Abstract
Alexander Krzyston x Alexander J Krzyston x Alex James Krzyston Alex Krzyston x Alex J Krzyston x Alexander James Krzyston x NORTHWESTERN UNIVERSITY x EVANSTON x BURR RIDGE
The cardiovascular system is responsible for the transport and distribution of essential nutrients, hormones, and compounds. During exercise, efficient cycling of oxygen and carbon dioxide is necessary, along with sufficient cardiac activity to support the exerted tissues.
In this lab, the effects of increasingly intense exercise on blood pressure, Mean Arterial Pressure(MAP), heart rate, cardiac output, Total Peripheral Resistance(TPR), oxygen flow, ECG intervals and the Ventilation-to-Perfusion Ratio were tested. This was done by measuring the cardiac activity of a test subject pedaling on stationary exercise bike, and increasing the target power output (resistance) approximately every four minutes by 50 watt intervals. Before each increase in resistance, the subject’s heart rate and blood pressure was recorded. From these recordings, MAP, stroke volume, cardiac output, TPR, and the Ventilation-to-Perfusion Ratio were calculated. Our results showed that everything except TPR increased as the workload increased. From these results, it was concluded that as the intensity of exercise increases, cardiovascular activity also increases to account for the increased demand for oxygen in the muscle tissues. TPR decreases because as the workload on the heart increases, the arteries dilate in order to decrease the resistance to blood flow and allow for better circulation and thus provide enough oxygen for the increased demand in muscle tissues. The cardiovascular system responds to exercise in such a way that the increased need for oxygen in the muscle tissues being exerted can be met.
Discussion
How do results compare with those of similar studies on other systems
Errors, limitations, and improvements
What questions and further hypotheses are generated by our work
Place study in broaders context and consider implications for the field
References
(Demonstrate understanding of topic and analytical)
Based on the results of this experiment, the null hypothesis that increased exercise has no effect on the cardiovascular system can be rejected. Therefore, it can be reasonably concluded from the results that exercise does have a profound effect on the cardiovascular system in such a way that blood pressure, diastolic, systolic, and MAP, all increased (in general) as a result of increased physical exertion. In addition, heart rate and cardiac output also increased, while total peripheral resistance decreased. All of these responses are to be expected because as a result of increased physical exertion, there is an increased demand for oxygen in the muscle tissues. Therefore, in order to supply the oxygen deprived muscles with more oxygen, via the bloodstream, the heart must pump faster.
Blood Pressure
For systolic blood pressure, our results reveal that as the exercise workload increases, the systolic blood pressure increases (shown in ‘Systolic Blood Pressure at Increasing Work Loads’ graph). These results support our alternative hypothesis which predicted that systolic blood pressure increases as the workload increases while refuting the null hypothesis that anticipated no change in systolic blood pressure due to increasing workload. Our investigation of diastolic blood pressure shows that as workload increases, the diastolic blood pressure also increases (as shown in the ‘Diastolic Blood Pressure at Increasing Work Loads’ graph). The results show a deviation from this trend, as the third measurement decreased dramatically. These observations support the hypothesis that diastolic blood pressure is proportional to workload. These results disprove the null hypothesis that predicted no effect of workload on diastolic blood pressure. The results agree with the alternative hypotheses because as workload increases, the active muscles needs more oxygen to function. To allow more blood to reach the working muscles, the heart must pump more blood and to do so, the systolic pressure increases to allow the heart to pump a higher volume of blood. The diastolic pressure must also increase because as more blood is being pumped out, more blood is in return entering the heart. Our investigation of MAP (mean arterial pressure) shows that as workload increases, MAP also increases. The results show an anomalous data point, as the third measurement is abnormally low. The MAP increases because the heart contracts and relaxes more rapidly due to higher activity in the muscles, in order to allow for the quicker filling of and ejection of blood from the heart. This increased activity therefore increases the pressure of blood on the arterial walls.
The Integrated Response
Based on the results of this experiment, it can be concluded that heart rate increases in response to exercise, and thus disproving the null hypothesis. Heart rate increases because the heart contracts and relaxes more rapidly in order to transport blood to and from active muscles more quickly. The investigation also displayed results that indicate that cardiac output (Q) increases with workload. The dependence of cardiac output on workload shows that the null hypothesis predicting no effect of workload on cardiac output, can be rejected. This confirms the hypothesis that increased workload has an effect on heart rate, increasing it, and rejects the null hypothesis that workload does not have an effect on it. This relationship between workload and cardiac output is supported by the fact that the stroke volume remains constant while heart rate increases. Since cardiac output is the product of heart rate and stroke volume, increased muscle activity and heart rate cause an increase in cardiac output. The results also indicate that total peripheral resistance (TPR) decreases with increasing workload. There was an anomaly in our data for this, as our fourth data point shows a small increase in TPR. These results confirm the hypothesis that TPR is affected by workload and rejects the null hypothesis that states the opposite. TPR decreases, because as a person exercises, their arteries dilate in order to decrease resistance. This allows for better and more efficient blood circulation with increased heart rate.
The Ventilation-Perfusion Ratio
The experimental results show increasing Ve / Q as the workload of the subject increases. This confirms the hypothesis that an increase in workload correlates with an increase in the Ve / Q ratio, refuting the null hypothesis that workload does not affect this ratio. Ve / Q ratio increases with larger workload, because active muscles need more oxygen. The heart pumps more blood more rapidly to the muscles in order to supply them with more oxygen. The need for more oxygen also causes the subject to breathe more rapidly. *There seems to be an error with the calculations of the excel sheet, but the first ratio should be a positive value.
The limiting factor to this ratio is that the heart beats faster that the respiratory system can take in air to exchange the carbon dioxide in the blood for oxygen in the muscles. This limiting minute ventilation factor is thus the cap on the cardiovascular system at which point increased physical exertion would lead to shut down of muscle function due to accumulation of lactic acid in the muscles because of the inability to supply them with adequate amounts of oxygen. Continued exercise at this level could result in death. In contrast to the human Ve/Q ratio, that of a horses in nearly perfect which is why they can run for long distances without their muscles shutting down, the cardiovascular system is in sync. This evident in the fact that a steady ventilation rate in a horse is reached in 60 seconds (Evans).
O2max
in the horses in this study was greater than in man, but is similar to or less than
maximal cardiac output in rats, dogs and possums.”
In horses, a steady state is reacted in the less than 60 seconds (Evans).
The Electrocardiogram
Because of the recordings of the test subject’s electrocardiogram throughout the duration of the exercise, the null hypothesis-that the ECG does not change in response to exercise- can be rejected. It can be concluded that as the workload increases, each interval in the ECG decreases accordingly. These results agreed with the hypothesis that the PR, ST, and TP intervals of the ECG would decrease as intensity increases. As a person exercises, the heart contracts and relaxes more rapidly to optimize the delivery of oxygen to active muscle tissues. Because of the need for more rapid contraction and relaxation, action potentials travel more quickly through the AV node, decreasing the delay between atrial and ventricular excitation. This decrease in the delay shortens the PR and TP intervals. Not only does exercise cause faster contraction, but ventricular contraction is also more forceful, causing the ST segment to be shorter. The first three data points confirm the hypothesis that the ST and TP intervals decrease; however, the fourth point instead shows a slight increase, likely as a result of human error, such as the subject slowing down for a short period of time.
Alexander Krzyston CC Alexander J Krzyston CC Alex James Krzyston
Alex Krzyston CC Alex J Krzyston CC Alexander James Krzyston
NORTHWESTERN UNIVERSITY CC EVANSTON CC BURR RIDGE
AlexanderJKrzyston.com Alexanderjkrzyston.com/Alexander_j_krzyston_links.html AlexanderjKrzyston.com/Alexander_j_krzyston_quotes.html AlexanderjKrzyston.com/contact_Alexander_j_krzyston.html AlexanderJKrzyston.com/index.html AlexanderKrzyston.com AlexanderKrzyston.com/Alexander_krzyston_links.html AlexanderKrzyston.com/Alexander_krzyston_quotes.html AlexanderKrzyston.com/contact_Alexander_krzyston.html AlexanderKrzyston.com/index.html AlexJKrzyston.com AlexJKrzyston.com/Alex_j_krzyston_links.html AlexJKrzyston.com/Alex_j_krzyston_quotes.html AlexJKrzyston.com/contact_Alex_j_krzyston.html AlexJKrzyston.com/index.html AlexKrzyston.com Alexkrzyston.com/Alex_krzyston_links.html AlexKrzyston.com/Alex_krzyston_quotes.html AlexKrzyston.com/contact_Alex_krzyston.html AlexKrzyston.com/index.html
