Diaphragm Electromyogram Research Articles

Diaphragmatic function in patients on continuous ambulatory peritoneal dialysis.

We investigated 8 patients undergoing continuous ambulatory peritoneal dialysis (CAPD) for diaphragmatic strength and the neuromechanical efficiency of the diaphragm while the abdomen was filled with dialysate and while it was empty. Maximum transdiaphragmatic pressure (Pdimax) served as parameter for diaphragmatic strength; diaphragmatic efficiency was assessed by simultaneously monitoring transdiaphragmatic pressure (Pdi) and diaphragmatic electromyogram (EMGdi) during room-air breathing and hyperoxic CO2-rebreathing. After instilling dialysate, Pdimax increased from 76.7 +/- 12.1 cmH2O to 92.2 +/- 16.3 cmH2O (P < 0.05). While the slopes of the regression lines relating minute ventilation (VE) to arterial CO2 tension, and the change in VE for a given change in Pdi during hypercapnic rebreathing were similar in both states, the slope of EMGdi vs Pdi was significantly steeper when the abdomen was filled (P < 0.05). The increase in Pdimax observed in the filled state may suggest an adaptive rightward shift in the diaphragm's force-length relationship in CAPD patients, although this mechanism is insufficient to prevent a reduction of neuromechanical efficiency of the diaphragm.

Effect of helium-induced ventilatory unloading on breathing and diaphragm EMG in awake ponies.

Two questions were addressed in this study: 1) Does respiratory resistive unloading (inspired O2 fraction = 0.21, inspired He fraction = 0.79) elicit a compensatory reduction in stimulation of the diaphragm? 2) Do diaphragm and lung afferents contribute to compensatory responses to unloading? Ten intact (I), five diaphragm-deafferented (DD), four hilar nerve-denervated (HND), and seven DD+HND adult ponies were studied at rest and during mild and moderate treadmill exercise. During steady-state unloading at rest, duration of the diaphragm electromyogram (EMGdi) was less (P < 0.05) than control in I ponies, but there were no additional significant changes in breathing or blood gases. Unloading during mild and moderate exercise increased (P < 0.05) pulmonary ventilation in all groups, and this response did not differ (P > 0.05) among the groups. With unloading during exercise, arterial PCO2 was within 1 Torr of control except in the DD+HND ponies, which were 1-2 Torr hypocapnic (P < 0.05). During exercise, the duration and rate of rise of the EMGdi were reduced (P < 0.05) below control, beginning at about the third unloaded breath. The decrease in rate of rise was usually not sustained, inasmuch as there was a gradual return toward control over 2 min of unloading. There were no consistent group differences in these EMGdi responses. We conclude that resistive unloading during mild and moderate exercise in ponies results in a transient reduction in neural drive to the diaphragm that is not critically dependent on diaphragm and pulmonary afferents.

Modification in activity of medullary respiratory-related neurons for vocalization and swallowing

1. The medullary ventral respiratory group (VRG) in and near the nucleus ambiguus contains neurons related to respiration. Also found here are neurons related to vocalization and swallowing as well as motoneurons of laryngeal, pharyngeal, palatal, and esophageal muscles. Previous reports in anesthetized animals have characterized discharge properties of neurons as they relate to a single behavior, e.g., respiration. Relatively few studies have documented discharge properties during more than one behavior, e.g., respiration and swallowing. Neurons were recorded extracellularly from awake Macaca nemestrina monkeys engaged in a vocalization task. The present paper describes how respiratory-related neurons (RRNs) modify their discharge during vocalization and swallowing. 2. The temporal relation between vocalization, subglottal pressure (SP), and diaphragm electromyogram (EMG) was established from recordings in anesthetized monkeys. Vocalization was elicited by electrical stimulation of the midbrain periaqueductal gray (PAG). Vocalization is preceded by deep inspiration and a brief pause in diaphragm EMG and begins with a rapid increase in positive SP. 3. Extracellularly recorded neural potential from the VRG in three awake monkeys were related to respiration by correlating their discharge with EMGs from the posterior cricoarytenoid or intercostal muscles during quiet respiration. Neurons were classified as inspiratory (INSP; N = 27), phase spanning (PS; N = 20), or expiratory (N = 6) on this basis. 4. A fourth category of cells was defined as a subgroup of INSP cells on the basis of their discharge during vocalization. This group, inspiratory-pause (INSP-PS; N = 10), paused for approximately 100 ms just before vocalization and resumed their activity during vocalization. 5. Of 63 fully analyzed RRNs, 40 (63%) also modulated their activity with vocalization and 3 (5%) with swallowing. Thirteen (21%) RRNs modulated with vocalization, respiration, and swallowing. Seven (11%) cells were modulated only with respiration. 6. Most cells demonstrated a shorter period of activity and a higher discharge rate associated with vocalization in comparison with quiet respiration. Six (30%) of the PS cells demonstrated an augmenting discharge pattern before vocalization, which was different from the other PS cells and different from their pattern during quiet respiration. Thirteen RRNs showed a pause in activity during vocal fold closure associated with swallowing, whereas three cells gave a burst at this time. 7. The higher discharge rate and shorter burst duration preceding vocalization, compared with quiet respiration, may be related to the greater positive SP necessary to support vocalization.(ABSTRACT TRUNCATED AT 400 WORDS)

Reflex effects of lung inflation on tracheomotor tone observed during apnea produced by the Hering-Breuer reflex

Reflex effects of static pressure lung inflation (SLI) on tracheomotor tone (TT) were studied during apnea produced by the Hering-Breuer expiratory-facilitatory reflex. Anesthetized dogs were placed on cardiopulmonary bypass, and diaphragm electromyogram was used as an indicator of central nervous system inspiratory output. Tracheomotor tone (TT) was reflexly produced by chemoreceptor stimulation. The volume and frequency of the ventilator [phasic lung inflation (PLI)] were adjusted to produce nearly a maximum reflex decrease in TT. The increase in TT observed while PLI was withheld (0 mmHg tracheal pressure) for 1-2 min was used as the control response. SLIs were interspersed among sets of PLIs. Although SLI produced apnea, TT returned toward the control TT recorded during 0 mmHg tracheal pressure. TT observed during apnea was reflexly sensitive to further increases in SLI and to changes in chemoreceptor stimulation, which also affected the time course of the tracheomotor responses. These results suggest that the reflex decrease in TT produced by SLI and the Hering-Breuer expiratory-facilitatory reflex are mediated by different central mechanisms but may be from the same or different pulmonary receptors.

Mechano- and chemoreceptor modulation of respiratory muscles in response to upper airway negative pressure.

To investigate the influence of phasic pulmonary stretch receptors (n = 6) and chemoreceptors (n = 7) on the reflex response of the genioglossus (GG) muscle and diaphragm (DIA) to upper airway (UAW) negative pressure, we measured the response of the GG and DIA electromyogram (EMG) to three challenges: 1) negative pressure applied to the UAW during normoxia and hypercapnia, 2) end-expiratory tracheal occlusion, and 3) application of UAW negative pressure simultaneous with tracheal occlusion in spontaneously breathing tracheotomized anesthetized cats. Peak GG EMG was greatest when UAW negative pressure and end-expiratory tracheal occlusion were combined. No GG EMG activity was seen when UAW negative pressure was applied alone unless the animal was vagotomized or hypercapnic. DIA EMG increased in response to UAW negative pressure combined with occlusion. However, the increase in peak GG EMG was significantly greater than for the DIA with the same challenge. DIA EMG amplitude increased in response to occlusion alone but did not change when UAW negative pressure was applied alone. In the cat, phasic feedback from phasic pulmonary stretch receptors is a potent inhibitor of reflex activation of the GG in response to negative pressure applied to the UAW, which can be overridden by an increase in chemoreceptor drive.

Spectrum analysis of diaphragmatic global electromyograms in cattle, with special regard to appropriate strategy for detection of fatigue

Summary Although the respiratory tract of healthy and diseased cattle has been intensively studied during the past few years, only a few attempts to detect dysfunctions of bovine inspiratory muscles have been reported. Such technique would be useful in assessing the possibility of inspiratory muscle fatigue in the context of ventilatory failure. Fatigue in skeletal muscle is associated with characteristic changes in the electromyographic power spectrum. Power spectral analysis was therefore applied to cattle diaphragmatic electromyograms (emgdi) to precisely determine the exact influence of motion and ecg artifacts, describe its basic frequency content, and extract a spectral index capable of providing an accurate warning of fatigue. The emgdi was recorded via intramuscularly placed fishhook electrodes in 5 healthy young bulls during resting and stimulated respiration. The emgdi and egc signals were analyzed by use of power spectral density analysis after band-pass filtering (20 to 1,800 Hz). The emgdi spectrum was concentrated in the band width 20 to 530 Hz. Electrode motion artifacts were absent, and it was always possible to find an electrode pair giving ecg-free emgdi. Of the 12 power and frequency values used to quantitate the spectrum, the most stable was the centroid frequency. It was reproducible within and between calves and was only minimally altered by changing inspiratory load. Though the clinical relevance of fatigue in the respiratory musculature in case of ventilatory failure is currently unknown, the method described here constitutes a possible approach to detection of such phenomenon in cattle.

Changes in respiratory muscle activity in ponies when end-expiratory lung volume is increased.

The objective of the present study was to determine whether lung and diaphragm afferents contribute to the changes in respiratory muscle activity when end-expiratory lung volume (EELV) is changed in ponies. We studied the responses of the diaphragm and the transversus abdominis (TA) muscles to passive increases in EELV in awake intact (I), diaphragm-deafferented (DD), pulmonary vagal- (hilar nerve) denervated (HND), and DD + HND ponies. Negative pressure of -10 or -20 cmH2O applied around the ponies' torsos [positive transrespiratory (TR) pressure] increased (P < 0.05) EELV in all ponies; the increases were more (P < 0.05) in HND and less (P < 0.05) in DD than in I ponies. In I ponies, positive TR pressure increased (P < 0.05) the rate of rise of the integrated diaphragmatic electromyogram (EMG), reflecting increased drive to the muscle. This increase was less (P < 0.05) in DD and HND than in I ponies. In DD + HND ponies, there was no significant (P > 0.10) change in drive to the diaphragm during positive TR pressure. In I ponies, positive TR pressure increased (P < 0.05) the duration and mean activity of the TA EMG. In HND and DD + HND ponies, the TA EMG was not altered by positive TR pressure. I and DD ponies decreased (P < 0.05) breathing frequency but maintained tidal volume (VT) during positive TR pressure. HND and DD+HND ponies increased breathing frequency (P < 0.05) and decreased (P < 0.05) VT during positive TR pressure. We conclude that, during positive TR pressure when the diaphragm is presumably at a mechanical disadvantage, diaphragm and vagal afferents mediate increased drive to the diaphragm to prevent VT from decreasing. In addition, during positive TR pressure, vagal afferents mediate an increase in duration of TA activity, which minimizes the increase in EELV.

Acoustically induced cortical arousal increases phasic pharyngeal muscle and diaphragmatic EMG in NREM sleep.

Six healthy subjects (3 males, 3 females) were studied to assess phasic inspiratory responses of upper airway (UA) and diaphragm muscles to electrocortical arousal independent of other potential respiratory stimulation. Transient electroencephalographic (EEG) arousal (abrupt EEG frequency shift > or = 3 s without awakening) was induced during supine stage 2 non-rapid-eye-movement (NREM) sleep with binaural tone bursts (0.5 s, 4 kHz, 25-95 dB). Electromyograms (EMG) of levator veli palatini (EMGlvp) and genioglossus (EMGgg) were obtained with intramuscular electrodes, and EMG of diaphragm (EMGdi) was obtained with esophageal electrodes. EMG signals were processed as moving time-averaged inspiratory activity over 100-ms windows. For each arousal, each of five consecutive postarousal breaths (R1-R5) was scored for peak inspiratory phasic EMG and normalized as percent averaged EMG of the three prearousal breaths for all muscles. After arousal, EMGlvp was increased for R1-R5 and EMGgg and EMGdi were increased for R1-R4. The increase in EMGlvp was greater than those of EMGgg and EMGdi for all response breaths. There was a significant increase in EMGlvp in all subjects, and EMGgg and EMGdi were significantly increased in three and two subjects, respectively. These data indicate that isolated transient electrocortical arousal is generally associated with phasic inspiratory recruitment of UA and diaphragm muscles in normal humans during NREM sleep; velopharyngeal muscle recruitment appears to be more consistent and of greater magnitude and duration than that of oropharyngeal muscle or diaphragm. We speculate that transient arousal from sleep may contribute to UA patency independent of chemical and mechanical respiratory stimuli.

Metabolic-ventilatory interaction in conscious rats: effect of hypoxia and ambient temperature.

Previous studies have indicated that the hypometabolic response to hypoxia depends on ambient temperature (Ta), being more pronounced in the cold. If metabolic rate were an important contributor to the level of ventilation (VE), the magnitude of the hyperpneic response to hypoxia should also depend on Ta. We tested this hypothesis on adult conscious male rats. In normoxia, a drop in Ta from 25 to 10 degrees C increased O2 consumption and CO2 production (VO2 and VCO2, respectively, measured by an open-flow technique) and VE (measured with the barometric method) by 80 and 60%, respectively, with no changes in blood gases. At both Ta, hypoxia (10% inspired O2, 33-35 Torr arterial PO2) induced the same degree of hyperventilation, i.e., the same drop in arterial PCO2 (about -13 Torr). The hyperventilation at 25 degrees C Ta was achieved exclusively by an increase in VE, whereas at 10 degrees C Ta the hyperpnea was minimal (+15%) and accompanied by a drop (-30%) in VO2 and VCO2. Diaphragmatic electromyograms confirmed the VE results. Changes in blood pressure were similar at both Ta. Addition of 3% CO2 to the inspired air further increased VE, indicating that the hypoxic rat was not breathing at its maximal VE at either Ta. We conclude that, in the rat, changes in metabolic rate play an important role in the VE response to hypoxia and that Ta influences the response because of its effect on the degree of hypoxic hypometabolism.

Diaphragmatic electrical activity during controlled and assisted mechanical ventilation in conscious human subjects.

Breathing during mechanical ventilation was analyzed in 8 conscious healthy volunteers by application of intermittent positive pressure ventilation through a mouthpiece. In controlled mechanical ventilation (CMV), the respiratory rate and tidal volume were fixed at 110 and 120% of the subject's corresponding spontaneous breathing parameters. The diaphragmatic electromyogram (EMGdi) decreased significantly but become synchronous with the rhythm of the CMV. In assisted mechanical ventilation (AMV), the EMGdi response developed prior to and during the inspiratory phase of AMV. Application of an unexpected mechanical breath elicited the EMGdi. As the triggering sensitivity was decreased, the EMGdi prior to and during a mechanical breath was augmented, however, its rate of rise was unaffected. Our results suggest that the EMGdi during mechanical ventilation in conscious subjects is initiated by the respiratory center, however, this activity is modulated strongly by input from the pulmonary afferents and from the cerebral cortex.

Diaphragmatic activity and ventilation in preterm infants. I. The effects of sleep state.

To determine the effects of sleep on diaphragmatic activity and ventilation we studied 10 preterm infants (birth weight 1,840 +/- 50 g, gestational age 33 +/- 0.6 weeks, and postnatal age 9.4 +/- 1.4 days). We measured surface and esophageal diaphragmatic electromyograms (EMGdi). Ventilation was measured using a nasal flowmeter and a flow-through system. Diaphragmatic activity was analyzed for total phasic activity, expiratory phasic activity, the expiratory to total phasic activity ratio, and the presence of 'tonic' activity. The latter was defined by the presence of electrical activity and the end of expiration. There was a decrease in the average total phasic activity (1.25 vs. 0.71 s, p = 0.001), expiratory phasic activity (0.67 vs. 0.21 s, p = 0.002), the expiratory to total phasic activity ratio (0.51:0.27 s, p = 0.001) and tonic activity (51 to 5%, p = 0.01) from quiet to REM sleep in the surface EMGdi. Similar changes were found in the esophageal EMGdi, except that tonic activity was rarely observed. In parallel with these changes in electrical activity of the diaphragm, minute ventilation and alveolar ventilation increased from quiet to REM sleep. This increase was primarily related to an increase in frequency with a negligible change in tidal volume. The increase in frequency was primarily due to shortening of inspiratory time. The findings that tonic activity recorded via surface electrodes decreased substantially from quiet to REM sleep and was not observed in the esophageal EMGdi suggests that this tonic activity may represent electrical activity of the postural muscles of the chest wall rather than the diaphragm.

Central chemosensitivity affects respiratory muscle responses to laryngeal stimulation in the piglet

Stimulation of laryngeal afferent fibers triggers reflex apnea, which can be very long in the neonatal period. The purpose of this study was twofold: 1) to determine the effect of superior laryngeal nerve (SLN) stimulation on expiratory as well as inspiratory muscle activity and 2) to compare the respiratory response to SLN stimulation under conditions that would appear to alter the level of central chemosensitivity in anesthetized spontaneously breathing piglets. In protocol 1, we measured electromyogram (EMG) responses from the diaphragm (DIA), triangularis sterni, and transversus abdominis muscles to graded SLN stimulation; in protocol 2, we compared the DIA response to different levels of SLN stimulation during normocapnia, hypercapnia, and cooling of the ventrolateral medullary surface (VMS). SLN stimulation performed during normocapnia caused significantly greater inhibition of both expiratory muscles (triangularis sterni and transversus abdominis) than of the DIA. During hypercapnia, laryngeal stimulation-induced inhibition of all three muscles was significantly diminished, and the degree of inhibition for the three muscles became equivalent. Inhibition of the DIA EMG was significantly greater with SLN stimulation during VMS cooling than with a VMS temperature of 38 degrees C. We conclude that the magnitude of respiratory inhibition induced by laryngeal stimulation during early postnatal life is inversely related to the level of central chemical input and speculate that functional deficiency of structures located in the VMS may contribute to potentially life-threatening apnea in infants.

Hypercapnia increases expiratory braking in preterm infants

In contrast to adults, newborn infants breathe from an elevated end-expiratory lung volume, determined by the interaction of airflow retardation (braking) by the diaphragm and larynx, and expiratory duration. To determine the effect of hypercapnia on this strategy, we examined changes in respiratory muscle activity and the ventilatory response to CO2 breathing in eight premature infants 33-34 wk gestational age in the first 3 postnatal days. We recorded tidal volume, airflow, and electromyograms (EMG) of the laryngeal abductor [posterior cricoarytenoid (PCA)], which abducts the vocal cords, and diaphragm during behaviorally determined quiet sleep in room air and during steady-state inhalation of 2% CO2 in air. As expected, tidal volume increased (P < 0.0005) without a change in inspiratory duration with hypercapnia. Unexpectedly, in all subjects, expiratory duration was longer during CO2 inhalation (P < 0.001), accompanied by marked changes in expiratory flow patterns consistent with increased expiratory braking. Diaphragm post-inspiratory EMG activity increased with hypercapnia (P < 0.005) with no change in baseline diaphragm or PCA EMG activity. Peak inspiratory EMG activity of the diaphragm and PCA increased with CO2 (10 and 37%, respectively; P < 0.05). We conclude that the mechanisms used to elevate end-expiratory lung volume are enhanced during hypercapnia in premature infants. This breathing strategy may be important in maintaining gas exchange in infants with lung disease.

RESPIRATORY ALTERATIONS WITH INTRAPERICARDIAL PROCAINE IN THE CONSCIOUS RABBIT

1. Intrapericardial procaine, used to produce cardiac nerve blockade in both conscious and anaesthetized animals, has been reported to also produce changes in respiration. This study systematically investigated the effects of two doses of intrapericardial procaine on respiration in the conscious rabbit. 2. Rabbits were pre-instrumented with a chronic diaphragm electromyogram (dEMG) recording electrode and intrapericardial catheter. Arterial pressure, heart rate, dEMG and respiratory excursions (recorded with a pneumograph) were monitored in the conscious rabbit before and after intrapericardial and intravenous infusion of 2 and 5% procaine. Efficacy of cardiac nerve blockade was tested by intravenous infusion of phenyl biguanide. Arterial blood gases were determined at rest and during changes in respiration. 3. Following a low dose of intrapericardial procaine (12 mg), dEMG and respiratory excursions increased (65 +/- 13 and 76 +/- 32%, respectively) with no change in breathing frequency or arterial blood gases. Following a high dose of intrapericardial procaine (30 mg), four of six animals exhibited a similar response. However, four of the six rabbits also exhibited a second type of response pattern characterized by a further increase in respiratory efforts (430 +/- 336%), abolition of dEMG, and a mild hypoxaemia. 4. Intravenous infusion of a low dose of procaine was without effect, whereas intravenous infusion of a high dose of procaine produced minor behavioural responses. 5. In four additional anaesthetized rabbits, it was demonstrated that high doses of intrapericardial procaine anaesthetized the phrenic nerve to produce the observed alterations in respiration. 6. We conclude that if intrapericardial procaine is used to block cardiac nerves in conscious rabbits, it should be used in a low concentration and at the lowest possible total dose to avoid complications due to changes in respiration.

Muscle temperature alters the EMG power spectrum of the canine diaphragm

Electromyogram (EMG) power spectral analysis has been widely used to detect muscle fatigue. Non-fatigue factors that influence the EMG power spectrum must be well understood to ensure accurate interpretation. We explored the effect of muscle temperature on the EMG power spectrum in an isolated canine diaphgram preparation with intact neuro-vascular supply. In 5 animals, diaphragm temperature was continuously recorded with an intramuscular thermocouple, and the EMG signal was recorded with intramuscular wire electrodes. Data were obtained from spontaneous isometric diaphragm contractions while the diaphragm underwent passive cooling from 40 to 30°C. The EMG power spectrum was determined using fast Fourier transform and each spectrum was characterized by its center frequency (fc). A direct linear relationship was found between diaphragm temperature and the EMG fc. The mean slope of the temperature-EMG fc relationship was 2.9 fc·°C −1. In conclusion, diaphragm temperature is a major determinant of the diaphragmatic EMG power spectrum, and should be controlled when this index is employed in the investigation of muscle fatigue.

Modeling human diaphragmatic electromyogram and airflow responses to imperceptible mechanical loads.

We used an esophageal electrode to measure the amplitude and timing responses of diaphragmatic electrical activity and airflow in response to flow resistive and elastic loads at or below the threshold for conscious detection, applied pseudorandomly to the oral airway of eight normal human subjects. The mechanical and neural parameter responses to mechanical loading were cross-correlated with the pseudorandom loading sequence to obtain estimates of the impulse responses. We convolved the resultant impulse response estimates with the loading sequence to obtain the responses predicted from the linear component of the generalized Wiener kernel model. Highly significant correlations and close correspondence were found between the model-predicted and ensemble-averaged experimental responses for nearly all neural and mechanical parameters in all subjects. For nearly every aspect of the pattern, with few exceptions, the response to these small load perturbations in all eight subjects was adequately explained by an impulse response, leaving negligible nonlinearity to require higher-order cross-correlations. These results indicate that the estimated impulse responses accurately model the dynamics of the neural and mechanical responses in human subjects for the types and magnitudes of loads applied. This study supports use of the pseudorandom loading technique to determine the neural and mechanical responses to imperceptible mechanical loads in conscious humans.

Upper airway obstruction induced by negative-pressure ventilation in awake healthy subjects

Negative-pressure ventilation (NPV) induces sleep-related upper airway obstruction. However, the precise mechanism and site of upper airway obstruction during NPV have not been worked out. We studied seven awake healthy volunteers (23-30 yr old) in an Emerson tank respirator. Subjects had the head outside the iron lung and breathed through a pneumotachograph, which yielded the airflow (V) signal. Supraglottic pressure (Psg) was measured with a catheter with the tip at the retroepiglottic level. Diaphragmatic electromyograms (EMGdi) were obtained from an esophageal bipolar electrode. Tidal volume was measured with an inductance plethysmograph. Measurements were done at -10, -20, and -30 cmH2O. At each pressure run subjects were asked to repeatedly relax or to actively breathe in phase with the respirator. Subjects had been previously trained to relax during NPV. During the relax runs there was no EMGdi activity. Stridor or wheezing occurred in all seven subjects during the relax runs but not during the active runs. Two patterns were associated with NPV during relax runs. One pattern was decreases in both V and Psg followed by zero values of these indexes, which corresponded to an inspiratory narrowing and closure of the glottis. These changes were visualized by fiber-optic bronchoscopy in one subject. The second pattern was a decrease in V and increase in Psg, which corresponded to an inspiratory supraglottic obstruction. In five subjects a supraglottic pattern was observed, whereas in two subjects glottic closure was seen. We conclude that muscular relaxation during NPV produces a decrease in the caliber of the upper airways at the glottic or supraglottic level. An uncoupling of upper airway muscle activity and the diaphragm might be the mechanism responsible for these changes.

Effects of high-frequency oscillating pressures on upper airway muscles in humans

We examined the effects of high-frequency- (30-Hz) low-pressure oscillations (< 1 cmH2O) applied to the upper airway, via a nose mask, on genioglossus (EMGgg), sternomastoid (EMGsm), and diaphragm electromyogram (EMGdia) activity in sleeping humans. Ten patients with sleep apnea and six normal subjects were studied. The pressure oscillations were applied through the mask for a single breath. The subjects were studied in non-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep. In the normal subjects, during NREM sleep, peak EMGgg, EMGsm, and EMGdia activity increased significantly in response to the oscillations in 63, 51, and 46%, respectively, of all trials. During REM sleep, significant increases occurred in 73, 88, and 13%, respectively, of all trials. Similar responses were observed in the patients with obstructive sleep apnea. Peak EMGgg, EMGsm, and EMGdia activity increased significantly in 74, 50, and 67%, respectively, of all NREM sleep trials and in 55, 81, and 76%, respectively, of all REM sleep trials. An important finding was that in 46% of the trials in the patients with sleep apnea the oscillation-induced increase in EMGgg activity was associated with a partial or complete reversal of the upper airway obstruction with an increase in tidal volume. This was observed in NREM and REM sleep. We conclude that there are upper airway receptors that respond to low-pressure-high-frequency oscillations applied to the upper airway that have input to the genioglossus and other muscles of respiration. These responses may be utilized in future treatment for sleep apnea.

The effect of opioids on inspiratory muscle fatigue during inspiratory resistive loading.

The effect of opioids on inspiratory muscle function under high mechanical load is still unknown. Even less clear is the extent to which opioids influence the shift of the electromyographic power spectrum of the inspiratory muscles to lower frequencies during ventilatory stress. We studied seven healthy subjects breathing against high inspiratory threshold loads until exhaustion while keeping the minute ventilation constantly high. We compared runs with and without administration of 0.2 mg kg-1 of morphine sulphate intramuscularly; two subjects were given 30 mg morphine sulphate so that we could study the effect of higher opioid concentration. The endurance time (Tlim), the diaphragmatic electromyogram (EMG), the transdiaphragmatic pressures (Pdi) and the ventilatory effort sensation were analysed. Morphine did not have any effect on Tlim or on the effort sensation elicited by the inspiratory resistance in both concentrations. Analysing the spectral shifts of the diaphragmatic EMG, we did not find any significant difference in the decrease of the centroid frequency between drug and control runs. Furthermore, the activation pattern of the diaphragm and the intercostal muscles, evaluated from the percentage contribution of oesophageal and gastric pressures on the transdiaphragmatic pressure swings, did not change following the administration of morphine. Our study shows that morphine does not change the function of the inspiratory muscles during high-resistive breathing. Morphine does not affect the electromyographic power spectrum of the diaphragm during those resistive breathing runs, either. This points out that during stressful ventilatory situations, the shift of the electromyographic power spectrum is attributed to a peripheral (muscular) event consequent to muscle fatigue and not to the elaboration of endogenous opioids.

Reflex control of diaphragm activation by thoracic afferents

Recent studies suggest that chest wall reflexes may have a role in modulating diaphragm activation. The purpose of this study was to more closely examine this issue by assessing the diaphragmatic motor response to airway occlusion. Studies were performed in vagotomized mongrel dogs anesthetized with pentobarbital sodium. Diaphragmatic electromyogram (EMG) and phrenic neurogram (ENG) responses to airway occlusion were evaluated at different precontractile respiratory muscle lengths, achieved by passive inflation and deflation with a volume syringe during the preceding expiration. Lung volume was expressed as the corresponding change in airway pressure. At functional residual capacity, deflation (-5 cmH2O), and large inflation (+25 cmH2O), phrenic ENG during occlusion was 90 +/- 2 (SE), 84 +/- 5, and 86 +/- 3% of the preceding control breaths, respectively (n = 9). Qualitatively similar, but somewhat more pronounced, responses were observed on diaphragmatic EMG. With small lung inflations, the degree of reduction of phrenic ENG with airway occlusion was less. Consequently, the relationship between airway pressure and degree of inhibition was best described as a reverse parabola with the maximum at approximately +10-15 cmH2O. Responses were not significantly affected by bilateral cervical phrenicotomy. Complete section of the spinal cord at the high thoracic level (T1-T2) abolished the observed reduction in phrenic ENG in response to airway occlusion. Our results demonstrate 1) the existence of nonvagal nonphrenic reflex control of diaphragm activation most likely secondary to activation of intercostal afferents and 2) that the magnitude of this reflex is highly dependent on factors related to lung volume.