Ganong’s Review of Medical Physiology, 24th Edition

CHAPTER 27 Gastrointestinal Motility


After studying this chapter, you should be able to:

image List the major forms of motility in the gastrointestinal tract and their roles in digestion and excretion.

image Distinguish between peristalsis and segmentation.

image Explain the electrical basis of gastrointestinal contractions and the role of basic electrical activity in governing motility patterns.

image Describe how gastrointestinal motility changes during fasting.

image Understand how food is swallowed and transferred to the stomach.

image Define the factors that govern gastric emptying and the abnormal response of vomiting.

image Define how the motility patterns of the colon subserve its function to desiccate and evacuate the stool.


The digestive and absorptive functions of the gastrointestinal system outlined in the previous chapter depend on a variety of mechanisms that soften the food, propel it through the length of the gastrointestinal tract (Table 27–1), and mix it with bile from the gallbladder and digestive enzymes secreted by the salivary glands and pancreas. Some of these mechanisms depend on intrinsic properties of the intestinal smooth muscle. Others involve the operation of reflexes involving the neurons intrinsic to the gut, reflexes involving the central nervous system (CNS), paracrine effects of chemical messengers, and gastrointestinal hormones.


TABLE 27–1 Mean lengths of various segments of the gastrointestinal tract as measured by intubation in living humans.



Peristalsis is a reflex response that is initiated when the gut wall is stretched by the contents of the lumen, and it occurs in all parts of the gastrointestinal tract from the esophagus to the rectum. The stretch initiates a circular contraction behind the stimulus and an area of relaxation in front of it (Figure 27–1). The wave of contraction then moves in an oral-to-caudal direction, propelling the contents of the lumen forward at rates that vary from 2 to 25 cm/s. Peristaltic activity can be increased or decreased by the autonomic input to the gut, but its occurrence is independent of extrinsic innervation. Indeed, progression of the contents is not blocked by removal and resuture of a segment of intestine in its original position and is blocked only if the segment is reversed before it is sewn back into place. Peristalsis is an excellent example of the integrated activity of the enteric nervous system. It appears that local stretch releases serotonin, which activates sensory neurons that activate the myenteric plexus. Cholinergic neurons passing in a retrograde direction in this plexus activate neurons that release substance P and acetylcholine, causing smooth muscle contraction behind the bolus. At the same time, cholinergic neurons passing in an anterograde direction activate neurons that secrete NO and vasoactive intestinal polypeptide (VIP), producing the relaxation ahead of the stimulus.


FIGURE 27–1 Patterns of gastrointestinal motility and propulsion. An isolated contraction moves contents orally and aborally. Segmentation mixes contents over a short stretch of intestine, as indicated by the time sequence from left to right. In the diagram on the left, the vertical arrows indicate the sites of subsequent contraction. Peristalsis involves both contraction and relaxation, and moves contents aborally.


When the meal is present, the enteric nervous system promotes a motility pattern that is related to peristalsis, but is designed to retard the movement of the intestinal contents along the length of the intestinal tract to provide time for digestion and absorption (Figure 27–1). This motility pattern is known as segmentation, and it provides for ample mixing of the intestinal contents (known as chyme) with the digestive juices. A segment of bowel contracts at both ends, and then a second contraction occurs in the center of the segment to force the chyme both backward and forward. Unlike peristalsis, therefore, retrograde movement of the chyme occurs routinely in the setting of segmentation. This mixing pattern persists for as long as nutrients remain in the lumen to be absorbed. It presumably reflects programmed activity of the bowel dictated by the enteric nervous system, and can occur independent of central input, although the latter can modulate it.


Except in the esophagus and the proximal portion of the stomach, the smooth muscle of the gastrointestinal tract has spontaneous rhythmic fluctuations in membrane potential between about –65 and –45 mV. This basic electrical rhythm (BER) is initiated by the interstitial cells of Cajal, stellate mesenchymal pacemaker cells with smooth muscle-like features that send long multiply branched processes into the intestinal smooth muscle. In the stomach and the small intestine, these cells are located in the outer circular muscle layer near the myenteric plexus; in the colon, they are at the submucosal border of the circular muscle layer. In the stomach and small intestine, there is a descending gradient in pacemaker frequency, and as in the heart, the pacemaker with the highest frequency usually dominates.

The BER itself rarely causes muscle contraction, but spike potentials superimposed on the most depolarizing portions of the BER waves do increase muscle tension (Figure 27–2). The depolarizing portion of each spike is due to Ca2+ influx, and the repolarizing portion is due to K+ efflux. Many polypeptides and neurotransmitters affect the BER. For example, acetylcholine increases the number of spikes and the tension of the smooth muscle, whereas epinephrine decreases the number of spikes and the tension. The rate of the BER is about 4/min in the stomach. It is about 12/min in the duodenum and falls to about 8/min in the distal ileum. In the colon, the BER rate rises from about 2/min at the cecum to about 6/min at the sigmoid. The function of the BER is to coordinate peristaltic and other motor activity, such as setting the rhythm of segmentation; contractions can occur only during the depolarizing part of the waves. After vagotomy or transection of the stomach wall, for example, peristalsis in the stomach becomes irregular and chaotic.


FIGURE 27–2 Basic electrical rhythm (BER) of gastrointestinal smooth muscle. Top: Morphology, and relation to muscle contraction. Bottom: Stimulatory effect of acetylcholine and inhibitory effect of epinephrine. (Modified and reproduced with permission from Chang EB, Sitrin MD, Black DD: Gastrointestinal, Hepatobiliary, and Nutritional Physiology. Lippincott-Raven, 1996.)


During fasting between periods of digestion, the pattern of electrical and motor activity in gastrointestinal smooth muscle becomes modified so that cycles of motor activity migrate from the stomach to the distal ileum. Each cycle, or migrating motor complex (MMC), starts with a quiescent period (phase I), continues with a period of irregular electrical and mechanical activity (phase II), and ends with a burst of regular activity (phase III) (Figure 27–3). The MMCs are initiated by motilin. The circulating level of this hormone increases at intervals of approximately 100 min in the interdigestive state, coordinated with the contractile phases of the MMC. The contractions migrate aborally at a rate of about 5 cm/min, and also occur at intervals of approximately 100 min. Gastric secretion, bile flow, and pancreatic secretion increase during each MMC. They likely serve to clear the stomach and small intestine of luminal contents in preparation for the next meal.


FIGURE 27–3 Migrating motor complexes (MMCs). Note that the complexes move down the gastrointestinal tract at a regular rate during fasting, that they are completely inhibited by a meal, and that they resume 90–120 min after the meal. (Reproduced with permission from Chang EB, Sitrin MD, Black DD: Gastrointestinal, Hepatobiliary, and Nutritional Physiology. Lippincott-Raven, 1996.)

Conversely, when a meal is ingested, secretion of motilin is suppressed (ingestion of food suppresses motilin release via mechanisms that have not yet been elucidated), and the MMC is abolished, until digestion and absorption are complete. Instead, there is a return to peristalsis and the other forms of BER and spike potentials during this time. The antibiotic erythromycin binds to motilin receptors, and derivatives of this compound may be of value in treating patients in whom gastrointestinal motility is decreased.



In the mouth, food is mixed with saliva and propelled into the esophagus. Peristaltic waves in the esophagus move the food into the stomach.


Chewing (mastication) breaks up large food particles and mixes the food with the secretions of the salivary glands. This wetting and homogenizing action aids swallowing and subsequent digestion. Large food particles can be digested, but they cause strong and often painful contractions of the esophageal musculature. Particles that are small tend to disperse in the absence of saliva and also make swallowing difficult because they do not form a bolus. The number of chews that is optimal depends on the food, but usually ranges from 20 to 25.

Edentulous patients are generally restricted to a soft diet and have considerable difficulty eating dry food.


Swallowing (deglutition) is a reflex response that is triggered by afferent impulses in the trigeminal, glossopharyngeal, and vagus nerves (Figure 27–4). These impulses are integrated in the nucleus of the tractus solitarius and the nucleus ambiguus. The efferent fibers pass to the pharyngeal musculature and the tongue via the trigeminal, facial, and hypoglossal nerves. Swallowing is initiated by the voluntary action of collecting the oral contents on the tongue and propelling them backward into the pharynx. This starts a wave of involuntary contraction in the pharyngeal muscles that pushes the material into the esophagus. Inhibition of respiration and glottic closure are part of the reflex response. A peristaltic ring contraction of the esophageal muscle forms behind the material, which is then swept down the esophagus at a speed of approximately 4 cm/s. When humans are in an upright position, liquids and semisolid foods generally fall by gravity to the lower esophagus ahead of the peristaltic wave. However, if any food remains in the esophagus, it is cleared by a second wave of peristalsis that occurs by the mechanisms discussed above. It is therefore possible to swallow food while standing on one’s head.


FIGURE 27–4 Movement of food through the pharynx and upper esophagus during swallowing. (a) The tongue pushes the food bolus to the back of the mouth. (b) The soft palate elevates to prevent food from entering the nasal passages. (c) The epiglottis covers the glottis to prevent food from entering the trachea and the upper esophageal sphincter relaxes. (d) Food descends into the esophagus.


Unlike the rest of the esophagus, the musculature of the gastroesophageal junction (lower esophageal sphincter; LES) is tonically active but relaxes on swallowing. The tonic activity of the LES between meals prevents reflux of gastric contents into the esophagus. The LES is made up of three components (Figure 27–5). The esophageal smooth muscle is more prominent at the junction with the stomach (intrinsic sphincter). Fibers of the crural portion of the diaphragm, a skeletal muscle, surround the esophagus at this point (extrinsic sphincter) and exert a pinchcock-like action on the esophagus. In addition, the oblique or sling fibers of the stomach wall create a flap valve that helps close off the esophagogastric junction and prevent regurgitation when intragastric pressure rises.


FIGURE 27–5 Esophagogastric junction. Note that the lower esophageal sphincter (intrinsic sphincter) is supplemented by the crural portion of the diaphragm (extrinsic sphincter), and that the two are anchored to each other by the phrenoesophageal ligament. (Reproduced with permission, from Mittal RK, Balaban DH: The esophagogastric junction. N Engl J Med 1997;336:924. Copyright © 1997 by the Massachusetts Medical Society. All rights reserved.)

The tone of the LES is under neural control. Release of acetylcholine from vagal endings causes the intrinsic sphincter to contract, and release of NO and VIP from interneurons innervated by other vagal fibers causes it to relax. Contraction of the crural portion of the diaphragm, which is innervated by the phrenic nerves, is coordinated with respiration and contractions of chest and abdominal muscles. Thus, the intrinsic and extrinsic sphincters operate together to permit orderly flow of food into the stomach and to prevent reflux of gastric contents into the esophagus (Clinical Box 27–1).


Motor Disorders of the Esophagus

Achalasia (literally, failure to relax) is a condition in which food accumulates in the esophagus and the organ can become massively dilated. It is due to increased resting LES tone and incomplete relaxation on swallowing. The myenteric plexus of the esophagus is deficient at the LES in this condition and the release of NO and VIP is defective. The opposite condition is LES incompetence, which permits reflux of acid gastric contents into the esophagus (gastroesophageal reflux disease). This common condition is the most frequent digestive disorder causing patients to seek care from a physician. It causes heartburn and esophagitis and can lead to ulceration and stricture of the esophagus due to scarring. In severe cases, the intrinsic sphincter, the extrinsic sphincter, and sometimes both are weak, but less severe cases are caused by intermittent periods of poorly understood decreases in the neural drive to both sphincters.


Achalasia can be treated by pneumatic dilation of the sphincter or incision of the esophageal muscle (myotomy). Inhibition of acetylcholine release by injection of botulinum toxin into the LES is also effective and produces relief that lasts for several months. Gastroesophageal reflux disease can be treated by inhibition of acid secretion with H2 receptor blockers or proton pump inhibitors (see Chapter 25). Surgical treatment in which a portion of the fundus of the stomach is wrapped around the lower esophagus so that the LES is inside a short tunnel of stomach (fundoplication) can also be tried, although in many patients who undergo this procedure the symptoms eventually return.


Some air is unavoidably swallowed in the process of eating and drinking (aerophagia). Some of the swallowed air is regurgitated (belching), and some of the gases it contains are absorbed, but much of it passes on to the colon. Here, some of the oxygen is absorbed, and hydrogen, hydrogen sulfide, carbon dioxide, and methane formed by the colonic bacteria from carbohydrates and other substances are added to it. It is then expelled as flatus. The smell is largely due to sulfides. The volume of gas normally found in the human gastrointestinal tract is about 200 mL, and the daily production is 500–1500 mL. In some individuals, gas in the intestines causes cramps, borborygmi (rumbling noises), and abdominal discomfort.


Food is stored in the stomach; mixed with acid, mucus, and pepsin; and released at a controlled, steady rate into the duodenum.


When food enters the stomach, the fundus and upper portion of the body relax and accommodate the food with little if any increase in pressure (receptive relaxation). Peristalsis then begins in the lower portion of the body, mixing and grinding the food and permitting small, semiliquid portions of it to pass through the pylorus and enter the duodenum.

Receptive relaxation is, in part, vagally mediated and triggered by movement of the pharynx and esophagus. Intrinsic reflexes also lead to relaxation as the stomach wall is stretched. Peristaltic waves controlled by the gastric BER begin soon thereafter and sweep toward the pylorus. The contraction of the distal stomach caused by each wave is sometimes called antral systole and can last up to 10 s. Waves occur 3–4 times per minute.

In the regulation of gastric emptying, the antrum, pylorus, and upper duodenum apparently function as a unit. Contraction of the antrum is followed by sequential contraction of the pyloric region and the duodenum. In the antrum, partial contraction ahead of the advancing gastric contents prevents solid masses from entering the duodenum, and they are mixed and crushed instead. The more liquid gastric contents are squirted a bit at a time into the small intestine. Normally, regurgitation from the duodenum does not occur, because the contraction of the pyloric segment tends to persist slightly longer than that of the duodenum. The prevention of regurgitation may also be due to the stimulating action of cholecystokinin (CCK) and secretin on the pyloric sphincter.


The rate at which the stomach empties into the duodenum depends on the type of food ingested. Food rich in carbohydrate leaves the stomach in a few hours. Protein-rich food leaves more slowly, and emptying is slowest after a meal containing fat (Figure 27–6). The rate of emptying also depends on the osmotic pressure of the material entering the duodenum. Hyperosmolality of the duodenal contents is sensed by “duodenal osmoreceptors” that initiate a decrease in gastric emptying, which is probably neural in origin.


FIGURE 27–6 Effect of protein and fat on the rate of emptying of the human stomach. Subjects were fed 300-mL liquid meals. (Reproduced with permission from Brooks FP: Integrative lecture. Response of the GI tract to a meal. Undergraduate Teaching Project. American Gastroenterological Association, 1974.)

Fats, carbohydrates, and acid in the duodenum inhibit gastric acid and pepsin secretion and gastric motility via neural and hormonal mechanisms. The messenger involved is probably peptide YY. CCK has also been implicated as an inhibitor of gastric emptying (Clinical Box 27–2).


Consequences of Gastric Bypass Surgery

Patients who are morbidly obese often undergo a surgical procedure in which the stomach is stapled so that most of it is bypassed, and thus the reservoir function of the stomach is lost. As a result, such patients must eat frequent small meals. If larger meals are taken, because of rapid absorption of glucose from the intestine and the resultant hyperglycemia and abrupt rise in insulin secretion, gastrectomized patients sometimes develop hypoglycemic symptoms about 2 h after meals. Weakness, dizziness, and sweating after meals, due in part to hypoglycemia, are part of the picture of the “dumping syndrome,” a distressing syndrome that develops in patients in whom portions of the stomach have been removed or the jejunum has been anastomosed to the stomach. Another cause of the symptoms is rapid entry of hypertonic meals into the intestine; this provokes the movement of so much water into the gut that significant hypovolemia and hypotension are produced.


There are no treatments, per se, for the dumping syndrome, other than avoiding large meals, and particularly those with high concentrations of simple sugars. Indeed, its occurrence may account for the overall success of bypass surgery in reducing food intake, and thus obesity, in many patients who undergo this operation.


Vomiting is an example of central regulation of gut motility functions. Vomiting starts with salivation and the sensation of nausea. Reverse peristalsis empties material from the upper part of the small intestine into the stomach. The glottis closes, preventing aspiration of vomitus into the trachea. The breath is held in mid inspiration. The muscles of the abdominal wall contract, and because the chest is held in a fixed position, the contraction increases intra-abdominal pressure. The lower esophageal sphincter and the esophagus relax, and the gastric contents are ejected. The “vomiting center” in the reticular formation of the medulla (Figure 27–7) consists of various scattered groups of neurons in this region that control the different components of the vomiting act.


FIGURE 27–7 Neural pathways leading to the initiation of vomiting in response to various stimuli.

Irritation of the mucosa of the upper gastrointestinal tract is one trigger for vomiting. Impulses are relayed from the mucosa to the medulla over visceral afferent pathways in the sympathetic nerves and vagi. Other causes of vomiting can arise centrally. For example, afferents from the vestibular nuclei mediate the nausea and vomiting of motion sickness. Other afferents presumably reach the vomiting control areas from the diencephalon and limbic system, because emetic responses to emotionally charged stimuli also occur. Thus, we speak of “nauseating smells” and “sickening sights.”

Chemoreceptor cells in the medulla can also initiate vomiting when they are stimulated by certain circulating chemical agents. The chemoreceptor trigger zone in which these cells are located (Figure 27–7) is in the area postrema, a V-shaped band of tissue on the lateral walls of the fourth ventricle near the obex. This structure is one of the circumventricular organs (see Chapter 33) and is not protected by the blood–brain barrier. Lesions of the area postrema have little effect on the vomiting response to gastrointestinal irritation or motion sickness, but abolish the vomiting that follows injection of apomorphine and a number of other emetic drugs. Such lesions also decrease vomiting in uremia and radiation sickness, both of which may be associated with endogenous production of circulating emetic substances.

Serotonin (5-HT) released from enterochromaffin cells in the small intestine appears to initiate impulses via 5-HT3 receptors that trigger vomiting. In addition, there are dopamine D2 receptors and 5-HT3 receptors in the area postrema and adjacent nucleus of the solitary tract. 5-HT3 antagonists such as ondansetron and D2 antagonists such as chlorpromazine and haloperidol are effective antiemetic agents. Corticosteroids, cannabinoids, and benzodiazepines, alone or in combination with 5-HT3 and D2 antagonists, are also useful in treatment of the vomiting produced by chemotherapy. The mechanisms of action of corticosteroids and cannabinoids are unknown, whereas the benzodiazepines probably reduce the anxiety associated with chemotherapy.


In the small intestine, the intestinal contents are mixed with the secretions of the mucosal cells and with pancreatic juice and bile.


The MMCs that pass along the intestine at regular intervals in the fasting state and their replacement by peristaltic and other contractions controlled by the BER are described above. In the small intestine, there are an average of 12 BER cycles/min in the proximal jejunum, declining to 8/min in the distal ileum. There are three types of smooth muscle contractions: peristaltic waves, segmentation contractions, and tonic contractions. Peristalsis is described above. It propels the intestinal contents (chyme) toward the large intestines. Segmentation contractions (Figure 27–1), also described above, move the chyme to and fro and increase its exposure to the mucosal surface. These contractions are initiated by focal increases in Ca2+ influx with waves of increased Ca2+ concentration spreading from each focus. Tonic contractions are relatively prolonged contractions that in effect isolate one segment of the intestine from another. Note that these last two types of contractions slow transit in the small intestine to the point that the transit time is actually longer in the fed than in the fasted state. This permits longer contact of the chyme with the enterocytes and fosters absorption (Clinical Box 27–3).



When the intestines are traumatized, there is a direct inhibition of smooth muscle, which causes a decrease in intestinal motility. It is due in part to activation of opioid receptors. When the peritoneum is irritated, reflex inhibition occurs due to increased discharge of noradrenergic fibers in the splanchnic nerves. Both types of inhibition operate to cause paralytic (adynamic) ileus after abdominal operations. Because of the diffuse decrease in peristaltic activity in the small intestine, its contents are not propelled into the colon, and it becomes irregularly distended by pockets of gas and fluid. Intestinal peristalsis returns in 6–8 h, followed by gastric peristalsis, but colonic activity takes 2–3 days to return.


Adynamic ileus can be relieved by passing a tube through the nose down to the small intestine and aspirating the fluid and gas for a few days until peristalsis returns. The occurrence of ileus has been reduced by more widespread use of minimally invasive (eg, laparoscopic) surgery. Post-surgical regimens also now encourage early ambulation, where possible, which tends to enhance intestinal motility. There are also ongoing trials of specific opioid antagonists in this condition.


The colon serves as a reservoir for the residues of meals that cannot be digested or absorbed (Figure 27–8). Motility in this segment is likewise slowed to allow the colon to absorb water, Na+, and other minerals. By removing about 90% of the fluid, it converts the 1000–2000 mL of isotonic chyme that enters it each day from the ileum to about 200–250 mL of semisolid feces.


FIGURE 27–8 The human colon.


The ileum is linked to the colon by a structure known as the ileocecal valve, which restricts reflux of colonic contents, and particularly the large numbers of commensal bacteria, into the relatively sterile ileum. The portion of the ileum containing the ileocecal valve projects slightly into the cecum, so that increases in colonic pressure squeeze it shut, whereas increases in ileal pressure open it. It is normally closed. Each time a peristaltic wave reaches it, it opens briefly, permitting some of the ileal chyme to squirt into the cecum. When food leaves the stomach, the cecum relaxes and the passage of chyme through the ileocecal valve increases (gastroileal reflex). This is presumably a vago-vagal reflex.

The movements of the colon include segmentation contractions and peristaltic waves like those occurring in the small intestine. Segmentation contractions mix the contents of the colon and, by exposing more of the contents to the mucosa, facilitate absorption. Peristaltic waves propel the contents toward the rectum, although weak antiperistalsis is sometimes seen. A third type of contraction that occurs only in the colon is the mass action contraction,occurring about 10 times per day, in which there is simultaneous contraction of the smooth muscle over large confluent areas. These contractions move material from one portion of the colon to another (Clinical Box 27–4). They also move material into the rectum, and rectal distention initiates the defecation reflex (see below).


Hirschsprung Disease

Some children present with a genetically determined condition of abnormal colonic motility known as Hirschsprung disease or aganglionic megacolon, which is characterized by abdominal distention, anorexia, and lassitude. The disease is typically diagnosed in infancy, and affects as many as 1 in 5000 live births. It is due to a congenital absence of the ganglion cells in both the myenteric and submucous plexuses of a segment of the distal colon, as a result of failure of the normal cranial-to-caudal migration of neural crest cells during development. The action of endothelins on the endothelin B receptor (see Chapter 7) are necessary for normal migration of certain neural crest cells, and knockout mice lacking endothelin B receptors developed megacolon. In addition, one cause of congenital aganglionic megacolon in humans appears to be a mutation in the endothelin B receptor gene. The absence of peristalsis in patients with this disorder causes feces to pass the aganglionic region with difficulty, and children with the disease may defecate as infrequently as once every 3 weeks.


The symptoms of Hirschsprung disease can be relieved completely if the aganglionic portion of the colon is resected and the portion of the colon above it anastomosed to the rectum. However, this is not possible if an extensive segment is involved. In this case, patients may require a colectomy.

The movements of the colon are coordinated by the BER of the colon. The frequency of this wave, unlike the wave in the small intestine, increases along the colon, from about 2/min at the ileocecal valve to 6/min at the sigmoid.


The first part of a test meal reaches the cecum in about 4 h in most individuals, and all the undigested portions have entered the colon in 8 or 9 h. On average, the first remnants of the meal traverse the first third of the colon in 6 h, the second third in 9 h, and reach the terminal part of the colon (the sigmoid colon) in 12 h. From the sigmoid colon to the anus, transport is much slower (Clinical Box 27–5). When small colored beads are fed with a meal, an average of 70% of them are recovered in the stool in 72 h, but total recovery requires more than a week. Transit time, pressure fluctuations, and changes in pH in the gastrointestinal tract can be observed by monitoring the progress of a small pill that contains sensors and a miniature radio transmitter.



Constipation refers to a pathological decrease in bowel movements. It was previously considered to reflect changes in motility, but the recent success of a drug designed to enhance chloride secretion for the treatment of chronic constipation suggests alterations in the balance between secretion and absorption in the colon could also contribute to symptom generation. Patients with persistent constipation, and particularly those with a recent change in bowel habits, should be examined carefully to rule out underlying organic disease. However, many normal humans defecate only once every 2–3 days, even though others defecate once a day and some as often as three times a day. Furthermore, the only symptoms caused by constipation are slight anorexia and mild abdominal discomfort and distention. These symptoms are not due to absorption of “toxic substances,” because they are promptly relieved by evacuating the rectum and can be reproduced by distending the rectum with inert material. In western societies, the amount of misinformation and undue apprehension about constipation probably exceeds that about any other health topic. Symptoms other than those described above that are attributed by the lay public to constipation are due to anxiety or other causes.


Most cases of constipation are relieved by a change in the diet to include more fiber, or the use of laxatives that retain fluid in the colon, thereby increasing the bulk of the stool and promoting reflexes that lead to evacuation. As noted above, lubiprostone has recently joined the armamentarium for the treatment of constipation, and is assumed to act by enhancing chloride, and thus water, secretion into the colon thereby increasing the fluidity of the colonic contents.


Distention of the rectum with feces initiates reflex contractions of its musculature and the desire to defecate. In humans, the sympathetic nerve supply to the internal (involuntary) anal sphincter is excitatory, whereas the parasympathetic supply is inhibitory. This sphincter relaxes when the rectum is distended. The nerve supply to the external anal sphincter, a skeletal muscle, comes from the pudendal nerve. The sphincter is maintained in a state of tonic contraction, and moderate distention of the rectum increases the force of its contraction (Figure 27–9). The urge to defecate first occurs when rectal pressure increases to about 18 mm Hg. When this pressure reaches 55 mm Hg, the external as well as the internal sphincter relaxes and there is reflex expulsion of the contents of the rectum. This is why reflex evacuation of the rectum can occur even in the setting of spinal injury.


FIGURE 27–9 Responses to distention of the rectum by pressures less than 55 mm Hg. Distention produces passive tension due to stretching of the wall of the rectum, and additional active tension when the smooth muscle in the wall contracts. (For Internal, Adapted from Denny-Brown D, Robertson EG: An investigation of the nervous control of defaecation. Brain 1935; 58:256–310; For external, Adapted from Schuster MM et al: Simultaneous manometric recording of internal and external anal sphincteric reflexes. Bull Johns Hopkins Hosp 1965 Feb;116:79–88.)

Before the pressure that relaxes the external anal sphincter is reached, voluntary defecation can be initiated by straining. Normally, the angle between the anus and the rectum is approximately 90° (Figure 27–10), and this plus contraction of the puborectalis muscle inhibits defecation. With straining, the abdominal muscles contract, the pelvic floor is lowered 1–3 cm, and the puborectalis muscle relaxes. The anorectal angle is reduced to 15° or less. This is combined with relaxation of the external anal sphincter and defecation occurs. Defecation is therefore a spinal reflex that can be voluntarily inhibited by keeping the external sphincter contracted or facilitated by relaxing the sphincter and contracting the abdominal muscles.


FIGURE 27–10 Sagittal view of the anorectal area at rest (above) and during straining (below). Note the reduction of the anorectal angle and lowering of the pelvic floor during straining. (Modified and reproduced with permission from Lembo A, Camilleri, M: Chronic constipation. N Engl J Med 2003;349:1360.)

Distention of the stomach by food initiates contractions of the rectum and, frequently, a desire to defecate. The response is called the gastrocolic reflex, and may be amplified by an action of gastrin on the colon. Because of the response, defecation after meals is the rule in children. In adults, habit and cultural factors play a large role in determining when defecation occurs.


image The regulatory factors that govern gastrointestinal secretion also regulate its motility to soften the food, mix it with secretions, and propel it along the length of the tract.

image Two major patterns of motility are peristalsis and segmentation, which serve to propel or retard/mix the luminal contents, respectively. Peristalsis involves coordinated contractions and relaxations above and below the food bolus.

image The membrane potential of the majority of gastrointestinal smooth muscle undergoes rhythmic fluctuations that sweep along the length of the gut. The rhythm varies in different gut segments and is established by pacemaker cells known as interstitial cells of Cajal. This basic electrical rhythm provides for sites of muscle contraction when stimuli superimpose spike potentials on the depolarizing portion of the BER waves.

image In the period between meals, the intestine is relatively quiescent, but every 90 min or so it is swept through by a large peristaltic wave triggered by the hormone motilin. This migrating motor complex presumably serves a “housekeeping” function.

image Swallowing is triggered centrally and is coordinated with a peristaltic wave along the length of the esophagus that drives the food bolus to the stomach, even against gravity. Relaxation of the lower esophageal sphincter is timed to just precede the arrival of the bolus, thereby limiting reflux of the gastric contents. Nevertheless, gastroesophageal reflux disease is one of the most common gastrointestinal complaints

image The stomach accommodates the meal by a process of receptive relaxation. This permits an increase in volume without a significant increase in pressure. The stomach then serves to mix the meal and to control its delivery to downstream segments.

image Luminal contents move slowly through the colon, which enhances water recovery. Distension of the rectum causes reflex contraction of the internal anal sphincter and the desire to defecate. After toilet training, defecation can be delayed till a convenient time via voluntary contraction of the external anal sphincter.


For all questions, select the single best answer unless otherwise directed.

1. In infants, defecation often follows a meal. The cause of colonic contractions in this situation is

A. histamine.

B. increased circulating levels of CCK.

C. the gastrocolic reflex.

D. increased circulating levels of somatostatin.

E. the enterogastric reflex.

2. The symptoms of the dumping syndrome (discomfort after meals in patients with intestinal short circuits such as anastomosis of the jejunum to the stomach) are caused in part by

A. increased blood pressure.

B. increased secretion of glucagon.

C. increased secretion of CCK.

D. hypoglycemia.

E. hyperglycemia.

3. Gastric pressures seldom rise above the levels that breach the lower esophageal sphincter, even when the stomach is filled with a meal, due to which of the following processes?

A. Peristalsis

B. Gastroileal reflex

C. Segmentation

D. Stimulation of the vomiting center

E. Receptive relaxation

4. The migrating motor complex is triggered by which of the following?

A. Motilin



D. Somatostatin

E. Secretin

5. A patient is referred to a gastroenterologist because of persistent difficulties with swallowing. Endoscopic examination reveals that the lower esophageal sphincter fails to fully open as the bolus reaches it, and a diagnosis of achalasia is made. During the examination, or in biopsies taken from the sphincter region, a decrease would be expected in which of the following?

A. Esophageal peristalsis

B. Expression of neuronal NO synthase

C. Acetylcholine receptors

D. Substance P release

E. Contraction of the crural diaphragm


Barrett KE: Gastrointestinal Physiology. McGraw-Hill, 2006.

Cohen S, Parkman HP: Heartburn—A serious symptom. N Engl J Med 1999;340:878.

Itoh Z: Motilin and clinical application. Peptides 1997;18:593.

Lembo A, Camilleri M: Chronic constipation. N Engl J Med 2003;349:1360.

Levitt MD, Bond JH: Volume, composition and source of intestinal gas. Gastroenterology 1970;59:921.

Mayer EA, Sun XP, Willenbucher RF: Contraction coupling in colonic smooth muscle. Annu Rev Physiol 1992;54:395.

Mittal RK, Balaban DH: The esophagogastric junction. N Engl J Med 1997;336:924.

Sanders KM, Ward SM: Nitric oxide as a mediator of noncholinergic neurotransmission. Am J Physiol 1992;262:G379.

Ward SM, Sanders KM: Involvement of intramuscular interstitial cells of Cajal in neuroeffector transmission in the gastrointestinal tract. J Physiol 2006;576:675.