Costal and crural diaphragm, and intercostal and genioglossal electromyogram activities during spontaneous augmented breaths (sighs) in kittens

Spontaneously occurring augmented breaths (sighs) are common in infants. The pattern of electrical activity of the inspiratory muscles of the thorax and upper airway during augmented breaths, however, has not been fully characterized in this less than fully mature age group. We therefore examined costal and crural diaphragm and external intercostal and genioglossal EMG activities during spontaneous augmented breaths (n = 46) in 10 anesthetized (1.35% halothane) 1-month-old kittens breathing room air. EMG responses were assessed by comparing the spontaneous augmented breaths (AB) to the five immediately preceding breaths (control). The peak moving time average EMG activity observed during the AB was 240 +/- 32% (mean +/- SD) of control for the costal diaphragm, 279 +/- 66% of control for the crural diaphragm, and 274 +/- 68% of control for the external intercostal muscle. The mean increase in EMG activity during the AB was not significantly different among these three muscle groups (P greater than 0.25). Genioglossal EMG activity during AB was observed in only 1 of 10 study animals. These results document that during AB in anesthetized kittens, activity of the thoracic inspiratory muscles (costal/crural diaphragm and external intercostal muscles) increase in parallel, suggesting that they are modulated in a uniform manner. The infrequent observance of genioglossal activity during AB suggests that either 1) halothane anesthesia depresses genioglossal activity more than diaphragmatic and intercostal activity during AB or 2) that genioglossal recruitment is not necessary to maintain upper airway patency during this period of heightened respiratory drive.     

Vagal afferent dysfunction in naturally occurring canine esophageal motility disorder

Few studies have examined the vagal afferent innervation of the esophagus in naturally occurring esophageal motility disorders. The present study assessed the integrity of distension-sensitive vagal afferents innervating the esophagus in naturally occurring canine megaesophagus. In the dog, esophageal distension induces reflex inhibition of crural diaphragm electromyographic activity that is mediated by vagal afferents innervating esophageal mechanoreceptors. This reflex was measured during stepwise esophageal distension in six dogs with congenital idiopathic megaesophagus, two dogs with megaesophagus secondary to esophageal striated muscle disease, and eight matched controls. In contrast to control dogs, inhibition of crural electromyographic activity was not observed in megaesophagus dogs with esophageal distension within the control volume range. With esophageal distensions far in excess of the control volume range, inhibition of crural electromyographic activity was not observed in five of six dogs with congenital idiopathic megaeosphagus, while crural inhibition was observed in the two dogs with secondary megaesophagus. These findings indicate that a defect is present in the vagal afferent innervation to the esophagus in a majority of dogs with congenital idiopathic megaesophagus.The present study was funded by a Clive and Vera Ramaciotti Foundations research grant. Christopher T. Holland was the recipient of a Jean Walker Trust Fellowship from the University of Sydney.     

Effect of head-up tilt on neural inspiratory drive in the anesthetized dog

To examine how anesthetized dogs compensate for the diaphragmatic shortening that occurs during head-up tilting, we measured the electroneurogram (ENG) of the C5 phrenic root and the electromyographic (EMG) activity of the parasternal intercostal and transversus abdominis muscles in eight spontaneously breathing animals during postural changes between supine (0 degree) and 80 degrees head-up. Both steady state ENG and EMG activities and first breath responses to tilting from 80 degrees head-up to supine were studied. These experiments have shown that: (1) anesthetized dogs respond to head-up tilting by increasing the neural drive to the costal diaphragm and parasternal intercostals; (2) this response, however, does not occur on the first breath and therefore cannot compensate for the immediate changes in diaphragmatic length; (3) the abdominal muscles, in contrast, show a first breath response to tilting and their activation is primarily responsible for the maintenance of tidal volume. Unlike in humans, increases in neural inspiratory drive in head-up anesthetized dogs are mediated by a chemoreceptive, rather than proprioceptive, feedback mechanism.     

Electrical and mechanical inhibition of the crural diaphragm during transient relaxation of the lower esophageal sphincter

Electrical and mechanical correlates of crural diaphragm activity during swallow-induced and transient lower esophageal sphincter relaxation were monitored in 12 healthy subjects. Simultaneous esophageal manometric, pH, and crural diaphragm electromyogram recordings were performed for 1 hour in the postprandial period. Swallow-induced lower esophageal sphincter relaxation was associated with minimal inhibition of the crural diaphragm, but transient lower esophageal sphincter relaxation was accompanied by marked inhibition of the crural diaphragm. The degree of lower esophageal sphincter relaxation appeared to correlate with the degree of crural diaphragm inhibition during transient lower esophageal sphincter relaxation. Inhibition of crural diaphragm during transient lower esophageal sphincter relaxation may play an important role in facilitating flow across the gastroesophageal junction.     

Regional training-induced alterations in diaphragmatic oxidative and antioxidant enzymes

We examined the relationship between the intensity and duration of exercise training and the up-regulation of diaphragmatic oxidative and antioxidant enzyme activities. Nine groups of rats exercised for 10 weeks (4days/week). Groups of animals exercised at three intensities (low, moderate, and high); at each exercise intensity, a group of animals ran at one of three exercise durations (30, 60, and 90 min/day). Sedentary animals served as controls. Muscle oxidative capacity was assessed by citrate synthase (CS) activity while antioxidant capacity was evaluated by total superoxide dismutase (SOD) and total glutathione peroxidase (GPX) activities. All intensities and durations of exercise training promoted significant (P<0.05) increases in costal diaphragmatic CS, SOD, and GPX activities. Increases in costal CS, SOD, and GPX activity were independent of the exercise intensity and duration. High and moderate intensity exercise of 90 min duration significantly elelevated (P<0.05) crural diaphragm CS activity. Further, high and moderate intensity exercise of durations ≥60 min promoted significant (P<0.05) increases in crural diaphragm SOD activities. Exercise did not influence (P>0.05) crural diaphragm GPX activity. We conclude that the training threshold for up-regulation of oxidative and antioxidant enzyme activities differs between the costal and crural diaphragm.     

Effect of lung inflation and upright posture on diaphragmatic shortening in dogs

In an earlier study (Road and Leevers (1988), J. Appl. Physiol. 65: 2283-2389), the application of continuous positive airway pressure (CPAP) produced a marked reduction in diaphragm initial length (LFRC) and tidal diaphragmatic shortening (%LFRC), tidal volume (VT) and transdiaphragmatic pressure swings (delta Pdi) in supine dogs after vagotomy. We postulated that the reduced diaphragmatic shortening was mainly a result of the decrease in diaphragm LFRC but an increase in afterload could not be excluded. In this study, we attempted to define the role of these two mechanisms during postural change. Eight, pentobarbital-anaesthetized, vagotomized dogs were studied in the supine position during CPAP and during postural change (tilting towards upright). As before, CPAP produced a prompt reduction in diaphragm LFRC and tidal %LFRC, VT and delta Pdi. Tilting produced similar decreases in crural diaphragm LFRC (23% from control values) as the weight of the abdominal contents was removed, but less decrease in costal LFRC (17% during CPAP compared to 10% during tilting). A given reduction in crural diaphragm initial length (15%) resulted in less tidal shortening during tilting compared to CPAP, whereas costal diaphragm shortening was similar at a given reduction in initial length (10%). Both CPAP and tilting reduced tidal volumes (47.8 +/- 5.1 and 56.5 +/- 3.1% of control), however, delta Pdi decreased less during tilting (20%) than CPAP (47%). There was no significant change in the level of diaphragmatic EMG with either CPAP or tilting.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reverse-perfused sleeve: an improved device for measurement of sphincteric function of the crural diaphragm

The sphincteric function of the crural diaphragm has been difficult to measure in humans. The authors recently reported the use of a Dent sleeve device to measure esophagogastric junction pressure during contraction of the crural diaphragm. However, the major limitation of the conventional sleeve device is its slow response rate, and sustained diaphragmatic contractions of 6-8 seconds must be induced to measure the true pressure. In this article, the principles of a reverse-perfused sleeve device and the theoretical basis for its fast response rate are reported. The reverse-perfused sleeve is validated in an in vitro model of the lower esophageal sphincter. Furthermore, in vivo studies were performed in seven healthy human subjects. Standardized Muller maneuvers and straight-leg raises were performed to induce diaphragmatic contractions. Pressure increases of 50-150 mm Hg during diaphragmatic contractions were attained in less than 1 second. The delay between the actual contraction of the diaphragm as measured by simultaneously recorded crural diaphragm electromyography and pressure recorded by the sleeve was only 0.25-0.50 seconds. Increasing the rate of infusion of the sleeve from 0.5 to 1.0 mL/min did not further improve the response rate of the reverse perfused sleeve. It was concluded that the reverse-perfused sleeve is a considerable improvement over the conventional sleeve for quantitating the sphincteric function of the crural diaphragm. The role of the crural diaphragm in reflux esophagitis may be easily investigated using a reverse-perfused sleeve device.     

The effects of locomotion on respiratory muscle activity in the awake dog

Using 6 chronically-instrumented awake dogs, we characterized the response of the respiratory muscles to mild and moderate treadmill exercise in terms of (1) the magnitude and timing of the EMGs of the costal and crural diaphragm, triangularis sterni and transverse abdominal muscles, and (2) the concomitant changes in esophageal (PE) and gastric (PG) pressures during treadmill exercise. Dogs wore a bivalved breathing mask which constrained breathing frequency and prevented some of the exercise-induced hypocapnia. Inspiratory and chest expiratory muscle EMGs increased linearly with a 1.5-fold tidal volume (VT) change during exercise. Abdominal muscle recruitment occurred during most exercise levels and exhibited (1) phasic activity coincident with footplant and (2) tonic activation evidenced by a baseline shift in PG and EMG activities. During control, inspiratory and expiratory flow preceded the onset of respiratory muscle EMG activity, but during exercise, electrical activation of these muscles coincided with the onset of mechanical flow. We conclude that phasic and tonic activation of expiratory muscles during exercise in the dog is significantly influenced by both respiratory and locomotory requirements. These patterns of expiratory muscle recruitment may assist inspiration by lengthening inspiratory muscles through decrements in end-expiratory lung volume and by passive recoil of the rib cage and abdominal compartments.     

Vector analysis in partitioning of inspiratory muscle action in dogs.

We considered the displacements and the pressure changes resulting from isolated contraction of 2 muscles as analogous to 2 vectors and those during simultaneous contraction as resultants. These were resolved into contributing components to calculate the contribution of each muscle group and partition the action of inspiratory muscles. Relative displacements of rib cage (delta RC) and abdomen (delta AB) and changes in transpulmonary (delta PL) and abdominal (delta Pab) pressures were obtained during spontaneous breathing, isolated contraction of rib cage muscle (RCM), diaphragmatic (DI), costal and crural diaphragm and passive inflation in 7 dogs. The diaphragm accounted for 58 +/- 19.8% SD of the chest wall displacement and 90 +/- 6.6% SD of the pressure swings during spontaneous breathing. The costal diaphragm accounted for 61 +/- 28.9% SD of the displacement produced by contraction of the entire diaphragm. Despite wide variability in the action of the diaphragm and its components, all animals breathed close to their relaxation characteristic. We conclude that there are marked differences in the degree of RCM recruitment between dogs in order to prevent chest wall distortions.     

External intercostal muscle activity during acute hypoxia in the kitten

The effects of acute hypoxia on the recruitment of external intercostal muscle activity were determined in 12 kittens, aged 14 to 36 days. The animals were anesthetized with 1.23 +/- 0.23% halothane and bipolar electrodes were placed in the costal and crural diaphragm and in dorsal external intercostal muscles. Acute hypoxia was induced by the animals breathing 13% oxygen; arterial gases were sampled during baseline conditions and at 1 and 5 min after induction of hypoxia. Peak-moving average (PA) and minute electromyogram (EMG) activity (PA x f) were recorded during baseline conditions and at 1 and 5 min after onset of acute hypoxia. At 1 min of acute hypoxia, PA and PA x f of the costal diaphragm, crural diaphragm, and external intercostal muscles were significantly increased above baseline values (P less than 0.01). After 5 min of acute hypoxia, PA of all three muscles remained elevated above baseline values (P less than 0.05) but PA x f returned toward baseline levels. Respiratory frequency remained unchanged during the hypoxic stimulus. These data document that the newborn is capable of increasing inspiratory external intercostal muscle EMG activity during acute hypoxia. We speculate that this phasic recruitment could be of physiologic benefit to the newborn by stabilizing the complaint chest wall and by increasing the contribution of rib cage expansion to tidal breathing.     

Phrenic afferents and ventilatory control

It has been understood since the late 1800s that the diaphragm has significant sensory innervation. The role of phrenic afferents in the control of breathing, however, has been obscure. The phrenic nerve has been shown to contain a full array of afferent fibers. However, proprioceptive (group 1 fibers) afferents are few compared to postural muscles or the intercostals. The diaphragm, unlike the inspiratory intercostal muscles, has a small complement of spindle afferents and not all of these spindles are supplied with fusorial fibers. Reduced spindle afferents under gamma control help to explain previous studies of the diaphragm that have failed to reveal autogenic facilitation, that is, a reflex-mediated increase in drive during inspiratory loading. Nevertheless, some clinical studies have revealed increased activation of the diaphragm when its length is reduced. Group 1 fibers, which are predominantly tendon organ afferents in the diaphragm, have been shown to have a phasic inhibitory function. A reduction in this inhibition brought about by a reduction in diaphragmatic length during lung inflation may explain the increased diaphragmatic activation reported in clinical studies. Phrenic afferents have been shown to have multiple spinal and supraspinal projections. Recent studies have explored the ventilatory effects of thin fiber afferents (group III and IV fibers) in the phrenic nerve. Stimulation of these afferents has been shown both to inhibit and excite ventilation. These afferents arise from polymodal receptors that respond to both mechanical and chemical stimulation. Activation of these receptors may occur in a variety of conditions and the ventilatory response may be determined by the specific receptor activated.     

Phrenic afferents and ventilatory control

It has been understood since the late 1800s that the diaphragm has significant sensory innervation. The role of phrenic afferents in the control of breathing, however, has been obscure. The phrenic nerve has been shown to contain a full array of afferent fibers. However, proprioceptive (group 1 fibers) afferents are few compared to postural muscles or the intercostals. The diaphragm, unlike the inspiratory intercostal muscles, has a small complement of spindle afferents and not all of these spindles are supplied with fusorial fibers. Reduced spindle afferents under gamma control help to explain previous studies of the diaphragm that have failed to reveal autogenic facilitation, that is, a reflex-mediated increase in drive during inspiratory loading. Nevertheless, some clinical studies have revealed increased activation of the diaphragm when its length is reduced. Group 1 fibers, which are predominantly tendon organ afferents in the diaphragm, have been shown to have a phasic inhibitory function. A reduction in this inhibition brought about by a reduction in diaphragmatic length during lung inflation may explain the increased diaphragmatic activation reported in clinical studies. Phrenic afferents have been shown to have multiple spinal and supraspinal projections. Recent studies have explored the ventilatory effects of thin fiber afferents (group III and IV fibers) in the phrenic nerve. Stimulation of these afferents has been shown both to inhibit and excite ventilation. These afferents arise from polymodal receptors that respond to both mechanical and chemical stimulation. Activation of these receptors may occur in a variety of conditions and the ventilatory response may be determined by the specific receptor activated.     

Contractile and histochemical characteristics of the rabbit diaphragm in elastase-induced emphysema

The effects of elastase-induced emphysema on diaphragmatic force output and fiber composition were studied in 7 rabbits given 600 IU porcine pancreatic elastase intratracheally (E group), and 8 untreated rabbits (U group) under pentobarbital anesthesia. The presence of emphysema was confirmed by histologic and pathologic criteria and by documented changes in lung mechanics 7 months posttreatment. Histochemical characteristics (size and proportions of muscle fibers) of the costal part of the diaphragm were assessed by staining myofibrillar ATPase. In the E group, maximal tracheal pressure (Ptr max) developed during tetanic stimulation of the phrenic nerves was significantly lowered at volumes greater than functional residual capacity, throughout the inspiratory capacity (IC): the IC % vs. Ptr max curve was shifted to the left when compared to the U group. This phenomenon may be attributed to a change in position on the length-force curve of the diaphragm, secondary to lung inflation rather than to alterations of intrinsic properties of this muscle in the E group, because the sizes and proportions of diaphragmatic fibers were not affected in these animals.     

Age-related changes in enzyme activity in the rat diaphragm

Limited data exist concerning the effect of growth and aging on the metabolic properties of the diaphragm. Therefore, we investigated age-related changes in protein concentration and glycolytic and Krebs cycle enzyme activity in the diaphragm as well as the plantaris muscle of female Sprague-Dawley rats ranging in age from 1 to 12 months. Samples from the costal and crural diaphragm and the plantaris muscle were obtained from 38 animals in the following age groups: (1) 1 month old (N = 7); (2) 4 month old (N = 6) (3) 6 month old (N = 13); and (4) 12-month-old (N = 12). Body weight and diaphragm weight increased rapidly by a factor of 6 and in parallel during 1-4 months postpartum before reaching a plateau at 6 months of age. No significant difference (P greater than 0.05) existed in the ratio of diaphragm weight to body weight among age groups. Protein concentration was significantly higher (P less than 0.05) in the costal diaphragm and plantaris at 4 and 6 months when compared to 1 and 12 months of age. In the crural diaphragm, protein concentration was significantly lower (P less than 0.05) at 1 month postpartum when compared to all other age groups. Succinate dehydrogenase (SDH) activity was significantly higher (P less than 0.05) at 1 month of age in the plantaris, the costal diaphragm and the crural diaphragm when compared to older animals. In contrast, the activity of lactate dehydrogenase (LDH) in the plantaris, the costal diaphragm and the crural diaphragm was significantly lower (P less than 0.05) in the 1-month-old animals when compared to all other ages.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in diaphragmatic EMG spectra during hyperpneic loads

Changes in electromyographic (EMG) activity of the diaphragm were examined in human subjects during different levels of voluntary hyperpnea. Diaphragmatic EMG was recorded using both surface and esophageal electrodes. The power spectra density (PSD) of the EMG signal was calculated and characterized by the high frequency to low frequency (H/L) ratio and by the centroid frequency (Fc). During high levels of voluntary hyperpnea, a significant decrease in both the H/L ratio and Fc occurred, which was similar in diaphragmatic EMG recorded by either surface or esophageal electrodes. This similarity in EMG spectral changes suggested that when diaphragmatic EMG was recorded using surface electrodes, there was only minimal contamination from the activity of other chest wall muscles. Changes in EMG Fc were detected during levels of hyperpnea which could be readily sustained. Thus, diaphragmatic EMG spectral changes were not characteristic of imminent ventilatory failure (i.e., an inability to sustain a target level of ventilation). In contrast, significant changes in EMG H/L ratio were observed only during hyperpneic loads which could not be sustained. This difference in sensitivity between the Fc and H/L ratio was due to the increased variability of H/L ratio and suggests that the H/L ratio may fail to detect small but significant shifts in EMG spectra. The relationship between the rate of decrease in EMG Fc and the level of hyperpnea was not statistically significant. We conclude that diaphragmatic EMG spectral changes do occur during hyperpneic loads, but we question the specificity of using diaphragmatic EMG spectral changes in predicting ventilatory failure.     

The effects of chemical versus locomotory stimuli on respiratory muscle activity in the awake dog

Using 6 chronically instrumented awake dogs, we contrasted the ventilatory and respiratory muscle EMG responses to steady-state normoxic hypercapnia with those occurring at similar levels of ventilation during steady-state treadmill exercise. During hypercapnia, increases in ventilatory output were primarily due to increments in VT whereas during exercise, increases in minute ventilation were due primarily to increases in frequency. With either hyperpnea, augmentation of both inspiratory and expiratory muscle EMG activity occurred but only diaphragmatic EMG activity was strongly correlated with tidal volume changes in both conditions. Using both EMGs and thoraco-abdominal pressures, we found that with increasing chemical or locomotory stimuli, during inspiration (1) diaphragmatic EMG activation occurred sooner relative to the onset of mechanical flow and (2) that respiratory muscles other than the diaphragm contributed significantly to the generation of inspiratory flow and VT either actively or passively through recoil. Post-inspiratory inspiratory activity of the crural diaphragm shortened relative to control in hypercapnia but did not change in exercise. Finally, during mild hyperpneas, end-expiratory lung volume did not change significantly in either hypercapnia or exercise but decreased at the higher levels of hyperpnea only during exercise. This may reflect differences not in the magnitude of phasic expiratory muscle activity, but rather in the degree of tonic abdominal muscle activation between the two conditions.     

Distal and deglutitive inhibition in the rat esophagus: role of inhibitory neurotransmission in the nucleus tractus solitarii

BACKGROUND & AIMS: This study aimed to show the presence of deglutitive and distal inhibition in the rat esophagus and to differentiate the underlying neural mechanisms. METHODS: Under urethane anesthesia, the pharyngoesophageal tract was fitted with water-filled balloons for luminal distention and pressure recording. Neural activity was recorded in the nucleus tractus solitarii subnucleus centralis and rostral nucleus ambiguous. RESULTS: Distal esophageal distention evoked both rhythmic local contractions and burst discharges of ambiguous neurons that were simultaneously inhibited by a swallow or proximal esophageal distention. In subnucleus centralis interneurons, type I rhythmic burst discharges correlated with distal esophageal pressure waves and were suppressed by midthoracic esophageal distention; type II non-rhythmic excitatory responses, like type III inhibitory responses, were evoked by distention of either the thoracic or distal esophagus. When applied to the surface of the solitarius complex, bicuculline and, less effectively, strychnine suppressed distal inhibition, and 2-(OH)-saclofen and 3-aminopropylphosphonic acid were ineffective. None of the drugs tested, including systemic picrotoxin, affected deglutitive inhibition. CONCLUSIONS: Distal and deglutitive inhibition are present in the rat esophagus. The former, unlike the latter, depends on activation of ligand-gated chloride channels associated with subnucleus centralis premotor neurons. Inhibitory aminoacidergic local interneurons are a probable source of type II responses.     

Recruitment of intercostal muscle activity during hypercapnia in kittens

Little is known about the respiratory behavior of the intercostal muscles within a neonatal and developmental context. We, therefore, examined intercostal muscle electromyographic (EMG) activity in kittens (1 month old, n = 8; 2 months old, n = 7) during eupnea and heightened respiratory drive induced by hypercapnia. The kittens were anesthetized with halothane (1.25-1.50%) at comparable minimum alveolar concentrations and were studied in the prone position during an acute exposure to hyperoxic hypercapnia (8% CO2, 50% O2, balance N2) for 7 min. We recorded EMG activities from bipolar electrodes embedded in the intercostal (dorsolateral thorax, 4th-5th interspace) (EMGic) and costal diaphragm (EMGdi) muscles. Peak moving time average EMG measurements served as our index of muscle activity. Phasic inspiratory EMGic activity was present during eupnea in all animals. EMGic and EMGdi increased significantly above baseline levels during hypercapnic exposure with the increase in EMGic (133 +/- 27%) being comparable to that observed in EMGdi (141 +/- 28%) (P = 0.40). No differences in EMGic (P = 0.64) or EMGdi (P = 0.88) recruitment were noted between age groups. These data indicate that hypercapnia augments intercostal muscle EMG activity in kittens and suggest that such activity parallels costal diaphragmatic EMG recruitment. We conclude that EMGic recruitment is a frequent respiratory phenomenon associated with hypercapnically stimulated diaphragmatic muscle activity in kittens. We speculate that intercostal muscle recruitment stabilizes the compliant chest wall of the newborn and helps sustain inspiratory force generation during stimulated breathing.     

Diaphragm length and breathing pattern changes during hypoxia and hypercapnia

In this study diaphragmatic length changes were measured during quiet breathing and during augmentation of breathing with hypoxia and hypercapnia in supine anesthetized dogs. The breathing pattern and the VT-TI relationship during hypoxia were different than those during hypercapnia. The crural diaphragm shortened more than the costal diaphragm with both stimuli, and the amount of shortening in relation to the tidal volume implied that there was considerable distortion of the chest wall during hyperventilation. The velocity of shortening of both parts of the diaphragm at similar levels of ventilation was greater during hypoxia than hypercapnia. The velocities found with hyperventilation suggested that force-velocity considerations did not reduce force generation. Hypoxic stimulation resulted in a reduction in the resting length of both parts of the diaphragm, and was associated with a positive shift in baseline pleural pressure which implied gas trapping. The large tidal diaphragmatic shortening found with augmented breathing and the shorter resting length with hypoxia indicated that length-force properties are important in force generation.     

Current concepts of the antireflux barrier

The lower esophageal sphincter, crural diaphragm, and phrenoesophageal ligament are the anatomic structures that constitute the antireflux barrier. The intraluminal pressure at the esophagogastric junction (EGJ) reflects the strength of the antireflux barrier. The end-expiratory pressure is a result of the tonic activity of the smooth muscles of the lower esophageal sphincter. The EGJ pressure increases during inspiration owing to the effect of the crural diaphragm. There is a reflex increase in the EGJ pressure during periods of increased intra-abdominal pressure, and the crural diaphragm contributes to this reflex contraction of the EGJ. Based on the contribution of the lower esophageal sphincter and crural diaphragm to the EGJ pressure, a two sphincter hypothesis of the antireflux barrier competence is suggested.