HUMAN PHYSIOLOGY

LAB REPORT

ABCT2326

Respiration

Name: Cheung Chi Ming

Student Number: 23086215D
Program: Physiotherapy
Team member’s names:
Chau Cho Hin, Chen Hao, Cheung Chak Lam, Cheung Chi Kit
 Results
a) Atmospheric pressure=760 mmHg
b) Results sheet

Alveolar Gas Samples

Time to % CO2 % O2 PCO2(mmHg) PO2 (mmHg)
Breaking Point
(1) Normal Breathing - 1.28 18.97 9.73 144.17
(2) Breath holding after 36.00s 1.44 18.40 10.94 139.84
Normal breathing
(3) Breath holding after 53.05s 5.32 59.99 40.43 455.92
Breathing O2
(4) Hyperpnoea - 1.12 19.31 8.51 146.76
(5) Breath holding after 47.85s 3.12 14.21 23.71 108.00
Hyperpnoea
(6) Breath holding after 1 min and 9.07s 3.97 37.39 30.17 284.16
Hyperpnoea and breathing O2
Discussion

Basic concepts
When CO2 is breathed in, they enter the bloodstream by dissolving into plasma, binding to
hemoglobin and formation of carbonic acid. Carbonic acid formed will dissociate into H+ and
HCO3-, and the H+ ions will then lower blood pH, then stimulate the chemoreceptors in aortic and
carotid bodies. Carbonic acid can also diffuse into cerebrospinal fluid and lower its pH, so the
chemoreceptors in medulla are stimulated.

What can you observe by comparing the following data?

I) Experiments (1) and (2)

Based on experiments (1) and (2), the percentage carbon dioxide (CO2) and partial pressure of CO2
in alveolar air in experiment (1) is lower than that in experiment (2) by 0.16% and 1.21 mmHg
respectively, while the percentage oxygen (O2) and partial pressure of O2 in alveolar air in
experiment (1) is higher than that in experiment (2) by 0.57% and 4.33 mmHg respectively.

The independent variable in experiments (1) and (2) is breath holding. Breath holding prevents the
ex. of gas from the body
The higher partial pressure of CO2 in experiment (2) indicates that holding breath after normal
breathing would increase the CO2 concentration in alveolar air. During normal breathing, CO2
continuously produced from cellular respiration of somatic cells is transported to the lung by blood
through systemic and pulmonary circuit. Higher partial pressure of CO2 in blood in the network of
capillary membrane surrounding the alveolar membrane causes CO2 to diffuse from blood, passing
through capillary wall and alveolar wall, to the alveolar space. In breath holding, the air with higher
partial pressure and concentration of CO2 cannot be exhaled. The accumulated CO2 exhaled during
the first breath after breath holding contributes to the higher concentration and partial pressure of
CO2.

The lower partial pressure of O2 in experiment (2) indicates that holding breath after normal
breathing would lower O2 concentration. During normal breathing, O2 inhaled continuously
diffuses from the alveolar space, passing through alveolar wall and capillary wall, to the blood in
capillaries surrounding the alveoli down the O2 partial pressure gradient. As the somatic cells
continuously undergo cellular respiration, the O2 dissolved in blood eventually diffuses to the
somatic cells. Holding the breath stops the O2 supply from external environment due to no
inhalation, while the somatic cells continue to consume O2 from blood to undergo cellular
respiration. Therefore, the concentration of O2 in blood drops and the remaining O2 in alveolar air
with higher concentration further diffuses from the alveoli to blood, and the partial pressure and
concentration of O2 in alveolar air decrease. In the first breath after breath holding, the exhaled air
contains lower concentration and partial pressure of O2, so the partial pressure and concentration of
O2 in experiment (2) is lower than that in experiment (1).

By simply comparing experiments (1) and (2), no relationship between the gases and the breaking
point can be concluded, because experiment (1) does not involve breath holding.

II) Experiments (2) and (3)

Percentage CO2 in (3) is higher than (2) by 3.88%, while the percentage O2 in experiment (3) is
much higher than (2) by 41.59%. The partial pressure of CO2 and O2 in experiment (3) are both
higher than that in (2). Moreover, the time to breaking point of (3) is longer than (2) by 17.05s,
which is an increase of 47.4%. The independent variable is whether breathing O2 before breath
holding. Hence, the results indicate that breathing O2 can lengthen the time to breaking point.

During breath holding, somatic cells need to carry out cellular respiration, which consumes O2 and
gives out CO2, to produce energy. In experiment (3), the cells have more O2 supply as the subject
breathes O2 before holding breath, so there is more O2 for the somatic cells to carry out cellular
respiration continuously before taking another breath. As a result, more CO2 is produced and then
transported to the alveolar space through the bloodstream. In experiment (2), the somatic cells have
less O2 to continue the aerobic respiration when O2 concentration in blood is lowered during
continuous consumption of O2 by the cells. Less CO2 is produced from the aerobic respiration of
the somatic cells. The expired air therefore contains higher concentration and partial pressure of
CO2 in experiment (3). Furthermore, the time to breaking point in experiment (3) is longer, so there
is longer time for CO2 to accumulate to a higher concentration and partial pressure than that in
experiment (2).
The higher partial pressure of O2 in experiment (3) suggests that holding breath after breathing O2
will increase the O2 concentration in the alveolar air. When breathing in pure O2, the partial
pressure of O2 in alveolar space is much higher, steeper partial pressure gradient of O2 causes more
O2 to diffuse into the blood in pulmonary capillaries, when compared to normal breathing. The high
partial pressure of O2 in blood desensitizes the chemoreceptors in aortic and carotid bodies. The
desensitized chemoreceptors cause less or delayed signals to be sent to the external intercostal and
diaphragm muscles, so the time to breaking point in experiment (3) is longer than that in (2).
Percentage O2 remains high in experiment (3) as not all inhaled O2 enters the alveoli and
undergoes gas exchange in the alveoli. Pure O2 remained in the conducting passage mixes with the
exchanged gas during exhalation, the diluted O2 still has a higher concentration than experiment (2)
due to the pure O2 remaining in the conducting passage of the respiratory tract.

III) Experiments (2) and (5)

Partial pressure and percentage of CO2 in alveolar air in experiment (5) is higher than that in (2),
while partial pressure and percentage of O2 in alveolar air in experiment (5) is lower than that in
experiment (2). Time to breaking point in experiment (5) is longer than that in experiment (2) by
11.85s, which is a 32.9% increase. The independent variable between experiment (2) and (5) is
hyperpnoea, which is suggested to increase the time to break point.

Hyperpnoea, as known as deep breathing which increases the depth of ventilation, removes more air
from the lung. During hyperpnoea, frequent and deep breathing removes CO2 from alveolar space
by exhalation more rapidly, so the CO2 concentration and partial pressure in alveolar gas is
lowered. During breath holding afterwards, concentration and partial pressure gradient of CO2
between alveolar gas and blood in pulmonary capillaries become steeper, so the diffusion of CO2
from the blood to alveolar space is more rapid. Therefore, the CO2 concentration and partial
pressure in alveolar gas increases more rapidly. In the first breath after breath holding, the CO2
concentration and partial pressure is higher in experiment (5).

Time to breaking point in experiment (5) is longer than that in (2). The decrease in partial pressure
of CO2 inhibits the chemoreceptors in aortic, carotid bodies and medullar oblongata. Less action
potential is generated from the respiratory center in the medullar oblongata to external intercostal
and diaphragm muscles. The lower initial CO2 allows the somatic cells to have longer time to
produce CO2 in cellular respiration until the partial pressure of CO2 in blood reaches the threshold
which breathing is forcibly initiated. As a result, the time to breaking point in experiment (5) is
longer than that in (2).

In light of the longer time to breaking point in experiment (5), O2 concentration in the exhaled air
in (5) is lower than that in (2). During breath holding with a longer time to breaking point in
experiment (5), body cells have a longer time to consume oxygen for cellular respiration from
blood, so the concentration and partial pressure of O2 in blood drops. Thus, the O2 partial pressure
gradient down the gas in alveolar gas in blood to the blood in pulmonary capillaries becomes
steeper. O2 then diffuses from the alveolar gas to the blood in pulmonary capillaries more rapidly,
causing the lower concentration and partial pressure of O2 in the exhaled air in experiment (5).
 IV) Experiments (2), (3), (5), (6)

From the results, the time to breaking point in experiment (6) is the longest, followed by experiment
(3), (5) and finally (2). Both experiments (3) and (5) show a longer time to breaking point than
normal breathing in (2). Experiment (6) combines breathing O2 in (3) and hyperpnoea in (5),
eventually shows the longest time to the breaking point among these 4 experiments due to the
effects of both breathing O2 and hyperpnoea.

Breathing pure O2 can supply more oxygen for the somatic cells to carry out respiration, and also
significantly increase the O2 partial pressure in blood. The increase in O2 partial pressure in blood
desensitizes the chemoreceptors in aortic, carotid bodies and medulla oblongata. During breath
holding, cellular respiration continues, and the somatic cells continue to consume oxygen and
produce CO2 to produce energy for survival. Consider the hyperpnoea which lowers the CO2
partial pressure in blood, alveolar gas and cerebrospinal fluid, the chemoreceptors in the aortic,
carotid bodies and medulla oblongata are desensitized by the lower CO2 partial pressure. The
decrease in CO2 partial pressure and the increase in O2 partial pressure together give a combination
of inhibitory effects on the chemoreceptors in experiment (6). The least action potential from the
respiratory center in medulla oblongata is sent to the external intercostal muscles and diaphragm
muscles, so much longer time is needed for the action potential sent to the external intercostal
muscles and diaphragm muscles to be strong enough to force the subject to breath. Therefore, the
subject gives the longest time to breaking point in experiment (6).

Abnormality of the data

The subject of our group in this experiment has previously experienced pneumothorax condition,
the vital capacity of the subject is therefore lowered. As a result, he demonstrated a much shorter
time to breaking point in all the experiments. As the vital capacity of the subject is lower, the
amount of O2 in each breath of him is less than that of the normal person, less O2 is diffused to the
blood in pulmonary capillaries from the alveolar space, so the O2 partial pressure in blood
decreases and the chemoreceptors in aortic, carotid bodies and medulla oblongata are stimulated.
The respiratory center in medulla oblongata then sends more action potential to the external
intercostal muscles and diaphragm muscles, the subject then is forced to breathe in a shorter time,
and has the shorter time to breaking point.