Geniohyoid muscle activity in normal men during wakefulness and sleep

Reduction in the activity of upper airway "dilator" muscles during sleep may allow the pharyngeal airway to collapse in some individuals. However, quantitative studies concerning the effect of sleep on specific upper airway muscles that may influence pharyngeal patency are sparse and inconclusive. We studied seven normal men (mean age 27, range 22-37 yr) during a single nocturnal sleep study and recorded sleep staging parameters, ventilation, and geniohyoid muscle electromyogram (EMGgh) during nasal breathing throughout the night. Anatomic landmarks for placement of intramuscular geniohyoid recording electrodes were determined from a cadaver study. These landmarks were used in percutaneous placement of wire electrodes, and raw and moving-time-averaged EMGgh activities were recorded. Sleep stage was determined using standard criteria. Stable periods of wakefulness and non-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep were selected for analysis. The EMGgh exhibited phasic inspiratory activity during wakefulness and sleep in all subjects. In six of seven subjects, mean and peak inspiratory EMGgh activities were significant (P less than 0.05) reduced during stages 2 and 3/4 NREM sleep and REM sleep compared with wakefulness. This reduction of EMGgh activity was shown to result from a sleep-related decline in the level of tonic muscle activity. Phasic inspiratory EMGgh activity during all stages of sleep was not significantly different from that during wakefulness. Of interest, tonic, phasic, and peak EMGgh activities were not significantly reduced during REM sleep compared with any other sleep stage in any subject. In addition, the slope of onset of phasic EMGgh activity was not different during stage 2 NREM and REM sleep compared with wakefulness in these subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Postinspiratory activity of the parasternal and external intercostal muscles in awake canines.

Previous studies have shown in awake dogs that activity in the crural diaphragm, but not in the costal diaphragm, usually persists after the end of inspiratory airflow. It has been suggested that this difference in postinspiratory activity results from greater muscle spindle content in the crural diaphragm. To evaluate the relationship between muscle spindles and postinspiratory activity, we have studied the pattern of activation of the parasternal and external intercostal muscles in the second to fourth interspaces in eight chronically implanted animals. Recordings were made on 2 or 3 successive days with the animals breathing quietly in the lateral decubitus position. The two muscles discharged in phase with inspiration, but parasternal intercostal activity usually terminated with the cessation of inspiratory flow, whereas external intercostal activity persisted for 24.7 +/- 12.3% of inspiratory time (P < 0.05). Forelimb elevation in six animals did not affect postinspiratory activity in the parasternal but prolonged postinspiratory activity in the external intercostal to 45.4 +/- 16.3% of inspiratory time (P < 0.05); in two animals, activity was still present at the onset of the next inspiratory burst. These observations support the concept that muscle spindles are an important determinant of postinspiratory activity. The absence of such activity in the parasternal intercostals and costal diaphragm also suggests that the mechanical impact of postinspiratory activity on the respiratory system is smaller than conventionally thought.     

Geniohyoid muscle properties and myosin heavy chain composition are altered after short-term intermittent hypoxic exposure.

Patients with obstructive sleep apnea (OSA) often exhibit fatigued or inefficient upper airway dilator and constrictor muscles; an upper airway dilator, the geniohyoid (GH) muscle, is a particular example. Intermittent hypoxia (IH) is a frequent concomitant of OSA, and it may trigger muscle fiber composition changes that are characteristic of a fatigable nature. We examined effects of short-term IH on diaphragmatic and GH muscle fiber composition and fatigue properties by exposing 24 rats to alternating 10.3% O(2)-balance N(2) and room air every 480 s (240 s duty cycle) for a total duration of 5, 10, 15, 20, or 30 h. Sternohyoid fiber composition was also examined. Control animals were exposed to room air on the same schedule. Single-fiber analyses showed that GH muscle fiber types changed completely from myosin heavy chain (MHC) type 2A to MHC type 2B after 10 h of exposure, and the conversion was maintained for at least 30 h. Sternohyoid muscle fibers showed a delayed transition from MHC type 2A/2B to MHC type 2B. In contrast, major fiber types of the diaphragm were not significantly altered. The GH muscles showed similar tension-frequency relationships in all groups, but an increased fatigability developed, proportional to the duration of IH treatment. We conclude that short-term IH exposure alters GH muscle composition and physical properties toward more fatigable, fast-twitch types and that it may account for the fatigable upper airway fiber types found in sleep-disturbed breathing.     

Thyroarytenoid muscle activity during hypoxia in awake lambs

It is generally accepted that hypoxia in early life results in active laryngeal braking of expiratory airflow via the recruitment of glottic adductor muscles. We examined the electromyogram expiratory activity of the thyroarytenoid muscle in seven 11- to 18-day-old awake nonsedated lambs exposed to an inspired O2 fraction of 0.08 for 18 min. The lambs breathed through a face mask and a pneumotachograph. During baseline prehypoxic breathing, the thyroarytenoid muscle was largely inactive in each awake lamb. Unexpectedly, no recruitment of the thyroarytenoid muscle was recorded during hypoxia in any of the seven lambs; simultaneous examination of the flow-volume curves revealed an absence of expiratory airflow braking. Also unexpectedly, marked expiratory activity of the thyroarytenoid muscle was recorded, with each expiration occurring within less than 10 s after the return to room air. The resulting delay of expiration was apparent in the flow-volume loops. Thus, in awake 11- to 18-day-old lambs, 1) active expiratory glottic adduction is absent during hypoxia and 2) a return from hypoxia to room air results in prolonged expiration as well as active glottic adduction that controls end-expiratory lung volume.     

Vagal contributions to respiratory muscle activity during eupnea in the awake dog.

We examined the effects of reversible vagal cooling on respiratory muscle activities in awake chronically instrumented tracheotomized dogs. We specifically analyzed electromyographic (EMG) activity and its ventilatory correlates, end-expiratory lung volume (EELV) and diaphragmatic resting length via sonomicrometry. Elimination of phasic and tonic mechanoreceptor activity by vagal cooling doubled the EMG activity of the costal, crural, and parasternal muscles, with activation occurring sooner relative to the onset of inspiratory flow. Diaphragmatic postinspiration inspiratory activity in the intact dog coincided with a brief mechanical shortening of the diaphragm during early expiration; vagal blockade removed both the electrical activity and the mechanical shortening. Vagal blockade also doubled the EMG activity of a rib cage expiratory muscle, the triangularis sterni, but reduced that of an abdominal expiratory muscle, the transversus abdominis. Within-breath electrical activity of both muscles occurred sooner relative to the onset of expiratory flow during vagal blockade. Vagal cooling was also associated with a 12% increase in EELV and a 5% decrease in end-expiratory resting length of the diaphragm. We conclude that vagal input significantly modulates inspiratory and expiratory muscle activities, which help regulate EELV efficiently and optimize diaphragmatic length during eupneic breathing in the awake dog.     

Vagal modulation of respiratory muscle activity in awake dogs during exercise and hypercapnia.

Using chronically instrumented awake tracheotomized dogs, we examined the contributions of vagal feedback to respiratory muscle activities, both electrical and mechanical, during normoxic hypercapnia (inspired CO2 fraction = 0.03, 0.04, 0.05, and 0.06) and during mild treadmill exercise (3, 4.3, and 6.4 km/h). Cooling exteriorized vagal loops eliminated both phasic and tonic mechanoreceptor input during either of these hyperpneas. At a given chemical or locomotor stimulus, vagal cooling caused a further increase in costal, crural, parasternal, and rib cage expiratory (triangularis sterni) muscles. No further change in abdominal expiratory muscle activity occurred secondary to vagal cooling during these hyperpneas. However, removal of mechanoreceptor input during hypercapnia was not associated with consistent changes in end-expiratory lung volume, as measured by the He-N2 rebreathe technique. We conclude that during these hyperpneas 1) vagal input is not essential for augmentation of expiratory muscle activity and 2) decrements in abdominal expiratory muscle activity may be offset by increments in rib cage expiratory muscle activity and contribute to the regulation of end-expiratory lung volume.     

Chemoreceptor and vagal influences on thyroarytenoid muscle activity in awake lambs during hypoxia.

This study was designed to identify the various controllers of thyroarytenoid (TA) activity in lambs during resting breathing, hypocapnic hypoxia, and isocapnic hypoxia. The TA muscle is known as the major adductor of the laryngeal aperture. We assumed that both the chemoreceptors and vagal nerves would interact to inhibit TA activity during hypoxia and to favor the occurrence of hyperpnea as a defense against hypoxia. We recorded TA activity directly in 11 awake lambs, aged 11 to 22 days, and studied them in three groups: four normals, four carotid body denervated, and three vagotomized. To test the contribution of the chemoreceptors to TA activity, we used pure O2 tests (Dejours' test) to silence the effects of the peripheral arterial chemoreceptors on the larynx during resting breathing and during the course of two hypoxia tests (the first: hypocapnic hypoxia; the second: isocapnic hypoxia). Our results confirmed 1) that both the peripheral arterial chemoreceptors and the vagal nerves inhibit the TA activity of 15-day-old lambs, during both resting and hypocapnic hypoxia conditions, and 2) that their effects override the hypocapnic effects that would otherwise recruit the TA muscle and close the glottis during hypocapnic hypoxia. We also found that vagotomy, or the pure O2 test, causes major recruitment of TA activity. These findings confirm that 15-day-old lambs are capable of using sustained hyperventilation as a means of fighting hypoxia, and that, because of the control of both the vagus nerves and the chemoreceptors, the laryngeal dynamic is able to keep the glottis aperture actively open, thereby favoring the hyperpnea.     

Respiratory muscle electromyogram responses to acute hypoxia in awake ponies

We determined the effect of acute hypoxia on the ventilatory (VE) and electromyogram (EMG) responses of inspiratory (diaphragm) and expiratory (transversus abdominis) muscles in awake spontaneously breathing ponies. Eleven carotid body-intact (CBI) and six chronic carotid body-denervated (CBD) ponies were studied during normoxia (fractional inspired O2 concn [FIO2] = 0.21) and two levels of hypoxia (FIO2 approximately 0.15 and 0.12; 6-10 min/period). Four CBI and five CBD ponies were also hilar nerve (pulmonary vagal) denervated. Mean VE responses to hypoxia were greater in CBI ponies (delta arterial PCO2 = -4 and -7 Torr in CBI during hypoxic periods; -1 and -2 Torr in CBD). Hypoxia increased the rate of rise and mean activity of integrated diaphragm EMG in CBI (P less than 0.05) and CBD (P greater than 0.05) ponies relative to normoxia. Duration of diaphragm activity was reduced in CBI (P less than 0.05) but unchanged in CBD ponies. During hypoxia in both groups of ponies, total and mean activities per breath of transversus abdominis were reduced (P less than 0.05) without a decrease in rate of rise in activity. Time to peak and total duration of transversus abdominis activity were markedly reduced by hypoxia in CBI and CBD ponies (P less than 0.05). Hilar nerve denervation did not alter the EMG responses to hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Differential respiratory muscle recruitment induced by clonidine in awake goats

The purpose of this study was to test thehypothesis that dysrhythmic breathing induced by the₂-agonist clonidine isaccompanied by differential recruitment of respiratory muscles. Inadult goats (n = 14) electromyographic(EMG) measurements were made from inspiratory muscles (diaphragm andparasternal intercostal) and expiratory muscles [triangularissterni (TS) and transversus abdominis (Abd)]. EMG of thethyroarytenoid (TA) muscle was used as an index of upper airway(glottal) patency. Peak EMG activities of all spinal inspiratory andexpiratory muscles were augmented by central and peripheralchemoreceptor stimuli. Phasic TA was apparent in the postinspiratoryphase of the breathing cycle under normoxic conditions. Duringdysrhythmic breathing episodes induced by clonidine, TS and Abdactivities were attenuated or abolished, whereas diaphragm andparasternal intercostal activities were unchanged. There was no tonicactivation of TS or Abd EMG during apneas; however, TA activity becametonic throughout the apnea. We conclude that1) ₂-adrenoceptor stimulationresults in differential recruitment of respiratory muscles duringrespiratory dysrhythmias and 2) apneas are accompanied by active glottic closure in the awake goat.

     

Expiratory muscle activity in the awake and sleeping human during lung inflation and hypercapnia.

Expiratory muscle activity has been shown to occur in awake humans during lung inflation; however, whether this activity is dependent on consciousness is unclear. Therefore we measured abdominal muscle electromyograms (intramuscular electrodes) in 13 subjects studied in the supine position during wakefulness and non-rapid-eye-movement sleep. Lung inflation was produced by nasal continuous positive airway pressure (CPAP). CPAP at 10-15 cmH2O produced phasic expiratory activity in two subjects during wakefulness but produced no activity in any subject during sleep. During sleep, CPAP to 15 cmH2O increased lung volume by 1,260 +/- 215 (SE) ml, but there was no change in minute ventilation. The ventilatory threshold at which phasic abdominal muscle activity was first recorded during hypercapnia was 10.3 +/- 1.1 l/min while awake and 13.8 +/- 1 l/min while asleep (P less than 0.05). Higher lung volumes reduced the threshold for abdominal muscle recruitment during hypercapnia. We conclude that lung inflation alone over the range that we studied does not alter ventilation or produce recruitment of the abdominal muscles in sleeping humans. The internal oblique and transversus abdominis are activated at a lower ventilatory threshold during hypercapnia, and this activation is influenced by state and lung volume.     

Mechanisms of sympathoexcitation: single-unit analysis of muscle vasoconstrictor neurons in awake OSAS subjects.

In congestive heart failure (CHF), muscle sympathetic activity (MSNA) is greatly elevated, but our laboratory has shown that single muscle vasoconstrictor neurons primarily fire only once per cardiac interval, as in normal subjects (Elam M and Macefield VG. J Appl Physiol 91: 717-724, 2001; Macefield VG, Rundqvist B, Sverrisdottir YB, Wallin BG, and Elam M. Circulation 100: 1708-1713, 1999). In this study, we used patients with obstructive sleep apnea syndrome (OSAS) to test the hypothesis that this firing pattern is maintained in other states of sympathoexcitation. Unitary recordings were made from muscle vasoconstrictor neurons in eight awake OSAS patients. The average firing frequency of 12 units was 0.96 Hz and the firing probability 51%, similar to previous observations in CHF patients (0.98 Hz, 55%) but higher than in healthy subjects (0.40 Hz, 31%). However, the percentages of cardiac intervals in which neurons generated one, two, three, or four spikes were 59, 27, 10, and 3% in OSAS, compared with 71, 18, 7, and 2% in CHF and 73, 18, 5, and 3% in healthy subjects. Thus the firing pattern is different in OSAS and CHF, leading to rejection of the hypothesis: although in both conditions individual neurons show an increase in firing probability, in OSAS patients they also fire more often within a cardiac interval. It is likely that differences may also be apparent in other states of sympathoexcitation.     

Breathing route influences upper airway muscle activity in awake normal adults

Both nasal obstruction and nasal anesthesia result in disordered breathing during sleep in humans, and bypassing the nasal route during tidal breathing in experimental animals produces decreased electromyographic activity of upper airway (UA) dilating muscles. To investigate UA responses to breathing route in normal awake humans, we studied eight healthy males (ages 21-38 yr) during successive trials of voluntary nose breathing (N), voluntary mouth breathing (M), and mouth breathing with nose occluded (MO). We measured genioglossus electromyographic activity (EMGgg) with perorally inserted bipolar electrodes, alae nasi (EMGan) and diaphragm EMG activity (EMGdi) with surface electrodes, and minute ventilation (VE) with a pneumotachograph. Mean phasic inspiratory EMG activity of both UA muscles was significantly greater during N than during M or MO, even when a 2.5-cmH2O.l-1.s inspiratory resistance was added to MO (P less than 0.01). In contrast, neither EMGdi nor VE was consistently affected by breathing route. EMGgg during N was significantly decreased after selective topical nasal anesthesia (P less than 0.002); a decrease in EMGan did not achieve statistical significance. These data suggest that peak UA dilating muscle activity may be modulated by superficial receptors in the nasal mucosa sensitive to airflow.