The tidal volume and corresponding efferent phrenic activity of spontaneously occurring and provoked "augmented" breaths, AB, and the subsequent post-augmented breaths were studied in cats anesthetized with pentobarbitone during hypercapnia and hypoxia. The augmentation phase (phase II) begins at, or close to, the crest of what appears as a "normal" inspiration (phase I). The amplitude and duration of phase II remained fairly constant whereas the amplitude and the duration of phase I changed with chemical drive just as in control breaths. The smaller amplitude and shorter duration of post-augmented breaths as compared to control breaths seems to be due to both a lower-than-normal inspiratory "off-switch" threshold following the AB and an increased rate of rise of inspiratory activity. With increasing hypercapnia and hypoxia both the time interval between AB and the refractory period following an AB during which a new AB cannot be provoked were reduced. Following bilateral vagotomy AB was temporarily abolished but reappeared after 1-2 h. The relatively low rates of occurrence after vagotomy still showed the same type of dependence on chemical stimuli. The refractory period was not abolished although usually decreased by gallamine paralysis or high thoracic spinalization.

The position of the hyoid arch suggests that it supports soft tissue surrounding the upper airway (UA) and can act to maintain UA patency. We also suspected that muscles inserting on the hyoid arch might show respiratory patterns of activity that could be affected by respiratory stimuli. To test these possibilities, we moved the hyoid arch ventrally in six anesthetized dogs either by traction on it or by stimulation of hyoid muscles. UA resistance was decreased 73 +/- (SE) 6% and 72 +/- 6% by traction and stimulation during expiration and 57 +/- 15% and 52 +/- 8% during inspiration. Moving averages of the geniohyoid (GH) and thyrohyoid (TH) obtained in six other dogs breathing 100% O2 showed phasic respiratory activity while the sternohyoid (SH) showed phasic respiratory activity in only two of these animals and no activity in four. With progressive hypercapnia, GH and TH increased as did SH when activity was already present. Airway occlusion at end expiration augmented and prolonged inspiratory activity in the hyoid muscles but did not elicit SH activity if not already present. Occlusion at end inspiration suppressed phasic activity in hyoid muscles for as long as in the diaphragm. After vagotomy activity increased and became almost exclusively inspiratory. Activity appeared in SH when not previously present. Duration and amplitude of hyoid muscle activity were increased with negative UA pressure and augmented breaths. We conclude that the hyoid arch and muscles can strongly affect UA flow resistance. Hyoid muscles show responses to chemical, vagal, and negative pressure stimuli similar to other UA muscles.

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SUMMARY1. We examined the interaction between central pattern generators for respiration and deglutition in decerebrate, vagotomized, paralysed and ventilated cats (n = 10), by recording activity from the following nerves: hypoglossal, phrenic, thyroarytenoid and triangularis sterni. Fictive breathing was spontaneous with carbon dioxide above the apnoeic threshold (end-tidal Pco2, 32 + 4 mmHg) and fictive swallowing was induced by stimulating the internal branch of the left superior laryngeal nerve (SLN) continuously (0-2 ms pulse duration, 10 Hz).2. In all ten animals, SLN stimulation evoked short bursts of thyroarytenoid and hypoglossal nerve activity indicative of fictive swallowing. In two of ten animals, respiration was inhibited completely during deglutition. In the other eight animals, fictive breathing and swallowing occurred simultaneously.3. With SLN stimulation below threshold for eliciting swallowing, the respiratory rhythm decreased, the duration of inspiration did not change but the duration of expiration, especially stage II, increased. Integrated nerve activities indicated that the rate of rise and peak of phrenic nerve activity decreased, stage I expiratory activity of the thyroarytenoid and especially that of the hypoglossal nerve increased and stage II expiratory activity of the triangularis sterni nerve was suppressed completely. However, if inspired carbon dioxide was increased, i.e. hypercapnic ventilation, stage II expiratory activity remained partially during continuous SLN stimulation.4. Fictive-swallowing bursts occurred only at respiratory phase transitions. At the minimal stimulus intensity that evoked repetitive swallowing bursts, the pattern of interaction between breathing and swallowing central pattern generators was consistent for each animal (n = 7) but was different across animals. In four animals, fictive swallows occurred at the phase transition between stage II expiration and inspiration, at the transition between inspiration and stage I expiration in one animal; and in two other animals, at the transition between stage I and II of expiration.

The effects of negative pressure applied to just the upper airway on nasal and laryngeal muscle activity were studied in 14 spontaneously breathing anesthetized dogs. Moving average electromyograms were recorded from the alae nasi (AN) and posterior cricoarytenoid (PCA) muscles and compared with those of the genioglossus (GG) and diaphragm. The duration of inspiration and the length of inspiratory activity of all upper airway muscles was increased in a graded manner proportional to the amount of negative pressure applied. Phasic activation of upper airway muscles preceded inspiratory activity of the diaphragm under control conditions; upper airway negative pressure increased this amount of preactivation. Peak diaphragm activity was unchanged with negative pressure, although the rate of rise of muscle activity decreased. The average increases in peak upper airway muscle activity in response to all levels of negative pressure were 18 +/- 4% for the AN, 27 +/- 7% for the PCA, and 122 +/- 31% for the GG (P less than 0.001). Rates of rise of AN and PCA electrical activity increased at higher levels of negative pressure. Nasal negative pressure affected the AN more than the PCA, while laryngeal negative pressure had the opposite effect. The effects of nasal negative pressure could be abolished by topical anesthesia of the nasal passages, while the effects of laryngeal negative pressure could be abolished by either topical anesthesia of the larynx or section of the superior laryngeal nerve. Electrical stimulation of the superior laryngeal nerve caused depression of AN and PCA activity, and hence does not reproduce the effects of negative pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

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Introduction We evaluated polysomnograms of chronic fatigue syndrome (CFS) patients with and without fibromyalgia to determine whether patients in either group had elevated rates of sleep-disturbed breathing (obstructive sleep apnea or upper airway resistance syndrome) or periodic leg movement disorder. We also determined whether feelings of unrefreshing sleep were associated with differences in sleep architecture from normal.