Physiology, Lower Esophageal Sphincter


The esophagus is a portion of the digestive system connecting the mouth to the stomach, allowing the passage of food for digestion. It is approximately 25 cm long, beginning at the inferior border of the cricoid cartilage in the neck (about at C6), descending in the posterior mediastinum through the esophageal hiatus of the diaphragm and terminating at the stomach (at T11 level). During its course, the esophagus encounters three anatomic constrictions - (1) at the level of the cricopharyngeus muscle, (2) as it travels posteriorly to the aortic arch/left mainstem bronchus, and (3) at the level of esophageal hiatus of the diaphragm. These constrictions are considered as the most frequent site for a foreign body or food impaction when encountered.

The esophagus has two functional sphincters, the upper and lower esophageal sphincters. The upper esophageal sphincter (UES) lies at the transition of the pharynx to the esophagus. It is composed of striated muscle - primarily the cricopharyngeus with assistance from the inferior pharyngeal constrictors that prevent the reflux of swallowed foods into the pharynx, thus reduces the risk of aspiration. The lower esophageal sphincter (LES), located at the distal end where it meets the stomach, is composed of a bundle of smooth muscle and functions to protect the reflux of gastric contents into the esophagus. The diaphragmatic crura and the phreno-esophageal ligament provide anatomical support to LES and further protection against gastric reflux. Impaired contraction or reduced tone of the LES leads to reflux, where increased pressure or impaired relaxation of the LES results in dysphagia.[1][2]


The esophagus has four histologic layers - the mucosa, submucosa, muscularis propria, and the adventitia.

  • Mucosa- Its the innermost layer can further subdivide into three layers, non-keratinized stratified squamous epithelium, the lamina propria, and a thin muscular layer, the muscularis mucosae, inside to outwards.
  • Submucosa - Deep to the mucosa, this is the most robust layer of the esophagus. The submucosa contains the majority of the esophageal vasculature, innervation, and lymphatics. Located in this layer is the submucosal (Meissner's) plexus, which primarily regulates GI secretions.
  • Muscularis Propria - smooth muscles of this layer are arranged into the inner circular muscle and the outer longitudinal muscle layers. Coordinated contraction of these muscle fibers assists in the propulsion of a food bolus through the esophagus. Proximally, this layer is primarily composed of striated muscle but transitions to smooth muscle distally. Thus, the middle esophagus is a mixture of striated and smooth muscle, while the distal esophagus is primarily smooth muscle. Within the muscular layer is the myenteric (Auerbach's) plexus, which regulates muscular contractions.
  • Adventitia - The outer-most layer of the esophagus; this loose layer of connective tissue connects the esophagus to adjacent structures. Unlike most structures in the GI tract, the esophagus does not have serosa.


The esophagus begins to develop around the fourth week of gestational age. Craniocaudal and lateral folding form the primitive gut tube that craniocaudally subdivides into foregut, midgut, and hindgut. The esophagus develops from the foregut, beginning with the development of the respiratory diverticulum (lung bud) on the ventral wall of the foregut. The tracheoesophageal septum is critical for anatomical separation of the two foregut derivatives, the trachea ventrally and the dorsal esophagus. The esophagus is initially very short in length that progressively elongates along with the descent of the heart and lungs. During week six, the muscularis propria begins to develop from the somatopleuric mesoderm around the developing foregut and the esophagus, which ultimately forms the circular and longitudinal muscle layers. The ganglion cells derived from neural crest cells give rise to the myenteric (Auerbach's) plexus within the muscle coat. The muscular layer is completed by week 9 of gestation. Embryologic development depends on many important genes, most crucially SOX2, which drives esophageal differentiation, and the Wnt signaling pathway, which drives esophageal/tracheal division and esophageal elongation.[3]


The Three Phases of Swallowing [4]

  • Oral phase - the only step that initiates voluntarily; the oral phase begins when food enters the mouth and ends when the tongue starts moving a food bolus into the oropharynx. During this phase, mastication decreases the size of food particles, and the food bolus is lubricated with saliva to facilitate swallowing.
  • Pharyngeal phase - this phase delivers food into the esophagus and protects the airway from aspiration. The pharyngeal phase begins when the food bolus reaches the palatoglossal arch and ends when it passes the UES into the esophagus. The airway is protected by the closure of the glottis and elevation of the larynx, while respiration is temporarily inhibited ("swallowing apnea"). Peristalsis begins in the pharynx, as the sequential contraction of the superior, middle, and inferior pharyngeal constrictor propels food toward the UES at a rate of 20 to 40 cm/s. A reflex arc causes relaxation of the UES, permitting transit of the food bolus into the esophagus.
  • Esophageal phase - this phase relies on peristaltic contractions to propel the food bolus through the esophagus into the stomach. Primary peristalsis occurs at a rate of 3 to 4 cm/s and requires precise coordination between the circular and longitudinal muscle layers.[5] Secondary peristaltic waves act as 'backup,' triggered by esophageal distention and irritation, and function to clear any remaining food.

The Lower Esophageal Sphincter (LES) [6]

The lower esophageal sphincter is crucial for proper swallowing, as it creates a high-pressure area of 2 to 4 cm at the distal esophagus. Similar to the entire esophagus, the LES is composed of circular and longitudinal muscle layers. The tonic contraction causes a thickened appearance of the LES. Still, a dissection of autopsy specimens has suggested that the muscle layers are, in reality, no thicker than the remainder of the esophagus. The LES is anatomically asymmetric, primarily due to the circular muscle layer. The right-sided circular layer is incomplete, forming semicircular C-shaped rings, termed clasp fibers. On the left, the circular layer is also incomplete, with semicircular rings joining with the fibers of the gastric sling, leading to an oblique orientation. There are also functional differences between clasp and sling fibers, leading to asymmetric pressure at the LES.[7][8]

The strength of the LES is further augmented by the crura of the diaphragm and the phreno-esophageal ligament. The diaphragmatic crura can be considered the 'external sphincter' of the LES and function to increase the pressure at the distal esophagus. The crura are particularly crucial during inspiration (when intrathoracic pressure decreases) or during periods of increased intraabdominal pressure - situations that predispose to gastric reflux. The right crus of the diaphragm is more extensive and thicker than the left. It arises from lumbar vertebrae L1-L3 and divides into a superficial and deep component. The outer part lies to the right of the esophageal hiatus, while the deep part lies to the left of the hiatus, lateral to the left crus. The left crus is smaller, arising from L1-L2, and lies to the left of the esophageal hiatus. The phreno-esophageal ligament is the continuation of the inferior diaphragmatic fascia and acts as a protective sleeve over the intraabdominal esophagus. The upper limb connects the distal esophagus to the superior aspect of the diaphragm, and the lower limb connects the cardia of the stomach to the inferior aspect of the diaphragm, allowing for independent movement of the diaphragm and the esophagus, protecting against gastric reflux and hiatal hernia.

The proper function of the LES occurs through two main mechanisms - myogenic and neural control. Myogenic control is the intrinsic rhythm of gastrointestinal smooth contraction/relaxation. Neural control is achieved through the autonomic and enteric nervous systems. The LES tonically contracts to an average pressure of 15 to 30 mmHg. After swallowing, inhibitory signals generated by peristalsis cause a reflex relaxation of the LES for approximately 5 seconds, allowing transit of the bolus into the stomach. During this time, the diaphragmatic crura also relax. After the passage of the bolus, the LES and crura return to their baseline contracted state. Transient LES relaxation (TLESR) is another physiologic relaxation of the LES that occurs outside of the swallowing mechanism. It is believed to be triggered by gastric distention and causes both the LES and the diaphragmatic crura to relax, allowing the release of excess gas. The process is followed by primary peristaltic waves distally to return any refluxed liquid into the stomach.[9]


Both sympathetic and parasympathetic fibers innervate the lower esophageal sphincter. Sympathetic afferents (sensory) have their cell bodies in the dorsal root ganglia of T1-L3 and detect nociceptive (painful) stimuli. Sympathetic efferents (motor) traverse through the sympathetic chain at the levels of T6-T10, converge into the greater splanchnic nerve and send fibers to the celiac ganglion. The sympathetic nervous system has only a minor effect on LES function, as bilateral cervical sympathectomy and greater splanchnicectomy do not affect baseline LES tone.

The vagus nerve mediates parasympathetic innervation of the esophagus. Parasympathetic afferents mediate non-nociceptive stimuli (stretch, swallow reflex) and synapse in the nucleus tractus solitarius. Parasympathetic efferents arise in the dorsal motor nucleus (DMN) and synapse with the myenteric plexus of the enteric nervous system. The parasympathetic system contributes to inhibitory and excitatory neurons, with excitatory nerves arising from the rostral portion of the DMN and inhibitory nerves arising from the caudal portion of the DMN. Excitatory impulses are primarily cholinergic-mediated via acetylcholine, with small contributions by tachykinins (substance P, neurokinin A/B). Inhibitory impulses are primarily nitrergic-mediated (nitric oxide) with smaller contributions by other compounds, including vasoactive inhibitory peptide (VIP), purine structures (particularly ATP), and carbon monoxide. Due to this dual innervation by the vagus, bilateral vagotomy or tetrodotoxin (pufferfish toxin blocks neural transmission via sodium-channel blockade) administration elicits no change in baseline LES tone. Conversely, blockade of the inhibitory neurons (with NO inhibitors) or excitatory neurons (with atropine - an anti-cholinergic) leads to unopposed action of the opposite system. While the vagus elicits dual effects, there have been suggestions that the inhibitory effect is greater, as studies have demonstrated that vagal stimulation leads to net LES relaxation.[10][11]

The baseline tone of the LES is primarily under myogenic, rather than neural, control. The smooth muscle cells of the LES differ from the smooth muscle of the esophageal body in several respects. The LES cells are relatively depolarized, maintained by an increased expression of voltage-gated calcium channels leading to spontaneous spike-like action potentials and increased tone. The clasp fibers of the LES contain a greater proportion of these calcium channels and are primarily under myogenic regulation. Sling fibers have a greater proportion of cholinergic and nitrergic channels and are primarily under vagal control. This neuronal arrangement leads to an asymmetric contraction pattern at the LES, with the right-sided clasp fibers contributing more to the baseline tone. In contrast, the left-sided sling fibers are more involved in contraction/relaxation. LES cells also have differential expression of structural proteins, including actin, light chains, and caldesmon, assisting in generating baseline tone. During normal swallowing, esophageal peristalsis leads to reflex relaxation of the LES, allowing passage of the swallowed bolus. Esophageal contraction follows relaxation and returns the LES to its resting pressure, which partially occurs through myogenic rebound, and partially via excitatory stimulation from the vagus nerve. In contrast to the swallowing mechanism, transient LES relaxations(TLESR) are mediated directly by the vagus nerve.[12][13]

Related Testing

Barium Esophagography - This is often the first study obtained in the workup of dysphagia, dyspepsia, or regurgitation. It is non-invasive and primarily assesses the structural integrity of the esophagus, identifying Hiatal hernias, leaks, diverticula, obstructions, and other structural malformations. This study can grossly assess esophageal motility, but a modified barium swallow performed with a speech pathologist better assesses functional swallowing. While barium provides better contrast than water-soluble solutions, in cases of suspected esophageal perforation, the use of barium increases the risk of inflammatory mediastinitis. Barium esophagogram should not be obtained in cases of acute chemical injury.[14]

Esophagogastroduodenoscopy (EGD) - Upper endoscopy allows for the direct visualization of the pathology in question. It is particularly useful to assess reflux esophagitis/Barrett's metaplasia, strictures/masses, suspected upper-GI bleeds, varices, and hiatal hernias. Endoscopy allows for select interventions, including biopsy, foreign body removal, stricture dilation, ligation of bleeding vessels, and pharmacologic injections. The most serious risk of this procedure is an esophageal perforation, but this occurs in fewer than 1% of cases.[15]

Esophageal pH Monitoring - The gold standard for diagnosis of gastroesophageal reflux disease. This test allows for 24-hr monitoring of the pH in the lower esophagus and measures 6 data points. These data points can help to calculate a DeMeester score, and scores >14.72 are an indication for anti-reflux surgery.[16]

  • The percentage of the total time that pH<4
  • The percentage of upright time that pH<4
  • The percentage of supine time that pH<4
  • The number of episodes of pH<4
  • The number of episodes lasting >5 mins of pH<4
  • The most extended episode (in minutes) where pH<4

Esophageal Manometry - This is a direct measurement of the intraluminal pressure at multiple levels within the esophagus. It assesses UES function, LES function, and motility within the esophageal body. Manometry is most useful in the workup of suspected achalasia, esophageal spasm, and GERD.


Gastroesophageal Reflux Disease (GERD) [17] - A very common condition in the western world, GERD's characteristic presentation shows the retrograde movement of gastric contents across the LES into the esophagus. Because some level of reflux is physiologic, particularly due to TLESR, it can be challenging to diagnose. Predisposing factors include an incompetent LES, hiatal hernia, a short intraabdominal esophagus, weakness of the diaphragmatic crura/phreno=esophageal ligament, or elevated intraabdominal pressure. Typical symptoms reported by patients are heartburn and regurgitation. Atypical (but still common) symptoms include cough, hoarseness, and chest pain. Esophageal pH monitoring is the gold standard for diagnosis, but barium studies and endoscopy can also play a role in evaluating for hiatal hernia and Barrett's metaplasia. Medical treatment is often preferable as a combination of behavioral modification and acid-reducing medications (PPIs, H2-antagonists) are effective in many cases. Surgery is an option for patients who fail conservative management, with the goal of restoring length to the intraabdominal esophagus, closing the crura of the diaphragm, and reinforcement of the LES via fundoplication. Complications of GERD include stricture formation and Barrett's metaplasia. Intestinal metaplasia can predispose patients to dysplasia and adenocarcinoma of the esophagus.

Achalasia [18] - An uncommon esophageal disease caused by denervation of the myenteric (Auerbach's) plexus, leading to failure of LES relaxation and loss of esophageal peristalsis.  Patients typically complain of dysphagia, progressing from solids to liquids, regurgitation, and possibly a foreign body sensation of the lower esophagus. Barium swallow reveals narrowing of the LES and proximal dilation of the esophagus ('bird's beak' sign). Esophageal manometry reveals a failure of LES relaxation and the absence of normal esophageal peristalsis. Endoscopy is necessary to rule out distal obstruction (pseudo-achalasia). While conservative treatment options with oral nitrates and calcium-channel blockers have been attempted, they are minimally effective. Endoscopic treatment options include balloon dilation of the LES, botox injections, and per-oral endoscopic myotomy (POEM). Balloon dilations and botox injections have shown to be effective, but only short-term and require repeat treatments. Repetitive dilations increase the risk of esophageal perforation. POEM involves submucosal tunneling with circular myotomy of the LES. POEM increases the risk for GERD, as the LES is rendered incompetent. Surgical management with Heller myotomy is possible via open or laparoscopic techniques and includes fundoplication to prevent reflux.

Hiatal hernia [19] - Hiatal hernias involves herniation of the esophagus, stomach, or other structures through the esophageal hiatus of the diaphragm. There are four types. Type I hernias, also known as sliding Hiatal hernias, involve the gastroesophageal junction and LES retracting superiorly above the diaphragm; this is the most common type and frequently occurs with the laxity of the phreno-esophageal ligament. Intermittent loss of tension from the diaphragmatic crura predisposes these patients to GERD. Types II-IV are all forms of para-esophageal hernia, which involves herniation of the stomach through the esophageal hiatus. Type II is purely para-esophageal, and the GE junction remains in place. Type III is a mixed sliding-para-esophageal hernia. And Type IV is a para-esophageal hernia with herniation of another GI organ (commonly the colon or spleen) through the hiatus. Paraesophageal hernias increase the risk for entrapment of the stomach, with subsequent ischemia/infarction. Diagnosis can be suggested by an abdominal X-ray, with the finding of an air-fluid level above the diaphragm, but is confirmed with contrast upper GI study. Treatment of asymptomatic sliding hernias is often conservative management, while symptomatic cases are treated surgically similarly to GERD. Asymptomatic para-esophageal hernias are controversial, with some advocating for surgical repair to remove the risk of incarceration, while others argue that this complication is rare, and watchful waiting can be appropriate. Symptomatic para-esophageal hernias require surgical repair.

Esophageal Foreign Body [20] - Foreign body ingestion is most common in pediatric patients and the mentally disabled. Three likely locations for esophageal entrapment are the areas of anatomic constriction, the UES/cricopharyngeus, the crossover of the aorta/left main-stem bronchus, and the LES. In pediatric patients, approximately 75% of foreign bodies ingested are trapped at the UES, while a distal esophageal stricture traps 67 % of foreign bodies in adults. Patients often present complaining of a foreign body sensation, chest pain, or inability to swallow. Drooling or the inability to handle secretions is a concerning feature indicative of an emergent obstruction. High-risk objects include batteries, magnets, and sharp objects. Batteries lodged in the esophagus can cause thermal injury to the mucosa, increasing the risk for bleeding and perforation. Sharp objects also increase the risk of perforation. Multiple magnets become a concern in the lower GI tract, where they can become separated and reattach across the bowel wall, increasing the risk for infarction and a bowel perforation. Diagnosis can often be made on chest X-ray, with anterior-posterior and lateral films to localize the object. Cervical or mediastinal emphysema are clues to esophageal perforation. Treatment is frequently endoscopic removal, but surgical removal can be performed with failure of endoscopic removal or in cases of esophageal perforation.

Clinical Significance

The lower esophageal sphincter plays an essential role in swallowing. Detailed knowledge of LES physiology can assist in the understanding and diagnosis of esophageal pathology, dysphagia, and related disorders. Normal LES function allows food transit from the esophagus into the stomach and prevents the reflux of gastric contents back into the esophagus. Improper relaxation of the LES can lead to food entrapment in the esophagus, achalasia, and an increased risk of esophageal squamous cell carcinoma. An incompetent LES can lead to GERD, increasing the risk for metaplasia and esophageal adenocarcinoma. Rapid identification of esophageal disorders can impact both a patient's quality of life and long-term morbidity and mortality.

(Click Image to Enlarge)
Esophagus, Incisor Teeth, Oropharynx, Epiglottis, Thyroid Cartilage, Cricoid Cartilage, Cricopharyngeus, Trachea, Arch of Aorta, Left Main Bronchus, Diaphram, Fundus of Stomach, Cardiac Part of Stomach, Abdominal Part of Stomach, Diaphragmatic Constriction, inferior esophageal sphincter, Thoratic, aortobronchial constriction, Pharyngoesophageal Constriction
Esophagus, Incisor Teeth, Oropharynx, Epiglottis, Thyroid Cartilage, Cricoid Cartilage, Cricopharyngeus, Trachea, Arch of Aorta, Left Main Bronchus, Diaphram, Fundus of Stomach, Cardiac Part of Stomach, Abdominal Part of Stomach, Diaphragmatic Constriction, inferior esophageal sphincter, Thoratic, aortobronchial constriction, Pharyngoesophageal Constriction
Contributed Illustration by Beckie Palmer
Article Details

Article Author

Ryan Rosen

Article Editor:

Ryan Winters


4/20/2021 2:52:27 PM



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