VENTILATION AND RESPIRATORY VOLUMES

Ventilation, or breathing, is the process of moving air into and out of the lungs.
There are two phases of ventilation:
(1) Inspiration, or inhalation, is the movement of air into the lungs;
(2) expiration, or exhalation, is the movement of air out of the lungs.
Ventilation is regulated by changes in thoracic volume, which produce changes in air pressure within the lungs.
Changing Thoracic Volume

• The muscles associated with the ribs are
responsible for ventilation.
• Inhaling requires a set of muscles called the
muscles of inspiration - include the diaphragm
and the muscles that elevate the ribs and
sternum, such as the external intercostals.
• The DIAPHRAGM , partition; is a large dome of
skeletal muscle that separates the thoracic cavity
from the abdominal.
• Forceful exhalation requires a set of muscles
called the muscles of expiration.
• The muscles of exhalation include the internal
intercostals and depress the ribs and sternum.
• At the end of a normal, quiet expiration, the
respiratory muscles are relaxed.
• During quiet inspiration, muscles of inspiration
contract to increase the volume of the thoracic
cavity.
• Contraction of the diaphragm causes the top of
the diaphragm to move inferiorly.
• Contraction of the external intercostals also
elevates the ribs and sternum to increase
thoracic cavity volume.
• The largest change in thoracic cavity volume is
due to contraction of the diaphragm

a. Expiration occurs when the thoracic cavity volume decreases.

b. During quiet expiration, the diaphragm and external intercostals relax.
c. The elastic properties of the thorax and lungs cause them to recoil into a relaxed state.
d. There are several differences between normal, quiet breathing and labored breathing.
e. During labored breathing, there is a much greater increase in thoracic cavity volume.
f. All the inspiratory muscles are active, and they contract more forcefully than during quiet breathing.
g. Also, during labored breathing, the internal intercostals and the abdominal muscles contract forcefully.
h. This decreases thoracic cavity volume more quickly and to a greater degree than during quiet breathing.
PRESSURE CHANGES AND AIRFLOW
Two physical principles govern the flow of air into and out of the lungs:
1. Changes in volume result in changes in pressure
• As the volume of a container increases, the pressure within the container decreases. The opposite is also true.
As the volume of a container decreases, the pressure within the container increases. In the same way, the
muscles of respiration change the volume of the thorax and therefore the pressure within the thoracic cavity.
2. Air flows from an area of higher pressure to an area of lower pressure.
• If the pressure is higher at one end of a tube than at the other, air or fluid flows from the area of higher pressure
toward the area of lower pressure.
• The greater the pressure difference, the greater the rate of airflow.
• Air flows through the respiratory passages because of pressure differences between the outside of the body and
the alveoli inside the body. These pressure differences are produced by changes in thoracic volume.
• The volume and pressure change responsible for one cycle of inspiration and expiration can be described as
follows:
1. At the end of expiration, alveolar pressure, which is the air pressure within the alveoli, is equal to atmospheric
pressure, which is the air pressure outside the body. No air moves into or out of the lungs because alveolar
pressure and atmospheric pressure are equal.
2. During inspiration, the volume of the thoracic cavity increases when the muscles of inspiration contract. The
increased thoracic volume decreases the pressure in the alveoli below atmospheric pressure. Air flows into
the alveoli.
3. At the end of inspiration, the thorax and alveoli stop expanding. When the alveolar pressure and atmospheric
pressure become equal, airflow stops.
4. During expiration, the thoracic cavity volume decreases. Consequently, alveolar pressure increases above
atmospheric pressure, and air flows out of the alveoli (figure 15.11, step 4). As expiration ends, the decrease
in thoracic volume stops, and the process repeats, beginning at step 1.

LUNG RECOIL
During quiet expiration, thoracic volume and lung volume decrease because of lung recoil, the tendency for an
expanded lung to decrease in size.
• Lung recoil is due to the elastic properties of its tissues and because the alveolar fluid has surface tension.
• Surface tension exists because the oppositely charged ends of water molecules are attracted to each other.
• As the water molecules pull together, they also pull on the alveolar walls, causing the alveoli to recoil and
become smaller.
• Two factors keep the lungs from collapsing:
(1) surfactant
(2) pressure in the pleural cavity.

a. Surfactant (ser-fak′tănt; surface acting agent)

• is a mixture of lipoprotein molecules produced by secretory cells of the alveolar epithelium.
• The surfactant molecules form a single layer on the surface of the thin fluid layer lining the alveoli, reducing
surface tension.
• Without surfactant, the surface tension causing the alveoli to recoil can be ten times greater than when
surfactant is present. Thus, surfactant greatly reduces the tendency of the lungs to collapse.

Infant respiratory distress syndrome (IRDS)

• is caused by too little surfactant.
• IRDS, also called hyaline membrane disease, is common in premature infants because surfactant is not
produced in adequate quantities u ntil about the seventh month of gestation.
• Thereafter, the amount produced increases as the fetus matures.
• Pregnant women who are likely to deliver prematurely can be given cortisol, which crosses the placenta
into the fetus and stimulates surfactant synthesis.

b. Pleural Pressure
• When pleural pressure, the pressure in the pleural cavity, is less than alveolar pressure, the alveoli tend to
expand. Normally, pleural pressure is lower than alveolar pressure.
• Pleural pressure is lower than alveolar pressure because of a suction effect caused by fluid removal by the
lymphatic system and by lung recoil.
• This difference in pressures—lower pleural pressure than alveolar pressure—keeps the alveoli expanded.

• If you have flown on a plane, or have been to the mountains, you may have experienced a situation similar
to that which keeps the alveoli expanded. At higher altitudes, the atmospheric pressure is much lower
than at sea level. If a bottle of liquid (such as shampoo) normally kept at sea level is rapidly taken to a high
altitude, it will “explode.” Because there is not as much force on the outside of the bottle at high altitude,
it expands. Similarly, because the pleural pressure pulls the pleura away from the outside of the alveoli,
the pressure on the alveoli is lower.
• The lower pressure allows the alveoli to expand. When pleural pressure is lower than alveolar pressure,
the alveoli tend to expand. This expansion is opposed by the tendency of the lungs to recoil.
• Therefore, the alveoli expand when the pleural pressure is low enough that lung recoil is overcome. If the
pleural pressure is not low enough to overcome lung recoil, the alveoli collapse, as is the case with a
pneumothorax
Changing Alveolar Volume

• Air moves into and out of the lungs due to changes in alveolar pressure.
• Alveolar pressure change is due to alveolar volume changes.
• Alveolar volume changes result from changes in pleural pressure.
• For example, during inspiration, pleural pressure decreases, and the alveoli expand.
The decrease in pleural pressure during inspiration occurs for two reasons:

1. Increasing the volume of the thoracic cavity results in a decrease in pleural pressure because a change in volume
affects pressure.
2. As the lungs expand, lung recoil increases, increasing the suction effect and lowering the pleural pressure. The
increased lung recoil of the stretched lung is similar to the increased force generated in a stretched rubber band.

The events of inspiration and expiration can be summarized as follows:

1. During inspiration, pleural pressure decreases because of increased thoracic volume and increased lung recoil. As
pleural pressure decreases, alveolar volume increases, alveolar pressure decreases, and air flows into the lungs.
2. During expiration, pleural pressure increases because of decreased thoracic volume and decreased lung recoil. As
pleural pressure increases, alveolar volume decreases, alveolar pressure increases, and air flows out of the lungs.

Respiratory Volumes and Capacities

• Spirometry (spī-rom′ĕ-trē) is the process of
measuring volumes of air that move into and
out of the respiratory system, and the
spirometer (spī-rom′ĕ-ter) is the device that
measures these respiratory volumes.
• Measurements of the respiratory volumes can
provide information about the health of the
lungs.
• Respiratory volumes are measures of the
amount of air movement during different
portions of ventilation,
• whereas respiratory capacities are sums of two
or more respiratory volumes.
• The total volume of air contained in the
respiratory system ranges from 4 to 6 L.
• The four respiratory volumes and their normal
values for a young adult male are shown in:
1. Tidal volume is the volume of air inspired or
expired with each breath. At rest, quiet
breathing results in a tidal volume of about 500
milliliters (mL).
2. Inspiratory reserve volume is the amount of air
that can be inspired forcefully beyond the
resting tidal volume (about 3000 mL).
3. Expiratory reserve volume is the amount of air
that can be expired forcefully beyond the
resting tidal volume (about 1100 mL).
4. Residual volume is the volume of air still
remaining in the respiratory passages and lungs
after maximum expiration (about 1200 mL).
• The tidal volume increases during physical
activity. The increase in the tidal volume
reduces the inspiratory and expiratory reserve
volumes, but total lung capacity stays relatively
constant
Values of respiratory capacities, the sum of two or more
pulmonary volumes,
1. Functional residual capacity is the expiratory
reserve volume plus the residual volume. This is
the amount of air remaining in the lungs at the
end of a normal expiration (about 2300 mL at
rest).
2. Inspiratory capacity is the tidal volume plus the
inspiratory reserve volume. This is the amount of
air a person can inspire maximally after a normal
expiration (about 3500 mL at rest).
3. Vital capacity is the sum of the inspiratory
reserve volume, the tidal volume, and the
expiratory reserve volume. It is the maximum
volume of air that a person can expel from the
respiratory tract after a maximum inspiration
(about 4600 mL).
4. Total lung capacity is the sum of the inspiratory
and expiratory reserves and the tidal and
residual volumes (about 5800 mL). The total lung
capacity is also equal to the vital capacity plus
the residual volume.
 Factors such as gender, age, and body size influence
the respiratory volumes and capacities.
For example, the vital capacity of adult females is
usually 20–25% less than that of adult males. The
vital capacity reaches its maximum amount in young
adults and gradually decreases in the elderly. Tall
people usually have a greater vital capacity than
short people, and thin people have a greater vital
capacity than obese people. Well-trained athletes
can have a vital capacity 30–40% above that of
untrained people. In patients whose respiratory
muscles are paralyzed by spinal cord injury or
diseases such as poliomyelitis or muscular dystrophy,
the vital capacity can be reduced to values not
consistent with survival (less than 500–1000 mL).
The forced expiratory vital capacity is the rate at
which lung volume changes during direct
measurement of the vital capacity. It is a simple and
clinically important pulmonary test. The individual
inspires maximally and then exhales maximally as
rapidly as possible into a spirometer. The spirometer
records the volume of air expired per second. This
test can help identify conditions in which the vital
capacity might not be affected but the expiratory
flow rate is reduced. Abnormalities that increase the
resistance to airflow slow the rate at which air can be
forced out of the lungs. For example, in people who
have asthma, contraction of the smooth muscle in
the bronchioles increases the resistance to airflow. In
people who have emphysema, changes in the lung
tissue result in the destruction of the alveolar walls,
collapse of the bronchioles, and decreased elasticity
of the lung tissue. The collapsed bronchioles increase
the resistance to airflow. In people who have chronic
bronchitis, the air passages are inflamed. The
swelling, increased mucus secretion, and gradual loss
of cilia result in narrowed bronchioles and increased
resistance to airflow.

GAS EXCHANGE

• Ventilation supplies atmospheric air to the alveoli. The next step in the process of respiration is the diffusion of
gases between the alveoli and the blood in the pulmonary capillaries.
• As previously stated, gas exchange between air and blood occurs at the respiratory membrane of the lungs.
• The major area of gas exchange is in the alveoli, although some takes place in the respiratory bronchioles and
alveolar ducts.
• Gas exchange between blood and air does not occur in other areas of the respiratory passageways, such as the
bronchioles, bronchi, and trachea. The volume of these passageways is therefore called anatomical dead space.
• The exchange of gases across the respiratory membrane is influenced by three factors:

(1) the thickness of the membrane

(2) the total surface area of the respiratory membrane,
(3) the partial pressure of gases across the membrane.

Factors That Affect Gas Exchange

Respiratory Membrane Thickness

• The thickness of the respiratory membrane increases during certain respiratory diseases.
• For example, in patients with pulmonary edema, fluid accumulates in the alveoli, and gases must diffuse through
a thicker than normal layer of fluid.
• If the thickness of the respiratory membrane is doubled or tripled, the rate of gas exchange is markedly
decreased. Oxygen exchange is affected before CO2 exchange because O2 diffuses through the respiratory
membrane about 20 times less easily than does CO2.
Surface Area

• The total surface area of the respiratory membrane is about 70 square meters (m2) in the normal adult, which is
approximately the floor area of a 25- × 30-ft room, or roughly the size of a racquetball court (20 × 40 ft).
• Under resting conditions, a decrease in the surface area of the respiratory membrane to one-third or one/fourth
of normal can significantly restrict gas exchange.
 • During strenuous exercise, even small decreases in the surface area of the respiratory membrane can adversely
affect gas exchange.
• Possible reasons for having a decreased surface area include the surgical removal of lung tissue, the destruction
of lung tissue by cancer, and the degeneration of the alveolar walls by emphysema.
• Collapse of the lung—as occurs in pneumothorax—dramatically reduces the volume of the alveoli, as well as the
surface area for gas exchange.
Partial Pressure
• Gas molecules move randomly from higher
concentration to lower concentration until an
equilibrium is achieved. One measurement of
the concentration of gases is partial pressure.
• The partial pressure of a gas is the pressure
exerted by a specific gas in a mixture of gases,
such as air. For example, if the total pressure of
all the gases in a mixture of gases is 760
millimeters of mercury (mm Hg), which is the
atmospheric pressure at sea level, and 21% of
the mixture is made up of O2, the partial
pressure for O2 is 160 mm Hg (0.21 × 760 mm Hg
= 160 mm Hg).
• If the composition of air is 0.04% CO2 at sea
level, the partial pressure for CO2 is 0.3 mm Hg
(0.0004 × 760 = 0.3 mm Hg) (table 15.1).
MOVEMENT OF GASES IN THE LUNGS
• The cells of the body use O2 and produce CO2.
• Thus, blood returning from tissues and entering
the lungs has a lower Po2 and a higher Pco2
compared to alveolar air Oxygen diffuses from
the alveoli into the pulmonary capillaries
because the Po2 in the alveoli is greater than
that in the pulmonary capillaries.
• In contrast, CO2 diffuses from the pulmonary
capillaries into the alveoli because the Pco2 is
greater in the pulmonary capillaries than in the
alveoli.
• When blood enters a pulmonary capillary, the
Po2 and Pco2 in the capillary are different from
the Po2 and Pco2 in the alveolus.
• By the time blood flows through the first third
of the pulmonary capillary, an equilibrium is
achieved, and the Po2 and Pco2 in the capillary
are the same as in the alveolus.
• Thus, in the lungs, the blood gains O2 and loses
CO2 (figure 15.13, step 2).
• During breathing, atmospheric air mixes with
alveolar air. The air entering and leaving the
• It is traditional to designated the partial pressure
of individual gases in a mixture with a capital P
followed by the symbol for the gas. Thus, the
partial pressure of O2 is Po2, and that of CO2 is
Pco2.
• When air is in contact with a liquid, gases in the
air dissolve in the liquid. The gases dissolve until
the partial pressure of each gas in the liquid is
equal to the partial pressure of that gas in the air.
• Gases in a liquid, like gases in air, diffuse from
areas of higher partial pressure toward areas of
lower partial pressure, until the partial pressures
of the gases are equal throughout the liquid. In
other words, gases diffuse down their pressure
gradient: from areas of higher partial pressure to
areas of lower partial pressure.
alveoli keeps the Po2 higher in the alveoli than
in the pulmonary capillaries. Increasing the
breathing rate makes the Po2 even higher in the
alveoli than it is during slow breathing.
• During labored breathing, the rate of O2
diffusion into the pulmonary capillaries
increases because the difference in partial
pressure between the alveoli and the
pulmonary capillaries has increased.
• There is a slight decrease in Po2 in the
pulmonary veins due to mixing with
deoxygenated blood from veins draining the
bronchi and bronchioles; however, the Po2 in
the blood is still higher than that in the tissues.
• Increasing the rate of breathing also makes the
Pco2 lower in the alveoli than it is during
normal, quiet breathing. Because the alveolar
Pco2 decreases, the difference in partial
pressure between the alveoli and the
pulmonary capillaries increases, which increases
the rate of CO2 diffusion from the pulmonary
capillaries into the alveoli
MOVEMENT OF GASES IN THE TISSUES

Blood flows from the lungs through the left side of the heart to the tissue capillaries. Figure 15.13 illustrates the partial
pressure differences for O2 and CO2 across the wall of a tissue capillary. Oxygen diffuses out of the blood and into the
interstitial fluid. The Po2 is lower in the interstitial fluid than in the capillary. Oxygen then diffuses from the interstitial fluid
into cells. The Po2 is less in cells than in the interstitial fluid (figure 15.13, step 4). Within the cells, O2 is used in cellular
respiration. There is a constant difference in Po2 between the tissue capillaries and the cells because the cells continuously
use O2 . There is also a constant diffusion gradient for CO2 from the cells. Carbon dioxide therefore diffuses from cells into
the interstitial fluid and from the interstitial fluid into the blood, and an equilibrium between the blood and tissues is
achieved

GAS TRANSPORT IN THE BLOOD

• Oxygen Transport
• After O2 diffuses through the respiratory membrane into the blood, about 98.5% of the O2 transported in the
blood combines reversibly with the iron-containing heme groups of hemoglobin (see chapter 11).
• About 1.5% of the O2 remains dissolved in the plasma.
• Hemoglobin with O2 bound to its heme groups is called oxyhemoglobin (ok′sē-hē-mō-glō′bin).
• The ability of hemoglobin to bind to O2 depends on the Po2.
• At high Po2, hemoglobin binds to O2, and at low Po2, hemoglobin releases O2. In the lungs, Po2 normally is
sufficiently high so that hemoglobin holds as much O2 as it can. In the tissues, Po2 is lower.
• Consequently, hemoglobin releases O2 in the tissues.
• Oxygen then diffuses into the cells, which use it in cellular respiration. At rest, approximately 23% of the O2
picked up by hemoglobin in the lungs is released to the tissues.
• The amount of O2 released from oxyhemoglobin is increased by four factors.
(1) low Po2
(2) high Pco2
(3) low pH
(4) high temperature.
• Increased muscular activity results in a decreased Po2, an increased Pco2, a reduced pH, and an increased
temperature. Consequently, during physical exercise, as much as 73% of the O2 picked up by hemoglobin in the
lungs is released into skeletal muscles.

Carbon Dioxide Transport and Blood pH

• Carbon dioxide diffuses from cells, where it is produced, into the blood.
• After CO2 enters the blood, it is transported in three ways:
(1) About 7% is transported as CO2 dissolved in the plasma;
(2) 23% is transported bound to blood proteins, primarily hemoglobin;
(3) 70% is transported in the form of bicarbonate ions. Carbon dioxide (CO2) reacts with water to form carbonic acid
(H2CO3), which then dissociates to form H+ and bicarbonate ions (HCO3 −):
• An enzyme called carbonic anhydrase (kar-bon′ik an-hī′drās) is located inside red blood cells and on the surface
of capillary epithelial cells.
• Carbonic anhydrase increases the rate at which CO2 reacts with water to form H+ and HCO3 − in the tissue
capillaries.
• Thus, carbonic anhydrase promotes the uptake of CO2 by red blood cells.
• In the capillaries of the lungs, the process is reversed, so that the HCO3 − and H+ combine to produce H2CO3,
which then forms CO2 and H2O. The CO2 diffuses into the alveoli and is expired.
• Carbon dioxide has an important effect on the pH of blood. As CO2 levels increase, the blood pH decreases
(becomes more acidic) because CO2 reacts with H2O to form H2CO3. The H+ that results from the dissociation of
H2CO3 is responsible for the decrease in pH. Conversely, as blood levels of CO2 decline, the blood pH increases
(becomes less acidic, or more basic).
RHYTHMIC BREATHING

• The normal rate of breathing in adults is between 12 and 20 breaths per minute. In children, the rates are higher
and may vary from 20 to 40 per minute.
• The rate of breathing is determined by the number of times respiratory muscles are stimulated.
• The basic rhythm of breathing is controlled by neurons within the medulla oblongata that stimulate the muscles
of respiration.
• An increased depth of breathing results from stronger contractions of the respiratory muscles caused by
recruitment of muscle fibers and increased frequency of stimulation of muscle fibers.
Respiratory Areas in the Brainstem

• Neurons involved with respiration are located in the brainstem.

• The neurons that are active during inspiration and those active during expiration are intermingled in these areas.
• The medullary respiratory center consists of two dorsal respiratory groups, each forming a longitudinal column
of cells located bilaterally in the dorsal part of the medulla oblongata, and two ventral respiratory groups, each
forming a longitudinal column of cells located bilaterally in the ventral part of the medulla oblongata (figure
15.15).
• The dorsal respiratory group is primarily responsible for stimulating contraction of the diaphragm.
• The ventral respiratory group is primarily responsible for stimulating the external intercostal, internal intercostal,
and abdominal muscles.
• A part of the ventral respiratory group, the pre-Bötzinger complex, is now known to establish the basic rhythm
of breathing.
• The pontine respiratory group is a collection of neurons in the pons (figure 15.15).
• It has connections with the medullary respiratory center and appears to play a role in switching between
inspiration and expiration.
Generation of Rhythmic Breathing

The medullary respiratory center generates the basic
pattern of normal breathing. Although the precise
mechanism is not well understood, the generation of
rhythmic breathing involves the integration of stimuli
that start and stop inspiration.
1. Starting inspiration.
The neurons in the medullary respiratory center that
promote inspiration are continuously active. The
medullary respiratory center constantly receives
stimulation from many sources, such as receptors that
monitor blood gas levels and the movements of muscles
and joints. In addition, stimulation can come from parts
of the brain concerned with voluntary respiratory
movements and emotions. When the inputs from all
these sources reach a threshold level, somatic nervous
system neurons stimulate respiratory muscles via action
potentials, and inspiration starts.
2. Increasing inspiration
Once inspiration begins, more and more neurons are
activated. The result is progressively stronger
stimulation of the respiratory muscles, which lasts for
approximately 2 seconds (s).
3. Stopping inspiration
The neurons stimulating the muscles of respiration also
stimulate the neurons in the medullary respiratory
center that are responsible for stopping inspiration.
The neurons responsible for stopping inspiration also
receive input from the pontine respiratory neurons,
stretch receptors in the lungs, and probably other
sources.
When the inputs to these neurons exceed a threshold
level, they cause the neurons stimulating respiratory
muscles to be inhibited. Relaxation of respiratory
muscles results in expiration, which lasts approximately
3 s. The next inspiration begins with step 1. Although
the medullary neurons establish the basic rate and
depth of breathing, their activities can be influenced by
input from other parts of the brain and from
peripherally located receptors.
Nervous Control of Breathing
• Higher brain centers can modify the activity
of the respiratory center (figure 15.16a).
• For example, controlling air movements out
of the lungs makes speech possible, and
emotions can make us sob or gasp.
• In addition, breathing can be consciously
controlled—that is, it is possible to breathe
or to stop breathing voluntarily. Some
people can hold their breath until they lose
consciousness due to lack of O2 in the
brain.
• Children have used this strategy to
encourage parents to give them what they
want.
• However, as soon as conscious control of
respiration is lost, automatic control
resumes, and the person starts to breathe
again. Several reflexes, such as sneeze and
cough reflexes, can modify breathing.
• The Hering-Breuer (her′ing broy′er) reflex
supports rhythmic respiratory movements
by limiting the extent of inspiration. As the
muscles of inspiration contract, the lungs
fill with air.
• Sensory receptors that respond to stretch
are located in the lungs, and as the lungs fill
with air, the stretch receptors are
stimulated.
• Action potentials from the lung stretch
receptors are then sent to the medulla
oblongata, where they inhibit the
respiratory center neurons and cause
expiration.
• In infants, the Hering-Breuer reflex plays an
important role in regulating the basic
rhythm of breathing and in preventing
overinflation of the lungs.
• In adults, however, the reflex is important
only when the tidal volume is large, as
occurs during heavy exercise. Touch,
thermal, and pain receptors in the skin also
stimulate the respiratory center, which
explains why we gasp in response to being
splashed with cold water or being pinched

Chemical Control of Breathing

• During cellular respiration, the body’s cells consume O2 and produce CO2 (see chapter 17).
• The primary function of the respiratory system is to add O2 to the blood and to remove CO2 from the blood.
Surprisingly, the level of CO2, not O2, in the blood is the major driving force regulating breathing.
• Even a small increase in the CO2 level (hypercapnia), such as when holding your breath, results in a powerful
urge to breathe. The mechanism by which CO2 in the blood stimulates breathing involves the change in pH that
accompanies an increase in CO2 levels.
• Receptors in the medulla oblongata called chemoreceptors are sensitive to small changes in H+ concentration.
• Recall from the section “Carbon Dioxide Transport and Blood pH” that blood CO2 combines with water, which
increases H+ concentration.
• Thus, it is the H+ that is detected by the medullary chemoreceptors

• Although O2 levels are not the major driving force of breathing, there are O2-sensitive chemoreceptors in the
carotid and aortic bodies.
• When blood O2 levels decline to a low level (hypoxia) such as during exposure to high altitude, emphysema,
shock, and asphyxiation, the aortic and carotid bodies are strongly stimulated.
• They send action potentials to the respiratory center and produce an increase in the rate and depth of breathing,
which increases O2 diffusion from the alveoli into the blood. Because CO2 levels affect blood pH, the medullary
chemoreceptors play a crucial role in maintaining blood pH.
• If blood CO2 levels decrease, such as during more rapid breathing, blood pH will increase (become more basic)
(figure 15.17). Thus, the homeostatic mechanism is that the medullary chemoreceptors signal a decreased
breathing rate, which retains CO2 in the blood. More CO2 in the blood causes H+ levels to increase, which causes
blood pH to decrease to normal levels. Alternatively, if blood CO2 levels increase, such as during increased
physical activity when the body’s cells are producing more CO2 as waste, blood pH will decrease (become more
acidic). The medullary chemoreceptors will detect the elevated H+ and signal a faster breathing rate. As
 breathing rate goes up, more CO2 will diffuse out of the blood and blood pH will return to normal. Thus, CO2
levels are very influential on breathing rate. The opposite is also true, which is why hyperventilation without
accompanying increases in CO2 levels due to physical exercise can cause someone to pass out.

EFFECT OF EXERCISE ON BREATHING

The mechanisms by which breathing is regulated during exercise are controversial, and no single factor can account
for all the observed responses. Breathing during exercise can be divided into two phases:
1. Breathing increases abruptly. At the onset of exercise, the rate of breathing immediately increases. This initial
increase can be as much as 50% of the total increase that will occur. The immediate increase occurs too quickly to
be explained by changes in metabolism or blood gases. As axons pass from the motor cortex of the cerebrum
through the motor pathways, numerous collateral fibers project to the respiratory center. During exercise, action
potentials in the motor pathways stimulate skeletal muscle contractions, and action potentials in the collateral
fibers stimulate the respiratory center.
Furthermore, during exercise, body movements stimulate proprioceptors in the joints of the limbs. Nerve fibers
from these proprioceptors extend to the spinal cord to connect with sensory nerve tracts ascending to the brain.
Collateral fibers from these nerve tracts connect to the respiratory center; therefore, movement of the limbs has
a strong stimulatory influence on the respiratory center (see figure 15.16e). There may also be a learned
component in the breathing response during exercise. After a period of training, the brain “learns” to match
breathing with the intensity of the exercise. Well-trained athletes match their respiratory movements more
efficiently with their level of physical activity than do untrained individuals. Thus, centers in the brain involved in
learning have an indirect influence on the respiratory center, but the exact mechanism is unclear
2. Breathing increases gradually. After the immediate increase in breathing, breathing continues to increase
gradually and then levels off within 4–6 minutes after the onset of exercise. Factors responsible for the immediate
increase in breathing may play a role in the gradual increase as well. Despite large changes in O2 consumption
and CO2 production during exercise, the average arterial O2, CO2, and pH levels remain constant and close to
resting levels as long as the exercise is aerobic (see chapter 7). This suggests that changes in blood gases and pH
do not play an important role in regulating breathing during aerobic exercise. However, during exercise, the values
of arterial O2, CO2, and pH levels rise and fall more than they do at rest. Thus, even though their average values
do not change, their oscillations may be a signal for helping control breathing. The highest level of exercise that
can be performed without causing a significant change in blood pH is the anaerobic threshold. If the exercise
intensity becomes high enough to exceed the anaerobic threshold, skeletal muscles produce lactate through the
process of anaerobic respiration (see figure 17.5). Lactate released into the blood contributes to a decrease in
blood pH, which stimulates the carotid bodies, resulting in increased breathing. In fact, ventilation can increase
so much that arterial CO2 levels fall below resting levels, and arterial O2 levels rise above resting levels.

RESPIRATORY ADAPTATIONS TO EXERCISE

• In response to training, athletic performance increases because the cardiovascular and respiratory systems
become more efficient at delivering O2 and picking up CO2.
• In most individuals, breathing does not limit performance because breathing can increase to a greater extent
than can cardiovascular function. With regular exercise, vital capacity increases slightly, and residual volume
decreases slightly.
• Tidal volume at rest and during normal activities does not change. However, the tidal volume increases during
maximal exercise. Increased efficiency of the respiratory system in response to regular exercise is evident.
• The respiratory rate at rest or during normal activities in athletes is slightly lower. However, at maximal exercise,
athletes’ respiratory rate is usually increased.
• Minute volume (total volume of air moved each minute) is affected by changes in tidal volume and breathing
rate. In athletes, minute volume is essentially unchanged or slightly reduced at rest, slightly reduced during
normal activities, but greatly increased at maximal exercise. For example, without regular exercise a person with
a minute volume of 120 liters per minute (L/min) can increase his or her minute volume to 150 L/min after
exercising regularly. Increases to 180 L/min are typical of elite athletes.
EFFECTS OF AGING ON THE RESPIRATORY SYSTEM

• Aging affects most aspects of the respiratory
system.
• Vital capacity, maximum ventilation rates, and
gas exchange decrease with age. However, the
elderly can engage in light to moderate exercise
because the respiratory system has a large
reserve capacity. With age, mucus accumulates
within the respiratory passageways.
• The movement of mucus by cilia in the trachea
is less efficient because the mucus becomes
more viscous and the number of cilia and their
rate of movement decrease.
• As a consequence, the elderly are more
susceptible to respiratory infections and
bronchitis. Vital capacity decreases with age
because of reduced ability to fill the lungs
(decreased inspiratory reserve volume) and to
empty the lungs (decreased expiratory reserve
volume).
• As a result, maximum minute ventilation rates
decrease, which in turn decreases the ability to
perform intense exercise.
• These changes are related to the weakening of
respiratory muscles and the stiffening of
cartilage and ribs.
• Residual volume increases with age as the
alveolar ducts and many of the larger
bronchioles increase in diameter.
• This increases the dead space, which decreases
the amount of air available for gas exchange.
• In addition, gas exchange across the respiratory
membrane declines because parts of the
alveolar walls are lost, which decreases the
surface area available for gas exchange, and the
remaining walls thicken, which decreases the
diffusion of gases.
• A gradual increase in resting tidal volume with
age compensates for these changes

ASTHMA

Asthma (az′ma˘; difficult
breathing) is characterized by
abnormally increased constriction
of the trachea and bronchi in
response to various stimuli, which
decrease ventilation efficiency.
Symptoms include rapid and
shallow breathing, wheezing,
coughing, and shortness of breath.
In contrast to many other
respiratory disorders, the
symptoms of asthma typically
reverse either spontaneously or
with therapy.
There is no definitive pathological
feature or diagnostic test for
asthma, but three important
characteristics of the disease are
chronic airway inflammation,
airway hyperreactivity, and airflow
obstruction.
The inflammation can block airflow
through the bronchi. Airway
hyperreactivity means that the
smooth muscle in the trachea and
bronchi contracts greatly in
response to a stimulus, thus
decreasing the diameter of the
airway and increasing resistance to
airflow. The effects of inflammation
and airway hyperreactivity
combine to cause airflow
obstruction. Many cases of asthma
appear to be associated with a
chronic inflammatory response by
the immune system. Inflammation
appears to be linked to airway
hyperreactivity by some chemical
mediators released by immune
cells. The stimuli that prompt
airflow obstruction in asthma vary
from one individual to another.
Some asthmatics react to particular
allergens, which are foreign
substances that evoke an
inappropriate immune system
response (see chapter 14).
Examples include inhaled pollen,
animal dander, dust mites, and
droppings and carcasses of
cockroaches. However, other
inhaled substances, such as
chemicals in the workplace or
cigarette smoke, can provoke an
asthma attack without stimulating
an allergic reaction. An asthma
attack can also be stimulated by
ingested substances such as some
medicines. Other stimuli, such as
strenuous exercise (especially in
cold weather) can precipitate an
asthma attack. Such episodes can
often be avoided by using a
bronchodilator prior to exercise.
Viral infections, emotional upset,
stress, air pollution, and even reflux
of stomach acid into the esophagus
are known to elicit asthma attacks.
Treatment of asthma involves
avoiding the causative stimulus and
taking medications. Steroids and
mast cell–stabilizing agents, which
prevent the release of chemical
mediators from mast cells, can
reduce airway inflammation.
Bronchodilators are used to
increase airflow.