Sleep of paradoxes

July 7, 2017 | Autor: W. Dunin-barkowski | Categoria: Biological Sciences, Humans, Respiration, Wakefulness, Sleep Stages
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2 Sleep of paradoxes

John Orem and Witali DuninBarkowski Department of Physiology, Texas Tech University School of Medicine, Lubbock, TX 79430, USA In this issue of The Journal of Physiology, Morrell et al. report their findings from a study of the response of human subjects to inspiratory resistive loading during sleep and wakefulness. At issue is a question of physiology in sleep that is important for understanding the pathophysiology of the obstructive sleep apnoea syndrome. These patients, and they are numerous, have recurring apnoeas during sleep. The apnoeas produce arousals that save the patient but disrupt sleep and cause excessive daytime sleepiness. They also produce repeated hypoxic episodes that lead to pulmonary and systemic hypertension. Most or all cases are the result of some anomaly in the structure of the upper airway that predisposes it to collapse in response to the negative pressure of inspiration. To the physiologist, one question is ‘Why does the airway collapse only in sleep?’ or ‘Why does it not collapse in wakefulness?’. There are several possibilities. Perhaps impending collapse is not sensed by the sleeping brain. Or perhaps it is sensed but a response is prevented. Or perhaps it has nothing to do with either of these and the problem is avoided in wakefulness but not in sleep because of differences in endogenous drive to airway dilating muscles in these states. For example, some have suggested that there is an endogenous drive that depends on wakefulness. In support of this idea, stimulation of the mesencephalic reticular activating system causes desynchronization of the electroencephalogram (arousal) and also causes an increase in the rate and depth of breathing and, perhaps more to the point of obstructive sleep apnoea, a preferential activation of muscles that dilate the upper airways (Orem & Lydic, 1978).

Perspectives Morrell et al. (2000) studied normal subjects, not patients with sleep apnoea, and they were interested in whether or not there was respiratory load compensation during sleep. In wakefulness, compensation is evident as a lengthened duration of inspiration and increase in tidal volume on the first breath following imposition of a load. The circuitry for the immediate prolongation of inspiration, that is, the sensory receptors, and central comparator that detects the difference between what was intended and what was achieved, is not known, but whatever the details, it involves sensory and motor limbs linked by central structures into a complex reflex. The authors findings for both rapid eye movement (REM) and non-REM (NREM) sleep were of interest. In REM sleep, but not NREM sleep, there was a prolongation of inspiration (but a decrease in tidal volume) on the first breath following the imposition of a resistance to breathing. The NREM sleep results (negative findings) are noteworthy because homeostasis is considered optimal in that state (Parmeggiani, 1980). For example, animals pant in response to high temperatures and shiver in the cold, and responses to changes in blood gases are easily demonstrated. The REM sleep results are noteworthy because homeostasis is absent in that state (Parmeggiani, 1980). Reflexes are variable and seem to depend on whether or not the brain is engaged with something endogenous such as the content of the dream or a primal pontine drive. Morrell et al. (2000) provide an interesting interpretation of this paradox of sleep states. Noting that there is desynchronization (excitation) of the EEG in both REM sleep and wakefulness, but not NREM sleep, they suggest that the response to a resistive load requires endogenous excitation. Thus, they come down clearly on the side of the idea that response to a load depends on the excitatory drives endemic to the state. Enigmas of REM sleep prevail throughout the work of Morrell et al. (2000). The search for differences in the response to a load in tonic versus phasic REM sleep led them to unexpected results and ultimately to the question of the

J. Physiol.

526.1

validity of the tonic—phasic distinction. The accompanying Fig. 1 from our experiments is offered as support for their skepticism. It shows two specific indices of REM sleep, firing frequency of a medullary neuron that was active only in REM sleep and frequency of pontogeniculo-occipital (PGO) waves, in relation to three respiratory parameters (diaphragmatic activity, respiration period and range of respiration periods) during two REM sleep periods, A and B. Although at times PGO activity and the discharge rate of the REMspecific cell are related to each other andÏor to one or more of the respiratory parameters, at other times they are not. In A (during the last minute of this REM sleep period), but not B, the discharge rate of the REM-specific neuron is highly correlated with diaphragmatic activity. In B but not A, PGO wave activity and REMspecific neuronal activity are correlated with the rate and irregularity of breathing. It is evident from the constantly varying parameters and their fleeting relations that REM sleep belongs to a multi-dimensional continuum that is not divisible into just two components of tonic and phasic REM sleep.

Morrell, M. J., Browne, H. A. K. & Adams, L. (2000). Journal of Physiology 526, 195—202. Orem, J. & Lydic, R. (1978). Sleep 1, 49—68. Parmeggiani, P. L. (1980). In Physiology in Sleep, ed. Orem, J. & Barnes, C. D., pp. 97—143.

Academic Press, New York.

Figure 1. Two periods of REM sleep

(A and B) in a cat

EMGdia, integrated diaphragmatic activity; Unit rate, activity of REM specific neuron in the medullary reticular formation; PGO waves rate, frequency of PGO waves; Ttot, breath duration; ÄTtot = Ttot,max − Ttot,min, difference between the shortest and longest breaths in a sliding 10 s period.

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