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The Effect of Exercise on Homeostatic Mechanisms in the Respiratory and Cardiovascular Systems

Introduction:
A 2006 study conducted by the CDC confirmed that heart disease is the leading cause of death for
American men and women. Resulting in the deaths of over 630,000 people in 2006, heart disease is the
cause of about one quarter of deaths of American citizens each year (Kulas). These statistics may seem
daunting, but there are many things Americans can do to dramatically decrease their risk of heart disease.
One of the easiest is to exercise regularly. A study published in the British Medical Journal found that
moderate daily exercise can reduce the risk of heart disease by up to 50% (Story).
By performing experiments on individuals exercising, biologists can determine the most effective
ways to exercise, and ultimately help to prevent heart disease. Experiments involving exercise also help
biologists to understand the mechanisms that bring the body back to homeostasis after exercise. During
exercise, body temperature, carbon dioxide concentration, heart rate, blood pressure, oxygen saturation,
and oxygen concentration all change in some manner. A complete understanding of the mechanisms that
return these values back to homeostasis is key for studying how to exercise most efficiently, and
eventually how to help prevent heart disease.
The exercise physiology lab to be performed by Biology 142 students at Penn State University
demonstrates many of these mechanisms through measurements of body temperature, heart rate,
hemoglobin saturation, mean arterial pressure, carbon dioxide clearance, and oxygen consumption
(Waters). For this experiment, one may hypothesize that body temperature will increase during exercise
when compared to the resting temperature, and then will start to return back to the resting temperature
during the recovery phase.
The lab features two measurements related to the respiratory system: carbon dioxide clearance
and oxygen consumption. For the carbon dioxide clearance, it is expected that the carbon dioxide
clearance during exercise will be higher than the resting and recovery rates. Similarly, one can predict that
oxygen consumption will also be greater during exercise when compared to the resting and recovery
values.

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Additionally, three measurements involving the cardiovascular system are taken during the

experiment. These measurements are heart rate, hemoglobin saturation, and mean arterial pressure.
During exercise one can expect that heart rate will be higher than when the subject is at rest or recovering.
Mean arterial pressure can be expected to follow the same trend of having a higher reading during
exercise than when compared to the readings during rest and recovery. Finally, one may hypothesize that
hemoglobin saturation measurements will be lowest during exercise, and higher during rest and recovery.
In all instances mentioned above, the recovery data will be much closer, if not identical, to the resting
data than to the data taken during exercise.

Methods:
The Exercise Physiology lab experiment features three test subjects and a wide variety of
measurements spanning the respiratory and cardiovascular systems (Waters). Before the experiment takes
place, the subjects age, height, and weight are written down.
After the preliminary measurements are taken, the resting data must then be recorded. While
sitting on a chair at rest, the subjects heart rate and hemoglobin saturation are taken using the pulse
oximeter. The target exercise heart rate is then calculated from this initial reading. Next, the subject
breathes into the spirometer to get a measurement for their tidal volume. Afterwards, the subject then
breathes into the capnometer to get a measurement for respiration rate, exhaled tidal CO2, and exhaled
tidal O2. CO2 Clearance is then calculated using the formula:
!"#$%&' !"#$% !"#
!"# !!"#

x Tidal Volume x Respiration Rate. Likewise, the O2 clearance is measured using the

formula: (0.209

!"#$%&' !"#$% !"


!"# !!"#

) x Tidal Volume x Respiration Rate. Following the capnometer

measurements, the body temperature is taken using a thermometer. The final resting measurements are the
systolic and diastolic blood pressures, which are taken using a sphygmomanometer. Mean Arterial
Pressure is then calculated using the formula: 2/3(Diastolic Pressure) + 1/3(Systolic Pressure). After three

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minutes, each measurement is taken once again. These data points are used as control data to compare to
the exercise and recovery values.
The subject then begins the exercise phase. The subject begins by jogging at a 0% incline with the
treadmill set at 5 miles per hour. Every three minutes the incline is increased by 3%, and the
measurements involving the pulse oximeter, spirometer, and capnometer are taken. Blood pressure and
temperature are not measured while the subject exercises because it is too difficult to get an accurate
reading while they are moving. Once the subject reaches the calculated target exercise heart rate or is
uncomfortable moving forward, the exercise phase is ended. The subject then immediately sits down and
is tested using the pulse oximeter, spirometer, capnometer, thermometer, and sphygmomanometer.
Finally, the recovery measurements are taken. After three minutes of sitting, the same five
devices are used to record the same measurements. This process is repeated one more time after another 3
minutes.

Results:
Figure 1: The effect of exercise on heart rate
250
200
Subject 1

150

Subject 2

100

Subject 3

50
0
0

10

20

30

Results are based on the heart rate measured by the pulse oximeter during rest, exercise, and recovery.
Each subject was resting between minutes 0 and 3. Subject 1 was exercising between minutes 3 and 15,
and was recovering between minutes 15 and 21. Subjects 2 and 3 exercised between minutes 3 and 18,
and were recovering between minutes 8 and 24.

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In general, it appears the subjects heart rates stayed constant during rest. Then they rose rapidly

during the beginning of exercise, but the slope became less steep as time went on. During the beginning
of the recovery phase, the heart rate dropped rapidly, and then the slope became less steep once again.
The ending recovery heart rate was higher than the resting heart rate, but was much closer to it than the
exercise heart rate.

Figure 2: The effect of exercise on carbon dioxide clearance


12
10
8

Subject 1

Subject 2

Subject 3

2
0
0

10

15

20

25

30

The results are based on the exhaled tidal CO2 measurements taken by the capnometer. The CO2
clearance was then calculated using the CO2 clearance formula. The subjects rested, exercised, and
recovered in the same time frames as in Figure 1.
While the subjects rested, the CO2 clearance stayed constant. At the beginning of exercise, there
was a very sharp increase in CO2 clearance, followed by a much more mild increase for the rest of the
exercise period. The CO2 clearance then decreased sharply at the beginning of recovery, and again
followed a more mild slope for the rest of the recovery period back to the resting values.

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Figure 3: The effect of exercise on oxygen consumption


20
15
10

Subject 1

Subject 2
Subject 3

0
0

10

15

20

25

30

-5
-10

The results are based off the exhaled tidal O2 measurement obtained by the capnometer. The oxygen
consumption is then calculated from these values using the oxygen consumption formula. The subjects
rested, exercised, and recovered during the same time frames as in Figure 1.
Although the graph for Figure 3 is a little less reliable, some trends can still be observed. It seems
that oxygen consumption stays constant during rest, and then follows a large spike at the beginning of
exercise. It seems to fluctuate a bit during the actual exercise portion. Following the exercise, the oxygen
consumption started to decrease, though at different rates for each subject.

Figure 4: The effect of exercise on body temperature


Time (min)
Resting:

0
3
Immediately After Exercise:
Recovery:
3
6

Subject 1:
36.8
36.6
35.5
35.9
36.4

Body Temperature (C)


Subject 2:
36.2
36.1
36
35.9
36.5

Subject 3:
36.2
36.2
34.9
36.5
36.6

The results are based on measurements taken by a thermometer during different increments of time during
rest and recovery, and immediately after the subjects exercised.

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For the most part, the body temperature stayed constant during the resting period, and then

decreased during exercise. The temperature then began to increase during the recovery phase back to the
resting temperature, or even higher.

Figure 5: The effect of exercise on hemoglobin saturation


120
100
80
Subject 1
60

Subject 2

40

Subject 3

20
0
0

10

15

20

25

30

The results are based on measurements of the subjects hemoglobin concentration taken by the pulse
oximeter. The subjects rested, exercised, and recovered during the same time frames as in Figure 1.
Again, the trend is a little more difficult to see this time. It appears the hemoglobin saturation
stays constant during rest, and then gradually decreases during exercise. The hemoglobin saturation then
increases during recovery almost back to the resting value.

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Figure 6: The effect of exercise on mean arterial pressure


Time (min)
Resting:

0
3
Immediately After Exercise:
Recovery:
3
6

Mean Arterial Pressure (mmHg)


Subject 1:
Subject 2:
Subject 3:
75
87
87
75
80
80
90
103
103
90
97
90
82
97
83

The results are based on the systolic and diastolic pressures obtained by the sphygmomanometer. The
mean arterial pressures were then calculated and recorded using the mean arterial pressure formula.
During exercise, it appears that the mean arterial pressure increases by quite a lot. The mean
arterial pressure then decreases during the recovery phase, but does not quite reach the resting pressure.

Discussion:
After the experiment, it is evident that the hypothesis regarding heart rate is supported by data.
The readings taken for subject 3 created the smoothest graph and are most representative of the heart rate
trend, though it is important to note that all of the data taken supported the hypothesis. Subject 3s resting
heart rate was 83 beats per minute. At the end of exercise, their heart rate had risen to 188 beats per
minute. At the end of the recovery period, their heart rate had fallen to 114 beats per minute. As
predicted, the subjects heart rate during exercise was significantly higher than the resting value. In
addition, the recovery heart rate was also below the exercise heart rate, and much closer to the resting rate
than to the exercise rate. This is strong evidence for the hypothesis because the graph was very smooth
and followed a defined trend. A physiological explanation for the trends regarding heart rate can be
explained by the increased need for oxygen by muscles during exercise. Since blood carries oxygen to
these muscles, the heart must beat faster to supply the muscles with adequate oxygen. After the exercise is
over, the muscles do not need as much oxygen, so the heart rate is slowed.
The data regarding the carbon dioxide clearance was a little less reliable, but still mostly
supported the hypothesis. Again, subject 3s data seems to be the most representative of the effect of

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exercise on CO2 clearance, though all of the data follows the same trend. The resting CO2 clearance
value for Subject 3 was 2.32 L/min. At the end of exercise, it was 5.82 L/min, and at the end of recovery
it was 1.15 L/min. As predicted, the CO2 clearance was higher during exercise than during rest, and the
recovery value was lower than the exercise value, and very close to the resting value. However, the
recovery value ended up being lower than the resting value, which contradicts the hypothesis. This can be
attributed to the fact that the data was not very reliable. All three graphs featured sharp spikes and dips
that did not follow any conceivable trend, which indicates that the equipment may have been faulty.
Removing some of these spikes and dips would make the data much more reliable. A physiological
explanation for the CO2 clearance trend can be explained by metabolism. When humans exercise,
muscles need more energy in the form of ATP, so more must be produced. CO2 is a waste product of
ATP production. In order to maintain homeostasis, more CO2 must be exhaled by the respiratory system.
Once exercise is complete, less ATP and CO2 is being produced, so less CO2 is exhaled.
Again, the data for O2 consumption was slightly less reliable, but still mostly supported the
hypothesis. Subject 1 appeared to illustrate the clearest trend for these measurements. When resting,
Subject 1 registered an O2 consumption of 1.62 L/min, and registered 15.93 L/min when exercising. At
the end of the recovery period, a value of 10.48 was recorded by the capnometer. The hypothesis seems to
be supported because the exercise value was higher than the resting value, and the recovery value was
lower than the exercise value. However, the recovery value for O2 consumption was much closer to the
exercise value than the resting value, which contradicts what was predicted. Again, this can probably be
attributed to faulty equipment, since the data fluctuated so much, and even registered negative values,
which is impossible. The O2 consumption trends can also be explained using metabolism. While
exercising, muscles need to use ATP for energy. In order to create ATP, O2 must be consumed. In order
to make more ATP for exercise, more O2 must be consumed. When the body is not exercising, less ATP
needs to be produced, so less O2 is consumed.
Measurements taken for body temperature almost completely contradict the hypothesis made in
the introduction section. Subject 3s measurements appear to be the most constant and consistent, though

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all three follow the same trend. Subject 3 registered a body temperature of 36.2C when resting, 34.9C
after exercise, and 36.6C while recovering. The recovery body temperature was only slightly higher,
almost identical in fact, to the resting temperature, which is in accordance with the hypothesis. However,
what was not expected was that the exercise body temperature would be significantly lower than the
resting and recovery values. However, since the data is very consistent with all three subjects, the data
seems to be valid. An explanation for the decrease in temperature could be attributed to the fact that more
blood is needed at the extremities during exercise since more oxygen needs to be delivered to the muscles.
Since less blood is present in the core areas of the body, it makes sense that the core body temperature
might be lower. If the measurements were taken with a thermometer on the skin as opposed to under the
tongue, the data would probably follow the hypothesis more closely.
Unlike in the body temperature section, the hemoglobin saturation measurements support the
hypothesis. Again, all three subjects follow the same trends, but Subject 2s data is most representative.
Subject 2 began with a resting hemoglobin saturation of 100%, registered a reading of 94% during
exercise, and then recorded 96% during exercise. As expected, the hemoglobin saturation was lowest
during exercise, and was higher and considerably close to the resting value during the recovery phase.
Since the data for all three subjects followed the same trend with little variation, this data is likely to be
very reliable. Once again, these trends can be explained using metabolism. As stated above, muscles
require more oxygen during exercise. Since hemoglobin saturation is a measurement of how much
oxygen is bound to hemoglobin, it makes sense that less would be bound to hemoglobin during exercise
because the muscles would be using more. When the body is not exercising, the muscles demand less
oxygen, so more stays bound to hemoglobin.
After the experiment, it is clear that the hypothesis regarding mean arterial pressure is supported
by data. Subject 3s resting MAP was 80 mmHg, exercise MAP was 103 mmHg, and recovery MAP was
83 mmHg. The exercise MAP is clearly much higher than the resting MAP, and the recovery MAP is in
between the resting and exercise values, and very close to the resting value. Since the data for all three
subjects clearly follows the same trend, this data is reliable. A physiological explanation for this trend is

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illustrated by the muscles need for oxygen. During exercise, the heart has to beat faster and harder to
deliver enough oxygen to the muscles. This increases both the systolic and diastolic pressures, and results
in a higher mean arterial pressure. When the body is done exercising, the heart does not need to beat as
hard or as fast, so the MAP falls.
Overall, the lab went very well and was very informative. All of the students supported each other
and worked well as a team. It was a shame the capnometer equipment was not working correctly, as it did
make the data a little bit more difficult to analyze. However, everything else seemed to go as planned.

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References:
Kulas, Michelle. "Exercise & Heart Disease Statistics." Livestrong.com. Demand Media, Inc., 20 Aug.
2013. Web. 1 Dec. 2014.
Story, Colleen. "Can Exercise Reverse or Prevent Heart Disease?" Healthline. Healthily Networks, Inc.,
10 Apr. 2012. Web. 1 Dec. 2014.
Waters, John R., and Nanette J. Tomicek. Exercise Physiology. Physiology Laboratory Manual.
Plymouth: Hayden-McNeil Publishing, 2015. Print.