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Properties of the Human Respiratory System

Kimberly Kavanaugh
Group: Cannon
Group Members: Harley Brinkman, Vickie Wong
Section 6
TA: Staci Cates
May 23, 2014

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Introduction
The human respiratory system is, without a doubt, the most vital part of the body.
The basic definition of respiration is the exchange of gas between the body and the
environment. The chief function of respiration is to supply the cells of the body with
needed O2 and eliminate CO2 produced during cellular respiration (Sherwood 2010, p.
461). Respiration can be split up into two components: internal and external respiration.
Internal respiration is what the cells throughout the body undergo while they are using
and producing different gases. External respiration is defined as gas exchange between
the alveoli in the lungs and the environment, or, better known as, breathing. The focus
of this experiment was on pulmonary ventilation, or, the movement of air in and out of
the lungs. In the few parts of this experiment, the effects of lung volume on breathing
were observed in different ways. For example, the subject was asked to perform various
types of breathing, asked to hold her breath, and also, exercise on a stationary bicycle.
From these tasks, the CO2 given off from the exhalation was analyzed.
There are many different components to the respiratory system, including: the
nose, mouth, pharynx, larynx, trachea, bronchi, lungs, respiratory muscles, and the
alveoli. The alveoli are sac like structures on the lungs and they interact with the
surrounding blood to regulate respiration. Respiration depends largely on the
relationship between atmospheric and intra-alveolar pressures. When the pressures
between the two differ, air will flow down its pressure gradient. Inspiration results when
atmospheric pressure is greater than that of the alveoli, and expiration occurs if
atmospheric pressure is lower. Analogous to that, partial pressure gradients promote
gas exchange between the blood and alveoli.

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Something referred to a lot in ventilation is a term called minute ventilation, or,


the amount of gas moved in and out of the lungs in a minutes time. Some other
components of ventilation include: Total Lung Capacity (TLC), Functional Residual
Capacity (FRC), and Vital Capacity (VC). Each of these is made up of a different
combination of Tidal Volume (TV), Inspiratory Reserve Volume (IRV), Expiratory
Reserve Volume (ERV), and Reserve Volume (RV). For the purposes of this lab, we will
focus on tidal volume, inspiratory reserve volume, expiratory reserve volume, and vital
capacity. VC is defined as the maximal amount of air one can breathe in or out. TV is
known as normal breathing, IRV is known as the volume of air one can inhale after
having already inhaled normally, ERV is similar to IRV except it applies to exhalation,
and lastly, RV is the amount of gas that is left in the lungs after forced exhalation. This
reserve volume is the reason that we cannot completely deflate our lungs; there is
always that small amount left inside.
Our hypothesis for the first part of this lab was that the higher the lung volume
was, the longer the duration of a breath-hold would be. To examine whether lung
volume contributes to breath-hold duration, the subject conducted variations of
breathing exercises followed by timed breath-holds. It was expected that the larger the
lung volume would result in a longer breath-hold. We also thought that as the CO2
concentration built up in the lungs, the subject would not have been able to hold her
breath for as long. For the exercise part of the lab, we hypothesized that as the
workload increased, the subjects CO2 production would increase as well. In order to
test this, the subject rode a stationary bicycle while breathing into a mouthpiece. This
mouthpiece was hooked up to a CO2 analyzer and the results were obtained via the

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student BioPac system. We expected to see the tidal volume and respiratory rate
increase as well as the minute ventilation and minute CO 2.
Materials and Methods
Specific details regarding the procedure for this lab can be found in Bautista and
Korbers lab manual (Bautista, Korber 2009, pp. 57-62). For this experiment, it should
be noted that for the duration of the lab, the subject had to wear a nose clip. There were
3 separate parts to this lab. Part 1 measured static lung volumes. In short, the subject
was instructed to breathe normally into a mouthpiece and then inhale as deeply as
possible. Afterwards, the subject was told to breathe normally again, and, this time,
exhale as deeply as possible. These steps provided data from which we could read the
inspiratory reserve volume, expiratory reserve volume, tidal volume, and vital capacity.
Part 2 of the experiment examined the effects of inspired gas composition and
lung volume on respiration. This part was split up into 4 different sections: normal
breathing, re-breathing, hyperventilation, and effects of lung volume on respiration.
Sections 1-3 looked at gas composition. During normal breathing, the subject was told
breathe normally and then exhale the last half of the tidal breath volume into a prepared
rubber bag. Next, the subject took a deep breath and held it for as long as possible and
followed the above procedure to exhale into a second rubber bag. The CO 2 composition
in each bag was then measured and recorded.
In re-breathing, the process was similar to before, but this time a large plastic
bag was inflated with atmospheric air and the subject breathed normally into it for 3
minutes. Afterwards, the subject followed the same exhalation procedure as before into
another rubber bag. The CO2 content in both bags was then analyzed and recorded.

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The hyperventilation part of the experiment was the same as normal breathing;
however, the subject was instructed to breathe deeply at a normal rate. The end-tidal
gas (after breathing normally) and end expired gas (after breath-hold) were captured in
the rubber bags and analyzed as before. In the last section of part 2, we looked at the
effects of lung volume on the duration of a breath-hold. The subject was told to breathe
normally and then hold her breath after a normal inhalation. This breath-hold was timed
and then repeated for normal exhalation, forced inhalation, and forced exhalation. Each
one was timed and recorded in the lab manual.
Finally, part 3 of the experiment looked at the subjects respiration during
exercise. To start, the subject was instructed to breathe normally, and then proceed to
start exercising. The subject rode a stationary bicycle while breathing into a mouthpiece
that was hooked up to a CO2 analyzer. Another group member increased the bicycle
resistance. The tidal volume, respiratory rate, minute ventilation, end tidal CO 2, and
minute CO2, were all measured and calculated.
Results
Raw data from this experiment can be found in the appendix of this paper.
Appendix 1 shows static lung volumes and Appendix 2 shows the exercise data at 2.0
kPa. This data point was selected because that is when respiration really started to
increase.
In part 1, static lung volumes were measured for our subject. After having the
subject perform normal breathing cycles followed by a deep inhalation and a deep
exhalation, we found the IRV, ERV, TV, and VC. We noticed that TV was the lowest
capacity (0.558 Liters), and that VC was the largest capacity (3.424 Liters). These

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values, plus ERV and IRV, can be found in Figure 1 below. VC was obtained by taking
the sum of these three values. TV, ERV, and IRV were all obtained via the student
BioPac software.
4.0
3.5
3.0
2.5

Liters

2.0
1.5
1.0
0.5
0.0
IRV

ERV

TV

VC

Lung Volumes
Figure 1: Static Lung Volumes measured in liters. IRV (Inspiratory Reserve Volume),
ERV (Expiratory Reserve Volume), TV (Tidal Volume), VC (Vital Capacity). VC= IRV +
ERV + TV. Each of the subjects lung volumes was obtained by breathing into a
mouthpiece hooked up to the student BioPac system.
In part 2 of the experiment, we looked at what effects CO 2 composition and lung
volume had on respiration. In sections 1-3, the subject exhaled end-tidal gas and endexpired gas into two separate rubber bags for each condition. Afterwards, the CO 2 was
analyzed, yielding various percentages. The CO2 percentages were taken before and
after the subjects breath hold. Figure 2a displays the percent CO 2 composition for three
conditions (normal breathing, re-breathing, and hyperventilation). We noticed that the
percent CO2 was greatest during the re-breathing exercise (about 5%) and the lowest
during the hyperventilation exercise (less than 1%). The CO 2 percentage in both normal

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breathing and hyperventilation increased after the breath-hold, by 2.64% and 0.424%,
respectively. We saw that re-breathing did not have this same outcome; there was only
about a 0.18% increase for this condition. Throughout each step of this section, the
subject was instructed to take a deep breath and hold it for as long as possible. These
breath-holds were timed and recorded. We saw that normal breathing yielded the
longest duration of 30 seconds, and re-breathing yielded the shortest duration of 17
seconds (Figure 2b).
6.00%
5.00%
4.00%
3.00%

% CO2

2.00%
% CO2 Before Breath Hold

1.00%

% CO2 After Breath Hold

0.00%

Condition
Figure 2a: Percent CO2 composition of end-tidal gas before a breath-hold, and endexpired gas after a breath-hold for three conditions (normal breathing, re-breathing, and
hyperventilation).

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35
30
25
20

Seconds 15
10
5
0
Normal Breathing

Re-Breathing

Hyperventilation

Condition
Figure 2b: Duration of Breath-Hold, in seconds, following 3 different conditions (normal
breathing, re-breathing, and hyperventilation).
For the last section of part 2, we looked at how different lung volumes affected
the duration of the subjects breath-hold. The breath-hold was conducted under four
conditions: normal expiration, normal inspiration, forced inhalation, and forced
exhalation. Of the four conditions, the breath-hold after normal inspiration had the
longest duration of 35.33 seconds, and the breath-hold after forced exhalation had the
shortest duration of 13.11 seconds (Figure 3).

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Seconds

40
35
30
25
20
15
10
5
0

Condition
Figure 3: Duration of breath hold (seconds) after breathing under four conditions
(normal expiration, normal inspiration, forced inhalation, and forced exhalation).
In the final part of this lab, we analyzed a subjects CO 2 production during
exercise. Various components of respiration were measured through the CO 2 analyzer:
tidal volume, respiratory rate, minute ventilation, and fraction of expired CO 2. Minute
CO2 was calculated using minute ventilation and the fraction of expired CO 2. When
analyzing the data, we noticed a common trend amongst each of these factors. We
noticed that for the most part, as the resistance, or workload, of the bicycle increased,
respiration increased as well. Each of the figures below displays this basic trend
(Figures 4a-4e).

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2.50

2.00

1.50

Liters
1.00

0.50

0.00

Workload (kPa)
Fig
ure 4a: Tidal Volume (Liters). Measured while the subject was exercising on a stationary
bicycle. The subject breathed into a CO2 analyzer that was hooked up to the student
BioPac software system. During rest, the subject was instructed not to exercise or talk.
25.0

20.0

15.0

Breaths/Minute
10.0

5.0

0.0

Workload (kPa)
Figure 4b: Respiratory Rate (Breaths/Minute). Calculated by multiplying the number of
breaths in a 30 second time period by 2.

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50.0
45.0
40.0
35.0
30.0

Liters/Minute 25.0
20.0
15.0
10.0
5.0
0.0

Workload (kPa)
Figure 4c: Minute Ventilation (Liters/Minute). These values were obtained using the
breathing mouthpiece and student BioPac system.
7.0
6.0
5.0
4.0

Percent CO2 (% )
3.0
2.0
1.0
0.0

Workload (kPa)
Figure 4d: Fraction of Expired CO2 (FECO2).

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3.5
3.0
2.5
2.0

Liters/Minute for end-tidal gas


1.5
1.0
0.5
0.0

Workload (kPa)
Figure 4e: Minute CO2. Calculated by multiplying the minute ventilation (
average end tidal CO2 (FECO2).

) by the

Discussion
The purpose of this experiment was to observe the basic functions of the human
respiratory system. The two main factors observed were, the effects of lung volume and
gas composition on respiration, and how performing exercise affected the subjects
respiration. These experiments displayed the different lung capacities and breath-hold
durations under certain conditions. Breath-hold duration is affected by different
concentrations of CO2 and O2 in the blood and alveoli. Plasma PO2 is sensed by the
peripheral chemoreceptors located in the carotid and aortic bodies, and P CO2 is sensed
by central chemoreceptors in the medulla. While respiration is strongly influenced by
PCO2 and pH, in certain cases, a drop in plasma PO2 can also drive it. Peripheral
chemoreceptors will only respond to a drop in P O2 if the concentration falls below 60
mmHg (Sherwood 2010, p. 502). This lab centered on breath-holds and the changes in
PCO2 and PO2 in the alveoli. Our subject was a 120 lb., active female, measuring about 5
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feet 6 inches tall. It was expected that for all parts of the lab, the subjects breath be
held to the same level of discomfort for each one.
Part 1 of the experiment was intended to measure the subjects static lung
volumes. The results of this part can be seen in Figure 1 above. Notice that the values,
except IRV, are around the expected averages of .500 L for TV, 3.0 L for IRV, 1.0 L for
ERV, and 4.5 L for VC (Sherwood 2010, p. 479). IRV is the volume of air that can be
taken in after a normal inhalation. It is important in respiration because if a person
needs to tap into that for a deeper breath, the lungs can handle that extra volume
without being over-inflated.
Figures 2a and 2b above show the relationship between CO 2 changes and
duration of breath-hold. During normal breathing, the observed CO 2 percentage
increased after the breath-hold from 1.13% to 3.77%. This was to be expected because
of the partial pressure of alveolar CO2. The alveoli and the plasma are always trying to
equilibrate the CO2 between them. For example, if the PCO2 of the plasma was 46 mmHg
and the PCO2 of the alveoli was 40 mmHg, then the PCO2 in the alveoli would increase.
When there is a breath-hold, PCO2 is higher in the blood than it is in the alveoli, causing
the PCO2 in the alveoli to increase. Once the subject lets the breath out, there will be a
larger amount of CO2 expelled than before the breath-hold. This is illustrated by normal
breathing in Figure 2a. Our data shows low numbers for normal breathing and this could
be due to the fact that we were misusing or misreading the software. However, we still
saw the expected increase in PCO2 after the breath-hold.
In a study done by Ferrigno et al., competitive divers increased their lung volume
before a dive in order to achieve a longer breath-hold. They performed a technique

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called glossopharyngeal insufflation (GI), which basically allowed them to get more
oxygen into their lungs (Ferrigno et al., 2007, pp. 841-846). By performing this pumplike action of the cheeks and pharynx, the breath-hold would be able to last longer due
to the decreased alveolar concentration of CO2. They saw that after GI, each of the
divers lung volumes increased. Our subjects lung volume increased due to forced
inhalation, however if we were to perform GI, we could expect similar results leading to
longer breath-holds.
During the re-breathing exercise, the subject was breathing into a bag filled with
atmospheric air. By doing so, she was inhaling her own previously exhaled CO 2. The
CO2 percentages were expected to be high here because the subject was breathing in
more CO2 than O2. The CO2 concentration before and after the breath-hold did not differ
by much for this condition, only by 0.18% (Figure 2a). This result is logical because the
CO2 concentration in the bag was the nearly the same as the CO 2 concentration in the
subjects breath. For this condition, the subjects breath-hold was the shortest of the 3
conditions and lasted only 17 seconds. This was to be expected because there was a
higher alveolar CO2 concentration, which caused the subject to exhale the built up CO 2
and inhale fresh O2.
Finally, we observed the effects of hyperventilation on breath CO 2 content.
Hyperventilation occurs when the plasma PCO2 falls below that of the alveoli, and the
body attempts to compensate by increasing CO2 production by faster ventilation. It was
observed that the percent CO2 before and after the breath-hold did not differ by much,
only by 0.424% (Figure 2a). It is important to note that both of the percentages here are
much smaller than the two preceding experiments. This is because the subject was

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breathing deeply and quickly, thus, letting off more CO 2 than she was when she was
breathing normally. The quick, deep breaths push more CO 2 out of the lungs, which
causes the alveolar CO2 concentration to decrease. This decrease should allow the
subjects breath-hold to last for a longer period of time because there is less CO 2 built
up, resulting in a later inhalation. Our subject only held her breath for 28 seconds, which
was shorter than the breath-hold after normal breathing (Figure 2b). It is likely that she
was not exhaling as strongly or as quickly as would have been expected, so there could
have been more CO2 in her lungs, making the breath-hold shorter.
Tancredi and Hoge conducted a study in which they observed the effects of
breath-holds, hyperventilation, and inspired CO 2 on cerebral blood flow (Tancredi &
Hoge, 2013, pp. 1066-1074). Now, even though we did not look at blood flow in the
brain, their study still pertains to respiration and can be compared with our results of
breath-hold and hyperventilation. Tancredi and Hoge found that the percent CO 2 after
hyperventilation their subjects was the lowest of their conditions and that it had a 50%
increased ventilation rate (Tancredi & Hoge, 2013, pp. 1066-1074). This is analogous to
our findings where our hyperventilation percent CO 2 was considerably lower than that of
normal and re-breathing.
The last section of part 2 looked at the effects of lung volume on respiration.
There were four conditions: normal expiration, normal inspiration, forced inhalation, and
forced exhalation. Each condition required the subject to perform the same procedure of
breathing normally and then holding her breath. Forced inhalation was expected to be
the longest duration, followed by normal inspiration, normal expiration, and then forced
exhalation being the shortest. The breath-hold after forced exhalation was expected to

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be the shortest duration because the subject had already exhaled deeply and then held
her breath, leaving a smaller lung volume. When the volume of the lungs is small, the
likelihood of inhalation is greater than if the lung volume was closer to being full. The
breath-hold following forced inhalation was expected to be the longest because the
lungs would be fully stretched, which creates a larger lung volume, resulting in a longer
breath-hold.
As seen in figure 3, the breath hold after normal inspiration was the longest (35.3
seconds), followed by the breath-hold after forced inhalation (30.7 seconds). This result
deviates from the expectation of forced inhalation described above. It is likely that the
Herring-Breuer reflex was activated during forced inhalation, making the subjects
breath-hold shorter. The Herring-Breuer reflex regulates respiration and works to
prevent over inflation of the lung. When the lungs stretch to a certain point, pulmonary
stretch receptors activate this reflex sending action potentials to the inspiratory area in
the medulla, inhibiting inspiration (Sherwood 2010, p. 500). Inversely, as observed in
forced exhalation, when there is no stretch on the lungs, the stretch receptors do not
activate and the inspiratory center is not inhibited. This causes the subject to want to
inhale after the breath-hold. We saw this trend in our results. Our subjects breath-hold
after forced exhalation lasted only 13.1 seconds (Figure 3), and this was indicative of
the smaller lung volume, which caused the subjects inspiratory center to be activated.
Finally, we looked at how exercise affects respiration. While the subject was
exercising on a stationary bicycle, she was breathing into a mouthpiece that was
hooked up to a CO2 analyzer. The bicycle was set at a resistance of 0 kPa and was
gradually increased every 2 minutes. As the workload increased, the subject began to

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breathe harder. It was right around 2.0 kPa that the subject began to increase breathing
efforts to keep up with the bodys demand for more O 2 (Figures 4a-4e). There is a
theory that a reflex called the Exercise Pressor Reflex contributes to increased
ventilation during exercise. Kaufman and Hayes state that the reflex that sends signals
to the medullary center originates in the contracting skeletal muscle during exercise
(Kaufman & Hayes, 2002). This theory held true during our experiment. The trend we
observed was that the subjects ventilatory efforts generally increased throughout this
part of the lab. Throughout the experiment, for each workload, we saw a total increase
of about 1.1 liters for TV, 5 breaths/minute for respiratory rate, 27 liters/minute for
minute ventilation, and about 1.3% for the fraction of expired CO 2 (Figures 4a-4d). All of
these increases were to be expected due to the exercise pressor reflex performing its
role in the subject.
Fontana et al. observed respiratory rate during spontaneous breathing, modified
breathing, and exercise (Fontana et al., 2014, pp. 60-66). Our lab can be linked to the
exercise portion of this study. As in our lab, Fontana et al. used spirometry to analyze
their subjects respiration. After analysis, they found that the subjects tidal volume
increased and saw a slight increase in respiratory rate at the end of exercise (Fontana
et al., 2014, pp. 60-66). This is parallel to what we saw in our subject. Our respiratory
rate increased more compared to their slight increase of 0.6 breaths per minute.
Many people may think that, during exercise, since the body is utilizing more O 2
that the PO2 would decrease. Similarly, many may think that since the body is producing
more CO2 that the PCO2 would increase. However, neither of those statements is true; it
is actually the opposite. The concentrations of O 2 and CO2 in the plasma generally stay

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constant; they may increase or decrease, respectively (Sherwood 2010, p. 504). Lactic
acid, or H+, builds up during heavy exercise, so only those peripheral chemoreceptors
will respond with an increase in ventilation. The peripheral chemoreceptors activate in
response to an increase in H+ that was not generated by CO 2. The central
chemoreceptors cannot sense the plasma H+ because the blood-brain barrier is
impermeable to it. However, they can sense H+ that was already in the extracellular
brain fluid after the presence of CO2. Because the plasma CO2 and O2 concentrations
primarily remain constant, the main factor that affects respiration during exercise is
ones body temperature. As more energy is being produced, it is getting lost as heat in
the body. Even though we sweat, our body still needs to maintain an internal
temperature, so respiration aids in cooling the body down.
In summary, the subjects breath-hold durations supported the expected trends
with respect to the changes in CO2 and O2 concentrations. When alveolar CO2
concentration was lower, the subjects breath-hold lasted longer, and when the alveolar
CO2 concentration was higher, the breath-hold duration was shorter. Also, various lung
volumes provided insight as to how long a breath-hold would last. When the lungs were
smallest, the subject was more likely to inhale sooner than when the lungs were largest.
During the exercise it was seen that the subjects pulmonary ventilation increased.
Those findings supported the thought that as the workload increased, so would the
subjects ventilation. However, we did not know or predict that CO 2 and O2 levels remain
pretty constant throughout exercise. It was after doing more research that I learned
about these gas levels.

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References
Bautista, E., & Korber, J. (2009). Properties of Skeletal Muscle. NPB 101L Physiology
Lab Manual (2 ed.,). : Cengage Learning.
Ferrigno, M., Loring, S. H., O'Donnell, C. R., Butler, J. P., Lindholm, P., & Jacobson, F.
Transpulmonary pressures and lung mechanics with glossopharyngeal
insufflation and exsufflation beyond normal lung volumes in
competitive breath-hold divers. Journal of applied Physiology, 841-846.
Fontana, G. A. Respiratory rate assessments using a dual-accelerometer device.
Respiratory Physiology & Neurobiology, 191, 60-66.
Hoge, R. D., & Tancredi, F. B. Comparison of cerebral vascular reactivity measures
obtained using breath-holding and CO2 inhalation. Journal of Cerebral Blood
Flow & Metabolism, 33, 1066-1074.
Kaufman, M. P., & Hayes, S. G. The Exercise Pressor Reflex. Clinical Autonomic
Research, 12, 429-439. Retrieved May 20, 2014, from
http://link.springer.com/article/10.1007/s10286-002-0059-1
Sherwood, L. (2010). Muscle physiology.Human physiology: from cells to systems(7th
ed., pp. 461-507). Belmont: Cengage Learning.

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