Abstract
Sleep is a vital component of health. When sufficient sleep durations are not obtained, health may be negatively affected in numerous ways, including an increased propensity for metabolic disease, cardiovascular disease, decreases in mood and cognitive performance, and reductions in physical performance. With approximately 30% of adults not achieving sufficient sleep durations (7h – 9h), developing and implementing effective strategies to augment sleep is prudent. Therefore, the overall aims of this thesis are to: 1) review the relationship between sleep, circadian biology, skeletal muscle, and metabolic health; 2) investigate how exercise and nutritional interventions interact with subsequent sleep; 3) investigate whether exercise-induced peripheral factors are potential mechanisms for changes in sleep observed after exercise; 4) determine the efficacy of a pre-sleep nutritional intervention for improving sleep outcomes, and next-morning cognitive function or physical performance.
The aim of study one was to review the literature pertaining to the relationship between sleep, circadian biology, and skeletal muscle. From this review, it became clear that insufficient sleep has a negative effect on metabolic health, with adverse effects observed on various cells, tissues, and organs. However, the underpinning mechanisms of these deleterious effects are often complex and not well understood. Additionally, exercise and nutrition emerged as potential strategies that show promise in mitigating some of the negative health consequences resulting from insufficient sleep durations.
The aim of study two was to investigate the effect of afternoon moderate-intensity (70% heart rate maximum) cycling exercise on objective and subjective sleep in healthy adult males. No statistically significant differences were observed in objective or subjective sleep quality or quantity assessed via polysomnography and subjective sleep questionnaires after exercise compared to no exercise. Wide inter-quartile ranges were observed for total sleep time (exercise: 51.50 min vs no exercise: 13.38 min) and sleep efficiency (exercise: 9.53% vs no exercise: 2.45%) which suggest there was more individual variability in subsequent sleep responses after afternoon exercise compared to no exercise. Consequently, healthy adult males can complete afternoon moderate-intensity exercise without compromising their subsequent sleep, but it is important to acknowledge and consider individual responses in sleep outcomes after exercise.
Study three explored components of a novel hypothesis suggesting exercise-induced peripheral factors may be potential mechanisms that explain exercise-induced changes in subsequent sleep. The aims of study three were: 1) to determine the effect of afternoon, moderate-intensity exercise (70% heart rate maximum) on metabolic factors suggested to be associated with sleep, tumour necrosis factor alpha (TNF-), interleukin-1, interleukin-1, interleukin-6 (IL-6), and brain-derived neurotrophic factor (BDNF); and 2) to investigate the relationship between exercise-induced peripheral factors and subsequent sleep in healthy, adult males measured using polysomnography. There was no effect of exercise on BDNF, interleukin-1, and interleukin-1, but a small amount of evidence for exercise increasing IL-6 (posterior probability = 0.650) and TNF- (posterior probability = 0.866). Additionally, there were no clear relationships between TNF-, interleukin-1, interleukin-1, IL-6, and BDNF levels measured at bedtime and sleep. Consequently, our findings do not support components of the proposed hypothesis that exercise-induced peripheral factors explain changes in sleep after exercise.
Study four extended the findings of study two and three by examining the effects of exercise performed in conjunction with a pre-sleep nutritional intervention on sleep. The aim of study four was to determine the effect two different doses of a formulated nutritional intervention, compared against a volume and colour-matched placebo consisting of non-nutritive sweetener, on objective and subjective sleep and next-morning physical performance (measure using a 10-minute maximal effort cycling time trial), cognitive function (measured using the psychomotor vigilance task), and balance (measured using a force plate) in trained adult males. The nutritional interventions consisted of high glycaemic index carbohydrate, whey, tryptophan, theanine, and 5’AMP. No improvements in objective or subjective sleep were observed with either dose of the nutritional intervention. Some aspects of sleep appeared to be affected by the supplement, the low-dose appeared to reduce N3 sleep duration compared to placebo (-13.6 min) and reduce the number of arousals experienced during non-rapid eye movement sleep (-7.6 count). The high-dose intervention appeared to increase N1 sleep duration compared to placebo (+7.4 min). No differences in subjective sleep, physical performance, cognitive function, or postural sway were observed after either dose. Whilst some components of sleep appeared to be negatively influenced by the interventions, the magnitude of changes observed were not likely to cause any meaningful reductions in sleep quality and quantity.
This thesis has contributed new knowledge elucidating the relationship between sleep, exercise, and nutrition. Four main outcomes were identified from this program of research: 1) sleep is consistent when measured using gold-standard techniques in highly controlled environments; 2) individual sleep responses after exercise vary but afternoon exercise does not appear to interrupt sleep; 3) certain peripheral exercise-induced metabolic factors may not be the underlying mechanism for changes in sleep following exercise; and 4) a proprietary nutritional intervention consumed in conjunction with afternoon exercise does not enhance sleep. These findings highlight the importance of considering an individualised approach to developing interventions to augment sleep and health.