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1 The Human Respiratory System Mary McKenna Lab Partners: Jennifer Daciolas-Semon Veronika Mach Colette Roblee TA: Pearl Chen NPB 101L Section 1 November 25, 2014

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The Human Respiratory System

Mary McKenna

Lab Partners: Jennifer Daciolas-Semon

Veronika Mach Colette Roblee

TA: Pearl Chen

NPB 101L Section 1

November 25, 2014

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Introduction

The average human will typically breath in and out at a rate of 22,000 times per day.

Although the act of breathing is an unconscious doing, the respiratory system allows for this gas

exchange between an organism and its environment. The respiratory system is a tightly governed

bodily process and has multiple processes in order to keep the body functioning properly

(Douglas & Haldane, 1909, pg. 420). In this experiment, multiple factors of the respiratory

system were looked into. Specifically, measuring lung volume, the effects of inspired gas

composition and lung volume on respiration, and exercise hyperpnea.

In order to understand the experiment at hand, the basic physiology of the human

respiratory system must be stated. Respiratory itself is defined as the act of obtaining oxygen

from the environment and eliminating carbon dioxide from the body. The key organs involved

are the lungs, which are composed of the respiratory passages, gas exchange surfaces, and

pulmonary circulation (Sherwood, 2013, pg. 457). There are two types of respiration; internal

and external. Internal involves the intracellular metabolism in mitochondria and the making of

ATP. External is the main type of respiration that was tested in this experiment and is the

exchange of oxygen and carbon dioxide. There are two main stages comprising external

respiration. The first being the most simple – breathing. The second includes the alveolar gas

exchange, which is the exchange of oxygen and carbon dioxide between gas in the alveoli and

blood in the pulmonary capillary. Alveoli are small, air-filled, thin-walled sacs where gas

exchange occurs. They are surrounded by capillaries and increase the surface area for exchange.

They are made of two types of cells. Type II cells secrete pulmonary surfactant that decreases

surface tension, preventing collapse of the lungs. Type I cells are very thin so gases can diffuse

through them easily. The method leading gas exchange is easily explained by the gradient in

pressure between the alveoli and the atmosphere. This provides the force to move air in and out.

Although this process appears to be relatively clear, respiration can be affected by various

factors. For the purpose of this experiment, a term that will be used often is ventilation. This is

normally expressed as an amount of time. For example, minute ventilation is the amount of gas

moved in and out of the lungs in one minute and is well controlled in a normal resting individual.

Now that there is an understanding of the major elements in respiration, there are three

parts of the experiment that test different mechanisms. The first deals with measuring static lung

volume by measuring four different volumes of air. There is a subject’s tidal volume (normal

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volume of entering and exiting air), the inspiratory reserve volume (additional volume above the

tidal volume), the expiratory reserve volume (air forcefully expired), and the residual volume

(the small amount of air left in the lungs). The vital capacity is the volume that best represents

our breathing range, and is found by adding together the volumes mentioned above. The

justification behind this portion is to determine which volumes exhibited large or small amounts

and to examine the reasons for the differences. The second aspect of this experiment was to

observe the differences between normal breathing, re-breathing, hyperventilation, and the effects

of lung volume on respiration. These exercises were done to examine the effects of altered

alveolar gases respiration. It was expected that hyperventilation would prove to be the best

option to have a longer duration of breath-hold. To examine the effects of exercising causing an

increase of respiration, the last part of the experiment dealt with exercise hyperpnea. These three

tests together provide an overall understanding of the mechanics of the human respiratory system

in regards to how it deals with carbon dioxide and additional environmental factors.

Materials and Methods

The tools and detailed procedures can all be found in the NPB 101L Physiology Lab

Manual 2nd Edition written by Bautista & Krober. The instruments that were needed included the

disposable cardboard mouthpieces, nose clip, spirometer, plastic bags, an exercise bicycle, and

the BioPac system to use for analysis. In all three parts of the experiment, the subject had to wear

a nose clip and breath into a disposable mouthpiece to capture the expelled air. Minute

ventilation and alveolar ventilation were the first values calculated and recorded. The following

values that were recorded were the percent of carbon dioxide before breath-hold, after breath

hold, and how long the duration of the breath hold was. The duration of breath hold in normal

expiration/inspiration and forced inhalation/exhalation was additionally recorded. It is important

to note that in all aspects of the second part of this experiment, the subject was given a minimum

of 2-3 minutes to recover between each breathing type. When using the exercise bike, the

increased workload was recorded along with the carbon dioxide expired. The workload started at

0 pKa and increased by 0.5 every two minutes until a final workload of 2 pKa was reached. All

the BioPac systems were calibrated prior to the beginning of testing and there were no

experimental changes that differed from the lab manual.

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Results

Part 1. Measuring Static Lung Volumes

To test static lung volume, the subject was required to use a nose clip and breath into a

mouthpiece that was connected to a spirometry station and the BioPac system. The program was

calibrated at the appropriate levels and the subject breathed normally and then had to inhale and

exhale deeply. During this time, the subject appeared to be calm and collected to guarantee there

was consistency in his normal breaths. As the data recorded, there was a large peak from the

normal breath from the inhalation, along with a large drop from the exhalation. The inspiratory

reserve volume (IRV) was calculated to be 1.62 L/min, the expiratory reserve volume (ERV) -

3.33 L/min, the tidal volume (TV) was 0.32 L/min, and the vital capacity (VC) was -1.43 L/min.

By using these values, the minute ventilation (VE) was analyzed to be 4.48 L/min. Since gas

exchange occurs only across alveoli and not the dead-space volume of the upper airways, this

amount needs to be removed in order to obtain the true value of alveolar ventilation. In order to

determine the dead-space volume, it had to be extrapolated because the weight of the subject was

not recorded. Instead, a weight of 165 lbs and height of 73 inches was used to do the

calculations. The alveolar ventilation (VA) was found to be at a volume of 2.5 L/min. These

values expressing the different static lung volumes can be seen in Table 1 and all calculations of

these can be found in the Appendix.

Table 1. Static Lung Volumes

Volume (L/min)

Inspiratory Reserve Volume (IRV) 1.62

Expiratory Reserve Volume ERV -3.33

Tidal Volume (TV) 0.32

Vital Capacity (VC) 4.48

Minute Ventilation (VE) 4.98

Alveolar Ventilation (VA) 2.5

L/min = Liters/minute

Part 2. Effects of Inspired Gas Composition and Lung Volume on Respiration

The results of this part of the experiment dealt with observing what happened to the

arterial pressure of carbon dioxide in the lungs by breathing into a bag or by hyperventilation.

One subject was used for the three different types of breathing conditions. The subject’s normal

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breath was first conducted and the last 20-50% of their air expired was collected in a bag and

contained 1.2% carbon dioxide. After a 56.5 second breath hold was done, the carbon dioxide

percentage increased to 3.6%. The next condition, which was the re-breathing exercise, soon

followed. After breathing in a bag for three minutes, the air in the bag had a measurement of

5.2% carbon dioxide. The subject then held their breath for 23.2 seconds, and the last 20-50% of

their air expired contained 5.5% carbon dioxide. The hyperventilation test was the next to follow

suit. The subject breathed deeply at their normal rate for four minutes and their percent carbon

dioxide before the breath hold was 3.6%. The subject was able to hold their breath longer, and

held it for 68.8 seconds and ended with have a carbon dioxide percentage of 2.7%. In table 2,

these varying carbon dioxide percentages and their corresponding durations of breath-hold can

be compared. Normal breathing had the largest increase in carbon dioxide and re-breathing had

the smallest. In hyperventilation, carbon dioxide percentage decreased and had the longest

duration of breath-hold. The relationship between ventilation type and breath hold can be seen in

Figure 1, and another relationship between ventilation type and percent carbon dioxide is

represented in Figure 2. Figure 2 clearly shows the dramatic rise of the percentage of carbon

dioxide before and after breath-hold, along with the decrease in carbon dioxide from

hyperventilation. After the subject was completely recovered from the two earlier challenges, the

effects lung volume on respiration was then observed. Table 3 shows the length of a breath hold

after four specific inhalations and exhalations. Each time the subject held their breath after a

specific effect, there was always a two-minute recovery period. The subject breathed normally as

a control for two minutes and held their breath after a normal inspiration for 51 seconds. The

subject then held their breath for 43 seconds after a normal expiration, for 79 seconds after a

forced inhalation, and for 32 seconds after a forced exhalation. Graph 3 shows this relationship

of static lung volume to breath hold.

Table 2. Percent Carbon Dioxide Before and After Breath Hold in Four Breathing Conditions: normal breathing, re-breathing, and hyperventilation.

Condition % Carbon Dioxide

Before Breath-Hold

% Carbon Dioxide

After Breath-Hold

Duration of Breath-

Hold (seconds)

Normal Breathing 1.2% 3.6% 56.6 secs

Re-Breathing 5.2% 5.5% 23.2 secs

Hyperventilation 3.6% 2.7% 68.8 secs

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Table 3. Duration of Breath Hold After Four Effects of Lung Volume: normal expiration, normal inspiration, forced inhalation, and forced exhalation.

Duration of Breath-Hold (seconds)

Normal Expiration 43 secs

Normal Inspiration 51 secs

Forced Inhalation 79 secs

Forced Exhalation 32 secs

Figure 1. The relationship between ventilation conditions (normal, re-breathing, and hyperventilation) versus the duration of breath-hold. Between each condition there was a three-minute rest period.

56.5  

23.2  

68.8  

0  

10  

20  

30  

40  

50  

60  

70  

Normal  Breathing   Re-­‐Breathing   Hyerventalation  Duration  of  Breath-­‐Hold  (seconds)  

Condition  

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Figure 2. The relationship between three ventilation conditions (normal, re-breathing, and hyperventilation) versus percent carbon dioxide before and after breath-hold. There is an increase of carbon dioxide percentage after normal breathing, and a decrease in carbon dioxide percentage after hyperventilation. Re-breathing had a relatively constant percentage of carbon dioxide. Part 3. Exercise Hyperpnea

The final aspect of this lab was to observe how exercise and the anticipation of it

influences respiration. At the beginning, the subject on the exercise bike did not breath heavily

and seemed to be relatively relaxed. As the workload increased, the subject began to breath more

forcefully and deeply. As seen in Table 4, and represented on Figure 3, in all ventilatory

responses there was a positive correlation with increased workload. These ventilatory responses

included tidal volume, respiratory rate, minute ventilation, percent-expired carbon dioxide, and

minute carbon dioxide. In comparing these, the greatest change in response was in the minute

ventilation. The minute ventilation at rest was 5.38 L/min, and increased to 32.48 L/min after a

workload of 2 pKa. Another notable response was minute carbon dioxide. The subject at rest had

a minute carbon dioxide reading of 0.36 L/min and amplified to 2.73 L/min after a workload of 2

pKa. The witnessed deep and faster breathing was also validated by the respiratory rate

increasing with the workload. The nature of all the curves in Figure 3 displays a linear

progression of change in response to workload.

1.2  

5.2  

3.6  3.6  

5.5  

2.7  

0  

1  

2  

3  

4  

5  

6  

Normal  Breathing   Re-­‐Breathing   Hyerventalation  

%  Carbon  Dioxide  

Condition  

%  Carbon  Dioxide  Before  Breath-­‐Hold  

%  Carbon  Dioxide  After  Breath-­‐Hold  

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Table 4. Ventilatory Responses from an Increase in Workload from Exercise. Workload increased in increments of 0.5 starting from 0 pKa and ending at 2.0 pKa. Respiratory responses include tidal volume (TV), respiratory rate (RR), minute ventilation (VE), percent-expired carbon dioxide (FECO2), and minute carbon dioxide.

Workload

(pKa)

TV (L/sec) RR

(Breaths/min)

VE (L/min) FECO2 (%) Minute CO2

(L/min)

Rest 0.38 14 5.38 6.6 % 0.36

0.0 0.50 24 11.95 6.8 % 0.81

0.5 0.61 20 12.1 6.9 % 0.84

1.0 0.69 20 13.76 7.0 % 0.96

1.5 0.85 26 22.2 7.7 % 1.71

2.0 1.16 28 32.48 8.4 % 2.73

L/sec = Liters/second; Breaths/min = Breaths/minute; L/min = Liters/minutes

Figure 3. The Relationship between Ventilatory Responses versus Increase in Workload during Exercise. Workload increased in increments of 0.5 starting from 0 pKa and ending at 2.0 pKa. Respiratory responses include tidal volume (TV), respiratory rate (RR), minute ventilation (VE), percent-expired carbon dioxide (FECO2), and minute carbon dioxide.

0  

5  

10  

15  

20  

25  

30  

35  

0   0.5   1   1.5   2  

Change  in  Response  

Workload  pKa  

TV  (L/sec)  

RR  (breaths/min)  

VE  (L/min)  

FE  CO2  %  

Minute  CO2  (L/min)  

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Discussion

There are several mechanisms that respond to various stimuli when placed on the lungs.

The intent of this study was to isolate these specific stimuli and observe what relationships

happen to these respiratory responses. We demonstrated the effects of static lung volumes, the

different durations of breath-hold following normal breathing, re-breathing, and hypertension, as

well as exercise hyperpnea.

Before the data is analyzed, let’s first recap the events that happen in respiratory

physiology. As stated previously, alveoli are the sites of gas exchange specifically in the Type I

cells. The pressure between the alveoli and the atmosphere creates a gradient that provides the

force to move air in and out. This process follows Boyle’s Law, which states that at constant

temperature, pressure is inversely related to volume (Sherwood, 2013, pg. 463). So as pressure

increases, volume decreases and vice versa. For the lungs, intra-pleural pressure is always below

intra-alveolar pressure, so the gradient always exists. If the intra-alveolar pressure is less than

atmospheric pressure, air will go into the lungs. If this pressure is greater than atmospheric

pressure then air will exit the lungs. The first portion of this experiment dealt with the various

volumes that the lungs can hold. The subject was a male who was roughly 165 lbs and 73 inches.

The calculated vital capacity was 4.48 liters. The tidal volume was at a normal level of 0.32

liters. When comparing the IRV and ERV, the ERV resulted in a larger volume ejected. This

could be because if there were more force exhibited to remove air, the air that would normally

stay in the dead space would also become expelled. Conversely, inhaling air above the tidal

volume is more difficult because there is already air that remains in the lungs. In another study

focused on lung volume, the body provides mechanisms to prevent over inflation (Albaiceta et

al., 2008). This could be another reason to why in this experiment exhalation had a larger volume

than inhalation. However, this is not to say that someone can fully deflate his or her lungs. The

principle reason to why we can never completely deflate our lungs is that otherwise the lungs

would collapse.

Continuing onto the next portion of the experiment, this dealt with the aspects of the

interactions of carbon dioxide and the duration of a breath-hold. The two key regulators in

noticing changes in pressure are the central and peripheral chemoreceptors. The central

chemoreceptors input into the respiratory control centers and are the major driver in ventilation

rate. More specifically, they respond to changes in partial pressures of carbon dioxide. Peripheral

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chemoreceptors are a last resort to maintain breathing, they respond when the partial pressure of

oxygen falls below normal levels (60 mmHg). During normal breathing, an increase of carbon

dioxide was seen after the subject held their breath for around 56 seconds. The amount of carbon

dioxide actually doubled from the start of the hold to the end. Hypoventilation, or re-breathing, is

breathing too slowly. The partial pressure of carbon dioxide increases to above normal and the

partial pressure of oxygen decreases below normal. The results showed that the amount of

carbon dioxide relatively stayed the same; it just had a minor increase. There was 5.12 % of

carbon dioxide at the beginning of the breath hold, and 5.5 % carbon dioxide at the end.

However, it is important to mention that the duration of the breath-hold was dramatically shorter

than in normal breathing, it was 23 seconds. Even though the amount of carbon dioxide didn’t

largely increase, it still was higher in levels than oxygen, thus shorting the ability to hold breath

for longer. The same result is found in a study about hypoventilation and also used a bag to

breath in from. It was found that when a subject was rebreathing their same air, carbon dioxide

accumulated and eventually increased its overall pressure (Domnik et al., 2013, pg. 361-369). On

the contrary, hyperventilation is breathing too quickly. This is when the partial pressure of

carbon dioxide decreases to below normal and the partial pressure of oxygen increases to slightly

above normal. It was hypothesized that this condition would allow the subject to hold their

breath for longer – and it did. The subject was able to hold their breath for about 69 seconds,

which is more than the normal breathing and almost triple the time than that of hypoventilation.

The second aspect of this part of the experiment involved the effects of lung volume on

the duration of breath-hold instead of carbon dioxide. Expiration and inspiration were the two

conditions that were tested. Inspiration is the act of breathing in, and is always an active process.

The diaphragm contracts and pulls down to increase vertical length or thoracic activity. The

external intercostal muscles elevate the ribcage and increase horizontal volume of thoracic

activity. Expiration is breathing out, and is a passive process. It is normally due to the elastic

recoil of the diaphragm and the relaxation of the intercostal muscles. The results showed that

forced exhalation had the shortest breath-hold at 32 seconds, then normal expiration at 43

seconds, followed by normal inspiration at 51 seconds, and finally forced inhalation being the

longest at 79 seconds. Since forced inhalation is largely an active process, there was an ample

amount of oxygen to prolong the breath-hold, so these results were expected.

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Exercise hyperpnea was the last item to be investigated in the experiment. Hyperpnea is

the increase in ventilation that corresponds to an increase in metabolic activity. Typically in the

event of hyperpnea, it will occur in two phases. The first phase involves a rapid ventilation

increase in response to exercise. The second is when the exercise is maintained at a certain level,

the increases become slower. Overall, the ventilation rate matches the demand for carbon dioxide

removal, and there isn’t a decrease in carbon dioxide pressure. Our results indicate that all

ventilatory responses as mentioned in Table 4 showed to increase in regard to an increase of

workload. However, this does not fall in line with the typical ventilatory response during

exercise. FECO2 should have remained constant, but our data indicates a steady linear increase as

seen in Figure 3. Another trend that is seen is the Herring Breuer reflex. In the event that the

lungs will try to expand more during exercise, the Herring-Breuer reflex is initiated. This is a

reflex that is enlisted to prevent the over-stretching of the lungs. The reflex is caused when

pulmonary stretch receptors indicate that an over inflation is occurring. In this lab, the tidal

volume is increasing, but not that much. The workload was getting intensely higher however the

normal volume of breathing in and out stayed relatively the same. Another crucial thing to

mention is that there was a steady increase of minute carbon dioxide. This is because exercise

increases the demand for oxygen and produces more carbon dioxide as a consequence. Carbon

dioxide will actually become more prevalent in the blood in order for more oxygen to be able to

go directly to the tissues. The results of the minute ventilation showed that it increased with

workload, and it was similar to another study examining the effects of hyperpnea. This study,

which intended to mimic hyperpnea, found that with exercise, minute ventilation increased in a

linear fashion (Dominelli et al., 2014, pg. 15-23), which can be also explicitly seen in the

observed data from our experiment and represented in Figure 3. Overall, this last portion of the

experiment shows how with vigorous exercise, total carbon dioxide pressures increase along

with respiratory rate in order to try to create more oxygen available throughout the body

compared to that of a body at rest.

Beyond the scope of this experiment there are a couple of outstanding questions that

should be addressed. One deals with the most efficient way to increase alveolar ventilation. The

best mechanism would be to increase the tidal volume since this would reduce the proportion of

each breath occupied by anatomical dead space. Another way that it could be increased is by

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raising the respiratory rate. Based on the trends in Table 4, our results show that with in increase

of respiratory rate there was an increase in alveolar ventilation.

Another thing to indicate is the potential errors that could have made an impact on the

data. A major error was that the height and weight of the subject was never recorded so both of

these numbers were based off of pure observation. Due to this approximation, it could explain

the reason why in Table 1 the vital capacity is larger than the minute ventilation. The vital

capacity in theory should be larger since it is the normal breathing range. The equation to

determine vital capacity involved both the height and weight, two values that were never

recorded, thus resulting in error. A last error, which could be negligible, is that the subject on the

bike dropped the mouthpiece at once point and caused the data to be skewed for about ten

seconds. However, other than these error mentioned above, the other values that were recorded

were on track.

The experiments in this study allowed for the investigation of the human respiratory

system. Expiratory reserve volume proved to encompass a greater volume than the inspiratory

reserve volume. This is what was hypothesized since the act of exhalation is a passive process

that allows the muscles to relax to resting position instead of the being forced to expand in the

case of inhalation. In the breathing exercises, hyperventilation was thought to allow for the

pressure of oxygen to increase and for the percentage of carbon dioxide to decrease. This proved

to be true and can be viewed in the numerical decrease of carbon dioxide along with the increase

duration of breath-hold. During exercise, an increase in workload caused an increase of

ventilatory responses, all of which were mentioned above. Minute ventilation had the most

significant increase as expected since it is directly proportional to the amount of oxygen and

carbon dioxide consumed. Further studies examining the potential effects of long term endurance

athletes and their minute ventilation could be done since it is common for these types of people

to exhibit a lower minute ventilation in response to strenuous activity. Although the act of

breathing goes unnoticed, it is proven to be a complex system that has specific responses geared

for changes in pressures, pH, and workload. All of which aid humans in various activities such as

exercise, blowing out candles on a cake, or just having the ability to take a breather at the end of

the day.

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References

Albaiceta, G., Blanch, L., & Lucangelo, U. (2008). Static pressure–volume curves of the

respiratory system: Were they just a passing fad? Current Opinion in Critical Care, 80-86.

Bautista, E., & Korber, J. (2009). The Human Respiratory System. In NPB 101L: Physiology

Lab Manual (2nd ed.). Ohio: Cengage Learning.

Dominelli, P., Render, J., Molgat-Seon, Y., Foster, G., & Sheel, A. (2014). Precise mimicking of

exercise hyperpnea to investigate the oxygen cost of breathing. Respiratory Physiology &

Neurobiology, 201, 15-23.

Domnik, N., Turcotte, S., Yuen, N., Iscoe, S., & Fisher, J. (2013). CO2 rebreathing: An

undergraduate laboratory to study the chemical control of breathing. AJP: Advances in

Physiology Education, 361-369.

Douglas, C. G., & Haldane, J. S. (1909). The regulation of normal breathing.The Journal of

physiology, 38(5), 420-440.

Sherwood, L. (2013). The Respiratory System. In Human physiology: From cells to systems(8th

ed.). Pacific Grove, Calif.: Brooks/Cole.

     

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Appendix

Normal Breathing: Inhale/Exhale

Normal Breathing, Re-Breathing, Hyperventilation

Exercise Hyperpnea Sample Calculations: Minute Ventilation VE = TV x RR = 0.32 L x 15.57 breaths/min = 4.98 L/min

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Alveolar Ventilation VDS = DS x RR VA = VE – VDS = 165 x 15.57 breaths/min = 4.98 L/min – 2475 mL = 2475 mL = 4980 mL/min – 2475 mL = 2505 mL/min = 2.5 L/min Minute CO2 Minute CO2 = VE x average end tidal CO2 = 5.38 L/min x 6.6 % = 0.36 L/min Respiratory Rate RR = # breaths in 30 seconds x 2 = 7 breaths/30 sec x 2 = 14 breaths/min