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Current recruitment and retention issues within the armed forces draw links with breach of the psychological contract – the dynamics of the employee–employer relationship. Compared with civilian contexts, a military position is unique, however, there is a dearth of conceptual investigation regarding the lived experiences of military personnel, particularly with respect to how such contracts form. This paper combined a phenomenological approach with the critical decision method to investigate the lived experiences informing contract formation and contract trajectory of ex-military personnel. Lived experiences pointed to the formulation of ‘fuzzy’ contracts, impressions from defence force recruitment, specific tipping points around organisational commitment, and large differences between the fidelity of the idealised and actualised self/job. Seven superordinate themes are elicited that trace the formation and trajectory of the contract. A schematised account of findings is developed to provide avenues to investigate how beliefs form in a military contract context and their outcomes.

Objectives: This study examines the impacts of peak summer demand on operator workload and fatigue in a maritime environment. Methods: Participants (n = 12) were senior shipboard personnel who were working during the summer “double sailing” period for a roll-on roll-off ferry service. Wrist actigraphy was used to determine sleep opportunity and sleep duration, as well as prior sleep, total wake time, performance and alertness at the beginning and end of work periods. Results: Contrary to expectations, sleep was significantly greater, and both subjective estimates of fatigue and objective neurobehavioral performance were not impacted negatively by periods of increased work intensity. Conclusions: This study highlights a number of features of a fatigue-risk management system that appear to have been instrumental in ensuring adequate sleep and performance was maintained throughout periods of increased operational intensity. As a simple colloquial description of the fatigue-risk management system at play in this operation, it was fine to “work hard” if you were able to “sleep hard” as well. Refereed/Peer-reviewed

This study investigates the effect of passenger and phone conversations on sleep-restricted driving. Six volunteers (50% male, mean age 24.8 +/- 4.3years) had their sleep restricted to 4h in bed followed by a 20-min simulated drive on three separate occasions. Each drive included either a passenger conversation, a mobile phone conversation or a quiet passenger. The effect size of a phone conversation on lane deviation was large while passenger conversation was small. The main effect of conversation on lane deviation was non-significant (F(2,10)=2.57, p=0.126). Combining sleep-restricted driving with conversations warrants further investigation. Refereed/Peer-reviewed

Around a fifth of all road accidents can be attributed to fatigued drivers. Previous studies indicate that driving performance is influenced by time of day and decreases with sustained wakefulness. However, these influences occur naturally in unison, confounding their effects. Typically, when people drive at a poor time of day and with extended wake, their sleep is also restricted. Hence, the aim of the current study was to determine the independent effects of prior wake and time of day on driving performance under conditions of sleep restriction. The driving performance of fourteen male participants (21.8 ± 3.8 years, mean ±SD) was assessed during a 10 min simulated driving task with speed/lane mean, variability and violations (speeding and crashes) measured. Participants were tested at 2.5 h intervals after waking, across 7 × 28 h days with a sleep:wake ratio of 1:5. By forced desynchrony each driving session occurred at 9 doses of prior wake and within 6 divisions of the circadian cycle based on core body temperature. A mixed models ANOVA revealed significant main effects of circadian phase, prior wake and sleep debt on lane violations. In addition, three significant two-way interactions (circadian phase × prior wake, prior wake × sleep debt, sleep debt × circadian phase) and one three-way interaction (circadian × prior wake × sleep debt) were identified. The presence of the large interaction effects shows that the influence of each factor is largely dependent on the magnitude of the other factors. For example, the presence of the time of day influence on driving performance is dependent on the length of prior wake or the presence of sleep debt. The findings suggest that people are able to undertake a low-difficulty simulated drive safely, at least for a short period, during their circadian nadir provided that they have had sufficient sleep and have not been awake too long. Refereed/Peer-reviewed

Conclusions: The performance consequence of sleep restriction in our study was prominent during the biological night, even when the prior wake duration was short, and this performance consequence was in forms of waking state instability. This result is likely due to acute homeostatic sleep pressure remaining high despite the sleep episode. Study Objectives: The homeostatic-circadian regulation of neurobehavioral functioning is not well understood in that the role of sleep dose in relation to prior wake and circadian phase remains largely unexplored. The aim of the present study was to examine the neurobehavioral impact of sleep dose at different combinations of prior wake and circadian phase. Design: A between-participant design involving 2 forced desynchrony protocols varying in sleep dose. Both protocols comprised 7 repetitions of a 28-h sleep/wake cycle. The sleep dose in a standard protocol was 9.33 h per 28-h day and 4.67 h in a sleep-restricted protocol. Setting: A time-isolation laboratory at the Centre for Sleep Research, the University of South Australia. Participants: A total of 27 young healthy males participated in the study with 13 in the standard protocol (age 22.5+- 2.2 y) and 14 in the sleep-restricted protocol (age 21.8 +-3.8 y). Interventions: Wake periods during both protocols were approximately 4 h delayed each 28-h day relative to the circadian system, allowing performance testing at different combinations of prior wake and circadian phase. The manipulation in sleep dose between the 2 protocols, therefore, allowed the impact of sleep dose on neurobehavioral performance to be examined at various combinations of prior wake and circadian phase. Measurements and Results: Neurobehavioral function was assessed using the psychomotor vigilance task (PVT). There was a sleep dose x circadian phase interaction effect on PVT performance such that sleep restriction resulted in slower and more variable response times, predominantly during the biological night. This interaction was not altered by prior wakefulness, as indicated by a nonsignificant sleep dose x circadian phase x prior wake interaction. Refereed/Peer-reviewed

Study Objectives: The state instability hypothesis posits that increasing sleep drive brings about escalating state instability in attention, making neurobehavioral performance increasingly variable. This hypothesis predicts that performance variability is a function of prior wake, circadian phase, and time on task. These predictions have been supported when wakefulness is beyond the habitual wake period. Our study aimed to test these predictions within the habitual wake period. Design: A 12-calendar-day 28-h forced desynchrony protocol consisting of 7 repetitions of a 28-h sleep/wake cycle, with two-thirds time awake and one-third time in bed. Each wake period included 7 equally spaced 1-h testing sessions. Setting: A time-isolation sleep laboratory. Participants: Thirteen young healthy males. Interventions: Wake periods during the protocol were 4 h delayed each 28-h "day" relative to the circadian system, such that they were distributed across the whole circadian cycle. This allowed performance testing at different combinations of prior wake of a habitual length (i.e., < 18 h) and circadian phase. Measurements and Results: Performance variability was indexed by standard deviation of response times within a 10-min psychomotor vigilance task. We found that response times became more variable with increasing wakefulness and towards circadian nadir, i.e., when sleep drive was increasing. These changes in response time variability were however not dependent on time on task, which is likely due to the modest level of sleep drive in our study. Conclusions: The state instability hypothesis, as an explanation for the responsiveness of neurobehavioral performance to increasing sleep drive, is supported during the habitual wake period. Refereed/Peer-reviewed

Shiftworkers are often required to sleep at inappropriate phases of their circadian timekeeping system, with implications for the dynamics of ultradian sleep stages. The independent effects of these changes on cognitive throughput performance are not well understood. This is because the effects of sleep on performance are usually confounded with circadian factors that cannot be controlled under normal day/night conditions. The aim of this study was to assess the contribution of prior wake, core body temperature, and sleep stages to cognitive throughput performance under conditions of forced desynchrony (FD). A total of 11 healthy young adult males resided in a sleep laboratory in which day/night zeitgebers were eliminated and ambient room temperature, lighting levels, and behavior were controlled. The protocol included 2 training days, a baseline day, and 7 × 28-h FD periods. Each FD period consisted of an 18.7-h wake period followed by a 9.3-h rest period. Sleep was assessed using standard polysomnography. Core body temperature and physical activity were assessed continuously in 1-min epochs. Cognitive throughput was measured by a 5-min serial addition and subtraction (SAS) task and a 90-s digit symbol substitution (DSS) task. These were administered in test sessions scheduled every 2.5 h across the wake periods of each FD period. On average, sleep periods had a mean (± standard deviation) duration of 8.5 (±1.2) h in which participants obtained 7.6 (±1.4) h of total sleep time. This included 4.2 (±1.2) h of stage 1 and stage 2 sleep (S1-S2 sleep), 1.6 (±0.6) h of slow-wave sleep (SWS), and 1.8 (±0.6) h of rapid eye movement (REM) sleep. A mixed-model analysis with five covariates indicated significant fixed effects on cognitive throughput for circadian phase, prior wake time, and amount of REM sleep. Significant effects for S1-S2 sleep and SWS were not found. The results demonstrate that variations in core body temperature, time awake, and amount of REM sleep are associated with changes in cognitive throughput performance. The absence of significant effect for SWS may be attributable to the truncated range of sleep period durations sampled in this study. However, because the mean and variance for SWS were similar to REM sleep, these results suggest that cognitive throughput may be more sensitive to variations in REM sleep than SWS. Read More: http://informahealthcare.com/doi/abs/10.3109/07420528.2010.488621 Refereed/Peer-reviewed

Neurobehavioral function deteriorates with increasing homeostatic sleep pressure during wakefulness. It has been claimed that some individuals exhibit a quicker rate of such deterioration than others, thus being more vulnerable than others to the detrimental impact of increasing homeostatic sleep pressure. Evidence supporting the claim, however, has been limited by methodological issues. To overcome these limitations, the current study used a 12-calendar-day, 28-h forced desynchrony (FD) protocol (sleep:wake period = 1:2) to study individual differences in the rate of change in neurobehavioral performance with increasing homeostatic sleep pressure. Neurobehavioral performance was assessed with a psychomotor vigilance task and a serial addition subtraction task. A significant performance decline on both tasks was revealed within as short as 17 h of wakefulness. The rates of decline of individual performance trajectories were, however, not different from the group average rate. This suggests that individuals are not differentially vulnerable to the detrimental impact of increasing homeostatic sleep pressure.