Lab #3 (1) (1)
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Wilfrid Laurier University *
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Course
111
Subject
Health Science
Date
Dec 6, 2023
Type
Pages
6
Uploaded by KidRock7053
KP322 Tuesday Lab, 1:00 pm
November 21st 2023, 11:59 PM
Ethan Bush, Student ID: 210936170
Kevin Kim, Student ID: 200662490
1i)
ii)
iii) As seen from the graphs in Chapter 9, one of our graphs looks like it should. What we should
expect is that the increase in blood pressure (MAP) during the arm workout is due to the
vasoconstriction in the blood vessels from inactive larger muscles and because of the smaller
muscle group, which causes the arm muscles to work harder to complete the exercise. But as
seen from our graph of BP (MAP), there was a higher BP during the leg exercises over the
workload than the arm exercises. This could be due to improper calculations, the ability to
exercise aerobically greater during arm exercises than leg exercises, higher peripheral resistance
in leg exercises than arm exercises, or the machine not properly giving the correct numbers.
There was also an increase in heart rate because of the sympathetic stimulation. Arm muscles are
relatively smaller than leg muscles, meaning that there is higher sympathetic stimulation, which
is required to recruit more active muscle fibers compared to the leg muscles. When performing
the exercise, there is lower peripheral resistance, causing the heart rate and blood pressure
(MAP) to be significantly lower during the leg exercise.
2. i)
ii) Our graph does look like it should; as the workload and exercise intensity increase, the
systolic blood pressure should increase while the diastolic blood pressure remains fairly constant,
holding at around 80 mm Hg throughout the exercise.
3. i)
ii) The graph that we made looks like it should because, as the workload increases, the heart rate
increases as well, having a positive linear relation from minimum workload to maximum.
iii) If we were to plot the stroke volume on this graph, we would see an initial increase in stroke
volume. As the workload increases, the stroke volume will continue to rise until they reach a
VO2 max between 40-60%. This indicates that the moderately trained subject does not increase
their stroke volume; rather, the rise in cardiac output is achieved by an increased heart rate alone.
Once the athlete reaches 40-60% VO2 max, the stroke volume reaches a plateau, and once that
slight decrease occurs, the heart rate increases to meet the oxygen demand. As seen from the
subjects' stroke volume during the arm exercise, their stroke volume remained relatively the
same after 120ml/beat which we can assume would be around 40-60% of their VO2 max.
4.
CV
Measure
s
Lying
Sitting
Standing
Wall Squat
Arm Ergo 50 W
Arm Ergo 100 W
HR
(bpm)
85
85
91
155
175
195
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SBP
(mmHg)
146
149
135
140
155
176
DBP
(mmHg)
82
81
85
80
80
79
VO
2
(L/min)
.370
0.213
.314
.800
1.140
1.5
Q
(L/min)
4.2
8
11
15
20
28
a-vO
2
diff
Vo2 / Q =
0.370 / 4.2 =
0.088 L O2/min
0.0266 L
O2/min
0.0285 L
O2/min
0.0533 L
O2/min
0.057 L O2/min
0.053 L O2/min
MAP
(mmHg)
DBP + 0.33
(SBP-DBP) 82 +
0.33(146-82) =
82 + 0.33(64) =
21.12 + 82 =
103.12 mm Hg
103.44 mm
Hg
101.5 mm Hg
99.8 mm Hg
104.75 mm Hg
111.01 mm Hg
SV
(L/beat)
SV = Q/HR
0.09411
(L/beat)
0.1208 (L/beat)
0.0967
(L/beat)
0.1142 (L/beat)
0.1435 (L/beat)
SV = 4.2/85 =
0.0494 (L/beat)
RPP
RPP = HR X
(SBP)
RPP = 85 X 146
= 12,410 mm
Hg/bpm
12,665 mm
Hg/bpm
12,285 mm
Hg/bpm
21,700 mm
Hg/bpm
27,125 mm
Hg/bpm
34,320 mm
Hg/bpm
TPR
TPR = (MAP) /
(Q)
TPR =
103.12/4.2 =
24.55 mm
Hg/min/L
12.93 mm
Hg/min/L
9.22 mm H
g/min/L
6.65 mm
Hg/min/L
5.23 mm
Hg/min/L
3.96 mm
Hg/min/L
5. i) From the calculations of stroke volume, we saw that there was a significant increase with
each body position. There was an increase in stroke volume from lying down to sitting because
of the effect of gravity, venous return, and increased end-diastolic volume. Once the body
transitioned from lying down to sitting, gravity helped the venous return to the heart, causing the
increase in stroke volume. When transitioning from lying down to sitting up, the increase in
stroke volume is due to the increase in end-diastolic volume, and gravity promotes pooling in the
legs. Another thing we noticed was that cardiac output increased every time the subject changed
positions. With this increase in cardiac output, more blood is ejected per beat, meaning that when
the subject was changing positions, more blood was ejected from the heart per beat. We then saw
another noticeable difference from sitting to standing; this is likely due to the same effect lying
down to sitting had on stroke volume. Gravity continued to assist with venous return, and there
could be an additional mechanism that helped maintain stroke volume, such as the sympathetic
nervous system, in response to the change in posture. The changes in stroke volume were all to
adjust the cardiovascular system to maintain proper blood flow. Something we also noticed was
that when the subject performed the wall sit, the stroke volume was around the same as it was
when they were sitting, which could indicate that the blood flow was adjusting to the different
position they had previously been in.
ii) These results are not typically what you would expect from stroke volume in relation to the
different changes in posture. As said previously, the cardiovascular system has an important role
in maintaining blood flow. Blood flow is evenly distributed in the veins, and when our subject
changes positions, the effect of gravity assisting with venous return is the main factor in stroke
volume. When compared to an upright position, end-diastolic and stroke volumes are expected to
be higher in a supine position rather than a prone position because the effect of gravity is
changing blood flow and is distributed in different areas of the body.
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