados pela priva??o de sono paradoxal na fisiologia end?crina tanto em machos quanto em f?meas.

Introdução: Embora a relação entre privação de sono e limiar de dor tenha sido estudada em condições patológicas de quadros álgicos agudos e crônicos, os mecanismos envolvidos neste processo ainda carecem de investigações. Nesse contexto, sabe-se que são crescentes as situações nas quais a restrição de sono aguda é induzida por atividades laborais cotidianas, e a compreensão desta relação demanda modelos que permitam observar o efeito em condições em que os estímulos sejam padronizados e controlados. Assim sendo, investigamos o efeito da restrição aguda de sono na função autonômica e sua relação com limiares de dor em indivíduos saudáveis. Objetivos: Avaliar a relação entre respostas autonômicas e percepção a estímulos nociceptivos térmicos e elétricos pós-restrição aguda de sono ocasionada por estresse laboral. Métodos: Foram avaliados 19 estudantes de Medicina saudáveis após noite de sono habitual (SN) e após plantão noturno de 12 horas (RS). Primeiramente examinamos características clínicas dos sujeitos utilizando escalas para avaliação de sono e sintomas psiquiátricos. Foram realizados também testes quantitativos de sensibilidade para sensações térmicas e elétricas e registradas respostas cutâneas simpáticas (RCS) induzidas por estímulo elétrico duplo com diferentes intervalos interestímulos (ISI). Resultados: A média de duração do sono durante as 12 horas de plantão noturno foi de 120+ 28 minutos. Os escores de ansiedade foram maiores na fase RS quando comparados com os da fase SN (p<0,01). Após restrição de sono, houve diminuição no limiar de dor, mas não nos limiares de calor e elétricos. Em relação às respostas autonômicas, foram evidenciadas maiores amplitudes da RCS bem como aumento do número de duplas respostas em ISI 2s na fase RS. Também foi observada moderada correlação inversa entre limiares de dor e amplitudes da RCS (r= -0,45; p<0,01). Não foi encontrada correlação entre escores de ansiedade e parâmetros RCS. No entanto, no modelo de regressão linear multivariada, a percepção do limiar de dor ao estímulo térmico foi significativamente correlacionada com a amplitude da resposta cutânea simpática (β = - 0.55; 95% CI, -0.65 to -0.07), mas não com escores de ansiedade (p>0.05). Conclusões: Os efeitos da restrição aguda de sono no limar de dor são específicos e parecem não estar relacionados com alterações na percepção sensorial geral. Hiperalgesia foi associada com respostas autonômicas anormais, mas não com aumento da ansiedade, sugerindo a existência de uma associação entre o sistema nociceptivo e o autonômico, independente do estado emocional. / Background: Although the relationship between sleep deprivation and pain threshold has been studied in pathological acute and chronic conditions, the mechanisms involved in this process still require investigation. In this context, it is known that there is an increasing of situations where acute sleep restriction is induced by daily working activities and to understand this relationship is necessary models that allow the observation of the effect in situations in which the stimuli are standardized and controlled. Therefore, we investigated the effect of the acute sleep restriction on autonomic function and its relation with pain thresholds in healthy subjects. Objectives: Evaluating the relationship between autonomic responses and perception of thermal and electrical nociceptive stimuli after acute sleep restriction caused by stressful work. Methods: We evaluated 19 healthy medical students after normal night of sleep (NS) and after 12-hour night shift (SR). First we examined clinical characteristics of the subjects using scales for assessment of sleep and psychiatric symptoms. Also, we performed quantitative tests of sensitivity to thermal and electrical sensations and recorded double-electric-induced sudomotor skin responses (SSR) at different inter-stimulus intervals (ISI). Results: The total mean duration of sleep was 120 ± 28 minutes out of 12 hours of night shift. The anxiety scores were higher in SR Phase in comparison with those from NS Phase (p<0.01). After SR, there was a decrease in heat pain, but not in warm neither electrical threshold. Regarding autonomic responses, SR subjects showed higher SSR amplitudes and increased number of double responses at ISI 2s. It was also observed a moderate inverse correlation between heat pain thresholds and SSR amplitude (r = -0.45; P<0.01). However, there was no correlation between anxiety scores and SSR parameters. Indeed, in the multivariate linear regression model, heat pain perception was significantly correlated with SSR amplitudes (β = - 0.55; 95% CI, -0.65 to -0.07), but not with anxiety scores (p>0.05). Conclusions: The effects of SR on pain are specific and seem to be not related to general changes in sensory perception. Hyperalgesia was associated with abnormal autonomic responses, but not with increased anxiety, suggesting an association between the nociceptive and autonomic systems, independent of the emotional state.

Objetivo: Evaluar si existe asociación entre el Síndrome de Desgaste Profesional (SDP) y la mala calidad de sueño (MCS) en médicos que laboran en Instituciones Prestadoras de Servicios de Salud en el Sistema de Salud Peruano (SSP), controlada por variables demográficas, sociales y laborales. Métodos: Realizamos un análisis secundario de datos del Cuestionario 2 de la Encuesta Nacional de Satisfacción de Usuarios en Salud (ENSUSALUD-2016), la cual contó con un muestreo probabilístico, estratificado, bietápico con representatividad nacional. El SDP lo medimos con la versión validada al español del Maslach Burnout Inventory - Human Services Survey, el cual se compone de tres dominios del SDP: Agotamiento Emocional, despersonalización y la falta de realización personal; categorizados en tres niveles de deterioro: alto, moderado y bajo. La MCS fue medida con la versión validad al español del cuestionario de Jenkins. Estimamos Odds Ratio (OR) con IC 95% mediante modelos lineales generalizados, familia binomial link (logit) para muestras complejas. Resultados: Incluimos 2216 médicos, 69,2% fueron varones y la edad promedio fue 45,5 años y de todos ellos, 14,4%, tuvieron agotamiento emocional alto y 16,9% agotamiento emocional moderado. En el caso de la despersonalización, 416 (16,8%) presentaron niveles altos y 337 (16,2%) tuvieron niveles moderados. Mientras que 243 (12,9%) tuvieron falta de realización personal alta y 571(27,1%) moderada. Por otro lado, 269 (10,9%) tuvieron MCS. Encontramos que un agotamiento emocional moderado (ORa1: 5,6; IC95%: 2,1-15,1) y alto (ORa1: 6,6; IC95%: 4,2-10,3) incrementaron la odds de MCS. Asimismo, un alto deterioro en la despersonalización (ORa1: 3,5; IC 95%: 2,0-6,0) se asoció con MCS. En el caso de falta de realización personal, no encontramos evidencia estadística de asociación. Conclusión: Los niveles moderados y altos de agotamiento emocional, así como los niveles altos de despersonalización se asociaron con MCS en médicos que laboran en el SSP. Nuestros hallazgos pueden orientar la toma de decisiones a nivel de recursos humanos en salud. / Objective: To evaluate the association between Burnout Syndrome (BS) and poor sleep quality (PSQ) in physicians working in the Peruvian Health System (PHS) controlled by demographic, social and working variables. Methods: We carried out a secondary analysis of data from questionnaire 2 of the National Survey of Health User Satisfaction (ENSUSALUD-2016), which has a probabilistic, stratified, two-stage sampling with national representativeness. We measured the BS with the validated version in Spanish of Maslach Burnout Inventory - Human Services Survey, which measured three domains of BS: Emotional Exhaustion, depersonalization and the lack of personal achievement; categorized into three deterioration levels: low, moderate and high. The PSQ was measured with the Spanish version of the Jenkins questionnaire. We performed generalized lineal models binomial family link (logit) for complex sampling to estimate Odds Ratio (OR) with 95% CI. Results: We included 2216 doctors, 69.2% were males, and the average age was 45.5 years. Of all of them, 14.4% had high levels of emotional exhaustion. In depersonalization domain, 16.8% had high levels. While 12.9% had high levels of lack of personal achievement. Proportion of doctors with was PSQ was 10.9%. We observed that moderate (ORa1: 5.6, 95% CI: 2.1-15.1) and high (ORa1: 6.6, 95% CI: 4.2-10.3) levels of emotional exhaustion increased the odds of PSQ. Likewise, a high level of depersonalization (ORa1: 3.5, 95% CI: 2.0-6.0) was associated with PSQ. In the case of lack of personal achievement, we did not found statistical evidence of association. Conclusion: Moderate and high levels of emotional exhaustion and high levels of depersonalization were associated with PSQ in doctors working in the PHS. This primary evidence can guide decision-making at the level of human resources in health. / Tesis

Syftet med studien var att undersöka hur individer som arbetar skift upplever att skiftarbetet påverkar dem fysiskt och psykiskt samt hur de upplever att det påverkar deras mattider och matvanor. Metoden som användes var en kvalitativ semistrukturerad intervju. Fyra skiftarbetande informanter deltog i studien, av dessa var tre personer män och en kvinna. Informanterna i studien var 24, 27, 45 samt 45. Intervjuerna spelades in och transkriberades för att sedan analyseras med hjälp av innehållsanalys. Meningsenheter ur det transkriberade materialet valdes ut, kondenserades och kodades. Koderna sammanställdes sedan till kategorier. Resultat som framkom av studien var att informanterna angav att de påverkades både fysiskt och psykiskt av att arbeta skift. De upplevda fysiska symptom som rapporterades till följd av att arbeta skift var trötthet och sömnsvårigheter. De upplevda bakomliggande faktorerna till de fysiska symptomen var svårigheter att koppla av, omställning mellan skift samt intensiteten på arbetet. De upplevda psykiska symptom som rapporterades var trötthet, nedstämdhet och stress. De upplevda bakomliggande faktorerna som informanterna angav till de psykiska symptomen var störd sömnrytm, rädsla för att göra fel i arbetet samt matvanor. Informanterna uppgav att de upplevde att deras mattider och matvanor påverkades av att de arbetar skift. Gällande skiftarbetets påverkan på mattiderna uppgavs problematiska mattider, hungrigare på kvällarna samt sockersug nattetid som påverkansfaktorer. Informanter angav svårigheter att äta nattetid, mättnad, rörligt schema samt sömnbrist som upplevda bakomliggande faktorer. Informanternas upplevelser av hur skiftarbetet påverkar deras matvanor uppgavs att de äter onyttigare kvällstid samt att de äter onyttigare nattetid. De upplevda bakomliggande orsakerna till skiftarbetets påverkan på matvanorna var snabb energipåfyllning samt lathet. Resultaten visade att det finns ohälsosamma effekter av skiftarbete för personer som arbetar skift, vilket motiverar och därför är det en viktig aspekt för folkhälsovetenskap att fortsätta sin ytterligare forskning om riskfaktorer och förebyggande åtgärder. / The aim of this study was to learn about how shift workers experience how the shiftwork affect them both physically and psychologically and to study if they experience that their mealtimes and eating habits are affected by the shift work. The method used was a qualitative semi-structured interview. Content analysis was used to analyze the interviews. The results showed that the informants were affected by working shift both physically and psychologically. Physical symptoms reported were fatigue and insomnia. Reported psychological symptoms were fatigue, stress and low mood. All informants reported that both their mealtimes and eating habits were affected. The results showed that mealtimes were affected by sleep deprivation and variable schedule. The eating habits were reported to be unhealthier when the informants were working evening or night shift. The results showed that there are unhealthy impacts from shiftwork on individuals who are working shift, which motivates further research on risk factors and preventive measures.

Mémoire numérisé par la Division de la gestion de documents et des archives de l'Université de Montréal

Sleepiness contributes to between 20 and 30% of all heavy vehicle accidents throughout the world each year. Professional drivers are particularly susceptible to the effects of sleepiness, due to chronic or acute sleep deprivation, time-on-task effects, driving at circadian low points, and increased daytime sleepiness resulting from sleep disorders. Population surveys of heavy vehicle drivers indicates that a small proportion of drivers use pharmaceutical means in order to help maintain alertness during long-haul trips. Despite the known benefits of amphetamine-type stimulants on reducing fatigue and sleepiness, epidemiological evidence suggests that a large percentage of fatally injured professional drivers test positive to amphetamines. The primary objective of the current thesis was to determine the underlying causes of these sleep- and drug-related accidents. Experimentally, driving performance can be broken down into specific components that can be examined independently. Measures of behavioural disposition provide an indication of the drivers’ mood, ability to determine a change in performance and sleepiness, and whether the driver can make appropriate decisions regarding their ability to drive safely when sleep-deprived. Simulated driving tasks are commonly used to detect driving-related performance in a controlled and safe environment. The task of driving involves a number of components, including attention and vigilance, processing speed and reaction time, visual processes, and executive functioning, which can be measured using neurocognitive tasks. Smaller, pre-conscious neural processes that are undetected by behavioural tasks may also be affected by sleep deprivation, and in turn, affect driving performance. Electrophysiological (eventrelated potentials; ERPs) and neuroimaging (functional magnetic resonance imaging; fMRI) measures can be used to determine the neural underpinnings of visual and auditory processes after sleep deprivation. The aim of this thesis was to determine the effects of one night of sleep deprivation on these driving-related processes in professional drivers. In Experiment 1, nineteen professional drivers underwent two randomised sessions; one session following a normal night of sleep and one session following 24-hours of sleep deprivation. Behavioural disposition, simulated driving performance, neurocognitive measures related to driving, and visual and auditory ERPs were examined in both sessions. Subjective ratings of sleepiness and sleepiness symptoms increased significantly following sleep deprivation. Simulated driving performance and neurocognitive measures of vigilance and reaction time were impaired after sleep deprivation, whereas tasks examining processing speed and executive functioning were less susceptible to sleep deprivation. Event-related potentials of visual and auditory processing indicated that early visual processes were unaffected by sleep deprivation, whereas the amplitude of later cognitive processing was attenuated after sleep deprivation. Driving also involves the ability of the driver to divide his or her attention between different sensory modalities in the driving environment. Experiment 2 presents a functional neuroimaging experiment examining the effect of sleep deprivation on neural activations that occur in response to a cross-modal divided attention task. There was no significant effect of sleep deprivation on behavioural performance. Following sleep deprivation, increased activation was observed in the temporal gyrus, cerebellum and precuneus, compared to activations observed after normal sleep. As no behavioural changes were observed, the results suggest that additional activation may act as a compensatory mechanism. The restorative effect of d-amphetamine on sleep deprivation related impairment was examined in Experiment 3. This pilot study examined eight professional drivers who were past or current users of amphetamine across four, randomised sessions; after normal sleep with oral placebo, after sleep deprivation with oral placebo, after normal sleep with 0.42mg/kg oral d-amphetamine, and after sleep deprivation and 0.42mg/kg oral d-amphetamine. Measures of behavioural disposition appeared to be more affected by d-amphetamine administration after sleep deprivation compared to simulated driving and neurocognitive performance, however these findings need further clarification in a larger sample. The results of the present thesis highlight the detrimental influence of sleep deprivation on a range of driving-related processes. The experienced, professional drivers in this study were able to recognise signs and symptoms of sleepiness, and acted upon these indicators appropriately. Measures of driving-related performance on both simulated driving, and simple neurocognitive tasks were negatively affected by sleep loss, although there is likely to be a discrepancy between on-road and laboratory behaviour. ERP and neuroimaging findings in the present thesis suggest that these sleep-related behavioural effects are caused by small changes in neural processing and neural recruitment. Sleep deprivation can have large implications for safe driving, and this study highlights the importance of promoting and educating the driving public about the dangers of driving when sleepy.

Thesis (Ph. D.)--University of Sydney, 2008. / Title from title screen (viewed Mar. 12, 2008). Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Discipline of Medicine, Faculty of Medicine. Degree awarded 2008; thesis submitted 2007. Includes bibliography. Also issued in print.