Respiration
Control of Breathing
Dynamics of Breathing
External/Internal Respiration
Gas Transport in Blood
Control of Breathing
PRIMARY MECHANISM
• [CO2] and [H+] within the blood are the primary
stimuli that affect a person’s breathing rate/depth.
• CO2 and H+ levels in the blood (including all ways that
they are carried) are detected by chemoreceptors
(chemical-sensitive nerve endings) in the
Respiratory Center of the MEDULLA OBLONGATA
in the brainstem (top of spinal cord).
•
•
The Medulla Oblongata is the part of the brain that
controls the body’s organ systems. (p.334-335)
The respiratory center is a cluster of nerve cells that
trigger inspiration through automatic, fairly rhythmic
discharges.
CO2 and H+ ions are also detected by Carotid Bodies
(chemoreceptors) in the carotid arteries, and by
Aortic Bodies (chemoreceptors) located in the aorta.
-- these bodies communicate (via nerves) with the
Respiratory Center when CO2/H+ levels are too
high/low.
• When the levels of CO2/H+ increase in the blood
(usually coupled with decreased O2), the RATE and
DEPTH of breathing increases. Vice versa too…
• The Respiratory Center receives signals from the
Carotid/Aortic Bodies and sends a nerve message to
the diaphragm and intercostal muscles to contract
more often and for longer (fig. 15.6 p. 290).
*** An increase of 0.3% CO2 in the blood DOUBLES the
breathing rate!!!
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SECONDARY MECHANISM
o O2 levels in the blood are detected by the same
Carotid and Aortic Bodies.
o Oxygen levels have little effect on the respiratory
center, unless there exists an extreme deficiency.
o Cases could be:
o
High Altitudes, CO poisoning, extreme blood loss.
o The Carotid/Aortic Bodies detect the extreme O2 deficiency and
signal the Respiratory Center to increase the rate/depth of
breathing (again, low O2 is usually coupled with high CO2/H+, but
not necessarily in extreme cases – some anaerobic respiration can
produce CO2 as a byproduct).
Hyperventilation lowers CO2 levels to below normal  increases
blood pH  constricts blood vessels in brain  lowers O2 levels in brain
 faint. Breathing into paper bag? Increases CO2 levels to keep pH
nearer to normal…
Synchronicity!!!
The respiratory center responds to a
variety of nervous and chemical signals,
adjusting the rate/depth of breathing
accordingly.
 Control of breathing is only effective if it is
synchronized with the circulatory system.

 eg.
During exercise, cardiac output is aligned
with the increased breathing rate, thus
enhancing the O2 supply and CO2 removal.
Dynamics of Breathing -- Inspiration
The respiratory center signals the diaphragm and the
intercostal (rib) muscles to contract.
 Results: normally ‘dome-shaped’ diaphragm flattens
out; intercostals contract to move ribcage up and out.

* during ‘rest’ (normalcy), only the diaphragm contracts; intercostals
contract during stressful/exertive situations.
Both of these contractions/movements serve to
increase the size of the thoracic cavity.
- Since the lungs are attached to the diaphragm and
the intercostals/ribs by pleural membranes, the
contraction of each (and the increased thoracic cavity
volume) increases the size of the lungs (and the
alveoli, themselves) as well.
-

So, the air pressure within the lungs decreases
to a point where it is less than atmospheric air
pressure (ie. the air pressure outside the body).
 A notable pressure gradient has now been
created and air flows from a region of higher
pressure (outside of body) to a region of
lower pressure (inside lungs/alveoli).
 Result: Air rushes into lungs/alveoli.
 Fig. 15.7a p. 291.
Humans breathe due to negative pressure –
air does not force the lungs open, they are
opened up before air enters; a negative
(relative to the ‘outside’ of the body) pressure
induces this.
 In other words, a partial vacuum is created in
the lungs/alveoli – air flows into this vacuumlike region of space.
 Inspiration is an active process since muscles
must contract in order for it to occur.
 The stretch receptors in the alveolar walls
signal the respiratory center to stop stimulating
the diaphragm/intercostals – end of inspiration.

Dynamics of Breathing -- Expiration

Upon ceased stimulation from the respiratory
center, the diaphragm and the intercostals
relax and return to their resting positions:
 The
diaphragm resumes its dome shape by pushing
upward;
 The intercostals relax, dropping the ribcage down
and inward. See fig. 15.7b p. 291.
 Both
of these actions serve to decrease the
size of the thoracic cavity, decrease the size
of the lungs (the lungs recoil), and increase
the air pressure in the lungs to greater than
that of atmospheric air.
Air, once again, flows from a region of higher
pressure (the lungs/alveoli) to a region of lower
pressure (the ‘outside’).
 Expiration is a passive process in that it simply
involves the relaxation of muscles.
 That said, expiration, at times, may be active
in nature when breathing is deeper and/or
more rapid (eg. during exercise).

 Intercostal
muscle contractions can FORCE the
ribcage down and in with more vigor;
 Contraction of abdominal muscles can push
diaphragm upwards with more force.
 Thus, more air might be expelled at a faster rate.
Lung Air Capacity
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The volume of air a human inhales and exhales with
each breath is called tidal volume (avg = 500 mL).
The maximum volume of air that can be
inhaled/exhaled during forced breathing is known as
vital capacity (avg = 4-5 L).
The lungs are actually able to hold more air than the
vital capacity, but since it is impossible to completely
empty (and thus, collapse) the alveoli, a residual
volume of air remains in the lungs after active
expiration (avg = 1.2 L). This air plays no role in gas
exchange. Certain respiratory disorders increase the
residual volume of the lungs (more useless air = less
chance to get useful air  weak, short of breath, etc).
Avg total lung capacity = 6 L.
See fig. 15.5 p. 288
Some inspired air (in all people) never reaches
the lungs; instead it fills the respiratory tract
where there exists no gas exchange functioning
 Known as ‘dead space’ air…
 To increase the chances of inspired air reaching
the lungs, and expired air actually reaching the
‘outside’, it is better to breathe slowly &
deeply – luckily, the medulla promotes this.

 This
idea is evident when getting a cramp while
running (the cramp is indicative of anaerobic
respiration taking place in certain muscles (usually
the abs)) – it is better to exhale deeply to rid body
of dead space air so that the next inhalations
contain mainly ‘fresh’ air with a higher % of O2.
External Respiration (Location: Lungs)
Refers to the exchange of O2 and CO2 between
the alveoli and the blood in the alveolar
(pulmonary) capillaries.
 Recall that the two structures are, at most, 0.2
micrometers apart and that each of them
possess walls that are only one cell thick –
excellent conditions for efficient exchange.
 Transfer occurs via simple diffusion, but the
gradient is based on gas pressures.
 All gases exert pressure (proportional to their
concentrations); each indiv. gas exerts its own
partial pressure (PP).

The PPO2 in the alveoli (due to the inspiration of
O2-laden air) is higher than the PPO2 in the lung
capillaries (due to the usage of/transfer of O2
by/to the tissue cell capillaries in the body).
 Thus, O2 flows (via the principles of diffusion)
from a region of higher PP (alveoli) to a region
of lower PP (blood).
 CO2 follows a similar gradient, except that it
moves, via diffusion (higher PP to lower PP),
from the lung capillaries into the alveoli for
expiration.

 CO2 is
produced as a byproduct of cellular
respiration by the body’s cells – high blood PPCO2
 PPCO2 in inhaled air is quite low.
Internal Respiration (Location: Body Cells)
Gas exchange that occurs at the tissue cell level is
between the blood in the capillaries and the ECF
(tissue fluid) – the material entering the ECF
eventually enters cells; the material ‘waiting’ in the
ECF to enter the blood originated within the cells.
 PPO2 in blood > PPO2 in ECF  O2 diffuses into ECF for
eventual entry into cells.
 PPCO2 in ECF > PPCO2 in blood  CO2 diffuses into
blood (in order to reach lungs for exhalation).
**Both external and internal respiration involve the
movement of water and other substances as well
(Capillary-Tissue exchange) – but here, in the
Respiration Unit, we are focusing primarily on the
driving force (gradient) behind the movement of
gases.

Transport of Gases in Blood
OXYGEN:
 Oxygen binds loosely and therefore reversibly to
hemoglobin (Hb) in RBCs.
 One Hb molecule can bind up to 4 O2 molecules
 Once this occurs, and it is saturated, it is referred to
as oxyhemoglobin (HbO2).
 Hb + O2  HbO2 (at lungs)
 HbO2  Hb + O2 (at tissue cells)
 Hb = Deoxyhemoglobin (purplish) whereas HbO2 =
Oxyhemoglobin (bright red).
 Within the lung capillaries, 98% of O2 joins Hb
whereas 2% simply dissolves in the plasma (oxygen is
fairly non-polar).
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Hb binds more readily to oxygen at a relatively cooler
temperature (370 C) and a higher pH (7.40) –
conditions that exist in the lung capillaries (since they
are ‘closer’ to the outside of the body). (See fig. 15.9
p. 294)
Once Hb has 1, 2, or 3 O2 molecules bound to it, its
‘attraction’ (affinity) for the 2nd, 3rd, and 4th molecule
increases exponentially. Thus, all Hb molecules are
saturated with O2.
Conditions at the tissue cells are warmer (380 C) and
more acidic (7.38 pH) than those in the lung
capillaries.
Hb tends to release an appreciable amount (~28%) of
its O2 in these conditions.
The difference in the affinity of Hb for O2 under
different temp./pH conditions = the Bohr Shift.

The ‘freed’ O2 then diffuses across the capillary walls
into the ECF, and eventually into cells, following its PP
gradient and traveling with water and other stuff
(recall Tissue/Capillary Exchange). *label Bohr shift!
TISSUES
LUNGS
During exercise, muscles heat up and produce lactic
acid (decr. pH) which promotes Hb to give up even
more of its O2 to the cells (sometimes up to 75%).
 INTERNAL SUFFOCATION – Carbon monoxide (CO)
binds to Hb 200x more readily than O2.
 Thus, oxygen is prevented from reaching the tissue
cells on any RBC ‘infested’ with CO.
 Therefore, the cells ‘suffocate’.
CARBON DIOXIDE (CO2)
 CO2 is transported through the blood in three ways:
1. 70% is transported as the bicarbonate ion (HCO3-)
in the plasma (more on this in a moment).
2. 23% attaches directly to Hb to form
carbaminohemoglobin (HbCO2)

CO2 + Hb
@ TISSUES
@ LUNGS
HbCO2
 The
lower temp./higher pH in the lungs
promotes CO2 release by Hb.
 The higher temp./lower pH at the tissue cells
promotes CO2 uptake by Hb.
3. 7% simply dissolves in the plasma (as
molecular CO2).
** Metaphor: Hb likes O2 in the winter (O2 is like
a snowman) and hates O2 at the beach. CO2 is
opposite…when Hb likes O2, it hates CO2, and
vice versa…
The ‘Beach’:
‘Winter’:
Higher temperature,
Lower pH
Lower temperature,
Higher pH
O2
“snowman”
Bicarbonate Ion Transport of CO2
As mentioned previously, 70% of the tissue cellproduced CO2 is transported in the plasma
(dissolved) as HCO3-. HCO3- acts as a blood buffer.
 Once CO2 leaves tissue cells and enters the ECF,
the blood, and eventually the RBCs, it reacts with
water to form carbonic acid (H2CO3) which then
dissociates slightly to form HCO3- and H+.
CO2 + H2O  H2CO3  H+ + HCO3- The RBC enzyme carbonic anhydrase acts to
catalyze the first portion of this reaction and the
higher tissue temperature promotes the 70%
production of the final products.
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The HCO3- diffuse out of the RBCs (Cl- ions move into
RBCs to balance the charge) and are carried in the
plasma to the lungs, leaving H+ behind.
The remaining H+ are picked up by Hb (or else the pH
would severely drop – blood proteins would be
denatured, as would vessel walls) to form reduced
hemoglobin (HHb), which is carried within RBCs to
the lungs.
H+ + Hb  HHb (at tissues, within RBCs).
Thus, Hb acts to buffer the blood and keep it at, or
near, its optimal pH.
FYI: optimal blood pH = 7.4 due to the fact that HCO3is a better base than it is an acid and that there is a
much higher concentration of it in the blood than CO2
and H2O (which, in combo, produce H2CO3).
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Once blood reaches the lungs, the HCO3- and H+
must be converted back to CO2 and water so that
the majority of the CO2 can be expired.
At the lower temp. and higher pH conditions in the
lung capillaries, Hb gives up H+ (so that Hb can
pick up O2), HCO3- diffuses back into the RBC (Clions diffuse back out), reacts with H+ to form
H2CO3, which then forms CO2 and water; the CO2
then diffuses into the alveoli from the blood.
Carbonic anhydrase helps again, but this time
catalyzes the reverse reaction at the cooler
temperature. Also, the diffusion of the other 30%
of the CO2 into the alveoli drives the following
reaction to the right:
H+ + HCO3-  H2CO3  CO2 + H2O
See fig. 15.8 p. 293 for summary diagram
 Read pp. 295-298 (for interest only) –
Respiratory Disorders…including figs.
15.10 p. 295 and 15.11 p. 296.
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Finished!!!