The effects of sleep restriction on glucose metabolism, the cortisol awakening response and subjective hunger

Sleep restriction is a risky behaviour that can increase chronic disease risk. Sleep restriction can sometimes be volitional; the behaviour of engaging in waking activities instead of sleeping (e.g., late to bed and/or early to rise). Volitional sleep restriction may damage the metabolic system either directly (e.g., sleep restriction causes impaired glucose metabolism or impaired cortisol regulation via the hypothalamic-pituitary-adrenal (HPA) axis) or indirectly (e.g., sleep restriction causes poor food choice leading to weight gain). Thus, sleep restriction may be an independent risk factor for the development of chronic conditions, including type 2 diabetes mellitus—a disease characterised by dysregulation of glucose metabolism. Due to the potential increased disease risk, it is critical to establish how sleep restriction can influence health parameters related to the development of chronic conditions such as diabetes. The broad aims of this thesis were to examine the direct influence of sleep restriction on glucose metabolism (Chapter 3) and the HPA axis (which regulates cortisol secretion and is thus linked to glucose regulation) via the cortisol awakening response (CAR; Chapter 4) and to examine the indirect effects of sleep restriction on subjective hunger (Chapter 5). Over 120 participants were recruited to an experimental, laboratory-based sleep study. Participants’ sleep was manipulated to 5, 6, 7, 8 or 9 hours of time in bed for seven nights. A validation analysis for the use of continuous blood glucose monitoring devices during an oral glucose tolerance test was performed (Chapter 2) to establish the devices as an effective tool to research the effects of sleep restriction on glucose metabolism in healthy individuals. The influence of sleep restriction on glucose metabolism (Chapter 3), the CAR (Chapter 4) and subjective hunger (Chapter 5) were also examined. ii Sleep restriction did not produce an immediate (i.e., after one night) or cumulative (i.e., after multiple nights) effect on glucose concentration during sleep (Chapter 3). Similarly, sleep restriction did not have a significant effect on the CAR (Chapter 4). However, the CAR was slightly higher on the first and final mornings of the study in all conditions. Finally, the most severe level of sleep restriction (five hours per night) caused only a slight increase in desire to consume sweet foods that was evident on the final morning of the sleep restriction period (Chapter 5). The observed effects of sleep restriction on health were minimal. Glucose metabolism and HPA axis activity were stable despite multiple nights of sleep restriction. Possibly, the level of sleep restriction imposed (no less than five hours of time in bed per night for seven nights) was not severe enough to elicit an effect on these parameters. The increased subjective desire to consume sweet foods indicated that subjective hunger may be more sensitive to the effects of sleep restriction than glucose metabolism or the HPA axis. The increased desire for sweet foods could potentially lead to negative health effects (e.g., weight gain) if it translated to increased consumption of sweet foods. The main implications of the findings in this thesis were that young healthy males may be somewhat resistant to some of the potentially deleterious effects of short-term, mild sleep restriction. However, if experiencing even mild sleep restriction, individuals would need to be mindful of not consuming excess calories from sweet foods. Finally, arriving at and leaving the sleep laboratory were both found to be stressors, as participants may have anticipated high-demand days associated with arriving or departing the study (e.g., returning to work or school commitments). Future investigations may determine if other changes in living circumstances, such as returning from holidays, are also a stressor.