The  Human  Respiratory  System    

 

 

 

 

 

 

 

 

Joy Chen

Lab Partners: Harvinder Kaur

Nina Zai Marylee Banzon

NPB101L- SEC 09 TA: Phung Thai

19 Nov 2012

 

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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

 

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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.

 

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Table 1. Static lung volumes, in liters, for a female subject using a spirometer

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

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

Volume (L)

Inspiratory Reserve Volume (IRV) 1.06

Expiratory Reserve Volume (ERV) 0.89

Tidal Volume (TV) 0.59

Vital Capacity (VC) 2.68

 

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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

largest %CO2

before breath-hold

in re-breathing, then

normal breathing,

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-

Conditions

%CO2 Before

Breath-Hold

%CO2 After Breath-Hold

Change in %CO2

Duration of Breath-Hold

(seconds) Normal Breathing 3.71 5.43 1.72 29.5

Re-Breathing 6.56 6.24 -0.32 34.0 Hyperventilation 3.28 6.09 3.01 32.8

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.

 

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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

visually represents

the results in table

2. The bars for after

breath-hold are

taller than before

breath-hold in

normal breathing

and re-breathing,

visually showing the

increase in %CO2

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

results for each category are

shown in figure 2. As we

expected, the duration of breath-

3.71  

6.56  

3.28  

5.43  6.24   6.09  

0  1  2  3  4  5  6  7  

Normal  Breathing  Hyperventilation   Re-­‐Breathing  

%CO

2  Com

position  

Ventilation  Type  

Ventilaton  Type  vs.  %CO2  Composition  Before  and  Ater  Breath-­‐Hold  

Before  Breath-­‐Hold  After  Breath-­‐Hold  

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.

 

29.5  

34  32.8  

27  28  29  30  31  32  33  34  35  

Normal  Breathing   Hyperventilation   Re-­‐Breating  

Time  (seconds)  

Ventilation  Type  

Ventilation  Type  vs.  Duration  of  Breath-­‐Hold  

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.

 

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hold for hyperventilation was the longest, exceeding normal breathing by 4.5 seconds and re-

breathing by 1.2 seconds. However, re-breathing has the second longest duration for breath-

hold, which is not what we expected. As shown in figure 2, our subject had the shortest breath-

hold 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.

By looking at the table, it is clear that

breath-hold after inhalation is longer

than breath-hold after exhalation. Forced

inhalation has the longest duration of

breath-hold and forced exhalation has

the shortest duration of breath-hold. The

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.

Duration of Breath-Hold (seconds)

Normal Expiration 44

Normal Inspiration 68

Forced Inhalation 59

Forced Exhalation 39

Table 3. The data for the duration of breath-hold time, in seconds after normal expiration, normal inspiration, forced inhalation, and forced exhalation.

 

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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

more than three times greater

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

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,

Workload (kPa)

TV (liters)

RR VE (liters/min)

FECO2 (% CO2)

Minute CO2 (liters/min)

Rest 0.59 16 9.5 5.64 0.54 0.0 1.43 16 22.9 5.58 1.33 0.5 1.50 20 30.0 5.79 1.74 1.0 1.60 20 32.0 5.65 1.81 1.5 1.73 20 34.6 5.59 2.04 2.0 1.81 26 47.2 6.45 3.04

0  0.2  0.4  0.6  0.8  1  

1.2  1.4  1.6  1.8  2  

Tidal  Volum

e  (liters)  

Workload  (kPa)  

Workload  vs.  Tidal  Volume  

rest                      0                    0.5                      1                    1.5                  2.0                    

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  

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.  

 

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there is no change in

respiratory rate as illustrated

by the plateau between 0.5

to 1.5 kPa. At the end of the

experiment, when we

increased the workload to

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

396.8% increase in minute ventilation

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

0  

5  

10  

15  

20  

25  

30  RR

 (breaths/m

inute)  

Workload  (kPa)  

Workload  vs.  Respiratory  Rate  

             rest              0                    0.5                  1                1.5            2.0                    

0  

10  

20  

30  

40  

50  

Minute  Ventilation  (L/m

in)  

Workload  (kPa)  

Workload  vs.  Minute  Ventilation  

                       rest                  0                    0.5              1                  1.5              2.0                    

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.

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.  

 

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respect to workload. Figure 6 is a graph of the data from table 4, showing the %CO2 expired with

respect to workload. The data

we have of the %CO2 expired is

different from what we

expected to measure. We

expected the %CO2 to increase

with increase in workload. From

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.

5.4  5.6  5.8  6  

6.2  6.4  6.6  

FECO2  (%

)  

Workload  (kPa)  

Workload  vs.  FECO2  

                             rest                    0                    0.5                    1                      1.5                2.0                    

0  

0.5  

1  

1.5  

2  

2.5  

3  

3.5  

Minute  CO

2  (L/min)  

Workload  (kPa)  

Workload  vs.  Minute  CO2  

 rest                    0                        0.5                    1                        1.5                    2.0                    

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.

 

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.

 

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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

 

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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.

 

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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 intra-

alveolar 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

 

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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

 

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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

 

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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

 

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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, re-

breathing, 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 breath-

hold is corresponds to what we expected to see in the lab. The reason why %CO2 before breath-

hold 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 breath-

hold. 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

 

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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

 

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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,

 

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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

 

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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).

 

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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.

 

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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%

 

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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.