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The Human Body Respiratory System (V)
(page 496 - 507)
Control of Ventilation (see Fig. 13.30 to 13.37)
Due to the different solubilities of O2 and CO2 in air and water, the basic chemo-chemistry of
control of respiration is different in water versus air breathers.
Control of respiration and thus ventilation is necessary in order to match the oxygen uptake with the
metabolic demands. In general, Respiratory systems have a group of pacemaker neurons that
spontaneously induce a basic respiratory cycle pattern. Such systems consist of a sensory detector
and a motor effector with possible intermediate neuronal processing. Thus, respiratory cycles have
an autonomic characteristic that can be modified by a voluntary contribution.
Control of breathing involves control of the diaphragm, the most important muscle of inspiration.
Remember that when our diaphragms contract, air flows into the lungs and when it stops contracting
(i.e. when it relaxes), air flows out of the lungs. So the diaphragm has to contract and it also has to
relax in order for us to breath.
The diaphragm is a skeletal muscle. The motor neurons that control the diaphragm have cell bodies
in the ventral horn of the spinal cord in cervical segments 4 through 6 (C4 to C6) and send their
axons to the diaphragm in the phrenic nerves. When action potentials are initiated in the phrenic
neurons, they release acetylcholine on the muscle cells, initiate action potentials in the muscle cells
and thereby produce contractions of the muscle.
These phrenic motor neurons do not just fire off action potentials all the time, they need to be
"driven" by other neurons that provide them with inputs. The basic respiratory cycle is governed by
pacemaker nuclei in the medulla (PN) of the brain stem (analogous to the pacemakers in the
heart). This area is called the respiratory center and it communicates with the dorsal respiratory
group (DRG) which in turns communicates with the phrenic nerves (see below). The autonomic
character of this center is indicated by the fact that trans-section of the brainstem anterior (above) to
the medulla (thus cutting the connection with the rest of the brain) does not stop the basic rhythmic
breathing. This is true for most air-breathing vertebrates. Nonetheless, this basic medullary
respiratory rhythm can be modulated by actions of the central nervous system.
One of the most important sources of excitatory input to the phrenic neurons comes from the
medulla oblongata where there is a group of neurons called the "dorsal respiratory group". These
neurons have axons that course down the spinal cord and make synapses on the phrenic neurons.
These dorsal respiratory group neurons fire rhythmically at around 10 to 12 times per minute,
stimulating the phrenic neurons which in turn activate the diaphragm, producing about 10 to 12
inhalations per minute, our normal resting breathing pattern. The rhythms in firing of the dorsal
respiratory group neurons probably comes from 'pacemaker neurons' that are also located in the
medulla oblongata.
medulla
PN
= stimulation
= inhibition
VRG
STN
DRG
Phrenic nerves
Diaphragm
Spinal Cord (C4-C6)
But that isn't all that happens. These dorsal respiratory group neurons send branches of their
axons to another group of cells called the "ventral respiratory group" (VRG) where they make
excitatory synaptic connections.
The ventral respiratory group neurons send some of their axons to another group of neurons in the
medulla oblongata called the "solitary tract nucleus" (STN) where they make excitatory
synaptic connections with neurons that send their axons to the dorsal respiratory group. The
solitary tract neurons help to turn off (inhibit) the dorsal respiratory group neurons so that the
phrenic neurons stop getting their excitatory inputs, so inspiration ceases and exhalation begins.
The dorsal respiratory group excites the phrenics (which cause inspiration) AND in the meantime,
the dorsal respiratory group excites the ventral respiratory group which excites the solitary tract
nucleus neurons which inhibit the dorsal respiratory group and stops inspiration. It's a little cycle of
activity in a neural circuit that keeps us inhaling and exhaling at a rate of about 10 to 12 breaths per
minute!
The ponds has additional control centers that can modulate the basic pattern of respiration.
• The Pneumotaxic center : provides inhibition to the DRG, resulting in shorter periods of
inspiration
• The Apneustic center : provides stimulation to the DRG; this would result in prolonged
periods of inspiration and could induce breathholding at the end of inspiration.
When the connections of the Pneumotaxic center are cut, breathing becomes deep and slow, and
irregular. This indicates that the PC in addtion, tends to inhibit the Apneustic center ( absence of the
PC influence, results thus in enhanced AC influence). The role of the PC is most probably a
mechanism to switch from inspiration to expiration.
Several reflexes mechanisms affect the respiratory centers.
• Hering-Breuer reflex : protective reflex initiated by stretch receptors in the lungs ;
overstretching of the lungs will terminate inspiration
• Cold reflex : extreme sudden cold can result in cessation of breathing.
Regulation in Mammals works by means of two chemo receptor groups (Fig. 13-30)
•
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peripheral chemoreceptors ( the aortic and carotid bodies located in aortic arch and carotid
arteries respectively).
central chemoreceptors in the medulla
Both areas are richly supplied by blood capillaries and respond to changing levels of important
respiratory indicator molecules. These are
For the chemoreceptors:
• changes in oxygen levels ( especially hypoxia)
• changes in pH ( thus arterial blood hydrogen ions)
• changes in carbon dioxide ( especially increases, resulting in acidocis condition)
For the central chemoreceptors the signal is
• increases in CO2 , which in turn result in cerebrospinal fluid increase in hydrogen ions
The central chemoreceptors in the medulla are more sensitive and thus exert the biggest effect on
respiration.
What chemical signal is used to control respiration Air breathers such as humans ?
There is a consistent trend in air-breathers for CO2 to become the primary respiratory stimulant.
Control of respiration by Oxygen
SEE Fig. 13-31, 13-32 and text
Control of respiration by CO2
SEE fig. 13-33, 13-34 and text
Remember that the central chemoreceptors are located in the medulla area. Hydrigen ions cannot
pass from blood into the cerebrospinal fluid area due to the blood brain barrier at the capillary level.
CO2 levels in the blood enters the cerebrospinal fluid where it reacts with water, producing
Hydrogen ions. The central; chemoreceptors in actuality do not respond to CO2 but are very sensitive
to H+. CSF does not contain many proteins (unlike blood) and thus does not buffer pH changes well.
Thus pH drops when CO2 increases in CSF and this increase in H+ levels is detected by the
chemoreceptors. Thus the effect of CO2 is indirect.
Increase levels of CO2 ( termed hypercapnia) stimulates the central chemoreceptors which in turn
stimulates the respiratory center and triggers contraction of the diaphragm. Usually results in
increasing depth and rate of respiration.
Control by changes in H+.
SEE fig 13-35 and text.
For summary , see Fig. 13-37
Additional notes :
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Anxiety can cause hyperventilation. This results in dropping CO2 levels to below normal
levels, pH increases and may constrict blood vessels to the brain ( dizzy, fainting). Breathing
in a paper bag allows the person to retain the blown off CO2 , preventing pH levels from
changing dramatically
One cannot suffocate by holding ones breath and stop breathing ( apnea). Rising CO2 levels
will induce automatic breathing once CO2 increase beyond a critical level
Odine's curse ( named after a German legend): disorder where the autonomic respiratory
function is disabled ( damage to the brainstem). Victims must remember to take each breath
and cannot go to sleep without the aid of a mechanical ventilator
Overdose of sleeping pills, alcohol… can completely inhibit the respiratory center