Abdominal Expiratory Activity Research Articles

Expiratory activity during sleep in children.

Sleep irregularities and respiratory events (apnea, O2 desaturation or a combination thereof) are often present in the infant population. While inspiration is the main active process in the act of breathing, expiration is generally thought to occur passively. Although commonly considered as quiet during sleep, expiratory abdominal muscles have been proposed to be recruited to promote ventilation, facilitate gas exchange, and reduce the work of breathing during conditions of increased respiratory drive, exercise, or airway obstruction. In this study, we investigated the occurrence of expiratory abdominal muscle activity in polysomnographic studies of subjects (aged 0-2years) suspected of sleep disordered breathing. Our results indicate that abdominal muscle activation occurs during sleep, most frequently during non-rapid eye movement and rapid-eye movement states compared to slow-wave sleep. Furthermore, abdominal muscle activity was present during regular breathing or associated with respiratory events (apneas or O2 desaturation). In the latter case, abdominal muscle recruitment more frequently followed the onset of respiratory events and terminated with recovery from blood O2 desaturation events. We conclude that expiratory abdominal muscle activity contributes to the pattern of respiratory muscle recruitment during sleep in infants and given its temporal relationship with respiratory events, we propose that its recruitment could facilitate proper ventilation by counteracting airway resistance and O2 desaturation in infancy across different stages of sleep.

Inhibitory control of active expiration by the Bötzinger complex in rats.

Contraction of abdominal muscles at the end of expiration during metabolic challenges (such as hypercapnia and hypoxia) improves pulmonary ventilation. The emergence of this active expiratory pattern requires the recruitment of the expiratory oscillator located on the ventral surface of the medulla oblongata. Here we show that an inhibitory circuitry located in the Bötzinger complex is an important source of inhibitory drive to the expiratory oscillator. This circuitry, mediated by GABAergic and glycinergic synapses, provides expiratory inhibition that restrains the expiratory oscillator under resting condition and regulates the formation of abdominal expiratory activity during active expiration. By combining experimental and modelling approaches, we propose the organization and connections within the respiratory network that control the changes in the breathing pattern associated with elevated metabolic demand. The expiratory neurons of the Bötzinger complex (BötC) provide inhibitory inputs to the respiratory network, which, during eupnoea, are critically important for respiratory phase transition and duration control. Here, we investigated how the BötC neurons interact with the expiratory oscillator located in the parafacial respiratory group (pFRG) and control the abdominal activity during active expiration. Using the decerebrated, arterially perfused in situ preparations of juvenile rats, we recorded the activity of expiratory neurons and performed pharmacological manipulations of the BötC and pFRG during hypercapnia or after the exposure to short-term sustained hypoxia - conditions that generate active expiration. The experimental data were integrated in a mathematical model to gain new insights into the inhibitory connectome within the respiratory central pattern generator. Our results indicate that the BötC neurons may establish mutual connections with the pFRG, providing expiratory inhibition during the first stage of expiration and receiving excitatory inputs during late expiration. Moreover, we found that application of GABAergic and glycinergic antagonists in the BötC caused opposing effects on abdominal expiratory activity, suggesting complex inhibitory circuitry within the BötC. Using mathematical modelling, we propose that the BötC network organization and its interactions with the pFRG restrain abdominal activity under resting conditions and contribute to abdominal expiratory pattern formation during active expiration observed during hypercapnia or after the exposure to short-term sustained hypoxia.

Feedforward discharges couple the singing central pattern generator and ventilation central pattern generator in the cricket abdominal central nervous system

We investigated the central nervous coordination between singing motor activity and abdominal ventilatory pumping in crickets. Fictive singing, with sensory feedback removed, was elicited by eserine-microinjection into the brain, and the motor activity underlying singing and abdominal ventilation was recorded with extracellular electrodes. During singing, expiratory abdominal muscle activity is tightly phase coupled to the chirping pattern. Occasional temporary desynchronization of the two motor patterns indicate discrete central pattern generator (CPG) networks that can operate independently. Intracellular recordings revealed a sub-threshold depolarization in phase with the ventilatory cycle in a singing-CPG interneuron, and in a ventilation-CPG interneuron an excitatory input in phase with each syllable of the chirps. Inhibitory synaptic inputs coupled to the syllables of the singing motor pattern were present in another ventilatory interneuron, which is not part of the ventilation-CPG. Our recordings suggest that the two centrally generated motor patterns are coordinated by reciprocal feedforward discharges from the singing-CPG to the ventilation-CPG and vice versa. Consequently, expiratory contraction of the abdomen usually occurs in phase with the chirps and ventilation accelerates during singing due to entrainment by the faster chirp cycle.

Influence of expiratory abdominal muscle activity during straight leg raise according to lumbar supplement thickness and angle of leg raise

The purpose of this study is to measure the comparative abdominal muscle activation during straight leg raise according lumbar supplement thickness and angle of leg raise. Healthy 14 male and 16 female adults, 30 people in total were recruited. When straight leg raise, lumbar supplement thickness and angle of leg raise. We measured abdominis with ultrasonograpy. All measurements of the experiments were performed by two-way ANOVA. According to a study when exercise straight leg raise, there are no interaction between lumbar supplement and angle of leg raise. But when apply only lumbar supplement or apply only angle of leg raise, external oblique and rectus abdominis are show statically significant. It is considered exercise straight leg raise with lumbar supplement or apply angle of leg raise are effective way for selective abdominal muscle exercise.

Cholinergic modulation of the parafacial respiratory group.

This study investigates the effects of cholinergic transmission on the expiratory oscillator, the parafacial respiratory group (pFRG) in urethane anaesthetized adult rats. Local inhibition of the acetyl cholinesterase enzyme induced activation of expiratory abdominal muscles and active expiration. Local application of the cholinomimetic carbachol elicited recruitment of late expiratory neurons, expiratory abdominal muscle activity and active expiration. This effect was antagonized by local application of the muscarinic antagonists scopolamine, J104129 and 4DAMP. We observed distinct physiological responses between the more medial chemosensitive region of the retrotrapezoid nucleus and the more lateral region of pFRG. These results support the hypothesis that pFRG is under cholinergic neuromodulation and the region surrounding the facial nucleus contains a group of neurons with distinct physiological roles. Active inspiration and expiration are opposing respiratory phases generated by two separate oscillators in the brainstem: inspiration driven by a neuronal network located in the preBötzinger complex (preBötC) and expiration driven by a neuronal network located in the parafacial respiratory group (pFRG). While continuous activity of the preBötC is necessary for maintaining ventilation, the pFRG behaves as a conditional expiratory oscillator, being silent in resting conditions and becoming rhythmically active in the presence of increased respiratory drive (e.g. hypoxia, hypercapnia, exercise and through release of inhibition). Recent evidence from our laboratory suggests that expiratory activity in the principal expiratory pump muscles, the abdominals, is modulated in a state-dependent fashion, frequently occurring during periods of REM sleep. We hypothesized that acetylcholine, a neurotransmitter released in wakefulness and REM sleep by mesopontine structures, contributes to the activation of pFRG neurons and thus acts to promote the recruitment of expiratory abdominal muscle activity. We investigated the stimulatory effect of cholinergic neurotransmission on pFRG activity and recruitment of active expiration in vivo under anaesthesia. We demonstrate that local application of the acetylcholinesterase inhibitor physostigmine into the pFRG potentiated expiratory activity. Furthermore, local application of the cholinomimetic carbachol into the pFRG activated late expiratory neurons and induced long lasting rhythmic active expiration. This effect was completely abolished by pre-application of the muscarinic antagonist scopolamine, and more selective M3 antagonists 4DAMP and J104129. We conclude that cholinergic muscarinic transmission contributes to excitation of pFRG neurons and promotes both active recruitment of abdominal muscles and active expiratory flow.

Generation of active expiration by serotoninergic mechanisms of the ventral medulla of rats

Abdominal expiratory activity is absent at rest and is evoked during metabolic challenges, such as hypercapnia and hypoxia, or after the exposure to intermittent hypoxia (IH). The mechanisms engaged during this process are not completely understood. In this study, we hypothesized that serotonin (5-HT), acting in the retrotrapezoid nucleus/parafacial respiratory group (RTN/pFRG), is able to generate active expiration. In anesthetized (urethane, ip), tracheostomized, spontaneously-breathing adult male Holtzman rats we microinjected a serotoninergic agonist and antagonist bilaterally in the RTN/pFRG and recorded diaphragm and abdominal muscle activities. We found that episodic (3 times, 5 min apart), but not single microinjections of 5-HT (1 mM) in the RTN/pFRG elicited an enduring (>30 min) increase in abdominal activity. This response was amplified in vagotomized rats and blocked by previous 5-HT receptor antagonism with ketanserin (10 µM). Episodic 5-HT microinjections in the RTN/pFRG also potentiated the inspiratory and expiratory reflex responses to hypercapnia. The antagonism of 5-HT receptors in the RTN/pFRG also prevented the long-term facilitation (>30 min) of abdominal activity in response to acute IH exposure (10 × 6-7% O for 45 s every 5 min). Our findings indicate the activation of serotoninergic mechanisms in the RTN/pFRG is sufficient to increase abdominal expiratory activity at resting conditions and required for the emergence of active expiration after IH in anesthetized animals.

Electrophysiological properties of abdominal muscle‐projecting expiratory motoneurons of rats

Expiration is considered a passive process during resting breathing condition. There is a lack of information about the intrinsic electrophysiological properties of expiratory motoneurons and their possible changes in conditions in which the expiration becomes an active process, such as hypoxia. Considering that abdominal expiratory muscle activity depends on excitability of these motoneurons, here we aimed to characterize the electrophysiological properties of abdominal muscle‐projecting expiratory motoneurons combining retrograde tracer, immunofluorescence and whole cell patch clamp, in thoraco‐lumbar spinal cord slices from juvenile Wistar rats. Three different types of cholinergic expiratory motoneurons with similar capacitance were recorded: neurons with spontaneous action potentials whose resting potential hyperpolarizes (−65 ± 5 mV vs −69.7 ± 4 mV, n=9) and firing frequency decreases (8.5 ± 2 Hz vs 1.7 ± 1.3 Hz, n=9) after synaptic blockade. The passive properties of these motoneurons, such as input resistance and excitability, did not change after synaptic blockade (Ri = 0.16 ± 0.03 GΩ vs 0.13 ± 0.03 GΩ; Excitability = 40 ± 10 Hz vs 32 ± 11 Hz, n=9). The second group of motoneurons also exhibited spontaneous action potentials, but showed spike frequency adaptation, slowing or ceasing firing frequency during a maintained stimulus. Their membrane potential also hyperpolarized (−60 ± 1 mV vs −66 ± 1 mV, n=4) and firing frequency was abolished by synaptic blockade. On the other hand, no differences in the input resistance was observed (0.13 ± 0.01 GΩ vs 0.11 ± 0.01 GΩ, n=4). The third group did not show spontaneous action potential and synaptic blockade did not change membrane potential (−72.2 ± 2 mV vs −76 ± 3 mV, n=6) or input resistance (0.1 ± 0.04 GΩ vs 0.06 ± 0.02 GΩ, n=6). However, synaptic blockade decreased their intrinsic excitability. Overall, our data show that there are three different populations of abdominal muscle‐projecting expiratory motoneurons in rats, which may contribute to recruitment of expiratory muscles in different physiological and pathophysiological conditions.Support or Funding InformationFAPESP, CAPES, CNPQ

Serotoninergic Antagonism in the Retrotrapezoid Nucleus Prevents the Expiratory Long‐Term Facilitation Induced by Acute Intermittent Hypoxia

Serotonin (5‐HT) plays an important role in the development of sympathetic and phrenic long‐term facilitation (LTF) elicited by acute intermittent hypoxia (AIH). Herein, we evaluated the role of 5‐HT in the retrotrapezoid nucleus (RTN) on the emergence of active expiratory pattern in response to AIH. Using anesthetized (urethane; 1.2 g/Kg, ip) male Holztmann rats (280‐290 g), we analyzed the changes in the arterial pressure, heart rate and in the diaphragmatic and abdominal (ABD) activities elicited by single and repeated (3 times, 5 min apart) bilateral microinjections of 5‐HT (1mM, 50nl) in the RTN. We also analyzed the effects of bilateral microinjections of ketanserin (5‐HT2A antagonist; 10 µM, 50 nl) in the RTN on the cardiorespiratory changes induced by AIH (10 times of 6‐7% O2, for 45 s, each 5 min). Repeated, but not single, microinjections of 5‐HT in the RTN (n=7) elicited a sustained increase in the abdominal expiratory activity (ΔABD: 85±33%, 60 min after microinjections, P<0.05) that was prevented by previous microinjections of ketanserin. The 5HT2A receptor antagonism in the RTN during AIH exposure also prevented the increase in ABD activity evoked by AIH (ΔEMGABD: 40±9 vs ‐1±1% 60 min after AIH, respectively vehicle and ketanserin; P<0.05). The other cardiorespiratory parameters were not affected by the 5‐HT and the ketanserin microinjections in the RTN. Our results indicate that, in anesthetized conditions, the activation of serotoninergic receptors in the RTN is sufficient to promote a sustained increase in abdominal activity and required for the emergence of expiratory LTF induced by AIH. Supported by FAPESP, CNPq, CAPES and PROPe.

Vagal afferent control of abdominal expiratory activity in response to hypoxia and hypercapnia in rats

In the present study, we tested the hypothesis that vagal afferent information modulates the pattern of expiratory response to hypercapnia and hypoxia. Simultaneous recordings of airflow, diaphragmatic (DIA) and oblique abdominal muscle (ABD) activities were performed in anesthetized (urethane, 1.2g/kg), tracheostomized, spontaneously breathing male Wistar rats (290–320g, n=12). The animals were exposed to hypercapnia (7 and 10% CO2 for 5min) and hypoxia (7% O2 for 1min) before and after bilateral vagotomy. We verified that the percentage increase in DIA burst amplitude elicited by hypercapnia and hypoxia episodes was similar between intact and vagotomized rats (P>0.05). In contrast, hypercapnia and hypoxia promoted a marked increase in ABD activity in vagotomized, but not in intact rats (P<0.01). These amplified expiratory motor changes after vagotomy were associated with enhanced expiratory airflow (P<0.01) and augmented tidal volume responses (P<0.01). Our data indicates that, in anesthetized conditions, the removal of peripheral afferent inputs facilitates the processing of active expiration in response to hypercapnia and hypoxia in rats.

Periodic Leg Movement, Nasal CPAP, and Expiratory Muscles

Periodic leg movements (PLMs) may appear during nasal CPAP titration, persisting despite the elimination of hypopneas. Systematic recordings of expiratory abdominal muscles on the right and left sides with surface electromyographic (EMG) electrodes lateral to navel, and close from the lateral side of abdomen, were added during nasal CPAP titration for treatment of obstructive sleep apnea (OSA). Positive airway pressure was titrated during nocturnal polysomnography, based on analysis of the flow curve derived from the CPAP equipment and EEG analysis, including persistence of phases A2 and A3 of the cyclic alternating pattern (CAP). The requirement was to eliminate American Association of Sleep Medicine (AASM)-defined hypopnea and also flow limitation and abnormal EEG patterns. When CPAP reached valid results, it was lowered at the time of awakening by 2 or 3 cm H(2)O, and titration was performed again. Data collected during a 7-month period on adults with a prior diagnosis of OSA who had received treatment with nasal CPAP regardless of age and sex were rendered anonymous and were retrospectively rescored by a blinded investigator. Eighty-one successively seen patients with PLMs during CPAP titration were investigated. Elimination of AASM-defined hypopnea was not sufficient to eliminate the PLMs observed during the titration; higher CPAP eliminated flow limitation and CAP phases A2 and A3 and persisting PLMs. PLMs were associated with simultaneous EMG bursts in expiratory abdominal muscles. The presence of PLMs during CPAP titration indicates the persistence of sleep-disordered breathing. PLMs during CPAP titration are related to the presence of abdominal expiratory muscle activity.

Essential Role of Phox2b-Expressing Ventrolateral Brainstem Neurons in the Chemosensory Control of Inspiration and Expiration

Phox2b-expressing neurons of the retrotrapezoid nucleus (RTN), located in the ventrolateral brainstem, are sensitive to changes in PCO(2)/pH, have excitatory projections to the central respiratory rhythm/pattern generator, and their activation enhances central respiratory drive. Using in vivo (conscious and anesthetized rats) and in situ (arterially perfused rat brainstem-spinal cord preparations) models, we evaluated the functional significance of this neuronal population for both resting respiratory activity and the CO(2)-evoked respiratory responses by reversibly inhibiting these neurons using the insect peptide allatostatin following transduction with a lentiviral construct to express the G-protein-coupled Drosophila allatostatin receptor. Selective inhibition of the Phox2b-expressing neurons in the ventrolateral brainstem, including the RTN, using allatostatin was without effect on resting respiratory activity in conscious rats, but decreased the amplitude of the phrenic nerve discharge in anesthetized rats and the in situ rat preparations. Postinspiratory activity was also reduced in situ. In the absence or presence of the peripheral chemoreceptor input, inhibiting the Phox2b-expressing neurons during hypercapnia abolished the CO(2)-evoked abdominal expiratory activity in anesthetized rats and in situ preparations. Inspiratory responses evoked by rising levels of CO(2) in the breathing air were also reduced in anesthetized rats with denervated carotid bodies and conscious rats with peripheral chemoreceptors intact (by 28% and 60%, respectively). These data indicate a crucial dependence of central expiratory drive upon Phox2b-expressing neurons of the ventrolateral brainstem and support the hypothesis that these neurons contribute in a significant manner to CO(2)-evoked increases of inspiratory activity.

Response of individual abdominal muscles to nasal CPAP in supine and standing positions in humans

The respiratory function of individual abdominal muscles in humans is not well known. Some workers have reported that abdominal muscles act as a single unit during breathing, whereas others have reported differential activation. In the present study, fine wire electrodes were inserted into the rectus abdominis (RA), external oblique (EO), internal oblique (IO), and transversus abdominis (TA) muscles in six healthy awake subjects under direct vision provided by high-resolution ultrasonography. Electromyographic (EMG) signals were then recorded in the supine and standing positions during resting ventilation without nasal continuous positive airway pressure (nCPAP), then on nCPAP at 5, 10, 15, and 20 cmH2O. Peak values of integrated EMG during expiration were measured. For each abdominal muscle, the number of subjects showing expiratory EMG activity increased with increasing nCPAP or with a change in posture from supine to standing or both. The number of subjects showing expiratory abdominal muscle activity under any condition followed the order: RA < or = EO < or = IO < or = TA. Peak expiratory EMG activity increased significantly with increasing nCPAP in the standing position for EO (p < 0.05), and in both positions for IO and TA (both p < 0.01). These results suggest that: 1) both the standing position and nCPAP imposed an expiratory load, 2) TA and IO are most sensitive to expiratory loading, and are the primary expiratory muscles, and 3) RA is least sensitive to expiratory loading, and is a secondary expiratory muscle. We conclude that individual abdominal muscles respond differently to expiratory loading.

Abdominal expiratory muscle activity in anesthetized vagotomized neonatal rats

The pattern of respiratory activity in abdominal muscles was studied in anesthetized, spontaneously breathing, vagotomized neonatal rats at postnatal days 0-3. Anesthesia (2.0% isoflurane, 50% O(2)) depressed breathing and resulted in hypercapnia. Under this condition, abdominal muscles showed discharge late in the expiratory phase (E2 activity) in most rats. As the depth of anesthesia decreased, the amplitude of discharges in the diaphragm and abdominal muscles increased. A small additional burst frequently occurred in abdominal muscles just after the termination of diaphragmatic inspiratory activity (E1 or postinspiratory activity). Since this E1 activity is not often observed in adult rats, the abdominal respiratory pattern likely changes during postnatal development. Anoxia-induced gasping after periodic expiratory activity without inspiratory activity, and in most rats, abdominal expiratory activity disappeared before terminal apnea. These results suggest that a biphasic abdominal motor pattern (a combination of E2 and E1 activity) is a characteristic of vagotomized neonatal rats during normal respiration.

GABAA and glycine receptors in regulation of intercostal and abdominal expiratory activity in vitro in neonatal rat.

The roles played by GABAA and glycine receptors in inspiratory-expiratory motor co-ordination and in tonic inhibitory regulation of expiratory motor activity were studied using brainstem-spinal cord (-rib) preparations from neonatal rats. Inspiratory activity was recorded from the C4 ventral root. Expiratory activity in internal intercostal muscle, internal oblique muscle or T13 ventral root was evoked by a decrease in perfusate pH from 7.4 to 7.1 (i.e. from normal to low pH conditions) and was limited to the first part of the expiratory phase. Under low pH conditions, bath application of 10 microM bicuculline, a GABAA receptor antagonist, caused the inspiratory burst to overlap the expiratory burst in 2/7 preparations. Overlapping of the expiratory burst with the inspiratory burst was observed in 7/7 preparations made under 10 microM bicuculline. Furthermore, such preparations exhibited expiratory bursts under bicuculline-containing normal pH conditions. Local application of 10 microM bicuculline to the brainstem under normal pH conditions evoked expiratory bursts, some of which overlapped the inspiratory bursts. Picrotoxin, another antagonist of the GABAA receptor, had similar effects. Under normal pH conditions, application of strychnine (0.2- 2.0 microM; a glycine receptor antagonist) to the brainstem did not evoke expiratory bursts. On subsequent application of strychnine-containing low pH solution, expiratory bursts were evoked and some (0.5 microM) or all (2.0 microM) of these overlapped the inspiratory burst. Simultaneous application of picrotoxin and strychnine to the brainstem evoked expiratory bursts that overlapped the inspiratory bursts and a subsequent decrease in perfusate pH to 7.1 increased the frequency of the respiratory rhythm. It was a characteristic finding that the duration of the expiratory burst exceeded that of the inspiratory burst under control low pH conditions. This remained true during concurrent blockade of GABAA and glycine receptors. The results suggest that in the in vitro preparation from neonatal rats: (1) GABAA and glycine receptors within the brainstem play important roles in the co-ordination between inspiratory and expiratory motor activity, (2) tonic inhibition via GABAA receptors, but not glycine receptors, plays a role in the regulation of expiratory motor activity and (3) inspiratory and expiratory burst termination is independent of both GABAA and glycine receptors.

Neck and abdominal muscle activity during a sniff

Measurement of sniff nasal inspiratory pressure (SNIP) is now used widely as a simple, non-invasive assessment of global respiratory muscle strength, even though the technique evolved originally from measurements of trans-diaphragmatic pressure ( P di) that reflect the status of the diaphragm. The relative participation of major respiratory muscles, apart from the diaphragm, in the generation of SNIP is not known. Therefore, we examined the activity during a sniff of both neck and abdominal “accessory” muscles. In seven young adults we implanted fine wire EMG electrodes under direct vision with high-resolution ultrasound into scalene, sternocleidomastoid, trapezius, and transversus abdominis. SNIP was measured during sniffs that were short and sharp, from low to maximal intensity, in both standing and supine postures. Mean maximum SNIP was −105.6 cm H 2O (SD 32.9) in supine and −94.5 cm H 2O (26.6) in the standing posture, (difference NS). In every subject, scalene activity appeared even at the lowest SNIP, and increased linearly with increasing SNIP. Sternomastoid activity appeared at higher SNIP levels in three of seven subjects. By contrast, trapezius activity was never present at low SNIP, and appeared in only 2 subjects at maximum SNIP. Sniff abdominal expiratory activity was inconsistent with no activity of transversus in four of seven subjects even at greatest SNIP. Thus, we observed differential activation among these non-diaphragm respiratory muscles during SNIP; while some accessory muscles were very active, others were unlikely to contribute to generation of SNIP. Clinically, this indicates SNIP will be impacted unequally by loss of function of specific respiratory muscles.

Abdominal Muscle Activity in Sleep Apnea During Continuous Positive Airway Pressure Titration

The aim of this study was to investigate whether presence of expiratory abdominal muscle activity (EAMA) in obstructive sleep apnea syndrome (OSAS) patients during nasal continuous positive airway pressure (nCPAP) is due to either nCPAP overprescription or nCPAP underprescription. Airflow, esophageal pressure (Pes), and gastric pressure (Pga) were routinely measured during polysomnography aimed at determining the optimal nCPAP level, and the magnitude of EAMA was evaluated in relation to the nCPAP level and to the conventional indexes of upper-airway obstruction used during nCPAP titration. The study was performed 12 patients with OSAS. Six patients displayed sustained EAMA, ie, EAMA lasting > 3 min, and characterized by a decrease in abdominal diameter and a paradoxical rise in Pga during expiration. In all six patients, EAMA decreased gradually as nCPAP neared optimal levels, and then disappeared when the optimal nCPAP level was achieved. The decrease in EAMA as nCPAP increased was associated with an increase in minute ventilation, decreases in both inspiratory and expiratory resistance, a decrease in Pes swing, and the normalization of the inspiratory flow contour. We conclude that the EAMA observed in some OSAS patients might be an indirect marker of upper-airway obstruction, and that the presence of EAMA during nCPAP titration might indicate a suboptimal nCPAP level rather than a deleterious effect of nCPAP.

Respiratory muscle activity and oxygenation during sleep in patients with muscle weakness

Patients with respiratory muscle weakness show nocturnal hypoventilation, with oxygen desaturation particularly during rapid eye movement (REM) sleep, but evidence in individuals with isolated bilateral diaphragmatic paresis (BDP) is conflicting. The effect of sleep on relative activity of the different respiratory muscles of such patients and, consequently, the precise mechanisms causing desaturation have not been clarified. We have studied eight patients, four with generalized muscle weakness and four with isolated BDP during nocturnal sleep with measurements including oxygen saturation and surface electromyographic (EMG) activity of various respiratory muscle groups. Nocturnal oxygenation correlated inversely with postural fall in vital capacity, an index of diaphragmatic strength. During REM sleep, hypopnoea and desaturation occurred particularly during periods of rapid eye movements (phasic REM sleep). In most subjects, such events were "central" in type and associated with marked suppression of intercostal muscle activity, but two subjects had recurrent desaturation due to "obstructive" hypopnoea and/or apnoea. Expiratory activity of the external oblique muscle was present whilst awake and during non-rapid eye movement (NREM) sleep in seven of the eight subjects in the semirecumbent posture. This probably represents an "accessory inspiratory" effect, which aids passive caudal diaphragmatic motion as the abdominal muscles relax at the onset of inspiration. Expiratory abdominal muscle activity was suppressed in phasic REM sleep, suggesting that loss of this "accessory inspiratory" effect may contribute to "central" hypopnoea. We conclude that, in patients with muscle weakness, nocturnal oxygenation correlates with diaphragmatic strength.(ABSTRACT TRUNCATED AT 250 WORDS)

Regulation of respiratory muscle activities during chemoreceptor stimulation in adult horses

SUMMARY We examined the electromyographic activity of the costal portion of the diaphragm and the transverse abdominal and external oblique muscles in 6 chronically instrumented awake adult horses during eupneic breathing, during 2 levels of hypercapnia (fractional concentration of inspired CO2; FICO2 = 0.4 and 0.6), and during 2 levels of hypocapnic hypoxia (FICO2 = 0.15 and 0.12). Using the inert gas technique, we also measured the end-expiratory lung volumes of the 6 horses during eupnea, 6% CO2 challenge, and 12% O2 breathing. During eupneic breathing, phasic electrical activity of these 3 muscles was always present and was preceded by the onset of mechanical flow. At progressive levels of hypercapnia, the magnitude of inspiratory and expiratory electrical activity increased, and for the expiratory muscles, this recruitment coincided with significant (P &lt; 0.05) increases in peak expiratory gastric pressure. However, during hypocapnic hypoxia, differential recruitment patterns of the respiratory muscles were found. The electrical activity of the diaphragm increased in magnitude and occurred sooner relative to the onset of mechanical flow. The magnitude and onset of abdominal expiratory activity failed to increase significantly during these episodes of hyperpnea and this pattern of activity coincided with decrements in peak expiratory gastric pressure. Despite alterations in muscle recruitment patterns during these hyperpneic episodes, end-expiratory lung volume remained unchanged. Thus, we conclude that adult horses respond similarly to awake dogs during peripheral and central chemoreceptor stimulation.

Effects of Midazolam on Respiratory Muscles in Humans

Midazolam at sedative doses alters the breathing pattern; however, its effects on respiratory load and respiratory muscle activity have not been established completely. Therefore, the effects of midazolam (0.1 mg/kg) on total pulmonary resistances and on diaphragmatic, intercostal, and abdominal muscle patterns were studied in nine volunteers. Measurements were performed during control, 5 and 10 min after midazolam, and then 2 min after 1.0 mg of intravenous flumazenil. After midazolam, total pulmonary resistance increased from 6.3 +/- 0.65 to 36.6 +/- 8.1 cm H2O-L-1 x s-1 (P < 0.01), a pattern associated with an increased intercostal electromyographic activity (peak and slope; P < 0.05). By contrast, the ratio of gastric pressure on esophageal pressure changes decreased from 65.5% +/- 6.2% to 16.3% +/- 3.9% (P < 0.01), indicating reduced diaphragmatic activity. In 7/9 subjects, there was expiratory abdominal muscle activity. Flumazenil reversed all these effects. We conclude that midazolam 0.1 mg/kg increases total pulmonary resistance and elicits a compensatory load response characterized by an increase in inspiratory intercostal and expiratory abdominal muscle activities whereas diaphragmatic contribution is reduced.

Asynchronous Chest Wall Movements during Non-Rapid Eye Movement and Rapid Eye Movement Sleep in Children with Bronchopulmonary Dysplasia

The aim of this study was to assess whether age-related changes in thoracic shape modify patterns of thoracoabdominal asynchrony (TAA) or applicability of phase angle analysis during sleep in young children with increased respiratory loads. We assessed TAA during polysomnographic monitoring in 14 young children (mean age 32 months, range 19 to 46; mean weight 12.5 kg, range 9.3 to 17) with severe bronchopulmonary dysplasia (BPD). Of the patients 10 were severely enough affected to require tracheostomy. We measured asynchrony of rib cage (RC) and abdominal (AB) movements at midinspiration and the corresponding phase angle from oscillographic recordings during both non-REM and REM sleep. We measured the amplitude of "paradoxical" displacement of either RC or AB during inspiration and expressed this as a percentage of the total displacement of the compartment. Of 9 children who manifested early inspiratory AB paradox during non-REM sleep, 7 showed a figure eight on the Konno-Mead diagram. The magnitude of abdominal paradox during non-REM sleep was significantly positively correlated with age (n = 14, r = 0.68; p < 0.01). Phase angle was significantly negatively correlated with dynamic lung compliance (n = 14, r = -0.66; p < 0.01). During REM sleep, expiratory abdominal muscle activity was abolished and all patients with abdominal paradox "converted" to an open loop with RC paradox during inspiration. Graphic assessment of the Lissajous figure on the Konno-Mead diagram indicated when midinspiratory phase angle analysis did not reflect the severity of TAA and can be used to infer patterns of respiratory muscle recruitment. We conclude that young children manifest patterns of TAA that differ from the early inspiratory RC paradox commonly observed in infants. Comparison of RC-AB loops between non-REM and REM sleep in the same child can assess increased thoracic inspiratory efforts and expiratory muscle activity as potential mechanisms for abdominal paradox, as distinct from diaphragm ineffectiveness.