Lab #3 (1) (1)

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Wilfrid Laurier University *

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111

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Health Science

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Dec 6, 2023

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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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