Lumbar sympathetic nerve activity and hindquarter blood flow during REM sleep in rats

The present study aimed to investigate the response of lumbar sympathetic nerve activity (LSNA) to the onset of rapid eye movement (REM) sleep and its contribution to the regulation of muscle blood flow during REM sleep in rats. Electrodes for the measurements of LSNA, electroencephalogram, electromyogram and electrocardiogram and a Doppler flow cuff for the measurements of blood flow in the common iliac and mesenteric arteries, also catheters for the measurements of systemic arterial and central venous pressures were implanted chronically. REM sleep resulted in a step increase in LSNA, by 22 ± 9% (mean ± s.e.m. , P < 0.05), a reduction of iliac vascular conductance, by −16 ± 3% ( P < 0.05) and a gradual increase in systemic arterial pressure, reaching a maximum value of 8.1 ± 2.0 mmHg ( P < 0.05) at 89 s after onset of REM sleep, while mesenteric vascular conductance increased simultaneously by 5 ± 2% ( P < 0.05). There was a significant (Pearson's correlation coefficient = 0.94, P < 0.05) inverse linear relationship between LSNA and the iliac blood flow. Unilateral lumbar sympathectomy blunted the reduction of iliac blood flow induced by the onset of REM sleep. The present observations suggest that the onset of REM sleep appears to be associated with a vasodilation in viscera and a vasoconstriction in skeletal muscle, such that systemic arterial pressure increases during REM sleep in rats.     

Role of differential changes in sympathetic nerve activity in the preparatory adjustments of cardiovascular functions during freezing behaviour in rats

Freezing behaviour is associated with a distinct pattern of changes in cardiovascular function, which has been considered as a preparatory reflex for 'fight or flight' behaviour. However, the detailed mechanisms underlying preparatory cardiovascular adjustments and their physiological implications have received less attention. We studied responses in renal and lumbar sympathetic nerve activity and cardiovascular function during freezing behaviour in conscious rats, which was induced by exposure to loud white noise. Freezing behaviour was associated with regionally specific alterations in sympathetic nerve activity, in that renal sympathetic nerve activity increased while lumbar sympathetic nerve activity did not change. Moreover, freezing behaviour was associated with differential shifts in baroreflex control of sympathetic outflows, which could help to explain the selective responses in renal and lumbar sympathetic nerve activity during freezing behaviour. These differential changes in sympathetic outflows would result in a visceral vasoconstriction without having any impact on the skeletal muscle vasculature. These cardiovascular adjustments during freezing behaviour may help to explain the immediate and massive increase in muscular blood flow that occurs at the onset of fight or flight behaviour. It is hypothesized that central command originating from the defence area could somehow modulate separate baroreflex pathways, causing differential changes in sympathetic nerve activity to generate the preparatory cardiovascular adjustments during the freezing behaviour.     

Skin sympathetic nerve activity and effector function during sleep in humans

Multi-unit sympathetic skin nerve activity (SSA) in the peroneal nerve was recorded together with electrical skin resistance, skin blood flow and (in some subjects) finger blood pressure during sleep in 22 sleep-deprived healthy subjects. The average strength of sympathetic activity in different sleep stages was measured during 5-min periods as the area-under-curve of the integrated neurogram. Stage 2 sleep was reached by 15 subjects, stages 3–4 by nine and rapid eye movement (REM) sleep by six subjects. Non-REM sleep was always associated with an increased skin resistance, which was larger in glabrous than in hairy skin (293±48 vs. 175±4% of awake control level, n= 10, P < 0.05). Skin blood flow also increased during sleep, with a mean maximal increase of 397±79% of the awake control level (n= 11, P < 0.05). In spite of these changes of effector function no significant difference in mean SSA was found between the awake control period and periods of non-REM sleep, but during REM sleep SSA increased with 34% (P < 0.05) compared with the immediately preceding stage 2 period. In stage 2 sleep, K-complexes were associated with bursts of SSA followed by transient changes of skin resistance, blood flow and arterial blood pressure. When both skin resistance and blood flow were recorded within the innervation area of the impaled fascicle, single bursts or short periods of increased SSA could be succeeded by increased skin blood flow without concomitant skin resistance change. This indicates the existence of specific sympathetic vasodilator fibres in the skin. Therefore the unchanged strength of multiunit SSA during non-REM sleep in the face of increases of skin resistance and blood flow may be a consequence of an increased sympathetic vasodilator nerve activity combined with decreases of vasoconstrictor and sudomotor traffic.     

Muscle activities are differently modulated between masseter and neck muscle during sleep-wake cycles in guinea pigs

Sleep bruxism is a sleep-related movement disorder characterized by an exaggerated jaw motor activity during sleep. Currently, the magnitude of jaw motor activation in normal sleep remains poorly understood. In this study, we aim to assess the state-dependent changes in the magnitude of electromyographic activities of the jaw-closing masseter muscle in comparison with those of a neck muscle (specifically, the obliquus capitis) during sleep-wake cycles in guinea pigs. These electromyographic activities were integrated for 10-s epochs during wakefulness, non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. The masseter activity per epoch was found to be five times lower in both sleep stages while the neck muscle activity also decreased to 30% in NREM sleep and was lowest (16%) in REM sleep. In the periods without motor activity, masseter tone did not differ between the three states, whereas neck muscle tone decreased from wakefulness to NREM sleep and further to REM sleep. Moreover, in the epochs with masseter activation, the neck muscle activity did not increase during sleep. These results suggest that masseter activity decreases but is occasionally activated during sleep, and that state-dependent changes in electromyographic activity can be differently modulated in time and intensity between the masseter and the obliquus capitis.     

Muscle nerve sympathetic activity during sleep and its change with arousal response

SUMMARY  Muscle nerve sympathetic activity (MSA) was recorded from the peroneal nerve during wakefulness and in different sleep states in healthy young adults. The burst rate (BR) of MSA significantly decreased in NREM, but not in REM sleep, compared with that during wakefulness. Transient increases of MSA frequently appeared in association with rapid eye movements during REM sleep. K-complexes in Stage 2 were almost always accompanied by a burst of MSA, and were followed by a transient elevation of arterial blood pressure. Auditory stimuli applied in sleep induced a burst of MSA followed by a transient increase of arterial blood pressure, only when they elicited an arousal response in the EEG, such as a K-complex, transient EEG desynchronization, or a short train of alpha waves. The same stimuli applied during wakefulness did not induce such changes in MSA and in arterial blood pressure.     

Manoeuvres Affecting Sympathetic Outflow in Human Muscle Nerves

Multi-unit sympathetic activity was recorded in human muscle nerves, together with measurements of intra-arterial blood pressure and forearm or calf blood flow, during manoeuvres causing circulatory adjustments. Manoeuvres causing an increased vascular resistance in the forearm or calf were regularly associated with an increase in sympathetic outflow, proving that the neural activity was dominated by vasoconstrictor impulses. The inverse changes of blood pressure and sympathetic activity observed during Valsalva's manoeuvre and mental stress are explicable in terms of baroreflex control of the neural outflow. However, during muscle work and hyperventilation the relation between blood pressure and sympathetic activity was more complex, indicating that the baroreflex influence was superimposed or modified by other regulatory mechanisms. Some manoeuvres known to affect sympathetic outflow in skin nerves caused no appreciable change in sympathetic muscle nerve activity.     

Biphasic effects of tonic stimulation of muscle nociceptors on skin sympathetic nerve activity in human subjects

Skin sympathetic nerve activity (SSNA) controls skin blood flow and sweat release, and acute noxious stimulation of skin has been shown to cause a decrease in SSNA in the anaesthetised or spinal cat. In awake human subjects, acute muscle pain causes a transient rise in SSNA, but the impact of long-lasting (tonic) stimulation of muscle nociceptors on skin sympathetic outflow, blood flow and sweat release is unknown. We tested the hypothesis that tonic stimulation of muscle nociceptors causes a sustained increase in sympathetic outflow to the skin. SSNA was recorded from the common peroneal nerve of 10 awake human subjects. Tonic muscle pain was induced by infusing hypertonic saline (7 %) into the tibialis anterior muscle over ~40 min, titrated to achieve a constant level of muscle pain. SSNA initially increased following the onset of the infusion, reaching a peak of 164 % of baseline within 5 min, but then showed a prolonged and sustained decrease, reaching a nadir of 77 % in 20 min. Conversely, skin blood flow (and vascular conductance) initially decreased, followed by a progressive increase; there were no consistent changes in sweat release. In 9 of 10 subjects, SSNA and skin blood flow were inversely related. We conclude that sympathetic outflow to the skin exhibits a biphasic response to long-lasting stimulation of muscle nociceptors: an initial increase presumably related to the ‘arousal’ or ‘alerting’ component of pain, characterised by increased SSNA and decreased skin blood flow, followed by a prolonged decrease in SSNA and increased skin blood flow. The latter may be a purposeful response that contributes to wound healing.     

Sympathetic transients caused by abrupt alterations of carotid baroreceptor activity in humans

We examined the role of carotid baroreceptors in the short-term modulation of sympathetic outflow to the muscle vascular bed and parasympathetic outflow to the heart in 10 healthy adults. Afferent carotid baroreceptor activity was modified with 30-mmHg neck suction or pressure applied during held expiration, and efferent sympathetic activity was measured with microelectrodes inserted percutaneously into peroneal nerve muscle fascicles. Sympathetic responses were conditioned importantly by directional changes of carotid transmural pressure: increased pressure (onset of neck suction or offset of neck pressure) inhibited (totally) sympathetic activity, and reduced pressure (offset of neck suction or onset of neck pressure) augmented sympathetic activity. Responses occurred after a latency of about 2 s and did not persist as long as changes of neck-chamber pressure. Cardiac intervals were prolonged by increased carotid transmural pressures and shortened by decreased carotid transmural pressures, but, in contrast to sympathetic responses, cardiac responses adapted only slightly during neck-chamber pressure changes. Our results suggest that in the human a common baroreceptor input is processed differently in central vagal and sympathetic networks. Muscle sympathetic responses to changing levels of afferent baroreceptor traffic are profound but transitory. They appear to be conditioned more by changes of arterial pressure than by its absolute levels.     

Cardiopulmonary sympathetic afferent influences on renal nerve activity.

Cardiopulmonary sympathetic afferent nerves may affect renal control of intravascular volume by influencing renal sympathetic nerve activity. This influence was evaluated in alpha-chloralose anesthetized, vagotomized, sino-aortic denervated cats. When the afferent nerves were activated with a single electrical stimulus, the renal nerve responded with an excitatory burst of activity followed by a long period of inhibition. This response had characteristics of a supraspinal reflex. Repetitive stimulation of the sympathetic afferent nerve either inhibited or excited renal nerves and increased or decreased systemic blood pressure. The direction of these changes depended on stimulus parameters. No obligatory correlation in the direction of change of nerve activity and blood pressure was observed. Activation of cardiopulmonary sympathetic afferent nerves by intravascular volume expansion inhibited renal nerve discharge. Inhibition was elminated by sectioning the sympathetic afferent nerves. Volume expansion had no effect on lumbar sympathetic discharge monitored simultaneously with renal nerve activity. This observation suggests specificity of reflex influences of these afferent nerves on the kidney. In conclusion, cardiopulmonary sympathetic afferent nerves can reflexly alter renal nerve activity, and therefore may affect renal control of intravascular volume.     

Effects of Exhaustive Exercise on the Sleep of Men and Women

The effects of exhaustive exercise on sleep were examined in 5 women and 4 men who performed an acute bout of submaximal exercise (50–70% Vo_2max) to the point of volitional exhaustion. Significant changes were observed in the quantity and temporal distribution of slow-wave sleep (SWS) on the exercise night. The duration of SWS prior to rapid eye movement (REM) sleep onset increased markedly, along with a moderate increase in stage 4 and total SWS. REM sleep variables were affected in the early portion of the night, with an increased latency to first REM onset and a decrease in the duration of the first REM period. Initial REM cycle length (from first to second REM period onset) decreased as well. The magnitude of the SWS increase prior to REM onset was sex-related, averaging 24 min for women and 5.7 min for men. A correlation of .85 was observed between this increase and total caloric expenditure during exercise for the women. Cardiovascular measures indicated significant elevations of heart rate and cardiac output during sleep on the exercise night. Analysis of urine samples revealed a significant drop in nocturnal cortisol excretion rates after exercise. The results suggest that exhaustive exercise affects sleep primarily in the early portion of the night, inducing an increase in SWS pressure at the expense of REM sleep.     

Sleep-waking discharge patterns of neurons recorded in the rat perifornical lateral hypothalamic area

The perifornical lateral hypothalamic area (PF-LHA) has been implicated in the control of several waking behaviours, including feeding, motor activity and arousal. Several cell types are located in the PF-LHA, including projection neurons that contain the hypocretin peptides (also known as orexins). Recent findings suggest that hypocretin neurons are involved in sleep-wake regulation. Loss of hypocretin neurons in the human disorder narcolepsy is associated with excessive somnolence, cataplexy and increased propensity for rapid eye movement (REM) sleep. However, the relationship of PF-LHA neuronal activity to different arousal states is unknown. We recorded neuronal activity in the PF-LHA of rats during natural sleep and waking. Neuronal discharge rates were calculated during active waking (waking accompanied by movement), quiet waking, non-REM sleep and REM sleep. Fifty-six of 106 neurons (53 %) were classified as wake/REM-related. These neurons exhibited peak discharge rates during waking and REM sleep and reduced discharge rates during non-REM sleep. Wake-related neurons (38 %) exhibited reduced discharge rates during both non-REM and REM sleep when compared to that during waking. Wake-related neurons exhibited significantly higher discharge rates during active waking than during quiet waking. The discharge of wake-related neurons was positively correlated with muscle activity across all sleep-waking states. Recording sites were located within the hypocretin-immunoreactive neuronal field of the PF-LHA. Although the neurotransmitter phenotype of recorded cells was not determined, the prevalence of neurons with wake-related discharge patterns is consistent with the hypothesis that the PF-LHA participates in the regulation of arousal, muscle activity and sleep-waking states.     

Application of histamine or serotonin to the hypoglossal nucleus increases genioglossus muscle activity across the wake–sleep cycle

The decrease in genioglossus (GG) muscle activity during sleep, especially rapid eye movement (REM) or paradoxical sleep, can lead to airway occlusion and obstructive sleep apnoea (OSA). The hypoglossal nucleus innervating the GG muscle is under the control of serotonergic, noradrenergic and histaminergic neurons that cease firing during paradoxical sleep. The objectives of this study were to determine the effect on GG muscle activity during different wake–sleep states of the microdialysis application of serotonin, histamine (HA) or noradrenaline (NE) to the hypoglossal nucleus in freely moving cats. Six adult cats were implanted with electroencephalogram, electro-oculogram and neck electromyogram electrodes to record wake–sleep states and with GG muscle and diaphragm electrodes to record respiratory muscle activity. Microdialysis probes were inserted into the hypoglossal nucleus for monoamine application. Changes in GG muscle activity were assessed by power spectrum analysis. In the baseline conditions, tonic GG muscle activity decreased progressively and significantly from wakefulness to slow-wave sleep and even further during slow-wave sleep with ponto-geniculo-occipital waves and paradoxical sleep. Application of serotonin or HA significantly increased GG muscle activity during the wake–sleep states when compared with controls. By contrast, NE had no excitatory effect. Our results indicate that both serotonin and HA have a potent excitatory action on GG muscle activity, suggesting multiple aminergic control of upper airway muscle activity during the wake–sleep cycle. These data might help in the development of pharmacological approaches for the treatment of OSA.     

Heart rate variability during waking and sleep in healthy males and females

STUDY OBJECTIVES: The study goal was to investigate autonomic activity with heart rate variability analysis during different sleep stages in males and females. DESIGN: The study utilized a 2 Groups (males, females) x 4 States (waking, stage 2 sleep, stage 4 sleep, rapid-eye movement sleep) mixed design with one repeated, within-subjects factor (i.e., state). SETTING: The study was carried out in the sleep laboratory of the Thomas N. Lynn Institute for Healthcare Research. PARTICIPANTS: Twenty-four healthy adults (fourteen females and ten males). INTERVENTIONS: NA. MEASUREMENTS AND RESULTS: All participants underwent polysomnographic monitoring and electrocardiogram recordings during pre-sleep waking and one night of sleep. Fifteen-minute segments of beat-to-beat heart rate intervals during waking, stage 2 sleep, stage 4 sleep, and REM sleep were subjected to spectral analysis. Compared to NREM sleep, REM sleep was associated with decreased high frequency (HF) band power, and significantly increased low frequency (LF) to (HF) ratio. Compared to females, males showed significantly elevated LF/HF ratio during REM sleep. Males also demonstrated significantly decreased HF band power during waking when compared to females. No significant sleep- or gender-related changes in LF band power were found. CONCLUSIONS: The results confirmed changes in autonomic activity from waking to sleep, with marked differences between NREM and REM sleep. These changes were primarily due to stage-related alterations in vagal tone. REM sleep was characterized by increased sympathetic dominance, secondary to vagal withdrawal. The data also suggested gender differences in autonomic functioning during waking and sleep, with decreased vagal tone during waking and increased sympathetic dominance during REM sleep in the males.     

Spectral analysis of all-night human sleep EEG in narcoleptic patients and normal subjects

To investigate the pathophysiology of narcoleptic patients' sleep in detail, we analysed and compared the whole-night polysomnograms of narcoleptic patients and normal human subjects. Eight drug-naive narcoleptic patients and eight age-matched normal volunteers underwent polysomnography (PSG) on two consecutive nights. In addition to conventional visual scoring of the polysomnograms, rapid eye movement (REM)-density and electroencephalograph (EEG) power spectra analyses were also performed. Sleep onset REM periods and fragmented nocturnal sleep were observed as expected in our narcoleptic patients. In the narcoleptic patients, REM period duration across the night did not show the significant increasing trend that is usually observed in normal subjects. In all narcoleptic patient REM periods, eye movement densities were significantly increased. The power spectra of narcoleptic REM sleep significantly increased between 0.3 and 0.9 Hz and decreased between 1.0 and 5.4 Hz. Further analysis revealed that non-rapid eye movement (NREM) period duration and the declining trend of delta power density in the narcoleptic patients were not significantly different from the normal subjects. Compared with normal subjects, the power spectra of narcoleptic NREM sleep increased in the 1.0-1.4 Hz and 11.0-11.9 Hz frequency bands, and decreased in a 24.0-26.9 Hz frequency band. Thus, increased EEG delta and decreased beta power densities were commonly observed in both the NREM and REM sleep of the narcoleptic patients, although the decrease in beta power during REM sleep was not statistically significant. Our visual analysis revealed fragmented nocturnal sleep and increased phasic REM components in the narcoleptic patients, which suggest the disturbance of sleep maintenance mechanism(s) and excessive effects of the mechanism(s) underlying eye movement activities during REM sleep in narcolepsy. Spectral analysis revealed significant increases in delta components and decreases in beta components, which suggest decreased activity in central arousal mechanisms. These characteristics lead us to hypothesize that two countervailing mechanisms underlie narcoleptic sleep pathology.     

Magnetic stimulation of the human brain during phasic and tonic REM sleep: recordings from distal and proximal muscles

SUMMARY  During REM sleep, a powerful postsynaptic inhibition of spinal motoneurons induces a generalized muscle hypotonia. Despite this inhibition, it has been shown that by transcranial magnetic stimulation of the brain (TMS), muscle responses of normal amplitude can be evoked in small hand muscles of humans. Tonic innervation during sleep is different in postural vs. limb muscles, and the spinal inhibition differs during tonic vs. phasic REM episodes. Both phenomena may affect muscle responses to TMS. In this study, muscle responses of 14 healthy subjects were compared to TMS in abductor digiti minimi, lumbar erector spinae, trapezius, and diaphragm during phasic and tonic REM sleep. In all four muscles, the amplitudes of the muscle responses were extremely variable, ranging for example in trapezius from -100% to +473% as compared to wakefulness. There was no systematic difference between the muscles. Moreover, no differences were found for TMS during phasic REM events compared to tonic REM sleep. Thus, responses to TMS during REM sleep may be preserved, with a decreased or increased amplitude. As a likely explanation, the cortical excitability and/or the spinal inhibition fluctuates during REM sleep in humans.     

A sedentary day: effects on subsequent sleep and body temperatures in trained athletes

Exercise effects on sleep in fit healthy people have been difficult to determine because their sleep is close to optimal, leaving little room for improvement. Another method for assessing exercise effects on sleep is to significantly reduce the degree of activity in highly active people. Fifteen trained athletes who exercised daily at a moderate to high intensity were employed. By requesting that subjects remain sedentary in the laboratory for an entire day, the effect of reduced exercise on subsequent sleep parameters was assessed. Sleep and temperature were recorded after a sedentary day and after a normal day of moderate to high activity (control condition) in a counterbalanced design. In the sedentary condition, slow-wave sleep (SWS) decreased by a mean of 15.5+/-7.0 min and slow-wave activity (SWA) differed significantly (P<.05) between conditions in the first hour of sleep only. Rapid eye movement (REM) sleep increased by a mean of 17.9+/-5.7 min in the sedentary condition, while sleep onset latency (SOL) to Stages 1 and 2 increased by 10.2 and 10.7 min, respectively, and REM sleep latency decreased by 24.0+/-6.8 min (all P<.05). Between conditions, there was no overall effect on total sleep time (TST), sleep efficiency, wake after sleep onset or core or foot temperatures (P>.05). With reduced exercise load, SWS pressure may have been reduced, resulting in lower levels of SWS and increased REM sleep. Thus, the data indicate that reducing exercise has significant effects on sleep that may have implications for athletes tapering for competition.     

Sympathetic Withdrawal Augments Cerebral Blood Flow During Acute Hypercapnia in Sleeping Lambs

Study Objectives:

Cerebral sympathetic activity constricts cerebral vessels and limits increases in cerebral blood flow (CBF), particularly in conditions such as hypercapnia which powerfully dilate cerebral vessels. As hypercapnia is common in sleep, especially in sleep disordered breathing, we tested the hypothesis that sympathetic innervation to the cerebral circulation attenuates the CBF increase that accompanies increases in PaCO₂ in sleep, particularly in REM sleep when CBF is high.

Design:

Newborn lambs (n = 5) were instrumented to record CBF, arterial pressure (AP) intracranial pressure (ICP), and sleep-wake state (quiet wakefulness (QW), NREM, and REM sleep). Cerebral vascular resistance was calculated as CVR = [AP-ICP]/CBF. Lambs were subjected to 60-sec tests of hypercapnia (FiCO₂ = 0.08) during spontaneous sleep-wake states before (intact) and after sympathectomy (bilateral superior cervical ganglionectomy).

Results:

During hypercapnia in intact animals, CBF increased and CVR decreased in all sleep-wake states, with the greatest changes occurring in REM (CBF 39.3% ± 6.1%, CVR −26.9% ± 3.6%, P < 0.05). After sympathectomy, CBF increases (26.5% ± 3.6%) and CVR decreases (−21.8% ± 2.1%) during REM were less (P < 0.05). However the maximal CBF (27.8 ± 4.2 mL/min) and minimum CVR (1.8 ± 0.3 mm Hg/ min/mL) reached during hypercapnia were similar to intact values.

Conclusion:

Hypercapnia increases CBF in sleep and wakefulness, with the increase being greatest in REM. Sympathectomy increases baseline CBF, but decreases the response to hypercapnia. These findings suggest that cerebral sympathetic nerve activity is normally withdrawn during hypercapnia in REM sleep, augmenting the CBF response.

Citation:

Cassaglia PA; Griffiths RI; Walker AM. Sympathetic withdrawal augments cerebral blood flow during acute hypercapnia in sleeping lambs. SLEEP 2008;31(12):1729–1734.     

Effects of sympathetic stimulation on the rhythmical jaw movements produced by electrical stimulation of the cortical masticatory areas of rabbits

The somatomotor and sympathetic nervous systems are intimately linked. One example is the influence of peripheral sympathetic fibers on the discharge characteristics of muscle spindles. Since muscle spindles play important roles in various motor behaviors, including rhythmic movements, the working hypothesis of this research was that changes in sympathetic outflow to muscle spindles can change rhythmic movement patterns. We tested this hypothesis in the masticatory system of rabbits. Rhythmic jaw movements and EMG activity induced by long-lasting electrical cortical stimulation were powerfully modulated by electrical stimulation of the peripheral stump of the cervical sympathetic nerve (CSN). This modulation manifested itself as a consistent and marked reduction in the excursion of the mandibular movements (often preceded by a transient modest enhancement), which could be attributed mainly to corresponding changes in masseter muscle activity. These changes outlasted the duration of CSN stimulation. In some of the cortically evoked rhythmic jaw movements (CRJMs) changes in masticatory frequency were also observed. When the jaw-closing muscles were subjected to repetitive ramp-and-hold force pulses, the CRMJs changed characteristics. Masseter EMG activity was strongly enhanced and digastric EMG slightly decreased. This change was considerably depressed during CSN stimulation. These effects of CSN stimulation are similar in sign and time course to the depression exerted by sympathetic activity on the jaw-closing muscle spindle discharge. It is suggested that the change in proprioceptive information induced by an increase in sympathetic outflow (a) has important implications even under normal conditions for the control of motor function in states of high sympathetic activity, and (b) is one of the mechanisms responsible for motor impairment under certain pathological conditions such as chronic musculoskeletal head-neck disorders, associated with stress conditions.     

CNS determinants of sleep-related worsening of airway functions: implications for nocturnal asthma

This review summarizes the recent neuroanatomical and physiological studies that form the neural basis for the state-dependent changes in airway resistance. Here, we review only the interactions between the brain regions generating quiet (non-rapid eye movement, NREM) and active (rapid eye movement, REM) sleep stages and CNS pathways controlling cholinergic outflow to the airways. During NREM and REM sleep, bronchoconstrictive responses are heightened and conductivity of the airways is lower as compared to the waking state. The decrease in conductivity of the lower airways parallels the sleep-induced decline in the discharge of brainstem monoaminergic cell groups and GABAergic neurons of the ventrolateral periaqueductal midbrain region, all of which provide inhibitory inputs to airway-related vagal preganglionic neurons (AVPNs). Withdrawal of central inhibitory influences to AVPNs results in a shift from inhibitory to excitatory transmission that leads to an increase in airway responsiveness, cholinergic outflow to the lower airways and consequently, bronchoconstriction. In healthy subjects, these changes are clinically unnoticed. However, in patients with bronchial asthma, sleep-related alterations in lung functions are troublesome, causing intensified bronchopulmonary symptoms (nocturnal asthma), frequent arousals, decreased quality of life, and increased mortality. Unquestionably, the studies revealing neural mechanisms that underlie sleep-related alterations of airway function will provide new directions in the treatment and prevention of sleep-induced worsening of airway diseases.     

Cardiac autonomic characteristics in infants sleeping with their head covered by bedclothes

The risk of Sudden Infant Death Syndrome is increased in infants sleeping with their head covered by bedding items. This study was designed to evaluate cardiac autonomic nervous controls in infants sleeping with the head covered by bedclothes. Sixteen healthy infants with a median age of 12 weeks (range 9-13 weeks) were recorded polygraphically for one night. While they slept in their usual supine position, a bedsheet was placed over their head for about 45 min. All infants were challenged with the head covered and with the head free during both rapid eye movement (REM) and non-rapid eye movement (NREM) sleep. Sleep, breathing and heart rate (HR) characteristics were recorded simultaneously, together with rectal and pericephalic temperatures. In both head-free and head-covered conditions, autoregressive spectral analysis of HR was evaluated as a function of sleep stages. During the head-covered periods, parasympathetic tonus decreased and sympathetic activity increased in both REM and NREM sleep. Compared with the head-free periods, the head-covered sleep periods were characterized by greater rectal (P = 0.012) and pericephalic temperatures (P = 0.002). Covering the infant's head with a bedsheet was associated with significant changes in autonomic balance. The finding could be related to an elevation in temperatures within the infant's microenvironment.