The sleep and the visceral function control

The review focuses on rapidly growing body of data indicating that disturbances of the natural sleep and sleep deprivation lead to various visceral disorders. The review mentions consequences of sleep disturbances on the gastro-intestinal system, cardio-vascular and respiratory, immune, endocrine and reproductive functions. In order to establish the functional link between the sleep and the visceral health it is proposed that during sleep the central nervous system including all cortical areas switches from the processing of the exteroceptive information to the processing of the interoceptive information. Review of the studies, which offer the direct confirmation of this hypothesis, is presented.     

On the respiratory function of the ribs.

To assess the respiratory function of the ribs, we measured the changes in airway opening pressure (Pao) induced by stimulation of the parasternal and external intercostal muscles in anesthetized dogs, first before and then after the bony ribs were removed from both sides of the chest. Stimulating either set of muscles with the rib cage intact elicited a fall in Pao in all animals. After removal of the ribs, however, the fall in Pao produced by the parasternal intercostals was reduced by 60% and the fall produced by the external intercostals was eliminated. The normal outward curvature of the rib cage was also abolished in this condition, and when the curvature was restored by a small inflation, external intercostal stimulation consistently elicited a rise rather than a fall in Pao. These findings thus confirm that the ribs play a critical role in the act of breathing by converting intercostal muscle shortening into lung volume expansion. In addition, they carry the compression that is required to balance the pressure difference across the chest wall.     

Changes in cardiovascular function during the sleep onset period in young adults.

Blood pressure (BP) and heart rate (HR) are influenced by the sleep-wake cycle, with relatively abrupt falls occurring in association with sleep onset (SO). However, the pattern and rate of fall in BP and HR during SO and the processes that contribute to the fall in these variables have not been fully identified. Continuous BP and HR recordings were collected beginning 1 h before lights out (LO) until the end of the first non-rapid eye movement sleep period in 21 young, healthy participants maintained in a supine position. Five consecutive phases were defined: 1) the 30 min of wakefulness before LO; 2) LO to stage 1 sleep; 3) stage 1 to stage 2 sleep; 4) stage 2 sleep to the last microarousal before stable sleep; and 5) the first 30 min of undisturbed stable sleep. The data were analyzed on a beat-by-beat basis and reported as 2-min periods for phases 1 and 5 and 10% epochs for phases 2, 3, and 4 (as participants had variable time periods in these phases). The level of baroreflex (BR) activity was assessed by the sequence technique and an autoregressive multivariate model. Furthermore, during phases 3 and 4, the BP and HR responses to arousal from sleep were determined. There were substantial falls in BP and HR after LO before the initial onset of theta;-activity (phase 3) and again after the onset of stable sleep after the cessation of spontaneous arousals. During phases 3 and 4 when there were repeated arousals from sleep, the fall in both variables was retarded. Furthermore, both the rate and magnitude of the fall in BP were negatively associated with the number of arousals during phases 3 and 4. There was a small increase in the sensitivity of the BR and indirect evidence of a substantial fall in its set point.     

Swallowing function and upper airway sensation in obstructive sleep apnea.

The objective of this study was to determine whether impaired upper airway (UA) mucosal sensation contributes to altered swallowing function in obstructive sleep apnea (OSA). We determined UA two-point discrimination threshold (2PDT) and vibratory sensation threshold (VST) in 15 men with untreated OSA and 9 nonapneic controls (CL). We then assessed swallowing responses to oropharyngeal fluid boluses delivered via a catheter. The threshold volume required to provoke swallowing and the mean latency to swallowing were determined, as was the phase of the respiratory cycle in which swallowing occurred [expressed as percentage of control cycle duration (%CCD)] and the extent of prolongation of the respiratory cycle after swallowing [inspiratory suppression time (IST)]. 2PDT and VST were significantly impaired in OSA patients compared with CL subjects. 2PDT was positively correlated with swallowing latency and threshold volume in CL subjects, but not in OSA patients. Threshold volume did not differ between the groups [median value = 0.1 ml (95% confidence interval = 0.1-0.2) for OSA and 0.15 ml (95% confidence interval = 0.1-0.16) for CL], whereas swallowing latency was shorter for OSA patients [3.3 (SD 0.7) vs. 3.9 (SD 0.8) s, P = 0.04]. %CCD and IST were similar for OSA patients and CL subjects. However, among OSA patients there was a significant inverse relation between VST and IST. These findings suggest that oropharyngeal sensory impairment in OSA is associated with an attenuation of inhibitory modulating inputs to reflex and central control of UA swallowing function.     

Diurnal variation in vascular function: role of sleep

Although vascular function is lower in the morning than afternoon, previous studies have not assessed the influence of prior sleep on this diurnal variation. The authors employed a semiconstant routine protocol to study the contribution of prior nocturnal sleep to the previously observed impairment in vascular function in the morning. Brachial artery vascular function was assessed using the flow-mediated dilation technique (FMD) in 9 healthy, physically active males (mean ± SD: 27 ± 9 yrs of age), at 08:00 and 16:00 h following, respectively, 3.29 ± .37 and 3.24 ± .57 h prior sleep estimated using actimetry. Heart rate and systolic and diastolic blood pressures were also measured. The data of the experimental sleep condition were compared with the data of the "normal" diurnal sleep condition, in which FMD measurements were obtained from 21 healthy individuals who slept only during the night, as usual, before the morning test session. The morning-afternoon difference in FMD was 1 ± 4% in the experimental sleep condition compared with 3 ± 4% in the normal sleep condition (p =?.04). This difference was explained by FMD being 3 ± 3% lower in afternoon following the prior experimental sleep (p =?.01). These data suggest that FMD is more dependent on the influence of supine sleep than the endogenous circadian timekeeper, in agreement with our previous finding that diurnal variation in FMD is influenced by exercise. These findings also raise the possibility of a lower homeostatic "set point" for vascular function following a period of sleep and in the absence of perturbing hemodynamic fluctuation.     

Neural reapportionment: an hypothesis to account for the function of sleep

Sleep is a ubiquitous component of animal life, and prolonged sleep deprivation is fatal in both vertebrates and invertebrates. The physiologic function of sleep, however, is not known. We propose here that sleep provides a period of time necessary to reapportion resources within neurons and neural systems that become sub-optimally distributed during active waking. Three specific examples of such reapportionment during sleep are suggested: (1) the return of the neurotransmitter, glutamate, to synaptic vesicles at presynaptic sites most active during waking, (2) the intracellular movement of mitochondria from neuronal processes to the cells soma where mitochondrial replication can occur, and (3) the readjustment of the level and distribution of neurotransmitters within the brainstem modulatory systems and elsewhere that must function in an integrated fashion during waking. Experimental approaches that might be utilized to test these hypotheses are suggested.