Slow-wave sleep, diabetes, and the sympathetic nervous system

Abstract

Sleep oscillates between two different states: non-rapid eye movement (NREM) sleep and rapid-eye movement (REM) sleep. Slow-wave sleep (SWS) is a substate of NREM sleep, and its identification is based primarily on the presence of slow waves, i.e., low-frequency, high-amplitude oscillations in the EEG. Quantification of SWS is accomplished by visual inspection of EEG records or computerized methods such as spectral analysis based on the fast Fourier transform (FFT). Slow-wave activity (SWA; also referred to as delta power) is a quantitative measure of the contribution of both the amplitude and prevalence of slow waves in the EEG. The EEG oscillations reflect the field potentials associated with synchronized burst-pause firing patterns in cortical neurons (1). In view of these brain-based defining characteristics of SWS, it is not surprising that most theories on the functional significance of SWS have focused on the brain. In a recent issue of PNAS, Tasali et al. (2) draw attention to another aspect of SWS: the effects of SWS disruption on glucose tolerance and insulin resistance. What do these new data tells us about SWS and its functional significance? Is it for the body as well as the brain? The notion that SWS is an important substate of sleep has its foundations in the early observations that it is regulated accurately in response to variation in the duration of wakefulness. SWS increases in response to wake extension and is reduced after daytime naps, and these changes are observed in all EEG derivations, although they are most pronounced in frontal derivations (3). Variations in the nature of the waking experience, which may be associated with activation of specific neuronal populations, exhibit a significant, but minor and localized, influence on SWS (4). SWS and SWA are predominant at the beginning of sleep and decline in the course of sleep. …