Far Eastern University
Nicanor Reyes Medical Foundation
Institute of Medicine
1D Batch 2020
Gastrointestinal Tract Physiology II
Motor Activity of the GIT
Dr. Leandro Vila November 2016
MASTICATION
Chewing
Mechanical digestion in the oral cavity
The muscle responsible:
o Masseter strongest muscle; this is
the reason why you can chew some
bones in the food 200 dynes of
force
o Temporalis
o Lateral pterygoid
o Medial pterygoid
CN V mandibular portion (the only motor
portion) innervates this action
Syrian or semilunar ganglion is the nucleus of
the CN V that is involved.
Nucleus is the collection of cell inside a nerve body
while ganglion is the collection of cell outside the nerve
body.
It is initially voluntary that eventually
becomes involuntary
o Ex. Chewing a gum, voluntary at first
and after a while you dont realized
o that you are chewing.
Cephalic nucleus is for proprioception so you know
where are your mandile when you are chewing.
SWALLOWING
Done by the oral cavity, pharyngeal and
esophagus.
Cranial nerves involve are 5, 7, 9, 10, 11 & 12
CN IX for sensory function
CN X for motor function
THERE ARE THREE PHASES OF SWALLOWING
1. Oral / bucal
Voluntary
The tounge (innervated by CN 12)
pushes the food bolus toward the
pharynx
CN 5 (sometimes) , 7 and 12
Swallowing needs to have a close
mouth.
The soft palate must be pushed
towards the posterior and superior
and close the epiglottis.
Associated neurons are nucleus
tractus solitarius (sensory) and
nucleus ambiguus (motor)
Nucleus Tractus solitarius sensory association
neurons formed by CN 7, 9 and 10
Nucleus Ambiguus motor association neuron
formed by CN 9, 10 and 11
Association neurons connects sensory to motor and it is
also known as interneurons.
2. Pharyngeal
Involuntary
CN 9 and 10
3. Esophageal
Involuntary
CN 9 & 10
Peristalsis happens here *remember
the myenteric reflex so youll know
what is happening*
CHOANAE common opening of the nasal and oral
cavity
At rest, when not swallowing, the choanae is closed by
the soft palate.
The epiglottis closes the common opening of the
digestive and respiratory system at the level of the
larynx.
When we swallow, we stop respiration for 1 to 2
seconds, same as when we speak, our respiration stops
for a while for the closing of the openings so the food
bolus will go to the esophagus.
Peristalis in the esophagus is divided into:
1. Primary
Continuation of the pharyngeal phase
of swallowing / pharyngeal
contraction
2. Secondary
Stimulation of the myenteric plexus
to squeeze the esophagus so that the
food will go to the stomach.
Example of Dr. Vila
When you feel that there is a food left in the esophagus,
eat jello but it will just go to the primary phase of
peristalsis.
Even when we dont eat jello, banana or drink water, the
esophagus have their brush cells that will detect left
food in the mucosa. This brush cells will signal the
myentric plexus to stimulate the tunica muscularis to
squeeze the esophagus so that the food will go to the
stomach.
When you are talking about swallowing, SPHINCTERS
are also involved. This is because the esophagus is
guarded by the:
1. Upper esophageal sphincters
Not a true sphinctes hypertrophied
circular muscle
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 2. Lower esophageal sphincters
Sometimes referred to
gastroesophageal sphincters
Not a true sphinctes hypertrophied
circular muscle.
Sphincters are big muscle that is TONICALLY
CONSTRICTED are TONICALLY CLOSED. They can
obstruct the lumen.
These sphincters are pressure gradient dependent,
they will only open if there is a difference in the
pressure. Example is there is a high pressure in the
pharynx, low pressure in the esophagus, it can open the
the upper esophageal sphincter so that the food bolus
can move aboral. On the other hand, if there is a higher
pressure in the esophagus than the pharynx, it will open
the upper esophageal sphincter so that it moves the
food bolus backward, vommitting occurs.
If there is a higher pressure in the esophagus than the
stomach, it will open the lower esophageal sphincter,
moving the food bolus towards the stomach.
Sphincters are also TONICALLY ACTIVE. They are just
functional sphincters and not anatomic sphincters that
it just happen that the muscles are hypertrophied.
In cases of Gastroesophageal Reflux Disease (GERD),
the sphincters are not tonically contracted, it is
SOMEHOW relax that is why even without the pressure
gradient, it is somehow opening, making the gastric
contents reflux to the esophagus. The simple columnar
tissue of the lower third of the esophagus is bathed with
acid causing it to undergo metaplasia (become stratified
squamous non-keratinized) so the patient develops
Barretts esophagus.
Metaplasia is reversible, just make sure that the patient
is always erect. He should have a bed where when he
sleeps, he is in semi-fowlers position while sleeping so
acid will not reflux. The patient can only drink water.
Any carbonated drink or food that will cause acid reflux
will further cause relaxation of the smooth muscles,
aggravating GERD.
Review:
When we talk about the motor activity of the GIT, we
have motor innervation:
Extrinsic Neurons Autonomic Nervous System
Intrinsic Neurons Myenteric Plexus
The motor activity of the oral cavity is MASTICATION
and SWALLOWING which involves oral or bucal phase
(voluntary ad involves the tounge), pharyngeal and
esophageal phase (both are involuntary).
MOTOR ACTIVITY OF THE STOMACH
The stomach is divided into:
a. Upper half / proximal stomach
Fundus up to the corpus or body
For storage
Generation of tone in this part is
important for gastric emptying low
tone = low intragastric pressure =
slow gastric emptying
b. Lower half / distal stomach
with motor activity
having 3 per minute motor activity
more developed myenteric plexus
compared to the proximal half
important for mixing of gastric
contents and propelling food towards
the pylorus and to duodenum
Law of plasticitty / receptive relaxation of the
stomach
same as the myenteric reflex
relaxation of the upper half of the stomach in
preparation for the coming of food from the
esophagus
as the food is propelled from the esophagus
towards the stomach, the myenteric plexus of
the proximal part of the stomach will be
inhibited thereby the proximal portion dilates
and relaxes.
Sphincters are pressure gradient dependent. If there
is a high pressure in the esophagus than the stomach,
the gastroesophageal or lower esophageal sphincter
will open so food can go to the stomach.
In vomiting, if there is an increase pressure in the
stomach than the esophagus, the lower esophageal
sphincter will open so that food will propel towards the
mouth. This will also increase the pressure of the
esophagus than the pharynx, opening the upper
esophageal sphincter.
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PARTS OF THE STOMACH AND FUNCTION In the figure you can see that the food in the pylorus is
squirted back into the antrum. The antrum put it back to
the pylorus and again the pylorus will bring back to the
antrum. THERE IS MIXING OF FOOD HAPPENING until
it is VERY LIQUID so now it will be squirted to the
duodenum via the pyloric sphincter.

What will regulate Gastric emptying?

Gastric emptying is regulated by the lower half of the

stomach that is REGULATED by:

A. GASTRIC FACTORS

a. Volume of food
More food meaning more stretched
stomach. If the stomach is stretched,
CHYME it is made up of partially digested food articles the myenteric plexus becomes
plus the enzyme coming from both mechanical and stimulated causing it to contract and
chemical digestion. facilitate gastric emptying
Regulation of emptying is more of the function of the
Gastrin
pylorus and antrum.
Endocrine regulation
Gastrin is secreted by the G cells of
How does this work?
the stomach (also secreted by the G
The pyloric sphincter is normally close. As the pressure
cells of the intestine)
increases in the pyloric area, it will open the pyloric
It goes into the circulation then goes
sphincter thereby there will squirting of chyme little
back to the stomach to affect the
by little because it is acidic.
parietal cells, affecting gastric
emptying
In the duodenum, there is no prostaglandin coating that
It will INHIBIT the PYLORIC
is why there is HCO3 and alkaline fluids from the
SPHINCTERS causing it to dilate or
pancreas and Brunners gland that will neutralize. If
open facilitating the motor activity of
there are much food is propelled to the duodenum from
the pylorus
the stomach, there are many acids and there is no
mucous protection, development of DUODENAL
B. DUODENAL FACTORS
ULCER. Remember that an increase in gastric acid will
not cause gastric ulcer.
a. Type of food
High carbohydrate food
In GASTRIC ULCER, the prostaglandin coating which is
Facilitates faster gastric
replaced every 8 10 days. When a person always
emptying
drinks NSAID and steroid, it inhibits the replacement of
In two hours, 100% of glucose
the prostaglandin, exposing the epithelium. The HCl
is already emptied as
produced by the stomach will go in contact with the
compared to protein
epithelium causing ulcer.
High protein food
Delays gastric emptying the
Streoids inhibits the phospholipase A2 pathway
MOST
NSAID inhibits the Cyclooxygenase enzyme
In two hours, 60% of protein
is emptied so you still feel full
Maalox one of the treatments for gastric ulcer
due to 40% remaining in the
Drinking milk will cause more HCL formation that is
stomach
why it is not a medicine for gastric ulcer.
High lipid or fatty food
Delays gastric emptying

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High carbohydrate diet can easily stimulate the FEEDING AND HUNGER CENTER the physiology of
production of serotonin of the EC cells. Serotonin food intake and it is multifactorial
inhibits the reticular activating system hence we fall
asleep. Lateral nucleus of the hypothalamus responsible
for the feeding and hunger center
Protein and Lipids delays the gastric emptying. This is
why during alcohol drinking session; we avoid eating This is stimulated by:
rice or bread due to carbohydrate facilitating faster
gastric emptying. The alcohol will go to the small 1. Neuropeptide y
2. Dopamine
intestine in a faster pace, facilitating alcohol absorption
3. GABA
also in a faster pace. This will cause faster stimulation
and eventually inhibiting the person. 4. Norepinephrine
5. Gallamine
Rehydration and B-complex will return the person in 6. Opiods
7. Ghrelin hormone secreted by parietal cells
its normal state.
or oxyntic cells in between meals so that
b. Form of food it will tell the hunger center that you are
Liquid form or soft form faster gastric hungry. This is not secreted during meals.
emptying 8. Orexins (seen in hypoglycemia)
Solid form solid food arriving to the 9. Cold temperature
duodenum, it will wait for its digestion,
delaying gastric emptying. Inhibited by:

c. Volume of food 1. Leptin

More food delivered to the duodenum,
gastric emptying is delayed
Less food delivered to the duodenum, faster
facilitation of gastric emptying
d. Temperature of food
Warm food will delay gastric emptying
In warm environment, it will delay
gastric environment so supposedly,
we are not eating too much in hot
weather.
Cold food will facilitate gastric emptying
When the cold food reaches the
duodenum, it will facilitate gastric
emptying
e. Acidic and Basic food
Acidic food that is delivered to the
duodenum, it will wait for the time for its
neutralization by the HCO3 of the pancreas
and Brunners glands so gastric emptying
is delayed
f. Tonicity of the food
Isotonic food is around 200 milliosmole.
Remember that the tonicity of the plasma
is 285 milliosmole per liter.
Hypertonic food greater than 200
milliosmole; delays gastric emptying MORE
Hypotonic food less than 200
milliosmole; delays gastric emptying
This is why when we eat dessert
(hypertonic food), we feel satisfied and we
dont want food anymore. The hypertonic
food will stimulate the satiety center to tell
us that we are already full. Salty foods, oil,
sugar and honey are also hypertonic food.
2. Calcitonin
3. Corticotrophin Releasing Hormone (CRH)
4. Serotonin
There are also factors that stimulate eating. This will
cause an increase in adipocytes causing an increase in
inhibitory stimuli.
Adipokine or Leptin found in adipocytes and inhibits
the feeding center and stimulates satiety center.
Supposedly, when you are fat, more adipocytes will
secrete leptin that will tell you that you are already full.
But the problem is that the fat people cant control
eating due to the axis of leptin (hypothalamic axis) is
destroyed. Even though there are lots of leptin that is
being secreted, there is no inhibition of hunger center
and no stimulation of the satiety center that is why they
eat a lot.
SATIETY CENTER
Center that tells you that you are full
Located at the ventromedial nucleus of the
hypothalamus
Stimulated by:
Melanocyte Stimulating hormone (MSH)
o Supposedly, when you are colored
(with skin color), it stimulates the
satiety center that tell you are full.
Drugs like cocaine & amphetamine will
stimulate the satiety center (cocaine and
amphetamine regulated transcript
Warm temperature and warm food
Hypertonic diet and hypotonic diet
Hyperglycemic diet

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 CRH
Glucagon like Peptide 1 (GLP1)
Gastric distention
Leptin
CCK
Inhibited by: - tells you that you are hungry
GABA
Gastrin
Food intake is multifactorial:
1. Emotion (depression, happy)
2. Food characteristic we like eating soft and
slimy food
3. Lifestyle depends on the affordability to buy
food.
4. Environmental cues cold, warm or fiesta.
5. Peripheral signals that will inhibit or stimulate
the satiety centers hormones or substances
(drugs)
The lower stomach is responsible for mixing and
regulation of emptying.
Transit time how much time the food will stay in the
stomach.
Increased transit time slower passage of food; more
time to stay.
Decreased transit time faster passage of food; less
time to stay.
The Transit time of food in the stomach is 4 6 hrs.
If you eat at 6 in the morning, youll feel hungry at
around 10am if it is high carbohydrate diet. If you are
eating high protein diet, youll feel hungry at around
after 6 hours.
General motor activities of the GIT are peristalsis,
segmentation contraction and tonic contractions.
MOTOR ACTIVITIES IN THE SMALL INTESTINES
Peristalsis is LEAST seen in the small
intestines because we all know that the small
intestines are PRIMARILY FOR
ABSORPTION.
the reason why the small intestine has less
peristalsis is because if peristalsis is done,
there will be less time for absorption leading
to malnourishment or diarrhea.
More of tonic contraction and
segmentation contraction is happening in
the small intestine.
Promixodistal & distalproximal reflex
Peristaltic rush urge to defecate
MOTOR ACTIVITIES IN THE COLON / LARGE
INTESTINE
Irritation of the Ileum will cause proximaldistal reflex to
the cecum then and to the large intestine, stimulating its
motor activities.
Pressure in the colon will inhibit the peristalsis in Ileum
Guyton
Movements involve:
Tonic contraction
Haustration segmentation contraction in the
colon
Mass movement peristalsis in the colon
The undigested particle is compact so they move
together/as a whole until they reach the rectum causing
rectal distention. The stretch receptors in the rectum
will send impulses to the sacral spinal cord stimulating
the motor neurons that will stimulate the myenteric
plexus on the proximal portion of the rectum causing
contraction and inhibition to the distal myenteric plexus
to be inhibited so the food can pass through.
The external anal sphincter is VOLUNTARY and will be
stimulated.
The voluntariness of the external anal sphincter has
limitations:
@18mmHg rectal pressure urge to defacate
@55mmHG rectal pressure as it accumulates, you
know have the reflective urge to defacate.
The food that you ate will be at the cecum by 6 hours.
The rest of the undigested food will be at the large
intestine by 8 9 hours. Not all of the undigested food
will be excreted through defecation. 25% of the
remnants may stay in the rectum for 72 hours.
If you eat less, you cant defecate every day. We can say
that it is constipation if the person does not defecate
after 72 hours if the food intake is small.
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