Physiology 5th Ed.

MOTILITY

Motility is a general term that refers to contraction and relaxation of the walls and sphincters of the gastrointestinal tract. Motility grinds, mixes, and fragments ingested food to prepare it for digestion and absorption, and then it propels the food along the gastrointestinal tract.

All of the contractile tissue of the gastrointestinal tract is smooth muscle, except for that in the pharynx, the upper one third of the esophagus, and the external anal sphincter, which is striated muscle. The smooth muscle of the gastrointestinal tract is unitary smooth muscle, in which the cells are electrically coupled via low-resistance pathways called gap junctions. Gap junctions permit rapid cell-to-cell spread of action potentials that provide for coordinated and smooth contraction.

The circular and longitudinal muscles of the gastrointestinal tract have different functions. When circular muscle contracts, it results in shortening of a ring of smooth muscle, which decreases the diameter of that segment. When longitudinal muscle contracts, it results in shortening in the longitudinal direction, which decreases the length of that segment.

Contractions of gastrointestinal smooth muscle can be either phasic or tonic. Phasic contractions are periodic contractions followed by relaxation. Phasic contractions are found in the esophagus, gastric antrum, and small intestine, all tissues involved in mixing and propulsion. Tonic contractions maintain a constant level of contraction or tone without regular periods of relaxation. They are found in the orad (upper) region of the stomach and in the lower esophageal, ileocecal, and internal anal sphincters.

Slow Waves

Like all muscle, contraction in gastrointestinal smooth muscle is preceded by electrical activity, the action potentials. Slow waves are a unique feature of the electrical activity of gastrointestinal smooth muscle. Slow waves are not action potentials but rather oscillating depolarization and repolarization of the membrane potential of the smooth muscle cells (Fig. 8-7). During the depolarization phase of the slow wave, the membrane potential becomes less negative and moves toward threshold; during the repolarization phase, the membrane potential becomes more negative and moves away from threshold. If, at the plateau or the peak of the slow wave, the membrane potential is depolarized all the way to threshold, then action potentials occur “on top of” the slow wave. For example, the slow waves shown in Figure 8-7 reach threshold and result in bursts of six action potentials at the plateau. As in other types of muscle, the mechanical response (contraction or tension) follows the electrical response. In Figure 8-7, notice that the contraction, or tension, occurs slightly after the burst of action potentials.

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Figure 8–7 Slow waves of the gastrointestinal tract superimposed by action potentials and contraction. A burst of action potentials is followed by contraction. A, Electrical activity; B, electrical and mechanical activity.

image Frequency of slow waves. The intrinsic rate, or frequency, of slow waves varies along the gastrointestinal tract, from 3 to 12 slow waves per minute. Each portion of the gastrointestinal tract has a characteristic frequency, with the stomach having the lowest rate (3 slow waves per minute) and the duodenum having the highest rate (12 slow waves per minute). The frequency of slow waves sets the frequency of action potentials and, therefore, sets the frequency of contractions. (Action potentials cannot occur unless the slow wave brings the membrane potential to threshold.) The characteristic frequency of slow waves is not influenced by neural or hormonal input, although neural activity and hormonal activity do modulate both the production of action potentials and the strength of contractions.

image Origin of slow waves. It is believed that slow waves originate in the interstitial cells of Cajal, which are abundant in the myenteric plexus. Cyclic depolarizations and repolarizations occur spontaneously in the interstitial cells of Cajal and spread rapidly to adjacent smooth muscle via low-resistance gap junctions. Just as the sinoatrial node is the pacemaker of the heart, the interstitial cells of Cajal can be considered the pacemaker for gastrointestinal smooth muscle. In each region of the gastrointestinal tract, the pacemaker drives the frequency of slow waves, which determines the rate at which action potentials and contractions can occur.

image Mechanism of slow waves. The depolarizing phase of the slow wave is caused by the cyclic opening of calcium (Ca2+) channels, which produces an inward Ca2+ current that depolarizes the cell membrane. During the plateau of the slow wave, Ca2+ channels open, producing an inward Ca2+ current that maintains the membrane potential at the depolarized level. The repolarizing phase of the slow wave is caused by opening of potassium (K+) channels, which produces an outward K+ current that repolarizes the cell membrane.

image Relationship between slow waves, action potentials, and contraction. In gastrointestinal smooth muscle, even subthreshold slow waves produce a weak contraction. Thus, even without the occurrence of action potentials, the smooth muscle is not completely relaxed but exhibits basal contractions, or tonic contractions. However, if slow waves depolarize the membrane potential to threshold, then action potentials occur on top of the slow waves, followed by much stronger contractions, or phasic contractions. The greater the number of action potentials on top of the slow waves, the larger the phasic contraction. In contrast to skeletal muscle (where each action potential is followed by a separate contraction or twitch), in smooth muscle individual action potentials are not followed by separate twitches; instead, the twitches summate into one long contraction (see Fig. 8-7B).

Chewing and Swallowing

Chewing and swallowing are the first steps in the processing of ingested food as it is prepared for digestion and absorption.

Chewing

Chewing has three functions: (1) It mixes food with saliva, lubricating it to facilitate swallowing; (2) it reduces the size of food particles, which facilitates swallowing (although the size of the swallowed particles has no effect on the digestive process); and (3) it mixes ingested carbohydrates with salivary amylase to begin carbohydrate digestion.

Chewing has both voluntary and involuntary components. The involuntary component involves reflexes initiated by food in the mouth. Sensory information is relayed from mechanoreceptors in the mouth to the brain stem, which orchestrates a reflex oscillatory pattern of activity to the muscles involved in chewing. Voluntary chewing can override involuntary or reflex chewing at any time.

Swallowing

Swallowing is initiated voluntarily in the mouth, but thereafter it is under involuntary or reflex control. The reflex portion is controlled by the swallowing center, which is located in the medulla. Sensory information (e.g., food in the mouth) is detected by somatosensory receptors located near the pharynx. This sensory, or afferent, information is carried to the medullary swallowing center via the vagus and glossopharyngeal nerves. The medulla coordinates the sensory information and directs the motor, or efferent, output to the striated muscle of the pharynx and upper esophagus (Fig. 8-8).

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Figure 8–8 Structures of the upper gastrointestinal tract. The pharynx, upper esophageal sphincter, and upper third of the esophagus are composed of striated muscle. The lower two thirds of the esophagus and lower esophageal sphincter are composed of smooth muscle.

Three phases are involved in swallowing: oral, pharyngeal, and esophageal. The oral phase is voluntary, and the pharyngeal and esophageal phases are controlled by reflexes.

image Oral phase. The oral phase is initiated when the tongue forces a bolus of food back toward the pharynx, which contains a high density of somatosensory receptors. As previously noted, activation of these receptors then initiates the involuntary swallowing reflex in the medulla.

image Pharyngeal phase. The purpose of the pharyngeal phase is to propel the food bolus from the mouth through the pharynx to the esophagus in the following steps: (1) The soft palate is pulled upward, creating a narrow passage for food to move into the pharynx so that food cannot reflux into the nasopharynx. (2) The epiglottis moves to cover the opening to the larynx, and the larynx moves upward against the epiglottis to prevent food from entering the trachea. (3) The upper esophageal sphincter relaxes, allowing food to pass from the pharynx to the esophagus. (4) A peristaltic wave of contraction is initiated in the pharynx and propels food through the open sphincter. Breathing is inhibited during the pharyngeal phase of swallowing.

image Esophageal phase. The esophageal phase of swallowing is controlled in part by the swallowing reflex and in part by the enteric nervous system. In the esophageal phase, food is propelled through the esophagus to the stomach. Once the bolus has passed through the upper esophageal sphincter in the pharyngeal phase, the swallowing reflex closes the sphincter so that food cannot reflux into the pharynx. Aprimary peristaltic wave, also coordinated by the swallowing reflex, travels down the esophagus (see discussion of peristalsis), propelling the food along. If the primary peristaltic wave does not clear the esophagus of food, a secondary peristaltic wave is initiated by the continued distention of the esophagus. The secondary wave, which is mediated by the enteric nervous system, begins at the site of distention and travels downward.

Esophageal Motility

The function of motility in the esophagus is to propel the food bolus from the pharynx to the stomach (see Fig. 8-8). There is overlap between the esophageal phase of swallowing and esophageal motility. The path of the food bolus through the esophagus is as follows:

1.          The upper esophageal sphincter opens, mediated by the swallowing reflex, allowing the bolus to move from the pharynx to the esophagus. Once the bolus enters the esophagus, the upper esophageal sphincter closes, which prevents reflux into the pharynx.

2.          A primary peristaltic contraction, also mediated by the swallowing reflex, involves a series of coordinated sequential contractions (Fig. 8-9). As each segment of esophagus contracts, it creates an area of high pressure just behind the bolus, pushing it down the esophagus. Each sequential contraction pushes the bolus further along. If the person is sitting or standing, this action is accelerated by gravity.

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Figure 8–9 Pressures in esophagus during swallowing.

3.          As the peristaltic wave and the food bolus approach the lower esophageal sphincter, the sphincter opens. Opening of the lower esophageal sphincter is mediated by peptidergic fibers in the vagus nerve that release VIP as their neurotransmitter. VIP produces relaxation in the smooth muscle of the lower esophageal sphincter.

  At the same time that the lower esophageal sphincter relaxes, the orad region of the stomach also relaxes, a phenomenon called receptive relaxation. Receptive relaxation decreases pressure in the orad stomach and facilitates movement of the bolus into the stomach. As soon as the bolus enters the orad stomach, the lower esophageal sphincter contracts, returning to its high resting tone. At this resting tone, the pressure at the sphincter is higher than the pressure in the esophagus or in the orad stomach.

4.          If the primary peristaltic contraction does not clear the esophagus of food, a secondary peristaltic contraction, mediated by the enteric nervous system, clears the esophagus of any remaining food. The secondary peristaltic contraction begins at the point of distention and travels downward.

An interesting problem is posed by the intrathoracic location of the esophagus (only the lower esophagus is located in the abdomen). The thoracic location means that intraesophageal pressure is equal to intrathoracic pressure, which is lower than atmospheric pressure. It also means that intraesophageal pressure is lower than abdominal pressure. The lower intraesophageal pressure creates two problems: (1) keeping air out of the esophagus at the upper end and (2) keeping the acidic gastric contents out at the lower end. It is the function of the upper esophageal sphincter to prevent air from entering the upper esophagus, and the lower esophageal sphincter functions to prevent the acidic gastric contents from entering the lower esophagus. Both the upper and lower esophageal sphincters are closed, except when food is passing from the pharynx into the esophagus or from the esophagus into the stomach. Conditions in which intra-abdominal pressure is increased (e.g., pregnancy or morbid obesity) may causegastroesophageal reflux, in which the contents of the stomach reflux into the esophagus.

Gastric Motility

There are three components of gastric motility: (1) relaxation of the orad region of the stomach to receive the food bolus from the esophagus, (2) contractions that reduce the size of the bolus and mix it with gastric secretions to initiate digestion, and (3) gastric emptying that propels chyme into the small intestine. The rate of delivery of chyme to the small intestine is hormonally regulated to ensure adequate time for digestion and absorption of nutrients in the small intestine.

Structure and Innervation of the Stomach

The stomach has three layers of muscle: an outer longitudinal layer, a middle circular layer, and an inner oblique layer that is unique to the stomach. The thickness of the muscle wall increases from the proximal stomach to the distal stomach.

The innervation of the stomach includes extrinsic innervation by the autonomic nervous system and intrinsic innervation from the myenteric and submucosal plexuses. The myenteric plexus serving the stomach receives parasympathetic innervation via the vagus nerve and sympathetic innervation via fibers originating in the celiac ganglion.

Figure 8-10 shows the three anatomic divisions of the stomach: fundus, body, and antrum. On the basis of differences in motility, the stomach also can be divided into two regions, orad and caudad. The orad region is proximal, contains the fundus and the proximal portion of the body, and is thin walled. The caudad region is distal, contains the distal portion of the body and the antrum, and is thick walled to generate much stronger contractions than the orad region. Contractions of the caudad region mix the food and propel it into the small intestine.

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Figure 8–10 Schematic drawing showing the three major divisions of the stomach: fundus, body, and antrum. The orad region includes the fundus and the upper body. The caudad region includes the lower body and the antrum.

Receptive Relaxation

The orad region of the stomach has a thin muscular wall. Its function is to receive the food bolus. As noted in the discussion about esophageal motility, distention of the lower esophagus by food produces relaxation of the lower esophageal sphincter and, simultaneously, relaxation of the orad stomach, called receptive relaxation. Receptive relaxation reduces the pressure and increases the volume of the orad stomach, which, in its relaxed state, can accommodate as much as 1.5 L of food.

Receptive relaxation is a vagovagal reflex, meaning that both afferent and efferent limbs of the reflex are carried in the vagus nerve. Mechanoreceptors detect distention of the stomach and relay this information to the CNS via sensory neurons. The CNS then sends efferent information to the smooth muscle wall of the orad stomach, causing it to relax. The neurotransmitter released from these postganglionic peptidergic vagal nerve fibers is VIP. Vagotomy eliminates receptive relaxation.

Mixing and Digestion

The caudad region of the stomach has a thick muscular wall and produces the contractions necessary for mixing and digesting food. These contractions break the food into smaller pieces and mix it with gastric secretions to begin the digestive process.

Waves of contraction begin in the middle of the body of the stomach and move distally along the caudad stomach. These are vigorous contractions that increase in strength as they approach the pylorus. The contractions mix the gastric contents and periodically propel a portion of the gastric contents through the pylorus into the duodenum. Much of the chyme is not immediately injected into the duodenum, however, because the wave of contraction also closes the pylorus. Therefore, most of the gastric contents are propelled back into the stomach for further mixing and further reduction of particle size, a process known as retropulsion.

The frequency of slow waves in the caudad stomach is from 3 to 5 waves per minute. Recall that slow waves bring the membrane potential to threshold so that action potentials can occur. Because the frequency of slow waves sets the maximal frequency of action potentials and contractions, the caudad stomach contracts 3 to 5 times per minute.

Although neural input and hormonal input do not influence the frequency of slow waves, they do influence the frequency of action potentials and the force of contraction. Parasympathetic stimulation and the hormones gastrin and motilin increase the frequency of action potentials and the force of gastric contractions. Sympathetic stimulation and the hormones secretin and GIP decrease the frequency of action potentials and the force of contractions.

During fasting, there are periodic gastric contractions, called the migrating myoelectric complexes, which are mediated by motilin. These contractions occur at 90-minute intervals and function to clear the stomach of any residue remaining from the previous meal.

Gastric Emptying

After a meal, the stomach contains about 1.5 L, which is composed of solids, liquids, and gastric secretions. Emptying of the gastric contents to the duodenum takes approximately 3 hours. The rate of gastric emptying must be closely regulated to provide adequate time for neutralization of gastric H+ in the duodenum and adequate time for digestion and absorption of nutrients.

Liquids empty more rapidly than solids, and isotonic contents empty more rapidly than either hypotonic or hypertonic contents. To enter the duodenum, solids must be reduced to particles of 1 mm3 or less; retropulsion in the stomach continues until solid food particles are reduced to the required size.

Two major factors slow or inhibit gastric emptying (i.e., increase gastric emptying time): the presence of fat and the presence of H+ ions (low pH) in the duodenum. The effect of fat is mediated by CCK,which is secreted when fatty acids arrive in the duodenum. In turn, CCK slows gastric emptying, ensuring that gastric contents are delivered slowly to the duodenum and providing adequate time for fat to be digested and absorbed. The effect of H+ is mediated by reflexes in the enteric nervous system. H+ receptors in the duodenal mucosa detect low pH of the intestinal contents and relay this information to gastric smooth muscle via interneurons in the myenteric plexus. This reflex also ensures that the gastric contents are delivered slowly to the duodenum, permitting time for neutralization of H+ by pancreatic HCO3, as is necessary for optimal function of pancreatic enzymes.

Small Intestinal Motility

The functions of the small intestine are digestion and absorption of nutrients. In this context, motility of the small intestine serves to mix the chyme with digestive enzymes and pancreatic secretions, expose the nutrients to the intestinal mucosa for absorption, and propel the unabsorbed chyme along the small intestine into the large intestine.

In the small intestine, as with other gastrointestinal smooth muscle, the frequency of slow waves determines the rate at which action potentials and contractions occur. Slow waves are more frequent in the duodenum (12 waves per minute) than in the stomach. In the ileum, the frequency of slow waves decreases slightly, to 9 waves per minute. As in the stomach, contractions (called migrating myoelectric complexes) occur every 90 minutes to clear the small intestine of residual chyme.

There is both parasympathetic and sympathetic innervation of the small intestine. Parasympathetic innervation occurs via the vagus nerve, and sympathetic innervation occurs via fibers that originate in the celiac and superior mesenteric ganglia. Parasympathetic stimulation increases contraction of intestinal smooth muscle, and sympathetic activity decreases contraction. Although many of the parasympathetic nerves are cholinergic (i.e., they release ACh), some of the parasympathetic nerves release other neurocrines (i.e., they are peptidergic). Neurocrines released from parasympathetic peptidergic neurons of the small intestine include VIP, enkephalins, and motilin.

There are two patterns of contractions in the small intestine: segmentation contractions and peristaltic contractions. Each pattern is coordinated by the enteric nervous system (Fig. 8-11).

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Figure 8–11 Comparison of segmentation contractions (A) and peristaltic contractions (B) in the small intestine. Segmentation contractions mix the chyme. Peristalsis moves the chyme in the caudad direction. For the peristaltic contraction, behind the bolus (orad) circular muscle contracts and longitudinal muscle relaxes; in front of the bolus (caudad), circular muscle relaxes and longitudinal muscle contracts.

Video: Peristalsis

Segmentation Contractions

Segmentation contractions serve to mix the chyme and expose it to pancreatic enzymes and secretions, as shown in Figure 8-11A. Step 1 shows a bolus of chyme in the intestinal lumen. A section of small intestine contracts, splitting the chyme and sending it in both orad and caudad directions (Step 2). That section of intestine then relaxes, allowing the bolus of chyme that was split to merge back together (Step 3). This back-and-forth movement serves to mix the chyme but produces no forward, propulsive movement along the small intestine.

Peristaltic Contractions

In contrast to segmentation contractions, which are designed to mix the chyme, peristaltic contractions are designed to propel the chyme along the small intestine toward the large intestine (see Fig. 8-11B). Step 1 shows a bolus of chyme. A contraction occurs at a point orad to (behind) the bolus; simultaneously, the portion of intestine caudad to (in front of) the bolus relaxes (Step 2). The chyme is thereby propelled in the caudad direction. A wave of peristaltic contractions occurs down the small intestine, repeating the sequence of contractions behind the bolus and relaxation in front of the bolus, which moves the chyme along (Step 3).

To accomplish such propulsive movements along the small intestine, circular and longitudinal muscles must function oppositely to complement each other’s actions. (Recall that contraction of circular muscle decreases the diameter of that small intestinal segment, whereas contraction of longitudinal muscle decreases the length of that small intestinal segment.) To prevent the conflict that would occur if circular and longitudinal muscle contracted at the same time, they are reciprocally innervated. Consequently, when the circular muscle of a segment contracts, the longitudinal muscle simultaneously relaxes; when the longitudinal muscle contracts, the circular muscle simultaneously relaxes.

Peristalsis therefore occurs as follows. The food bolus in the intestinal lumen is sensed by enterochromaffin cells of the intestinal mucosa, which release serotonin (5-hydroxytyptamine, 5-HT). The 5-HT binds to receptors on intrinsic primary afferent neurons (IPANs) that, when activated, initiate the peristaltic reflex in that segment of small intestine. Behind the bolus, excitatory transmitters (e.g., ACh, substance P, neuropeptide Y) are released in circular muscle, while these pathways are simultaneously inhibited in the longitudinal muscle; thus, this segment of small intestine narrows and lengthens. In front of the bolus, inhibitory pathways (e.g., vasoactive intestinal peptide, nitric oxide) are activated in circular muscle, while excitatory pathways are activated in longitudinal muscle; thus, this segment of small intestine widens and shortens.

Vomiting

vomiting center in the medulla coordinates the vomiting reflex. Afferent information comes to the vomiting center from the vestibular system, the back of the throat, the gastrointestinal tract, and the chemoreceptor trigger zone in the fourth ventricle.

The vomiting reflex includes the following events in this temporal sequence: reverse peristalsis that begins in the small intestine; relaxation of the stomach and pylorus; forced inspiration to increase abdominal pressure; movement of the larynx upward and forward and relaxation of the lower esophageal sphincter; closure of the glottis; and forceful expulsion of gastric, and sometimes duodenal, contents. In retching, the upper esophageal sphincter remains closed, and because the lower esophageal sphincter is open, the gastric contents return to the stomach when the retch is over.

Large Intestinal Motility

Material that is not absorbed in the small intestine enters the large intestine. The contents of the large intestine, called feces, are destined for excretion. After the contents of the small intestine enter the cecum and proximal colon, the ileocecal sphincter contracts, preventing reflux into the ileum. Fecal material then moves from the cecum through the colon (i.e., ascending, transverse, descending, and sigmoid colons), to the rectum, and on to the anal canal.

Segmentation Contractions

Segmentation contractions occur in the cecum and proximal colon. As in the small intestine, these contractions function to mix the contents of the large intestine. In the large intestine, the contractions are associated with characteristic saclike segments called haustra.

Mass Movements

Mass movements occur in the colon and function to move the contents of the large intestine over long distances, such as from the transverse colon to the sigmoid colon. Mass movements occur anywhere from1 to 3 times per day.Water absorption occurs in the distal colon, making the fecal contents of the large intestine semisolid and increasingly difficult to move. A final mass movement propels the fecal contents into the rectum, where they are stored until defecation occurs.

Defecation

As the rectum fills with feces, the smooth muscle wall of the rectum contracts and the internal anal sphincter relaxes in the rectosphincteric reflex. Defecation will not occur at this time, however, because the external anal sphincter (composed of striated muscle and under voluntary control) is still tonically contracted. However, once the rectum fills to 25% of its capacity, there is an urge to defecate. When it is appropriate, the external anal sphincter is relaxed voluntarily, the smooth muscle of the rectum contracts to create pressure, and feces are forced out through the anal canal. The intra-abdominal pressure created for defecation can be increased by a Valsalva maneuver (expiring against a closed glottis).

Gastrocolic Reflex

Distention of the stomach by food increases the motility of the colon and increases the frequency of mass movements in the large intestine. This long arc reflex, called the gastrocolic reflex, has its afferent limb in the stomach, which is mediated by the parasympathetic nervous system. The efferent limb of the reflex, which produces increased motility of the colon, is mediated by the hormones CCK and gastrin.