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Lab 4: The Human Cardiovascular System: Measuring the
Effects of Activity on Cardiovascular Properties and Function
Jana Wong
Group Members: Bryan Lairmore, Jessica Chang, Amanda Perez-Stires
TA: Nicholas Klug; Section 9
November 7, 2013
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INTRODUCTION
The cardiovascular system is a crucial part of the human body function, creating a never ending
cycle of nutrient transport to keep every cell alive. The cardiovascular system uses blood to transport
nutrients into tissues and waste out of tissues throughout the body via blood vessels. Blood vessels are
broken up into different types – arteries, arterioles, capillaries, venules, and veins. Through systemic
circulation, oxygen rich blood is carried from the heart, through the arteries which branch into arterioles,
then to capillaries, where nutrient and gas exchange can occur. After the exchange occurs, capillaries
then branch into venules and then to veins to allow blood to be carried back to the heart and go through
the pulmonary circulation to become oxygen rich once again. The heart utilizes the systemic and
pulmonary circulation to create a pressure system to pump blood through the body successfully
(Sherwood, 2010, p. 303). By measuring blood pressure, the pressure system that the heart creates can
be monitored for changes and abnormalities.
There are many circumstances in life that can cause changes in heart activity, ultimately altering
the pressure gradient that is created by the heart and its components. Many times, these changes in
cardiovascular properties are related to changes in the autonomic nervous system, particularly the
sympathetic and parasympathetic responses. Past studies have shown research linking the human
cardiovascular system with responses to changes in posture, physical activity, and temperature. In
postural changes, studies have shown that sympathetic activity is initiated in vertical postures
(Watanabe, Reece, & Polus, 2007) Other studies have shown that an increase in physical activity causes
an increase in skeletal muscle metabolic demand, stimulating sympathetic activity to increase heart
activity to meet the increased needs. Temperature can also be a factor in a survival response, activating
parasympathetic input causing a decrease in heart rate when receptors in the face sense cold water in
order to conserve oxygen (Jay, Christensen, & White, 2006, p. 199) Studies like these have shown that
various triggers can cause a change in cardiovascular behavior.
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In this experiment, changes in cardiovascular responses will be observed in different situations.
In posture change, it is expected that blood pressure and heart activity decreases when going from a
supine to upright position due to gravitational effects. Vasodilation in response to metabolites will be
observed and it is expected that when the arm is cuffed, the arm will lose its color and temperature, but
will return to normal once the cuff is removed. The different properties of the venous system will be
observed through occlusion of a vein to observe venous valves, inflation of a cuff on the bicep to
observe an increase in forearm circumference due to venous distensibility, and gravity effects on venous
return and congestion. The effects of exercise on cardiovascular properties will also be observed and it is
expected that increase in intensity of exercise will cause an increase in blood pressure, heart rate, etc.
Lastly, the dive reflex will be observed by having a student hold his/her breath in cold water and it is
expected that heart rate will decrease in this situation.
MATERIALS AND METHODS
Detailed procedures for each part of the experiment can be found in the second edition NPB 101L
Physiology Lab Manual compiled by Erwin Bautista and Julia Korber. There are six parts of this lab,
each with its own objective to be observed. In the first part of the lab, students practiced measuring
blood pressure on each other using a stethoscope and sphygmomanometer. This was done by inflating
the cuff to 180 mmHg and slowly releasing the pressure, listening for the first beat, correlating to the
systolic pressure, and the last beat, correlating to the diastolic pressure. This was done three times per
person, taking the average of the trials. This part of the lab has been omitted from this report. In the next
part, the subject was put in a supine position and tilted by one person instead of two as stated in the lab
manual, blood pressure was taking by two people but only the values from the left arm were used in data
analysis due to measurement errors. Biopac software was used to measure heart activity; from this, heart
rate was determined using an average of ten beats. In part three of the lab, the subject’s arm was cuffed,
he clenched his fist repeatedly with his arm above his head, and the cuff was inflated. After this, the cuff
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was ripped off and his arms were returned to the tabletop for observation. In part four of the experiment,
the subject did four separate studies. In the first, the subject held his arm above his head for one minute
and then returned his arms to the table for observations. In the next section, the subject held one arm
above his head and slowly lifted his other arm starting from his side and observers looked for a
protruding vein to collapse. In the next section, the subject’s arm was cuffed and inflated to protrude
veins further. A protruding vein was occluded and blood was pushed towards the heart and away from
the heart for observations. In the last section, the subject’s arm was cuffed, held over his head for two
minutes, and his forearm circumference was measured. After the measurement, the cuff was inflated to
20 mmHg and the procedures repeated; this was repeated for pressures of 30, 40, and 60 mmHg. In part
five of the lab, heart activity was recorded using the Biopac software while the subject pedaled on the
exercise bike at a constant rate and various workloads while two people measured blood pressure at
given times throughout the exercise. Heart rate was taking from the recorded heart activity from the
average of ten beats. P-T interval calculations have been excluded from this report. In the last part of the
lab, the subject first held her breath above a container of cold water for 30 seconds as a control trial and
then held her breath for as long as possible with her face in the container of cold water. Heart rate
activity during these trials was recorded with the Biopac software and heart rate was measured from an
average of three beats due to a heart rate being taken every five seconds (there were not ten beats
between every five seconds).
RESULTS
Part I: Measuring Blood Pressure – omitted from this report
Part II: Effects of Posture on Blood Pressure
In the next part, heart activity was recorded and blood pressure was measured from the left arm at
various times to see the effect of going from a supine position to an upright position had on blood
pressure and heart activity. Measurements were taken at the supine position, after the initial tilt, 30
5
seconds after the tilt and 2 minutes after the tilt. From blood pressure measurements and heart rate
measured by the Biopac program, MAP, PP, stroke volume (SV), cardiac output (CO), and total
peripheral resistance (TPR) were calculated. In the course of the experiment, blood pressure dropped
significantly from the supine position to the tilt, and rose back to about the starting measurements 30
seconds and 2 minutes post-tilt. Accordingly, MAP, PP, HR, SV, and CO saw the same trend –
measurements dropped at the tilt and then increased post-tilt, as seen in Figures 1-5. Conversely, TPR
increased at the tilt and then decreased post-tilt, shown in Figure 6. The experiment resulted in
unexpected outcomes with the pulse pressure decreasing 2 minutes post-tilt, as seen in Figure 2, instead
of increasing. This caused for unexpected values 2 minutes post-tilt in stroke volume, cardiac output,
and total peripheral resistance as well, shown in Figures 4-6, because the pulse pressure is a component
in calculating those values.
60
65
70
75
80
85
90
0 100 200 300
Mea
n A
rter
ial
Pre
ssu
re (
mm
Hg
)
Time (seconds)
Figure 1: Changes in Mean Arterial Pressure
(MAP) are plotted against time when the
subject is supine, after the initial tilt, 30
seconds post-tilt, and 2 minutes post-tilt.
25
30
35
40
45
50
55
0 50 100 150 200 250 300
Pu
lse
Pre
ssu
re (
mm
Hg
)
Time (seconds)
Figure 2: Changes in pulse pressure (PP) are
plotted against time when the subject is supine,
after the initial tilt, 30 seconds post-tilt, and 2
minutes post-tilt.
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Part III: Vasodilation in Response to Metabolite
In this part of the experiment, one arm of the subject was cuffed with the sphygmomanometer, the
subject clenched his fist 15 times, the cuff was inflated to 150mmHg, and then ripped off. Observations
were made before, during, and after cuffing the arm, as seen in Table 1. The arm and hand appeared to
be a pale pink color with veins protruding with a blue/purple color before cuffing and inflating. After
being cuffed, the arm lost all its color and warmth as it turned white and cold while the hand turned
yellow and the veins disappeared. After removing the cuff, the arm immediately regained a pink color
and the veins became more visible than before, and gradually regained its normal temperature.
60
65
70
75
80
85
0 100 200 300
Hea
rt R
ate
(B
PM
)
Time (seconds)
Figure 3: Changes in heart rate (HR) are
plotted against time when the subject is supine,
after the initial tilt, 30 seconds post-tilt, and 2
minutes post-tilt.
30
35
40
45
50
55
60
65
70
0 50 100 150 200 250 300
Str
ok
e V
olu
me
(mL
)
Time (seconds)
Figure 4: Changes in stroke volume (SV) are
plotted against time when the subject is supine,
after the initial tilt, 30 seconds post-tilt, and 2
minutes post-tilt.
2
2.5
3
3.5
4
4.5
5
5.5
6
0 100 200 300
Ca
rdia
c O
utp
ut
(L/m
in)
Time (seconds)
Figure 5: Changes in cardiac output (CO) are
plotted against time when the subject is supine,
after the initial tilt, 30 seconds post-tilt, and 2
minutes post-tilt.
12
17
22
27
0 100 200 300To
tal
Per
iph
era
l R
esis
tan
ce
(mm
Hg
/L/m
in)
Time (seconds)
Figure 6: Changes in total peripheral resistance
(TPR) are plotted against time when the subject
is supine, after the initial tilt, 30 seconds post-
tilt, and 2 minutes post-tilt.
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Table 1: Observations of the cuffed arm and control arm before cuffing, after inflation to 150mmHg,
and after removal of the cuff
Before Treatment (size
& contour of veins,
skin color,
temperature)
Cuffed and Inflated to
150mmHg (size &
contour of veins, skin
color, temperature)
After removing the
cuff (size & contour
of veins, skin color,
temperature)
Left Arm
and hand
(Control)
Skin is pale pink, cool-
warm to the touch (not
hot, not cold), hand is
pink in color. Veins
protrude from arm,
visibly blue/purple in
color.
No changes, arm not
cuffed (n/a)
No changes, arm not
cuffed (n/a)
Right Arm
and hand
Skin is pale pink, cool-
warm to the touch (not
hot, not cold), hand is
pink in color. Veins
protrude from arm,
visibly blue/purple in
color.
Entire arm turns white,
hand is yellow, veins
disappear, skin is
colder to the touch
Immediately after
removing the cuff, the
arm is flushed with
red/pink color, veins
come back and
become more visible
than in the left arm.
20 seconds after,
temperature is back to
normal.
Part IV: The Venous System
Next, the effects of gravity and venous congestion were observed by having the subject hold one arm up
straight above his head for one minute as displayed in Table 2. During the process, the arm loses color
and becomes white and the veins are less prominent and visible. After the arm is returned to the tabletop
level, it regains its pale pink color and the veins become more prominent compared to before the raise.
Table 2: Observations of the control arm and the arm being raised for 1 minute during the raise and after
returning to a normal position on the tabletop to see the effects of gravity and venous congestion.
During raise After – return both arms to
tabletop, palms side up
Left arm (at
side)
Skin is pale pink in color, veins
protruding and visible.
No changes
Right arm
(raised)
Skin becomes white in color,
veins not as visible.
Arm and hand regain color, veins
more prominent than before raise
In the next part, the effects of venous return are observed by having the subject hold one arm over his
head and slowly lifting the other arm up as seen in Table 3. While the arm is raised, the observed
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protruding vein disappears once it reaches the level of the heart. There were 5cm between the heart and
the point where the vein in the subject’s arm disappeared, equating to a pressure of 3.68mmHg.
Table 3: Observations of the veins in one arm being raised slowly while the other arm stays raised
above the head to see the effects of venous return.
Next, the role of one-way valves in veins was observed by pushing the blood in a vein toward and away
from the heart, as seen in Table 4. When the blood was pushed toward the heart, it was seen that the vein
collapses and does not regain its contour until it is no longer occluded. When the blood is pushed away
from the heart, the vein swells and bubbles up at different locations, indicating the locations of one-way
valves in the blood that prevent backflow.
Table 4: Observations of a vein while blood is being pushed toward the heart and away from the heart to
see the role of the valves in veins.
Push the blood from the
occlusion toward heart
Push the blood away from
heart toward the occlusion
Occluded vein on the
cuffed arm
The vein collapses The vein swells and bubbles
up, showing where the one-
way valves are
In the next part, observations of venous distention
are observed by taking the circumference of the
forearm at various cuff pressures. The general
observed trend was an increase in forearm
circumference with an increase of cuff pressure,
as seen in Figure 7. There were discrepancies in
Observation as slowly
raising the arm up
Distance between where
the vein collapse to the
heart
Right arm raised slowly As the arm is raised, the
vein seems to protrude a
little bit, and then
disappears once it reaches a
level near the heart
5cm between arm and heart
when vein collapsed,
equates to 3.68mmHg.
26.4
26.6
26.8
27
27.2
27.4
0 20 40 60
Cir
cu
mfe
ren
ce (
cm)
Cuff Pressure (mmHg) Figure 7: The effects of cuff pressure on
forearm circumference are plotted at 0, 20, 30,
40, and 60 mmHg.
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this trend seen at 20 mmHg and 60 mmHg as circumference decreased instead of the expected increase.
Part V: Cardiovascular Responses to Exercise
In the third part, heart activity and blood pressure was measured at various intensities of exercise. Blood
pressure measurements and heart rate measured by the Biopac program were then used to calculate
MAP, PP, SV, CO, and TPR. In the course of the experiment, a general trend of increased blood
pressure and heart rate as exercise intensity increased was observed. This then caused a trend of
increasing MAP, PP, SV, and CO with increasing workload, seen in Figures 8-12. This also caused TPR
to decrease as intensity increased, displayed in Figure 13. There were some unexpected results in the
experiment as the pulse pressure at workload 0.5 kPa decreased from workload 0 kPa instead of the
expected increase, shown in Figure 9 as the pulse pressure dipped at a workload of about 30 watts. This
caused similar unexpected results in stroke volume, shown also as the dip in stroke volume at a
workload of about 30 watts in Figure 11, because the pulse pressure was used to calculate the stroke
volume.
80
85
90
95
100
105
110
-20 0 20 40 60 80 100 120 140
Mea
n A
rter
ial
Prs
sure
(m
mH
g)
Workload (Watts)
Figure 8: The effect of exercise on mean
arterial pressure (MAP) at different workloads.
REST
30
40
50
60
70
80
-20 0 20 40 60 80 100 120 140
Pu
lse
Pre
ssu
re (
mm
Hg
)
Workload (Watts)
Figure 9: The effect of exercise on pulse
pressure (PP) at different workloads.
REST
10
Part VI: The Diving Reflex
In the last part, heart activity was measured as Amanda held her breath right above a container of ice
cold water (used as a control) and then as she held her breath again with her face in the water. Heart rate
was measured by the Biopac program and used to see the phenomenon of the dive reflex. It can be seen
in Figure 14 that heart rate decreased from a maximum at 97 BPM to minimum at 72 BPM while the
subject held her breath above water. Similarly, heart rate decreased while the subject held her breath
with her face in cold water, but it dropped more significantly, a maximum of 114 BPM and a minimum
of 51 BPM, as seen in Figure 15.
8090
100110120130140150160170
-20 0 20 40 60 80 100 120 140
Hea
rt R
ate
(B
PM
)
Workload (Watts)
Figure 10: The effect of exercise on heart rate
(HR) at different workloads.
REST
50
60
70
80
90
100
-20 0 20 40 60 80 100 120 140
Str
ok
e V
olu
me
(mL
)
Workload (Watts)
Figure 11: The effect of exercise on stroke
volume (SV) at different workloads.
REST
4
6
8
10
12
14
16
-20 0 20 40 60 80 100 120 140
Ca
rdia
c O
utp
ut
(L/m
in)
Workload (Watts)
Figure 12: The effect of exercise on cardiac
output (CO) at different workloads.
REST 6
8
10
12
14
16
18
20
-20 0 20 40 60 80 100 120 140To
tal
Per
iph
era
l R
esis
tan
ce
(mm
Hg
/L/m
in)
Workload (Watts)
Figure 13: The effect of exercise on total
peripheral resistance (TPR) at different
workloads.
REST
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DISCUSSION
Part I: Measuring Blood Pressure has been excluded from this report.
Part II: Effects of Posture on Blood Pressure
In this part of the experiment, the effect on blood pressure due to postural changes were studied
as the subject was put in a supine position and then tilted into an upright position. Blood pressure
changes were seen as the subject was tilted upright, blood pressure went from 112/70 mmHg at a supine
position to 90/60 mmHg after the tilt. This significant decrease in blood pressure was seen due to gravity
acting on arterial flow and venous return. Because gravity acts against venous return, blood pools in the
lower body and decreases the amount of blood being pumped back to the heart. This in turn, causes a
decrease in the amount of blood that is pumped out of the heart and into the body, causing a decrease in
mean arterial pressure, as seen in Figure 1. Mean arterial pressure factors in the systolic and diastolic
pressure of the system, controlled and regulated by baroreceptors.
Heart activity was measured through an ECG using Biopac software. In an ECG, the P-wave
corresponds to atrial depolarization, the QRS wave complex corresponds to the ventricular
depolarization and the T-wave corresponds to the ventricular repolarization. These waves were seen in
the produced ECG from this experiment. Similar to blood pressure, heart rate decreased from 79.6 BPM
while supine to 67 BPM after the initial tilt, seen in Figure 3. This was due to the decrease in venous
60
70
80
90
100
110
0 10 20 30
Hea
rt R
ate
(B
PM
)
Time (seconds)
Figure 14: Heart rate of subject holding her
breath with face right above water.
50
60
70
80
90
100
110
120
0 20 40 60
Hea
rt R
ate
(B
PM
)
Time (seconds)
Figure 15: Heart rate of subject holding her
breath with face in ice cold water.
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return, as more time is needed to fill the ventricle before it can pump the blood out again. As shown in
Figure 4, stroke volume decreased from 65.1 mL to 37.5 mL after the tilt because of the decreased
venous return, causing the heart to be filled less than before the tilt, thus causing the heart to eject less
blood out per pump. This embodies the Frank-Starling Law, which states that increased filling of the
ventricle causes increased output (stroke volume). Thus, the opposite is also true; decreased filling of the
ventricle causes decreased output. Cardiac output also decreased from 5.2 L/min to 2.5 L/min after the
tilt, displayed in Figure 5. This, again, was due to the decrease in venous return, causing the heart to fill
at a slower rate and pump less blood each cycle. Since cardiac output is a product of stroke volume and
heart rate, the decreased heart rate and stroke volume caused this decrease in cardiac output. Because the
above factors all decreased, the total peripheral resistance increased post-tilt since it factors in mean
arterial pressure and cardiac output. Total peripheral resistance increased because of the need for
increased flow to tissues that resulted in increased venous return.
Blood pressure, mean arterial pressure, pulse pressure, heart rate, stroke volume, cardiac output,
and total peripheral resistance all return to normal values by 2 minutes post-tilt because of the
stabilization of heart activity. This occurs because of the baroreceptor reflex. The stretch-sensitive
baroreceptors sense the decrease in mean arterial pressure after the initial tilt and acts to increase heart
rate and venous return (Lanfranchi & Somers, 2002). This is done by the increase in sympathetic
activity, releasing epinephrine that will increase contractility of the heart causing an increase in stroke
volume and heart rate. The increase in sympathetic activity also causes vasoconstriction, which acts as a
mechanism to increase resistance to allow venous return to increase and help heart function return to
normal.
A study done on heart rate variability of related to posture changes on an individual basis
confirms these results. In the study, the sympathovagal balance is studied in the supine and upright
positions and it is clearly concluded that in an upright position, baroreceptor restriction on sympathetic
13
activity is removed, allowing an increase in sympathetic activity (Malliani et al., 1997). As mentioned
above, the baroreceptors act in relation to arterial pressure. When a low arterial pressure is sensed,
baroreceptors allow the increase in sympathetic activity, which, as mentioned before, is the mechanism
behind increasing venous return and heart rate, thus increasing blood pressure, pulse pressure, stroke
volume, and cardiac output while decreasing total peripheral resistance.
Part III: Vasodilation in Response to Metabolites
In the next part of the experiment, vasodilation was observed in response to metabolites by
cuffing the forearm and observing changes of the occluded area once the cuff was removed. As seen in
Table 1, when the cuff was inflated after clenching the fist repeatedly, the arm lost all of its color, turned
white, dropped in temperature and the veins were not visible as they were before inflation. When the
arm is raised, gravity works with venous flow and allows the blood to be easily returned to the heart
while working against arterial flow, inhibiting blood flow to the forearm and hand, but since the arm
was cuffed to a pressure higher than arterial and venous pressure, the veins collapsed and circulation
was stopped in that area, causing a pale color and decrease in temperature. As the cuff was ripped off,
the blood was allowed to circulate normally again, causing the skin to flush pink. Vasodilation was
observed because local metabolites were built up from the occlusion and an increased blood flow is
necessary to restore the chemical balance and the normal flow of metabolites (Sherwood, 2010, p. 357).
This phenomenon is known as reactive hyperemia, which is induced by myogenic relaxation and
unbalanced metabolites, both of which occur during occlusion of an area that stops blood flow
temporarily.
Part IV: The Venous System
Next, the venous system was observed in four different parts. First, gravity and its effects on
venous congestion were observed by having the subject hold one arm over his head for one minute and
then quickly returning his arm to the tabletop for observation. As seen in Table 2, during the arm raise,
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the subject’s arm became pale and the veins were no longer visible and protruding. Once his arm was
returned to the tabletop, the color returned to his arm and the vein protruded once again. This was due to
the effect of gravity on blood flow; when the arm was raised, gravity worked with venous return and
against arterial flow. The effect against arterial flow caused venous congestion, which is a decrease of
local blood flow, in this case to the arm and hand (Okazaki et al., 2005). This caused the veins to
protrude less, almost taking on a collapsed look. Once the arm is no longer raised, the blood flow was
able to return to equilibrium, allowing the arm to regain color and the veins to regain normal dilation
and blood flow through them.
In the next study, observations were made of a vein collapsing by having the subject hold one
arm above his head and slowly lift the other arm up from his side. Once his arm reached an area near his
heart, the vein collapsed. This is due to the decreased effect of gravity once the arm is near horizontal
position, in line with the heart. Because gravitational effects are minimal on the arm in this position,
effective circulation is reestablished and blood can be pumped to the heart with ease, eliminating the
slight pooling of blood that causes vasodilation (Sherwood, 2010, p. 374). The vein collapse was
observed when the arm was 5 cm away from the heart, correlating to a pressure of 3.68 mmHg at that
point.
Next, the valves in veins were observed through occluding a protruding vein in the subject’s
forearm and pushing the blood towards and away from the heart. As seen in Table 3, when the blood in
the vein was pushed towards the heart, the vein collapsed since the blood freely flowed away from the
occlusion while it was inhibiting further blood flow through the vein. Conversely, when the blood in the
vein was pushed away from the heart, the vein protruded more and bubbled up at various spots. This was
due to the one-way valves in veins that prevent backflow. Veins contain one-way valves that serve
multiple functions; it helps in preventing deoxygenated blood from flowing back into tissues and mixing
15
with oxygenated blood and it aids in offsetting the effects of gravity in blood flow. The points where
bubbles were seen after pushing the blood away from the heart were the locations of the valves.
Finally, the effect of cuff pressure on venous distension was observed by cuffing the subject’s
arm in various increments while the arm is raised above the head. As seen in Figure 7, the general trend
of this increase in cuff pressure was a slight increase in forearm circumference. This increase in forearm
circumference was due to the distension of the veins due to the slight inhibition of venous return from
the arm as a result of the inflated cuff. Because the pressure of the cuff stays lower than the arterial
pressure, blood can still be delivered to the arm, but the blood pools slightly in the forearm as the cuff
prevents normal blood flow back to the heart. Veins are able to hold the extra blood due to their
distensible nature, without a large increase in pressure. The data collected showed the general trend of
increased forearm circumference, but there were unexpected decreases in circumference. These
unexpected results are most likely due to measurement errors because the measurer did not keep the
exact same tension of the measuring tape and location of measurement on the forearm throughout the
study.
Part V: Cardiovascular Response to Exercise
In the next part of the lab, active hyperemia was observed as the subject was observed under
exercise at different workloads while being hooked up to the Biopac software to measure heart activity.
Active hyperemia causes vasodilation to increase blood flow due to an increased need for nutrients and
waste removal from metabolically active cells (Sherwood, 2010, p.354). During exercise, cells have an
increased need for oxygen and various other nutrients, causing an increase in blood uptake to meet these
needs. This then causes an initial drop in blood pressure, but as mentioned before, the baroreceptor
reflect senses the drop in arterial pressure and stimulates sympathetic activity and decreases
parasympathetic activity in anticipation of continued exercise. The increase in sympathetic activity
16
causes an increase in vasoconstriction, heart rate and stroke volume, and thus an increase in cardiac
output. These factors then increase blood pressure to allow an increased arterial flow to target tissues.
As workload increased during exercise, the subject’s mean arterial pressure increased, as seen in
Figure 7. This was seen along with an increase in heart rate (Figure 9), stroke volume (Figure 10), and
cardiac output (Figure 11). All of these factors increased in order to account for the increased need for
blood supply to cells that were being worked. Total peripheral resistance decreased with an increase of
workload because as active hyperemia causes vasodilation, the peripheral resistance decreases in order
to allow an increase in blood flow. The exercise pressor reflex takes responsibility for these changes in
response to skeletal muscle contractions that increase arterial blood pressure (Mitchell, Kaufman, &
Iwamoto, 1983, 229).
Unexpected results did occur, however. During the increased workload of 0.5 kPa, or about 30
watts, there was a slight decrease in stroke volume. It is suspected that this was due to the subject’s body
feeling that the slight increase in workload was not significant to need an increase in blood supply to
target tissues.
Part VI: The Diving Reflex
In the last part of the lab, the dive reflex was observed by having the subject hold her breath with
her face in cold water. In the posture change and the exercise portions of the lab, activity stimulated an
increase in sympathetic activity which caused an increase in heart rate. Conversely, the dive reflex
shows an increase in parasympathetic activity as well as an increase in sympathetic activity when the
face is immersed in cold water. The dive reflex is a phenomenon activated by receptors in the face that
are sensitive to cold water. This occurs as a survival mechanism in which heart rate is decreased in order
to slow blood flow to conserve oxygen supply for as long as possible.
The comparison from the control trial of the subject holding her breath for 30 seconds above the
water and that of the trial holding her breath with her face immersed in the cold water shows this dive
17
reflex. As shown in Figure 13, during the control trial, her heart rate decreases, but only from 97 BPM to
72 BPM at the lowest point. On the contrary, the subject’s heart rate decreased to a more extreme degree
when she held her breath in the cold water, from a high of 114 BPM to a low of 51 BPM. Also while she
was holding her breath in the cold water, it was observed from the ECG that there were times when it
seemed like there was a skipped beat altogether, as shown in Figure 16, a portion of the raw data from
the ECG. This was due to high amounts of parasympathetic input, activating a survival mechanism.
Figure 16: Raw data during breath holding with face immersion in cold water shows abnormal heart
activity caused by parasympathetic input.
In literature, this same dive reflex phenomenon has been studied and results are consistent with
the previously explained outcomes. A face immersion in cold water results in a slowed heart rate and a
slower depletion of oxygen supply (Jay, Christensen, & White, 2006, p. 203).
In the six different parts of this lab, various responses in cardiovascular function were observed. It was
seen that an upright position causes an initial decrease in blood pressure along with heart rate, stroke
volume, mean arterial pressure, and cardiac output because of the effects of gravity that causes blood to
pool at the feet. Next, vasodilation was observed due to the need for chemical balance in metabolites. In
the fourth part of the lab, various properties of the venous system was observed including gravity
causing venous congestion, venous return without gravitational effects, the role of venous valves, and
the distensible nature of veins. Moving to the fifth part of the lab, it was observed that exercise caused
an increase in sympathetic activity which promoted an increase in heart rate, blood pressure, arterial
18
pressure, stroke volume, and cardiac output. Finally, the dive reflex was observed as facial immersion in
cold water caused a decrease in heart activity to conserve oxygen supply in a survival situation.
19
REFERENCES:
Bautista E., & Korder, J. 2009. NPB 101L Systemic Physiology Lab Manual (2nd ed.). Department of
Neurobiology, Physiology and Behavior, University of California, Davis.
Jay, O., Christensen, J.P.H., & White, M.D. (2006). Human face-only immersion in cold water reduces
maximal apnoeic times and stimulates ventilation. Experimental Physiology, 92, 197-206. doi:
10.1113/expphysiol.2006.035261
Lanfranchi, P.A, & Somers, V.K. (2002). Arterial baroreflex function and cardiovascular variability:
interactions and implications. American Journal of Physiology – Regulatory, Integrative, and
Comparative Physiology, 283 (R815-R826). doi: 10.1152/ajpregu.00051.2002
Malliani, A., Pagani, M., furlan, R., Guzzetti, S., Lucini, D., Montano, N., Cerutti, S., & Mela, G.S.
(1997). Individual Recognition by Heart Rate Variability of Two Different Autonomic Profiles
Related to Postre. Circulation, 96, 4142-4145. doi: 10.1161/01.CIR.96.12.4143
Mitchell, J.H., Kaufman, M.P, & Iwamoto, G.A. (1983). The Exercise Pressor Reflex: Its
Cardiovascular Effects, Afferent Mechanisms, and Central Pathways. Annual Review of
Physiology, 45, 229-242. doi: 10.1146/annurev.ph.45.030183.001305
Okazaki, K., Fu, Q., Martini, E.R., Shook, R., Conner, C., Zhang, R., Crandall, C.G., & Levine, B.D.
(2005).Vasoconstriction during venous congestion: effects of venoarteriolar response, myogenic
reflexes, and hemodynamics of changing perfusion pressure. American Journal of Physiology –
Regulatory, Integrative, and Comparative Physiology, 289 (R1354-R1359). doi:
10.1152/ajpregu.00804.2004
Sherwood, L. Human Physiology: From Cells to Systems (7th ed.). California: Brooks/Cole, Cengage
Learning.
Watanabe, N., Reece, J., Polus, B.I. (2007). Effects of body position on autonomic regulation of
cardiovascular function in young, healthy adults. Chiropractice & Osteopathy, 15(19).
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APPENDICES:
Sample Calculations:
Given BP 112/60 at rest, supine
MAP = 1/3 (SP) + 2/3 (DP) = 1/3(112) + 2/3(60) = 77.3 mmHg
PP = SP – DP = 112 – 60 = 52 mmHg
HR = an average of HR taken from Biopac: (84+81+78+74+67+72+80+82+75+64)/10 = 75.7 BPM
SV = PP*Arterial Distensibility = 52 * 1.5 (at rest) = 78mL
CO = SV*HR = 78 * 75.7 = 5904.6 mL/min / 1000mL/L = 5.9046 L/min
TPR = MAP/CO = 77.3mmHg / 5.9046L/min = 13.097 mmHg/L/min
Raw Data:
Supine
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Tilt
30 seconds post-tilt
2 minutes post-tilt
Bike Resting
Exercise 0kPa
22
Exercise 0.5 kPa
Exercise 1 kPa
Exercise 1.5 kPa
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Exercise 2 kPa
Control breath hold start
Control breath hold stop
Dive Reflex start
Dive Reflex during
24
Dive Reflex stop