Physiology, Gastrocolic Re ex

Malone JC, Thavamani A.

Introduction
The gastrocolic reflex is a physiological reflex that controls the motility of the lower gastrointestinal tract following a meal. As
a result of the gastrocolic reflex, the colon has increased motility in response to the stretch of the stomach with the ingestion of
food. The gastrocolic reflex allows room for the consumption of more food via control over peristalsis and movement of
ingested food distally toward the rectum. Myoelectric recordings demonstrate the reflex in the large intestine that shows a
spike in electrical activity within minutes of food consumption. The gastrocolic reflex initiates and controls migrating motor
complexes throughout the colon. These motor complexes act cyclically during the digestion process and can be broken up into
four phases.

The control of these phases is multifactorial, involving neurological, mechanical, and paracrine mediators.[1] Several
neuropeptides are suspected mediators of the reflex, including cholecystokinin, serotonin, neurotensin, and gastrin. Three
centers of control have been identified and studied and include myogenic control, hormonal control, and neural control. The
sigmoid colon is the region most affected during the phasic response of digestion, which consists of cyclical periods of
contraction followed by relaxation to propel food distally toward the rectum. These contractions are generated in the
myenteric plexus and accomplished by the muscularis externa — the gastrocolic reflex results in the urge to defecate after a
meal. When food enters the rectum and drives pressures up, the gastrocolic reflex stimulates expulsion of the contents of the
rectum via defecation.[2]

Issues of Concern
Alteration in the gastrocolic reflex has been a suspected etiology in patients with irritable bowel syndrome (IBS). Patients
with IBS have demonstrated a stronger colonic response to the gastrocolic reflex. These patients may experience a strong urge
to defecate following ingestion of a meal and may experience symptoms like abdominal distension, flatulence, pain, and
tenesmus.[3][4] Furthermore, alternations in the gut microbiome can cause a downstream effect that alters the
enteroendocrine cells' ability to sense and carry out paracrine functions, thus indirectly affecting the motility of the colon.

Profound gastrocolic reflex has been implicated in the idiopathic variant of dumping syndrome (DS). Although abdominal pain
is present in both DS and IBS, systemic signs including palpitations, hypotension, dizziness, diaphoresis often accompany DS.
Another key difference in the presentation of DS is that they often present with protein-calorie malnutrition due to increased
excess nutritional loss in diarrhea.[5]

Both IBS and DS are caused by profound gastrocolic reflex, whereas poor gastrocolic reflex results in constipation. Neuronal
dysfunction may lead to impaired gastrocolic reflex and poor gut motility. Diabetic patients with neuropathy often have
gastroparesis resulting in delayed gastric emptying and also impaired gastrocolic reflex leading to constipation.[6]

Cellular
The cellular makeup of the gastrocolic reflex is multisystemic and includes cell bodies from the nervous, endocrine, and
gastrointestinal systems. The primary mediators are neurons of the autonomic nervous system, neurons of the myenteric
(Auerbach’s) plexus, interstitial cells of Cajal, and enteroendocrine cells that line the GI tract.

Sympathetic nerve fibers contribute an inhibitory effect on the colon, while parasympathetic nerve fibers contribute a
stimulatory effect. The nerve supply to the colon is broken up between midgut and hindgut derived structures. Structures
derived from the midgut include the ascending colon and proximal two-thirds of the transverse colon. These midgut derived
structures receive their sympathetic supply from nerves that originate from the superior mesenteric plexus and their
parasympathetic supply via the vagus nerve. Structures derived from the hindgut include the distal one-third of the transverse
colon, the descending colon, and the sigmoid colon. These structures receive their sympathetic innervation from the inferior
mesenteric plexus and parasympathetic innervation via pelvic splanchnic nerves.

Located in between the inner and outer layers of the muscularis externa, the myenteric plexus generates and helps coordinate
gut motility. A sensory component of the myenteric plexus has been identified, and this is thought to help with coordination
and the propagation of migrating motor complexes. The myenteric plexus propels a food bolus distally by contracting the
radius of the lumen of the bowel and extending the length of the bowel.[2] The cell bodies of nerves located in the myenteric
plexus communicate using gap junctions with both an excitatory component, as well as an inhibitory component.[7]

Interstitial cells of Cajal are located between smooth muscle cells and nerve endings throughout the GI tract and are
responsible for the inherent pacemaker activity of the GI system. These cell bodies interact with smooth muscle cells to
transduce contributions from the enteric motor neurons and turn these signals into the stimulus needed for phasic smooth
muscle cells to propel the food bolus distally.[8]

Enteroendocrine cells (EECs) are cells derived from endoderm epithelial cells that are abundant throughout the GI tract. These
cells form the largest endocrine organ in the body and are responsible for many tasks, including GI secretion and motility.
These cells function via endocrine and paracrine roles. They sense the contents of the lumen of the bowel and excrete
neuropeptides that can act on distal organs or even act on cells nearby, including neurons of the enteric nervous system that
control motility. Research has shown that EECs can act directly on cells of the enteric nervous system to help initiate and
propagate the proper physiological response.[9]

Development
The vagus nerve derives from two separate origins depending on functionality. The motor aspect of the nerve derives from the
basal plate of the medulla oblongata, and the sensory aspect arises from the neural crest.[10] The neurons of the enteric
nervous system derive from neural crest cells that migrate to occupy the GI tract.[11] Interstitial cells of Cajal appear to arise
from mesenchymal precursor cells.[12] Enteroendocrine cells that are responsible for the management of GI hormones arise
from pluripotent intestinal stem cells. These stem cells are present within intestinal crypts.[13] Smooth muscles of the colon
derive from mesoderm.

Organ Systems Involved

The gastrocolic reflex is multisystemic in origin. The reflex involves the autonomic nervous system, the enteric nervous
system, and cells of the GI tract that regulate endocrine functions. Signals from the central nervous system communicate with
the enteric nervous system and vice versa controlling peristalsis. The enteric nervous system proves to be paramount and is
demonstrated by the morbid effects of enteric nervous system neuropathies; this is in contrast with the importance of vagal
and sympathetic inputs, which have shown not to carry as much of an effect if these connections become interrupted.[14]

Function
The gastrocolic reflex is essentially the colonic response to food ingestion. Through a series of coordinated signals via the
enteric nervous system and neuropeptides, the colon is stimulated via muscarinic pathways to contract, resulting in colonic
migratory motor complexes or high amplitude propagating contractions (HAPCs) which usually occur in bursts and often after
food intake.[15] These colonic contractions following meal consumption help propel the food bolus toward the rectum for
defecation. Neuropeptides like serotonin, gastrin, cholecystokinin, and prostaglandin E1 all have all implications as mediators
of the response.[4] According to a study enrolling “twenty-nine healthy volunteers with a colonoscopically positioned multi-
lumen manometric probe and low-compliance infusion system,” the motor activity of the large bowel was significantly
increased following consumption of a meal. This study also showed that the right colon and transverse colon showed a much
faster, stronger increase in motor activity when compared to a slower, steadier increase in distal segments.[16]

Mechanism
When food gets introduced into the stomach, a coordinated response via stretch receptors, neuropeptides, and the enteric
nervous system activate the gastrocolic reflex, which in turn increases the motility in the colon to make room for more food.
Migrating motor complexes induce food bolus movement through slow waves and faster segments of increased electrical
activity, know as spike waves; this is very similar to how the stomach and small intestine move food. The large bowel also
employs stronger, more frequent contractions known as mass movements in response to signals from mechanical stretch
receptors in the stomach and the products of digestion in the small intestine. The enteric nervous system controls these mass
movements and is most active in the transverse and left colon, which helps move food toward the rectum for defecation,
which is the reason behind the urge to defecate following ingestion of a meal.[17][2]

Related Testing
A colon transit study may be employed to test for the functionality of the gastrocolic reflex. The gold standard for measuring
colon transit time utilizes a radiopaque indicator that is easy to do and relatively low cost. The only downside to this test is that
it subjects the patient undergoing radiation exposure. Another test utilized is radionuclide scintigraphy. This is done using a
labeled radioisotope and viewed through a specialized camera. The patient swallows a labeled radioisotope, and it gets
followed throughout transit through the GI tract; this approach exposes a lesser degree of radiation. Both of these transit
studies are usually for research purposes and less often used in clinical practice. Colonic manometry and bead expulsion
are more frequently used to assess the contractility and motility of the colon. Colonic manometry is a more common modality
in children with colonic dysmotility, encopresis, and abdominal pain. They record various colonic motor contractions and
guide the further courses of treatment, including the need for surgical interventions.[18] Lastly, a test that uses wireless
motility capsules has been considered.[19]

Pathophysiology
Patients that have irritable bowel syndrome have been shown to have a heightened gastrocolic response to ingested food. A
common symptom of patients with IBS is the urge to defecate following a meal and the relief of symptoms like tenesmus,
distension, and abdominal pain following defecation. This phenomenon is believed to be due to, in part, a heightened
gastrocolic response. As discussed previously, any impairment of the neural or the hormonal mechanisms leading to decreased
or absent gastrocolic reflux will result in decreased colonic transit of fecal matter and will lead to functional constipation. This
presentation is more prevalent in older patients with spinal cord problems, and also diabetic neuropathy patients with
gastroparesis.

Clinical Signi cance

The gastrocolic reflex has correlations with the pathogenesis of irritable bowel syndrome. The act of food consumption can
provoke an overreaction of the gastrocolic response due to heightened visceral sensitivity seen in IBS patients, resulting in
abdominal pain, constipation, diarrhea, bloating, and tenesmus. It is also a known fact that ondansetron decreases the tonic
response to stretch, giving evidence toward its use in providing relief for patients with IBS. Commonly prescribed medications
to treat overreactive gastrocolic response include antispasmodics, tricyclic antidepressants, and SSRIs. Antibiotics and
probiotics have also been utilized to restore normal colonic flora, which in turn helps regulate the response of integral
components of the reflex.

The gastrocolic reflex is most active during morning time and immediately after meals. Using this physiological reflex to our
advantage helps treat constipation. For both children and geriatric patients with constipation, using the toilet immediately
after having breakfast and establishing a daily routine helps to improve constipation. The use of stimulant laxatives like
sennosides or bisacodyl will augment the gastrocolic reflex and helps in improved colonic contractions and defecation. 

Continuing Education / Review Questions

Access free multiple choice questions on this topic.
Earn continuing education credits (CME/CE) on this topic.
Comment on this article.

References
1. Deloose E, Janssen P, Depoortere I, Tack J. The migrating motor complex: control mechanisms and its role in health and
disease. Nat Rev Gastroenterol Hepatol. 2012 Mar 27;9(5):271-85. [PubMed: 22450306]
2. Tobias A, Sadiq NM. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Oct 2, 2020. Physiology,
Gastrointestinal Nervous Control. [PubMed: 31424852]
3. Simrén M, Månsson A, Langkilde AM, Svedlund J, Abrahamsson H, Bengtsson U, Björnsson ES. Food-related gastrointestinal
symptoms in the irritable bowel syndrome. Digestion. 2001;63(2):108-15. [PubMed: 11244249]
4. Deiteren A, Camilleri M, Burton D, McKinzie S, Rao A, Zinsmeister AR. Effect of meal ingestion on ileocolonic and colonic
transit in health and irritable bowel syndrome. Dig Dis Sci. 2010 Feb;55(2):384-91. [PMC free article: PMC2900583] [PubMed:
19949866]
5. Berg P, McCallum R. Dumping Syndrome: A Review of the Current Concepts of Pathophysiology, Diagnosis, and Treatment.
Dig Dis Sci. 2016 Jan;61(1):11-8. [PubMed: 26396002]
6. Shakil A, Church RJ, Rao SS. Gastrointestinal complications of diabetes. Am Fam Physician. 2008 Jun 15;77(12):1697-702.
[PubMed: 18619079]
7. Diamant NE. Physiology of esophageal motor function. Gastroenterol Clin North Am. 1989 Jun;18(2):179-94. [PubMed:
2668166]
8. Al-Shboul OA. The importance of interstitial cells of cajal in the gastrointestinal tract. Saudi J Gastroenterol. 2013 Jan-
Feb;19(1):3-15. [PMC free article: PMC3603487] [PubMed: 23319032]
9. Latorre R, Sternini C, De Giorgio R, Greenwood-Van Meerveld B. Enteroendocrine cells: a review of their role in brain-gut
communication. Neurogastroenterol Motil. 2016 May;28(5):620-30. [PMC free article: PMC4842178] [PubMed: 26691223]
10. Momose-Sato Y, Sato K. The embryonic brain and development of vagal pathways. Respir Physiol Neurobiol. 2011 Aug
31;178(1):163-73. [PubMed: 21296688]
11. Young HM, Hearn CJ, Newgreen DF. Embryology and development of the enteric nervous system. Gut. 2000 Dec;47 Suppl
4:iv12-4; discussion iv26. [PMC free article: PMC1766797] [PubMed: 11076897]
12. Young HM. Embryological origin of interstitial cells of Cajal. Microsc Res Tech. 1999 Dec 01;47(5):303-8. [PubMed:
10602289]
13. May CL, Kaestner KH. Gut endocrine cell development. Mol Cell Endocrinol. 2010 Jul 08;323(1):70-5. [PMC free article:
PMC2905316] [PubMed: 20025933]
14. Furness JB, Callaghan BP, Rivera LR, Cho HJ. The enteric nervous system and gastrointestinal innervation: integrated local
and central control. Adv Exp Med Biol. 2014;817:39-71. [PubMed: 24997029]
15. Smith TK, Park KJ, Hennig GW. Colonic migrating motor complexes, high amplitude propagating contractions, neural
reflexes and the importance of neuronal and mucosal serotonin. J Neurogastroenterol Motil. 2014 Oct 30;20(4):423-46.
[PMC free article: PMC4204412] [PubMed: 25273115]
16. Bassotti G, Betti C, Imbimbo BP, Pelli MA, Morelli A. Colonic motor response to eating: a manometric investigation in
proximal and distal portions of the viscus in man. Am J Gastroenterol. 1989 Feb;84(2):118-22. [PubMed: 2916518]
17. Li Z, Hao MM, Van den Haute C, Baekelandt V, Boesmans W, Vanden Berghe P. Regional complexity in enteric neuron
wiring reflects diversity of motility patterns in the mouse large intestine. Elife. 2019 Feb 12;8 [PMC free article:
PMC6391068] [PubMed: 30747710]
18. Rodriguez L, Sood M, Di Lorenzo C, Saps M. An ANMS-NASPGHAN consensus document on anorectal and colonic
manometry in children. Neurogastroenterol Motil. 2017 Jan;29(1) [PubMed: 27723185]
19. Kim ER, Rhee PL. How to interpret a functional or motility test - colon transit study. J Neurogastroenterol Motil. 2012
Jan;18(1):94-9. [PMC free article: PMC3271260] [PubMed: 22323993]

Publication Details

Author Information

Authors

Jordan C. Malone1; Aravind Thavamani2.

A liations
1 University of Pikeville - KYCOM
2 Case Western Reserve University

Publication History

Last Update: July 10, 2020.

Copyright
Copyright © 2020, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits use,
duplication, adaptation, distribution, and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, a link is provided
to the Creative Commons license, and any changes made are indicated.

Publisher
StatPearls Publishing, Treasure Island (FL)

NLM Citation

Malone JC, Thavamani A. Physiology, Gastrocolic Re ex. [Updated 2020 Jul 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-.