Electromyographic recordings in animal models indicate that tongue protrudor (genioglossus, GG) and retractor muscles (styloglossus, SG; hyoglossus, HG) are co-activated during inspiration (Yasui et al. 1993, Fregosi & Fuller, 1997. Moreover, recent experiments indicate that respiratory-related co-activation of protrudor and retractor muscles results in retraction of the tongue (Fregosi & Fuller, 1997;Fuller et al. 1998). The observation that tongue muscle co-activation causes retraction of the tongue implies that respiratory-related tongue-motor activity narrows, rather than dilates, the oropharynx. However, two groups of investigators have shown that co-activation of the protrudor and retractor muscles evoked by XIIth nerve stimulation results in increased inspiratory flow rates in obstructive sleep apnoea (OSA) patients, in spite of clear tongue retraction (Eisele et al. 1997;De Backer et al. 1998). Protrusion of the tongue, evoked by either medial XIIth nerve branch stimulation (Eisele et al. 1997) or direct GG muscle stimulation (Schwartz et al. 1996) is also associated with increased inspiratory flow rates in human subjects. These observations suggest that either co-activation of tongue protrudor and retractor muscles, or independent protrudor muscle activation will improve pharyngeal flow mechanics. This is in spite of the fact that the tongue retracts 1. The purpose of these experiments was to examine the mechanisms by which either coactivation or independent activation of tongue protrudor and retractor muscles influence upper airway flow mechanics. We studied the influence of selective hypoglossal (XIIth) nerve stimulation on tongue movements and flow mechanics in anaesthetized rats that were prepared with an isolated upper airway. In this preparation, both nasal and oral flow pathways are available. 2. Inspiratory flow limitation was achieved by rapidly lowering hypopharyngeal pressure (Php) with a vacuum pump, and the maximal rate of flow (ýI,max) and the nasopharyngeal pressure associated with flow limitation (Pcrit) were measured. These experimental trials were repeated while nerve branches innervating tongue protrudor (genioglossus; medial XIIth nerve branch) and retractor (hyoglossus and styloglossus; lateral XIIth nerve branch) muscles were stimulated either simultaneously or independently at frequencies ranging from 20-100 Hz. Co-activating the protrudor and retractor muscles produced tongue retraction, whereas independently activating the genioglossus resulted in tongue protrusion. 3. Co-activation of tongue protrudor and retractor muscles increased ýI,max (peak increase 44%, P < 0·05), made Pcrit more negative (peak decrease of 44%, P < 0·05), and did not change upstream nasopharyngeal resistance (Rn). Independent protrudor muscle stimulation increased ýI,max (peak increase 61%, P < 0·05), did not change Pcrit, and decreased Rn (peak decrease of 41%, P < 0·05). Independent retractor muscle stimulation did not significantly alter flow mechanics. Changes in Pcrit and ýI,max at all stimulation fr...

The high quality of data collected in TuCASA demonstrates that multi-channel polysomnography data can be successfully obtained in children aged 5-12 years in an unattended setting under a research protocol.

Tongue position is controlled primarily by the mechanical actions of the extrinsic tongue muscles, which are innervated by separate branches of the hypoglossal (XIIth) nerve. The genioglossus (GG) muscle, which causes tongue protrusion, is innervated by the medial XIIth branch, while the hyoglossus (HG) and styloglossus (SG) muscles, which cause retraction of the tongue, are innervated by the lateral XIIth branch. A recent study showed that stimulating the XIIth nerve before its bifurcation into medial and lateral branches (i.e. co-activating the tongue protrudor and retractor muscles) caused tongue retraction in human subjects (Eisele, Smith, Alam & Schwartz, 1997). Consistent with these data, Gilliam & Goldberg (1995), using a rat model, found that the retractor muscles produce 10-20 times more force than the GG muscle, which explains why co-activation of both muscles results in strong tongue retraction. Thus, in both humans and rats, when protrudor and retractor muscle groups are activated maximally and 1. Our primary purpose was to test the hypothesis that the tongue protrudor (genioglossus, GG) and retractor (styloglossus, SG and hyoglossus, HG) muscles are co-activated when respiratory drive increases, and that co-activation will cause retraction of the tongue. This was addressed by performing two series of experiments using a supine, anaesthetized, tracheotomized rat in which tongue muscle force and the neural drive to the protrudor and retractor muscles could be measured during spontaneous breathing. In the first series of experiments, respiratory drive was increased progressively by occluding the tracheal cannula for thirty respiratory cycles; in the second series of experiments, the animals were subjected to hyperoxic hypercapnia and poikilocapnic hypoxia. 2. Airway occlusion for thirty breaths caused progressive, quantitatively similar increases in efferent motor nerve activity to protrudor and retractor tongue muscles. Net tongue muscle force was always consistent with tongue retraction during occlusion, and peak force rose in parallel with the neural activites. When airway occlusion was repeated following section of the lateral XIIth nerve branch (denervation of retractor muscles) the tongue either protruded (15Ï21 animals; 10 ± 2 mN at the 30th occluded breath) or retracted weakly (6Ï21 animals; 6 ± 2 mN at 30th occluded breath). 3. To ensure that our findings were not the result of damage to the muscle nerves, occlusion experiments were also done in eight animals in which GG EMG activity was recorded instead of nerve activities. Changes in peak integrated GG electryomyogram (EMG) activity and peak retraction force during occlusion were highly correlated (r = 0·86, slope = 1·05). 4. In separate experiments in fourteen rats, we found that hyperoxic hypercapnia and poikilocapnic hypoxia also result in parallel increases in the respiratory-related EMG activity of the GG and HG muscles. Also, as in the occlusion experiments, augmentations of protrudor and retractor muscle EMG activities were associate...

4. Successive CSN stimulation episodes evoked a previously undescribed phenomenon.Although the peak integrated phrenic activity was unchanged (90-95 % of maximal), IIC activity increased progressively during successive stimulus episodes (66-90 % of maximal; P < 0 05). However, after methysergide treatment, the initial stimulus-evoked phrenic response decreased to 58 % of maximal and both neurograms exhibited progressive augmentation of the stimulus-evoked response. As stimulus-evoked augmentation does not require serotonin, it is independent of LTF.5. We conclude that CSN stimulation-evoked LTF of IIC activity exceeds that of phrenic activity. Since LTF requires the neuromodulator serotonin and is expressed predominantly by changes in burst pattern formation versus rhythm generation, serotonin may exert a greater influence on IIC relative to phrenic respiratory motor output. A unique mechanism is described whereby successive CSN stimulus episodes cause progressively increasing responses in both neurograms.Chemical or electrical stimulation of the peripheral chemo-stimulation reflects at least two distinct mechanisms, with receptors evokes an abrupt increase in ventilatory activity.

We examined the relationship between nocturnal respiratory disturbance and learning and compared learning in children with and without nocturnal respiratory disturbance. Subjects were 149 participants in a prospective cohort study examining sleep in children ages 6-12: The Tucson Children's Assessment of Sleep Apnea study (TuCASA). Sleep was assessed via home polysomnography. Intelligence, learning and memory, and academic achievement were assessed. Parents rated attention. Group comparisons were used to test the hypothesis that the group with an apnea/hypopnea index (AHI) of 5 or more (n = 77) would have weaker performance than the group with AHI less than 5 (n = 72). The group with AHI of 5 or more had weaker learning and memory though differences between groups decreased when arousals were taken into account. There was a greater percentage of Stage 1 sleep in the AHI 5 or more group, and Stage 1 percentage was negatively related to learning and memory in the sample (n = 149). There were negative relationships between AHI and immediate recall, Full Scale IQ, Performance IQ, and math achievement. Hypoxemia was associated with lower Performance IQ. Thus, findings suggest that nocturnal respiratory disturbance is associated with decreased learning in otherwise healthy children, that sleep fragmentation adversely impacts learning and memory, and that hypoxemia adversely influences nonverbal skills.

The Tucson Children's Assessment of Sleep Apnea study has shown that there are values of RDI based on polysomnography that correspond to an increased rate of clinical symptoms in children ages 6 to 11 years.

The primary aim of this study was to determine the influence of systemic hyperoxia on sympathetic nervous system behavior at rest and during submaximal exercise in humans. In seven healthy subjects (aged 19-31 yr) we measured postganglionic sympathetic nerve activity to skeletal muscle (MSNA) in the leg, antecubital venous norepinephrine concentrations, heart rate, and arterial blood pressure during normoxic rest (control) followed by 3- to 4-min periods of either hyperoxic (100% O2 breathing) rest, normoxic exercise (rhythmic handgrips at 50% of maximum force), or hyperoxic exercise. During exercise, isocapnia was maintained by adding CO2 to the inspirate as necessary. At rest, hyperoxia lowered MSNA burst frequency (12-42%) and total activity (6-42%) in all subjects; the average reductions were 25 and 23%, respectively (P less than 0.05 vs. control). Heart rate also decreased during hyperoxia (6 +/- 1 beats/min, P less than 0.05), but arterial blood pressure was not affected. During hyperoxic compared with normoxic exercise, there were no differences in the magnitudes of the increases in MSNA burst frequency or total activity, plasma norepinephrine concentrations, or mean arterial blood pressure. In contrast, the increase in heart rate during hyperoxic exercise (13 +/- 2 beats/min) was less than the increase during normoxic exercise (20 +/- 2 beats/min; P less than 0.05). We conclude that, in healthy humans, systemic hyperoxia 1) lowers efferent sympathetic nerve activity to skeletal muscle under resting conditions without altering venous norepinephrine concentrations and 2) has no obvious modulatory effect on the nonactive muscle sympathetic nerve adjustments to rhythmic exercise.

Our purpose was to test the hypothesis that hypoxia potentiates exercise-induced sympathetic neural activation in humans. In 15 young (20-30 yr) healthy subjects, lower leg muscle sympathetic nerve activity (MSNA, peroneal nerve; microneurography), venous plasma norepinephrine (PNE) concentrations, heart rate, and arterial blood pressure were measured at rest and in response to rhythmic handgrip exercise performed during normoxia or isocapnic hypoxia (inspired O2 concn of 10%). Study I (n = 7): Brief (3-4 min) hypoxia at rest did not alter MSNA, PNE, or arterial pressure but did induce tachycardia [17 +/- 3 (SE) beats/min; P less than 0.05]. During exercise at 50% of maximum, the increases in MSNA (346 +/- 81 vs. 207 +/- 14% of control), PNE (175 +/- 25 vs. 120 +/- 11% of control), and heart rate (36 +/- 2 vs. 20 +/- 2 beats/min) were greater during hypoxia than during normoxia (P less than 0.05), whereas the arterial pressure response was not different (26 +/- 4 vs. 25 +/- 4 mmHg). The increase in MSNA during hypoxic exercise also was greater than the simple sum of the separate responses to hypoxia and normoxic exercise (P less than 0.05). Study II (n = 8): In contrast to study I, during 2 min of exercise (30% max) performed under conditions of circulatory arrest and 2 min of postexercise circulatory arrest (local ischemia), the MSNA and PNE responses were similar during systemic hypoxia and normoxia. Arm ischemia without exercise had no influence on any variable during hypoxia or normoxia.(ABSTRACT TRUNCATED AT 250 WORDS)