The Human Respiratory System Joy Chen
Lab Partners:
Harvinder Kaur
Nina Zai
Marylee Banzon
NPB101L- SEC 09
TA: Phung Thai
19 Nov 2012
Chen 1 Introduction
The respiratory system plays an important role in the human body by allowing gas
exchange to occur between tissues and the external environment. The main role of respiration is
intake of oxygen for metabolic processes in cells and elimination of carbon dioxide, a waste
product of metabolism. The respiratory system can be divided into two main processes, cellular
and external respiration. Cellular respiration refers to intracellular reactions that use O2 in order
to form ATP and produce CO2 in the process. On the other hand, external respiration refers to
events in the body that allow O2 and CO2 exchange to occur between cells and the external
environment (Sherwood, 2010, p. 462).
The main components of the respiratory system include airways leading into the lungs,
the lungs, and the thorax involved in producing movement of air into and out of the lungs. The
respiratory airway begins with nasal passages and opens into the pharynx, or throat. From the
pharynx is the esophagus, a tube that allows food to reach the stomach. The pharynx also leads to
the trachea, the windpipe that is responsible for bringing air into the lungs. Further branching
occurs as the trachea divides into the right and left bronchi, which enter the right and left lungs.
Within the lungs the bronchi continue branching into more airways that have progressively
smaller diameters and lengths, but larger in number. The smallest branches are the bronchioles
that have alveoli clustered at the ends (Sherwood, 2010, p. 463).
Alveoli are small sacs that have thin walls contributing to efficient gas exchange between
the air and the blood. The thin walls of the alveoli consist of type I alveolar cells with capillaries
that are only one cell thick surrounding them. This thin barrier that separates the air from the
blood allows for gas exchange to readily occur. Alveoli also have large surface areas with dense
capillary networks that facilitate efficient gas exchange. In addition to type I cells, the alveoli
Chen 2 also have type II alveolar cells that reside on the surface and secrete surfactant, which permits
lung expansion (Sherwood, 2010, p. 464).
Ventilation is a mechanical action that allows air to flow in and out of the lungs, guided
by partial pressure gradients. Gases move down a pressure gradient from areas of higher to lower
partial pressure. In the lungs, the pressure differences between the atmosphere and the alveoli
aids in the movement of gases. Also, Boyle’s law states that at a constant temperature, an inverse
relationship exists between gas volume and gas pressure. For example, during inspiration the
diaphragm contracts, which increases the volume of the thoracic cavity. The alveolar pressure
corresponds to lung volume and as the lung expands, the pressure decreases. The low alveolar
pressure relative to atmospheric pressure drives the movement of air into the lungs. The converse
occurs during expiration (Sherwood, 2010, p. 463).
The purpose of this experiment is to measure the static lung volume, examine the effects
of alveolar gases on respiratory mechanics and the length of breath-holds, and examine the
effects of moderate exercise workloads on ventilation. We expect to see the largest amount of
%CO2 before breath-hold in re-breathing and the smallest amount of %CO2 before breath-hold
during hyperventilation. We expect to see the %CO2 after breath-hold to be the same for all three
conditions because the subject is holding their breath to the same discomfort. The duration of
breath-hold differs due to chemoreceptors sensing changes in PCO2 , PO2, H+ and controlling
inspiratory drive. The duration is expected to be greatest for hyperventilation, then normal
breathing, and lastly re-breathing. In the last part of this experiment, we expect to see an increase
in respiratory rate (RR), TV, and the amount of CO2 expired with increased workload during
exercise.
Chen 3 Materials and Methods
The subject of the first two parts of the experiment was a lean female, and the subject for
the last part of the experiment was an athletic male. Details about the materials and methods can
be found in Expriment 6: The Human Respiratory System in NPB 101L Systemic Physiology
Lab Manual (Bautista, 2009). In the first part of this experiment, we measured static lung
volumes with a nose clip, a mouthpiece tube, a stopwatch, a filter, a spirometer, and the Biopac
software on a computer. In the second part of this experiment we used a plastic bag, two rubber
bags, a small plastic mouthpiece, metal clips for the rubber bag, nose clip, and stopwatch. In the
third part of this experiment, we used an exercise bicycle, rubber mouthpiece, nose clip,
stopwatch, and the Biopac software to measure exercise hyperpnea. Deviations from this lab
occurred because the subject did not hold her breath to the same degree of discomfort for normal
breathing, re-breathing, and hyperventilation. Also, both the female and male subjects did not
always breath normally when needed because they were laughing.
Results
Part 1: Measuring Static Lung Volumes
In the first part of the experiment, we measured static lung volume during normal
breathing, forced inspiration, and forced
Table 1. Static lung volumes, in liters, for a
female subject using a spirometer
Volume (L)
Inspiratory Reserve Volume (IRV)
1.06
Expiratory Reserve Volume (ERV)
0.89
Tidal Volume (TV)
0.59
Vital Capacity (VC)
2.68
expiration. The results are shown in table 1. The
IRV value was obtained by finding the delta of the
peak of a normal inhalation to the peak of a
maximum inhalation. The ERV was the delta from
the trough of a maximum exhalation to the trough
of the last normal exhalation before it. And the TV value was the delta from the peak to the
Chen 4 trough of a normal breath. We calculated our subject’s minute ventilation using her TV and RR
(14.5 breaths/min), which was 8.66 L/min. Her dead space was estimated by using her weight,
which was 132 mL. Then we calculated her dead space volume by multiplying her dead space
with her respiratory rate, which was 1.91 L/min. Lastly, we calculated her alveolar ventilation by
subtracting her dead-space volume from her minute ventilation, which was 6.75 L/min.
Part 2: Effects of Inspired Gas Composition and Lung Volume on Respiration
After we measured our subject’s static lung volumes, we measured the %CO2 in end tidal
volume and after breath-hold in normal ventilation, re-breathing, and hyperventilation. We
measured the duration of breath-hold for each condition as well. The results are shown in table 2.
In this experiment,
we expected the
Table 2. Data for the % CO2 composition before and after breath-hold and the
duration of breath-hold (in seconds) in response to normal breathing, re-
breathing, and hyperventilation.
largest %CO2
before breath-hold
in re-breathing, then
normal breathing,
Conditions
Normal Breathing
Re-Breathing
Hyperventilation
%CO2
Before
Breath-Hold
3.71
6.56
3.28
%CO2 After
Breath-Hold
Change in
%CO2
5.43
6.24
6.09
1.72
-0.32
3.01
Duration of
Breath-Hold
(seconds)
29.5
34.0
32.8
and lastly hyperventilation. The measured data shown in table 2 aligns with what we expected. In
this experiment, we were also expecting to see the %CO2 after breath-hold to remain the same
for all three conditions. This was true for re-breathing and hyperventilation because they only
differed by 0.15%. However, %CO2 after breath-hold for normal breathing differs the most from
the other two conditions. It is by 0.81% less than re-breathing and 0.66% less compared to
hyperventilation. Also, we expected %CO2 after breath-hold to be higher than before breath-hold
for all three conditions. From table 2, it is evident that our subject had a positive change in %CO2
for normal breathing and hyperventilation, indicating an increase in amount of CO2 after breath Chen 5 hold for these two conditions. However, the negative change in %CO2 is not what we expected
and indicates that there was a decrease in CO2 after breath-hold in our subject. A bar graph
comparing %CO2 before breath-hold and after breath-hold for each condition is illustrated in
figure 1. Figure 1
Ventilaton Type vs. %CO2 Composition Before and Ater Breath-­‐Hold visually represents
2. The bars for after
breath-hold are
taller than before
%CO2 Composition the results in table
breath-hold in
7 6 5 4 3 2 1 0 6.56 6.24 5.43 6.09 Before Breath-­‐Hold 3.71 After Breath-­‐Hold 3.28 Normal Breathing Hyperventilation normal breathing
Re-­‐Breathing Ventilation Type visually showing the
Figure 1. A graph of the percent CO2 composition recorded for normal
breathing, re-breathing, and hyperventilation, before and after the subject
completed breath-hold.
increase in %CO2
and re-breathing,
composition for these conditions. Also, the bar graph emphasizes the high amount of %CO2
composition in hyperventilation before breath-hold. The last column in table 2, compares the
duration of breath-hold in seconds for each type of ventilation. We expected it to be the longest
for hyperventilation, the shortest for re-breathing, and normal breathing to be in the middle. The
Ventilation Type vs. Duration of Breath-­‐Hold shown in figure 2. As we
expected, the duration of breath-
Time (seconds) results for each category are
35 34 33 32 31 30 29 28 27 34 32.8 29.5 Normal Breathing Hyperventilation Re-­‐Breating Ventilation Type Figure 2. A graph of the time, in seconds, that the subject was
able to hold his breath after performing normal, re-breathing,
and hyperventilation with respect to the change in % CO2
composition from before and after breath hold.
Chen 6 hold for hyperventilation was the longest, exceeding normal breathing by 4.5 seconds and rebreathing by 1.2 seconds. However, re-breathing has the second longest duration for breathhold, which is not what we expected. As shown in figure 2, our subject had the shortest breathhold duration for normal breathing. In the next part of this experiment, we looked at the effects
of lung volume on respiration. We did this by timing the breath-hold after a normal inhalation,
normal exhalation, forced inhalation, and forced exhalation. The results are shown in table 3.
Table 3. The data for the duration of breath-hold
time, in seconds after normal expiration, normal
inspiration, forced inhalation, and forced
exhalation.
Duration of Breath-Hold (seconds)
By looking at the table, it is clear that
breath-hold after inhalation is longer
than breath-hold after exhalation. Forced
Normal Expiration
44
Normal Inspiration
68
Forced Inhalation
59
breath-hold and forced exhalation has
Forced Exhalation
39
the shortest duration of breath-hold. The
inhalation has the longest duration of
data we recorded and shown in table 3 is consistent with our expectations.
Part 3: Exercise Hyperpnea
In this last part of the lab, we observed the effects of exercise on ventilation. First we measured
ventilation at rest for 2 minutes, then we counted down and instructed the subject to exercise at 0
kPa for two minutes. We increased the workload every 2 minutes by 0.5 kPa up to 2.0 kPa. The
values for TV, RR, VE, FECO2, and minute CO2 were either observed from the original graph or
calculated. The data recorded is shown in table 4, which is shown on the next page.
Chen 7 Table 4 Ventilatory responses during exercise with respect to increasing workload, measured in kPa.
Respiratory responses include tidal volume, in liter, respiratory rate, in breaths per minute, minute
ventilation, in liters per minute, end tidal CO2, as a percentage of expired air, and minute CO2 production,
in liters of CO2 expired per minute Workload
(kPa)
Rest
0.0
0.5
1.0
1.5
2.0
TV
(liters)
0.59
1.43
1.50
1.60
1.73
1.81
RR
16
16
20
20
20
26
VE
(liters/min)
9.5
22.9
30.0
32.0
34.6
47.2
FECO2
(% CO2)
5.64
5.58
5.79
5.65
5.59
6.45
Minute CO2
(liters/min)
0.54
1.33
1.74
1.81
2.04
3.04
The overall trend comparing workload and tidal volume can be seen in table 4 and figure 3 as
well. Figure 3 shows a positive relationship between workload and tidal volume. The tidal
volume at workload 2.0 kPa is
than the tidal volume at rest.
Overall, our subject had a
206.8% increase in tidal
volume at the maximum
resistance compared to rest.
Not only is there a positive
relationship between tidal volume
Tidal Volume (liters) more than three times greater
2 1.8 1.6 1.4 1.2 1 0.8 0.6 0.4 0.2 0 Workload vs. Tidal Volume rest 0 0.5 1 1.5 2.0 Workload (kPa) Figure 3. A graph of the changes in tidal volume, in liters,
with respect to increasing workload in increments of 0.5 kPa
during exercise. and workload, but figure 4 shows a
positive relationship between respiratory rate and workload as well. The figure is located on the
next page. In figure 4, there is a plateau between rest and 0 kPa. From table 4, we see that this
plateau is results from no change in the subject’s respiratory rate when he was resting and when
he initially began exercising. The respiratory rate increases by 4 breaths per minute when the
workload increases from 0 to 0.5 kPa. As we continued to increase the workload by 0.5 kPa,
Chen 8 30 Workload vs. Respiratory Rate there is no change in
RR (breaths/minute) 25 respiratory rate as illustrated
20 15 by the plateau between 0.5
10 to 1.5 kPa. At the end of the
5 0 experiment, when we
rest 0 0.5 1 1.5 2.0 Workload (kPa) increased the workload to
Figure 4. A graph of the changes in respiratory rate, in
breaths/minute, with respect to increasing workload, increments
of 0.5 kPa, during exercise.
2.0 kPa, we observed an
increased in respiratory rate by
6 beats/minute. The respiratory rate increased from rest to the maximum workload, but we did
not observe an increase at each workload. Overall, figure 4 shows a positive relationship
between respiratory rate and workload, which is the outcome we expected to see. Not only can
we observe a positive relationship between tidal volume and respiratory rate, but this relationship
exists between minute ventilation and workload as well. Minute ventilation is calculated by
multiplying tidal volume by respiratory rate. By looking at figure 5, we can see that as workload
increased for the subject, his minute ventilation increased as well. The subject’s minute
ventilation at 2.0 kPa is five times as much as his minute ventilation at rest. Overall, he had a
during the experiment, which
corresponds to what we expected to
observe. The next variable we looked
at is the %CO2 expired. Figure 6 is a
graph of the data from table 4,
showing the %CO2 expired with
Minute Ventilation (L/min) 396.8% increase in minute ventilation
50 Workload vs. Minute Ventilation 40 30 20 10 0 rest 0 0.5 1 1.5 2.0 Workload (kPa) Figure 5. A graph of the changes in minute ventilation, in
L/minute, with respect to increasing workload, increments of 0.5
kPa, during exercise. Chen 9 respect to workload. Figure 6 is a graph of the data from table 4, showing the %CO2 expired with
respect to workload. The data
FECO2 (%) Workload vs. FECO2 we have of the %CO2 expired is
6.6 6.4 6.2 6 5.8 5.6 5.4 different from what we
expected to measure. We
expected the %CO2 to increase
rest 0 0.5 1 1.5 2.0 with increase in workload. From
Workload (kPa) Figure 6. A graph of the changes in end tidal CO2, in percent,
with respect to increasing workload, increments of 0.5 kPa,
during exercise.
table 4, we see that there is an
increase of 0.81% CO2 expired.
However,
figure 6 shows that from rest to 1.5 kPa, the %CO2 expired does not increase
progressively, instead it is sporadic and the data points show no clear pattern. The graph in figure
6 is not what we expected to observe. Lastly, we were able to calculate the minute CO2 by
multiplying the minute ventilation and %CO2 expired. The calculated minute CO2 or each
workload is recorded in table 4. The values recorded values in table 4 for minute CO2 with
respect to workload is graphed in figure 7. From rest to 2.0 kPa there is a 462.9% increase in
minute CO2.
Minute CO2 (L/min) Workload vs. Minute CO2 3.5 3 2.5 2 1.5 1 0.5 0 rest 0 0.5 1 1.5 2.0 Workload (kPa) Figure 7. A graph of the changes in minute CO2, in L/minute, with
respect to increasing workload, increments of 0.5 kPa, during
exercise.
Chen 10 Discussion
This experiment highlighted the mechanics of ventilation and its ability to be changed by
activity, particularly different breathing patterns and exercise. In order to appreciate the methods
and observations that have been outlined, it is necessary to understand the physiology at work
that governs these results.
As previously stated in the introduction, the anatomy of the respiratory system begins at
the nasal passages, or the nose. The nasal passages open into the pharynx, which leads into the
esophagus and the trachea. The esophagus is a necessary passageway for the digestive system, as
food passes through it and enters the stomach. In the process of respiration, the trachea plays an
important role by allowing air to pass through and reach the lungs. The trachea then divides into
the right and left bronchi that enters the right and left lungs respectively. The bronchi continue to
branch within each lung, and the smallest of these branches are termed bronchioles. At the end of
bronchioles are alveoli, which are small air sacs and the major site of gas exchange. The trachea,
bronchi, bronchioles, and terminal bronchioles make up the conducting zone because no gas
exchange occurs there. This region is also called anatomical dead space. The respiratory
bronchioles, alveolar ducts, and alveolar sacs make up the respiratory zone because that is where
gas exchange occurs. (Sherwood, 2010, p. 463).
The anatomy of alveoli is optimal for gas exchange and is the reason why it is the major
site of gas exchange. Primarily, alveoli have thin walls composed of type I alveolar cells
surrounded by capillaries that are only one cell thick. Fick’s law of diffusion states that there is
an inverse relationship between the rate of diffusion and the distance that diffusion must take
place. Alveoli are ideal for gas exchange because there is a thin separation between blood from
the capillaries and air inside the alveoli. The oxygen can easily diffuse from the alveoli and into
the pulmonary capillary, where it is able to bind to hemoglobin in red blood cells. A second
Chen 11 reason why diffusion can readily occur at alveoli is because of its large surface area. As
branching occurs from the trachea to the alveolar sacs, the diameter and length of each branch
decreases, but the number of each increases significantly. This is why inside the lungs there are
500 million alveoli each only 300µm in diameter. Furthermore, capillaries densely surrounding
each alveolus, allowing gas exchange to occur efficiently. Lastly, alveoli contain type II alveolar
cells that secrete pulmonary surfactant that allows the lungs to easily expand. (Sherwood, 2010,
p. 463).
In the human body, there are two lungs that each have branched airways, alveoli, bloods
vessels, and connective tissue. The right and left lung each has a pleural sac that surrounds and
adheres to the surface of the lung. The pleural sac is double-walled and closed, allowing the
lungs to be separated from the thoracic wall. Inside the pleural sac is a space called the pleural
cavity. Intrapleural fluid is secreted by the pleura and it allows the pleural surfaces to be
lubricated and move easily during respiration. (Sherwood, 2010, p. 470).
Although the lungs contain smooth muscle in the walls of arterioles and bronchioles,
there is no muscle in the alveolar walls. Because the alveolar walls do not have muscle, they rely
on changes in the thoracic cavity to change lung volume during breathing. The thoracic cavity,
also known as the chest, has most of its volume occupied by the lungs. The thoracic cavity also
includes the thorax, or outer chest wall, which is formed by ribs. The rib cage plays an important
role in the thoracic cavity because it protects the lungs and the heart. At the bottom of the
thoracic cavity resides the diaphragm, a sheet of skeletal muscle that separates the thoracic cavity
from the abdominal cavity. The diaphragm is important because it is able to change lung volume
and alter alveolar pressure in the process of respiration. (Sherwood, 2010, p. 470).
The flow of air into and out of the lungs is dependent on the changes in alveolar pressure.
Chen 12 Because air flows down a pressure gradient, the intra-alveolar pressure must be lower than
atmospheric pressure flow air to flow into the lungs. Similarly, in order for air to flow out of the
lungs, the intra-alveolar pressure must be greater than the atmospheric pressure. The flow of air
out of the lungs is called expiration. Change in alveolar pressure is controlled by respiratory
muscles that indirectly change lung volume by altering the volume of the thoracic cavity.
(Sherwood, 2010, p. 470).
During inspiration, the diaphragm and external intercostal muscles are the inspiratory
muscles that allow inspiration during quiet breathing. Prior to inspiration the inspiratory muscles
are relaxed, the intra-alveolar and atmospheric pressures are equal, and thus no airflow is
occurring. The phrenic nerve innervates the diaphragm and when it is stimulated the diaphragm
descends downward, and the thoracic cavity volume increases by expanding vertically. The
abdominal wall will also bulge during inspiration due to the diaphragm pushing it outward
during contraction. The external intercostal muscles are located between the ribs and accessory
inspiratory muscles. Accessory inspiratory muscles are used to further increase the thoracic
cavity for deeper inspiration, which is necessary during exercise for example. When the thoracic
cavity increases, it causes the lung volume to increase as well, dropping the intra-alveolar
pressure. When the intra-alveolar pressure is less than the atmospheric pressure, air moves down
its pressure gradient into the lungs. The movement of air continues to move into the lungs until
the intra-alveolar pressure is equivalent to the atmospheric pressure (Sherwood, 2010, p. 471).
At the end of inspiration, the inspiratory muscles relax and the chest wall and lungs return
back to their preinspiratory size. The lungs recoil and decrease in volume, which causes intraalveolar pressure to rise and become greater than atmospheric pressure. Air will now leave the
lungs as it goes down its pressure gradient and will continue until a pressure gradient no longer
Chen 13 exists. This process of air leaving the lungs is expiration, which is a passive process, does not
involve inspiratory muscles and energy. However, forced expiration involves expiratory muscles,
which includes the abdominal muscles and internal intercostal muscles. When the abdominal
muscles contract, they push the diaphragm upward into the thoracic cavity, which decreases the
volume of the thoracic cavity. When the internal intercostal muscles contract, they push the ribs
inward and downward, which flattens the chest wall, causing the thoracic cavity to decrease the
further. When the thoracic cavity decreases in volume, the lungs recoil to a smaller volume and
this causes the intra-alveolar pressure to increase. During forced expiration the pressure
difference is greater between the alveoli and the atmosphere than in passive expiration. A greater
pressure difference allows more air to leave the lungs before equilibrium is established
(Sherwood, 2010, p. 472).
Part 1: Measuring Static Lung Volumes
In the first part of the experiment, we measured the static lung volume of the subject. Individual
factors can influence a person’s total lung capacity, such as anatomic build, age, dispensability of the
lungs, and presence of a respiratory disease. An individual’s total lung capacity can be quantified as the
sum of the TV, IRV, ERV, and RV. Tidal volume (TV) is defined as the volume of air that enters and
leaves the lungs during normal breathing. Additional air can be taken in into the lung following tidal
inspiration, and this is defined as inspiratory reserve volume (IRV). Similarly, the expiratory reserve
volume can be exhaled past the TV (Hlastala, 1996, p. 41). The expiratory reserve volume
(ERV) is the additional volume of air can leave the lung after passive expiration. However, even past
forceful expiration there is air that remains in the lungs and it is termed residual volume (RV).
Other capacities besides the total lung capacity are functional residual capacity, inspiratory
reserve capacity, and vital capacity. Functional reserve capacity (FRC) is the sum of ERV and
RV. FRC is the amount of air in the lungs at the end of passive expiration. It provides a reservoir
Chen 14 of oxygen and prevents the lung to collapse after each breath. The inspiratory reserve capacity
(IRC) is the sum of TV and IRV. IRC represents the total volume inspired during maximal
inspiration. The vital capacity (VC) is the sum of TV, IRV, and ERV. It is the maximum volume of
air that can be moved in and out of the lungs (Sherwood, 2010, p. 479).
In lab we measured our subject’s IRV, ERV, TV, and VC. In looking at the values gathered
and calculated in the results, the majority of our lung volumes are smaller than the average lung
volumes provided by Sherwood (Sherwood, 2010, p. 479). For an average healthy young adult
male, IRV is 3000 mL, the ERV is 1000 mL, the TV is 500 mL, and the VC is 4500 mL. Our
subject’s IRV was 1060 mL, her ERV was 890 mL, her TV was 590 mL, and her VC was 2680
mL. Her IRV, ERV, and VC were lower compared to the values listed in Sherwood, which is
expected because values for females are typically lower. Her TV was higher than the average
male’s TV by 90 mL, which is not what we would have expected. Her higher than expected TV
value can be due to the fact that she is 5’5” and 132 pounds. Her body frame is not small and
may be larger than the average female her age, which contributed to her larger TV value.
However, because her TV does not deviate exceed the standard TV by much, this 90 mL
difference can be due to random error during the experiment.
Part 2: Effects of Inspired Gas Composition and Lung Volume on Respiration
After measuring our subject’s static lung volume in the first part of the experiment, we
looked at the effects of normal breathing, re-breathing, and hyperventilation on respiration.
These three conditions alter gas composition differently and allow us to look at the effects of gas
composition on respiration. Carbion dioxide plays a significant role in changing the composition
of blood because it participates in reactions that produce bicarbonate and carbaminohemoglobin.
Both of these reactions form H+ as a byproduct, and the buildup of H+ effectively lowers pH. In
Chen 15 the body, changes in PCO2, PO2, and pH of arterial blood is regulated by peripheral and central
chemoreceptors.
Peripheral chemoreceptors are located in the carotic and aortic bodies and regulate
ventilation by sensing a decrease in PO2, increase in PCO2, and increase in [H+]. PO2 needs to
decrease past 60 mm Hg in order to have an effect on the peripheral chemoreceptors. When the
peripheral chemoreceptors sense decrease in PO2, increase in PCO2, and increase in [H+], they will
increase firing to the medullary inspiratory neurons. The medullary inspiratory neurons will in
turn increase firing to the diaphragm and inspratory intercostals. The diaphragm and inspiratory
intercostals will respond to this by contracting, which leads to ventilation.
The central chemoreceptors are located in the medulla and are sensitive to changes in pH
of the cerebrospinal fluid. CO2 has the ability to freely diffuse from the arterial blood to the
cerbral spinal fluid. CO2 interacts with water to produce bicarbonate and H+. The central
chemoreceptors directly sense the increase in H+ in the brain’s extracellular fluid. The increase in
H+ causes central chemoreceptors to increase firing to medullary inspiratory neurons, leading to
ventilation. The decrease in pH due to build up of H+ ultimately results in increased breathing
rate, which will bring PCO2 back to normal.
Furthermore, the medulla oblongata regulates breathing through its respiratory control
centers. The dorsal respiratory group (DRG) processes information from the central and
peripheral chemoreceptors and lungs. Its primary responsibility is control of inspiration and
generates the rhythm for breathing. There another group of neurons called the ventral respiratory
group (VRG) that receives input from the DRG and responds to changes in arterial gases. The
VRG is primarily responsible for expiration.
The pneumotaxic and apneustic respiratory centers in the pons also send signals to the
Chen 16 medullary center. The pneumotaxic center signals the inactivation of the neurons in the DRG.
Conversely, the apneustic center prevents the inspiratory neurons from inactivation. The
pneumotaxic center takes precedence over the apneustic center in order for inspiration to pause
so expiration can occur.
In our experiment, we measured the %CO2 before breath-hold in normal breathing, rebreathing, and hyperventilation. The data shows that our subject had the greatest amount of
%CO2 before breath-hold in re-breathing, hyperventilation had the lowest amount of %CO2
before breath-hold, and normal breathing was in the middle. The data for %CO2 before breathhold is corresponds to what we expected to see in the lab. The reason why %CO2 before breathhold is highest for re-breathing is because the subject is breathing in already breathed air. The air
in the bag has a large amount of expired CO2, which contributed to the large %CO2 in her breathhold. On the other hand, for hyperventilation, our subject had the lowest amount of %CO2 before
breath-hold because hyperventilation is a mechanism to increase O2 and decrease CO2.
Hyperventilation increases alveolar ventilation achieved by increasing respiratory frequency
and/or tidal volume. It is ultimately an increased pulmonary ventilation greater than the
metabolic needs of the body. Because of this, there is a decrease in arterial PCO2, as the body is
exhaling CO2 at a faster rate than it is being produced (Sherwood, 2010, p. 582). Therefore, we
observed the lowest %CO2 before breath-hold for this breathing condition.
For the % CO2 composition after breath-hold for the breathing conditions, we expected
the values to be similar. In other re-breathing experiments carried out in bags, it has been
concluded that even if O2 was added, the subjects would stop breathing at about 10% CO2.
Oxygen did not make a difference in the subject distress level (Haldane, 1935, p.16). Regardless
of the starting levels of CO2 after normal breathing, re-breathing, or hyperventilation, if the
Chen 17 subject held his breath to the same level of discomfort, the CO2 level at which the
chemoreceptors invade voluntary inhibition should be the same. However, our data shows that
while re-breathing and hyperventilation have similar %CO2, normal breathing did not have a
similar value. There are many possible source of error such as not fully emptying and cleaning
the rubber collecting bags or from the psychological effect of the subject being surprised after
peering at the breath-hold duration.
We also measured breath-hold duration for each breathing condition. We expected to
observe the shortest duration with re-breathing, the longest duration for hyperventilation and
normal breathing to be in the middle. Breath-hold duration is limited by the dominance of central
chemoreceptors of the CNS. During breath-hold, the body does not cease to produce CO2 so
there is an increase in PCO2 and, eventually, a buildup of H+ in the brain. These high levels of
PCO2- H+ continue to increase and stimulate firing in the central chemoreceptors until they can
overcome the voluntary inhibition to initiate breathing (Sherwood, 2010, p. 469). At a certain
breakpoint during breath-hold when the body is forced to take an involuntary breath, this is due
to the arterial PO2 falling below or the PCO2 rising above and certain threshold pressure in which
chemoreceptors are signaled (Parkes, 2006). Hyperventilation decreases the amount of PCO2 and
decreases it further from threshold, thus allowing more space for CO2 to be produced. In
contrast, during re-breathing, the increase in PCO2 starts breath-hold closer to threshold, leaving
less room for CO2 to accumulate.
Our results showed that the subject had the longest breath-hold duration for re-breathing,
then hyperventilation, and lastly normal breathing. These results are not what we expected to
observe because her re-breathing had the largest amount of %CO2, so her breath-hold should
have been the shortest. With increased levels of CO2 inside the bag, there is an elevated arterial
Chen 18 PCO2 that is detected by the central chemoreceptors. The central chemoreceptors send a signal to
the apneustic center and stimulate an increase in respiratory drive (Sherwood, 2010, p. 471). This
increase in respiratory drive is the reason why the subject should not have been able to hold her
breath for a long period of time. Furthermore, her %CO2 for hyperventilation was the lowest so
we expected to see the longest breath-hold for this breathing condition. In hyperventilation, there
is a decrease in arterial PCO2, as the body is exhaling CO2 at a faster rate than it is being
produced. Consequently, less CO2 is converted into H+ and HCO3¯, which leads to an increase in
pH (Sherwood, 2010). This decreases firing in the central chemoreceptors and, in addition to
increased arterial O2, the peripheral chemoreceptors. The subject reported slight dizziness while
performing active hyperventilation. An explanation for this could be that the increase in PO2 can
cause constriction of the blood supply to the brain due to a higher level of PO2 as compared to
the level of PCO2. In order for the brain to maintain the pH by monitoring the PCO2, the supply
of PO2 from the blood is slowed through constriction of blood vessels (Kety, 1946). This could
also provide an explanation for the shorter duration of breath-hold. We expected the duration of
breath-hold to be longer after the subject actively hyperventilation to decrease the PCO2, but the
constriction of the blood vessel to the brain due to the lowered pH could result in the subject
feeling the same amount of discomfort as when holding his breath.
At the end of this portion of the lab we also measured the effects of lung volume on
respiration, which involves the Hering-Breuer reflex. This negative feedback reflex involves
mechanoreceptors and responds to change in lung volume. When the lungs expand during large
pulmonary stretch receptors in smooth muscle cells will respond to excessive stretching. These
stretch receptors will fire and send action potentials to the medulla and apneustic area, located in
the pons. The inspiratory area is inhibited directly by inhibiting the apenustic area. Also,
Chen 19 inflation inhibits the output of phrenic motor neurons. The end result is inhibited inspiration and
expiration occurs. There are two of pulmonary stretch receptors (PSR) in the body: slowly
adapting PSRs and rapidly adapting PSRs. As their name suggests, slowly adapting PSRs
respond to stretch with a sudden increase in firing that adapts slowly over time. On the other
hand, rapidly adapting PSRs increase their firing rate due to maintain lung inflation and they
adapt quickly by decreasing their firing rate. This mechanism acts to protect lungs from over
inflation (Sherwood, 2010, p. 494).
We expected to observe the duration of breath-hold to be longest in forced inhalation.
second longest in normal inspiration, second shortest in normal expiration and shortest in forced
exhalation. Our subject’s data is consistent with our expectations because the gas composition
largely affected her ability for duration of breath-hold. The Hering-Breuer reflex did not play a
large role in this exercise because the gas composition controlled how long she could hold her
breath. The subject had the longest breath-holds for forced inhalation and normal inspiration
because the O2 in the lungs prior to breath-hold are greater in these conditions. Forced inhalation
had the greatest duration because there is an even greater amount of O2 being taken in, which
decreases inspiratory drive. On the other hand, normal expiration and forced exhalation had the
shortest durations because the largest amounts of CO2 relative to O2were present in these
conditions. Build up of CO2 in the subject causes an increased firing rate from chemoreceptors,
which increases inspiratory drive.
Part 3: Exercise Hyperpnea
In the last part of this lab, we examined how exercise and the anticipation of exercise
influences respiration. Hyperpnea refers to the increased depth of breathing because of an
increased metabolic demand by body tissues. This occurs during exercise or when there is a lack
Chen 20 of oxygen in the body. Variables that were measured during this experiment were TV, RR,
minute ventilation (VE ), fraction of expired carbon dioxide, and minute carbon dioxide. During
muscular exercise, the increase in alveolar ventilation maintains the normal levels of PCO2, PO2,
and pH. The body’s demand for O2 increases in order to keep up with the rate of consumption in
the tissues. The CO2 built up in the tissues as a result of internal respiration need to be removed
more rapidly from the body (Sherwood, 2010, p. 504). Therefore, in our experiment, we
expected all variables, except fraction of expired CO2, to increase with an increase in workload.
Our subject showed an increase in TV, RR, VE, and minute carbon dioxide during
exercise. In our subject we did saw a consistent increase in the VE as a product of the increase in
TV and RR. Being that either factor can be altered, in our experiment, the TV underwent a much
greater change overall than the RR, demonstrating that the subject preferred to change the
magnitude of the TV instead of RR when accommodating for the increased VE. In determining
the most effect combination for ventilation, for TV, it is necessary to consider the energy
necessary for the work of breathing and the stimulation of stretch receptors; for RR, the a large
volume of breath can wasted as dead space (Braun, 1990, p. 227-228). The Hering-Breuer reflex
plays a key role in the regulation of the work of breathing by calculating the most effective
combination of TV and RR for an optimal VA that costs the least amount of energy. There are
pulmonary stretch receptors in the wall of the bronchioles which are activated by the stretching
of the lungs to a large TV usually greater than 1 L. If hyperinflation occurs, the receptors send a
signal through the afferent nerves to the medulla. From the medulla, the inspiratory muscle
neurons are inhibited to allow for an extended expiratory response (Peters, 1969, p. 187;
Sherwood, 2010, p. 500).
Chen 21 The minute CO2 which is related to the VE and FE CO2, increased consistently in our
subject, showing that the volume exhaled per minute increases as workload increases. This is due
to the rise in the amount of CO2 produced by the metabolizing muscle during exercise. Exercise
elevates plasma CO2 because it is a byproduct of cellular respiration occurring in the
mitochondria. The high production of CO2 in the exercising muscle, particularly during intense
exercise, results in an increase in PCO2, acidity, and temperature. Similar to the way CO2 and
H2O converted to H+ and HCO3¯ in the brain ECF, this reaction also occurs in the blood as the
primary form of transportation of CO2 and H+ is bound to hemoglobin while HCO3¯ is diffused
out of the cell. Lactate produced as a product of anaerobic metabolism also contributes to acidity
(Sherwood, 2010, p. 494). Acidity in combination with the binding of CO2 to the subunits of
hemoglobin, these two factors contribute to the Bohr Effect, which decreases the affinity for O2
to favor the unloading at the tissue level.
Conclusion
In this experiment, the purpose was to measure the static lung volume, the effects of
alveolar gases on respiratory mechanics and the length of breath-holds, and examine the effects
of moderate exercise workloads on ventilation. This experiment emphasized the mechanisms and
physiological principles of the respiratory system. We observed the effects of gas composition
and lung volume as well as the neurological control on respiration. In addition, we saw the effect
of exercise hyperpnea on ventilation.
Chen 22 References
Bautista, Erwin and Korber, Julia. NPB101L Physiology Lab Manual. 2nd Edition. United
States: Cengage Learning, 2009.
Kety, Seymour S., and Carl F. Schmit. "The Effect of Active and Passive Hyperventilation on
Cerebral Blood Flow, Cerebral Oxygen Consumption, Cardiac Output, and Blood
Pressure of Normal Young Men." Laboratory of Pharmacology 25.1 (1946): 107-19.
Lausted, Christopher G., Johnson Arthur T., and Bronzino Joseph D. Biomedical Engineering
Fundamentals. 3rd ed. Floria: CRC Press, 2006.
Parkes M J. Breath-holding and its breakpoint. Experiemental Phyisology. 2006; 91.1: 1-15
Peters, Richard M. The Mechanical Basis of Respiration. 1st Ed. Great Britain: J. & A. Churchill
Ltd., 1969.
Sherwood, L. Human Physiology: From Cells to Systems. 7th Edition. Thomson Brooks/Cole.
Pgs 460-507.
Calculations
IRV = 3.12L – 1.32L = 1.8L
ERV = 1.32L – 0.57L = 0.75L
VC = 1.8L + 0.75L + 1.32L = 3.87L
VE = 0.93L x 10 = 9.3L
Minute CO2 = 9.3L/min x 5.08% = 0.47L/min
%CO2 change = 4.25% – 2.60% = 1.65%
Chen 23 Raw Data
Data 1 Raw data for the static lung volume of subject Harvinder.
Data 2 Raw data for the exercise hyperpnea of subject Timothy.