This mini-review focuses on the effects of exercise on sleep. In its early days, sleep research largely focused on central nervous system (CNS) physiology using standardized tabulations of several sleep-specific landmark electroencephalogram (EEG) waveforms. Though coarse, this method has enabled the observation and inspection of numerous uninterrupted sleep phenomena. The research on the effects of exercise on sleep began, in the 1960s, with a focus primarily on sleep related EEG changes (CNS sleep). Those early studies found only small effects of exercise on sleep. However, more recent sleep research has explored not only CNS functioning, but somatic physiology as well. Sleep should be affected by daytime exercise, as physical activity alters endocrine, autonomic nervous system (ANS), and somatic functions. Since endocrinological, metabolic, and autonomic changes can be measured during sleep, it should be possible to assess exercise effects on somatic physiology in addition to CNS sleep quality, evaluated by standard polysomnographic (PSG) techniques. Additional measures of somatic physiology have provided enough evidences to conclude that the auto-regulatory, global regulation of sleep is not the exclusive domain of the CNS, but it is heavily influenced by inputs from the rest of the body.

Recently, several new materials for mattresses have been introduced. Although some of these, such as low rebound (pressure-absorbing/memory foam) and high rebound mattresses have fairly different characteristics, effects of these mattresses on sleep have never been scientifically evaluated. In the current study, we have evaluated effects of a high rebound mattress topper [HR] on sleep and its associated physiology, and the effects were compared to those of a low rebound mattress toppers (LR) in healthy young (n = 10) and old (n = 20) adult males with a randomized, single-blind, cross over design. We found that sleeping with HR compared to LR induced a larger decline in core body temperature (CBT) in the initial phase of nocturnal sleep both in young (minimum CBT: 36.05 vs 36.35°C) and old (minimum CBT: 36.47 vs. 36.55°C) subjects, and declines in the CBT were associated with increases in deep sleep/delta power (+27.8% in young and +24.7% in old subjects between 11:00–01:00). We also found significantly smaller muscle activities during roll over motions with HR (-53.0 to -66.1%, depending on the muscle) during a separate daytime testing. These results suggest that sleeping with HR in comparison to with LR, may facilitate restorative sleep at the initial phase of sleep.

The effects of exercise on sleep have been explored from various perspectives, but little is known about how the effects of acute exercise on sleep are produced through physiological functions. We used a protocol of multiple daytime sessions of moderate-intensity aerobic exercise and examined the subsequent effects on sleep structure, core body temperature (CBT), distal-proximal skin temperature gradient (DPG), and subjective parameters. Fourteen healthy men who did not exercise regularly were evaluated under the baseline (no exercise) and exercise conditions on a within-subject crossover basis. Under the exercise condition, each participant performed a 40-min aerobic workout at 40% of maximal oxygen intake, four times between morning and early evening. We observed a 33% increase in slow-wave sleep (SWS; P = 0.005), as well as increases in slow-wave activity (SWA; P = 0.026), the fast-sigma power/SWA ratio ( P = 0.005), and subjective sleep depth and restorativeness the following morning. Moreover, both CBT and the DPG increased during sleep after exercise ( P = 0.021 and P = 0.047, respectively). Regression analysis identified an increased nocturnal DPG during sleep after exercise as a factor in the increase in SWA. The fast-sigma/SWA ratio correlated with CBT. The performance of acute exercise promotes SWS with nocturnal elevation in the DPG. Both CBT and fast-sigma power may play a role in the specific physiological status of the body after exercise. NEW & NOTEWORTHY We used multiple daytime sessions of moderate-intensity aerobic exercise to examine the effects on the sleep structure, core body temperature (CBT), distal-proximal skin temperature gradient (DPG), and subjective parameters. Significant increases in slow-wave activity (SWA), CBT, DPG, fast-sigma power, and subjective parameters were observed during the night and the following morning. Nocturnal DPG is a factor in the increased SWA.

This review focuses on the effects of exercise on sleep. In its early days, sleep research largely focused on central nervous system (CNS) physiology using standardized tabulations of several sleep-specific landmark electroencephalogram (EEG) waveforms. This method has enabled the observation and inspection of numerous uninterrupted sleep phenomena. Research on the effects of exercise on sleep began, in the 1960's, with a focus primarily on sleep related EEG changes (CNS sleep). Those early studies only found small effects of exercise on sleep. However, more recent sleep research has explored not only CNS functioning, but somatic physiology as well. Sleep should be affected by daytime exercise, as physical activity alters circadian pacemaker, endocrine, autonomic nervous system (ANS) and other somatic functions. Since endocrinological, metabolic and autonomic changes can be measured during sleep, it should be possible to assess exercise effects on somatic physiology in addition to CNS sleep quality, evaluated by standard polysomnographic (PSG) techniques. Additional measures of somatic physiology have provided enough evidence to conclude that the auto-regulatory, global regulation of sleep is not the exclusive domain of the CNS, but is heavily influenced by inputs from the rest of the body.

The present study evaluated whether slow-wave sleep and whole-night delta power of the non-rapid eye movement (NREM) sleep electroencephalogram (EEG) decrease during sleep at a simulated altitude of 2000 m, and whether such changes related to measures of hypoxic ventilatory response (HVR). This study consisted of two parts; in the first, HVR was measured in 41 subjects and each seven subjects with the lowest or the highest HVR were selected for the subsequent sleep study. In the second part, polysomnogram, arterial oxygen saturation (SpO2) and respiratory events are recorded on the selected subjects under normoxic and hypoxic conditions. Hypoxia decreased SpO2 and increased respiratory disturbances for both groups. The low HVR group, but not the high HVR group, showed decreases in the whole-night delta power of NREM sleep EEG under hypoxia. On the other hand, two subjects in the high HVR group, who showed relatively high apnoea indices, also showed lower SpO2 nadirs and decreases in the whole-night delta power under hypoxia. These results suggest that acute hypoxia equivalent to that at a 2000 m altitude decreases slow-wave sleep in individuals that show low HVR. However, low HVR may not be the only, but one of some factors that decrease the whole-night delta power under hypoxia. Therefore, it was not sufficient to identify individuals likely to be susceptible to deteriorated sleep quality at a simulated altitude of 2000 m only using the HVR test. Other factors, which relate to respiratory instabilities, should be taken into consideration to identify them.