GI Motility, Swallowing & Vomiting Reflex
The rhythms, reflexes, and receptors that move food, or send it back
The electrical basis of motility
Slow waves. Interstitial cells of Cajal, pacemaker cells within the muscularis externa, generate slow waves: rhythmic oscillations of membrane potential that set the maximum possible contraction rate for each region. Neural and hormonal input changes how strongly the muscle responds, not the slow-wave rate.
Spike potentials. A slow wave alone does not cause contraction. When its plateau reaches threshold, spike (action) potentials fire, Ca2+ enters the smooth muscle, and it contracts; the number of spikes sets the force. Acetylcholine brings the plateau closer to threshold and adds spikes, while norepinephrine does the opposite.
Swallowing and the stomach
- Oral phaseVoluntary: the tongue pushes the bolus into the pharynx
- Pharyngeal phaseMedullary reflex (afferents in CN IX and X): soft palate seals the nasopharynx, larynx rises under the epiglottis, breathing pauses
- UES opensThe cricopharyngeus relaxes to admit the bolus
- Esophageal phasePrimary peristalsis carries the bolus; secondary peristalsis, triggered by distension, clears residue
- LES relaxesVagal inhibitory neurons release VIP and nitric oxide
Sphincters. The upper esophageal sphincter (cricopharyngeus, skeletal muscle) stays closed between swallows so air does not enter the esophagus. The lower esophageal sphincter is tonically contracted smooth muscle that limits reflux; acetylcholine and gastrin raise its tone, and it relaxes at the start of each swallow. Loss of its inhibitory NO/VIP neurons prevents relaxation in achalasia.
Receptive relaxation. Swallowing and gastric stretch trigger a vagovagal reflex, with afferent and efferent limbs in the vagus and VIP and NO as transmitters, that relaxes the fundus and proximal body so the stomach fills with little rise in pressure. The distal stomach grinds and mixes food by retropulsion against a closing pylorus. Truncal vagotomy abolishes receptive relaxation, so small meals raise gastric pressure, causing early satiety and rapid emptying of liquids.
Gastric emptying. Liquids empty faster than solids, and the duodenum sets the pace. Fat releases CCK, the strongest brake, along with GIP; acid releases secretin and triggers the enterogastric reflex; hyperosmolar chyme also slows emptying. All weaken antral contractions and tighten the pylorus, matching delivery to what the duodenum can neutralize and digest.
Fasting motility and the colon
Migrating motor complex. Between meals, a band of intense contractions sweeps from stomach to terminal ileum about every 90–120 minutes, clearing debris and bacteria. Motilin released from the duodenum triggers its strong phase, and eating abolishes the cycle. Erythromycin is a motilin-receptor agonist used as a prokinetic, although tachyphylaxis limits long-term use.
Loss of the migrating motor complex, as in diabetes, scleroderma, or opioid use, predisposes to small-intestinal bacterial overgrowth.
Colon. The colon mixes contents by haustral segmentation and propels them with only a few mass movements a day. Gastric distension triggers the gastrocolic reflex (parasympathetic input plus gastrin and CCK), bringing mass movements and the urge to defecate soon after meals; it is prominent in infants and exaggerated in IBS.
Defecation. Rectal distension triggers the rectoanal inhibitory reflex: the internal anal sphincter (smooth, involuntary) relaxes while the external sphincter (skeletal, pudendal nerve) contracts to preserve continence. Defecation follows voluntary relaxation of the external sphincter and puborectalis plus a Valsalva push, with pelvic splanchnic (S2–S4) parasympathetic input. The rectoanal inhibitory reflex is absent in Hirschsprung disease, a key finding on anorectal manometry.
The vomiting reflex
Central control. The vomiting center in the medulla (nucleus tractus solitarius and nearby reticular formation) integrates four inputs. The chemoreceptor trigger zone lies in the area postrema, a circumventricular organ on the floor of the fourth ventricle outside the blood-brain barrier, so it can sample blood for chemotherapy, opioids, digoxin, and uremic toxins.
| Input | Typical triggers | Receptors | Blocking drugs |
|---|---|---|---|
| CTZ (area postrema) | Drugs, toxins, uremia | D2, 5-HT3, NK1, opioid | Metoclopramide, ondansetron, aprepitant |
| Gut vagal afferents | Chemotherapy, radiation, gastroenteritis (serotonin from enterochromaffin cells) | 5-HT3 | Ondansetron, granisetron |
| Vestibular system | Motion sickness | H1, M1 | Meclizine, scopolamine |
| Cortex and limbic system | Anticipation, smells, pain, raised intracranial pressure | Higher-center pathways | Benzodiazepines for anticipatory nausea |
The motor program. Nausea brings salivation, sweating, pallor, and tachycardia. A retrograde giant contraction returns small-bowel contents to the stomach; the glottis closes and the soft palate rises to protect the airway; the stomach and LES relax; then the diaphragm and abdominal muscles contract forcefully to expel the contents.
Diabetic gastroparesis. Autonomic (vagal) neuropathy, together with loss of interstitial cells of Cajal, weakens antral contractions and pyloric coordination. Patients have early satiety, fullness, bloating, vomiting of food eaten hours earlier, and erratic glucose control. A scintigraphic gastric emptying study confirms delayed emptying once endoscopy excludes obstruction. Treatment is small low-fat meals, glucose control, and prokinetics such as metoclopramide or erythromycin.
Metoclopramide, a D2 antagonist, carries a boxed warning for tardive dyskinesia with long-term use.