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Anthony Khong

The effects of smoking on four cardiorespiratory variables at
University of California Irvine
Abstract: The effects of smoking on physiological variables are widely
known and well established in academia and medical intuitions, and for
educational purposes, this experiment was done to test and reevaluate the
findings and results of those intuitions. On January 2014, UCI declared itself
to be a non-smoking campus and prohibited the use of cigarettes on campus;
using E112L UCI students, basic physiological variables were tested and
compared among smoking and non-smoking populations. The subjects from
both populations mounted on an exercise bike of varying work intensities,
and strapped on a spirometer, connected to gas analyzers, to record various
physiological variables, which include VO2 peak, heart rate, MAP

rest and peak

, and

the partial alveolar pressure of oxygen. The results showed no significance
between the two populations for all physiological variables, except in the
difference of resting and peak MAP values in the non-smoking population.
With a small sample size of 12 individual for each population and control for
only gender and smoking demographics in the experiment design, the results
does not accurately portray the physiological effects of smoking on the UCI
population.
Introduction:

Recent studies by American . From an epidemiological viewpoint. from early discovery of opium to cigarettes. but also the surrounding population. but blood pressure plummeted to bradycardic levels at rest. supplying a network of essential fuel for humans to do work.Breaths of air are taken everyday to sustain basal cellular metabolism and life. greater insight on how exercise affects physiology is gained. The University of Ohio conducted a study where chronic smokers were tested for several physiological and psychological factors. Exercise physiology examines what deters human health and reports those findings in hopes for educating the public. Smoking has existed throughout human history. limitations of the human body can be evaluated. the effects of smoking not only affect the individual. Exercise physiology is a specific field within physiology that is centered two core systems: the circulatory and respiratory systems. However. the essential gases permeate throughout the body. The results showed that blood pressure elevated rapidly while dealing with stress. how to thrive as a health human being. as well as. the opposite holds true as well. As the air diffuses down the lungs. one including blood pressure (Blackburn. Exercise physiology keenly scrutinizes this model of fuel transport. the hazardous habit is notorious for causing an array of complications and diseases. Questions on the limitations of the human body can be answered and understood. 2). but when metabolic rates elevate and hyperventilation forces more air in and out of the body. and by studying the variables surrounding these systems.

Materials and Methods: Individuals of random demographics voluntarily elected to perform the exercise physiology experiment. I hypothesize that during exercise the smoker population will have a decreased level in peak O2 consumption peaks (VO2 peak). a greater change in heart rate (responsiveness/sensitivity) will be associated in the smoking population. Though it seems as if the question of the effects of smoking on health is not debatable. Only two factors were controlled in the experiment. which were smoking and gender. but also of animals and insects (Omvik. which measured respiratory and . the difference from rest to peak of mean arterial pressure will be lower in the smoker group. 41). and a greater change in the partial alveolar pressure of oxygen in the smoker group.College of Physicians found that the second hand smoke not only affects the physiological states and performance on humans. the experiment randomly selected twelve other males and compared different physiological variables. what are its immediate physiological effects on an individual during exercise? Within the E112L population. all other demographics were not controlled. Among the smoker and nonsmoker population in the E112L dataset. Scientific articles ranging of Johns Hopkins School of Medicine to Annual Review of Plant Physiology and Plant Molecular Biology note the damaging effects of the toxic gases on living organisms. twelve males identified with smoking while the rest of the population did not.

and gas percentages were taken and continued to be measured with increasing intensities. blood pressures. After a two-minute warm-up. The biking apparatus constantly measured the heart rate or pulse. Mean arterial pressure (MAP) was statistically analyzed by both an unpaired and paired t-test. The biker was required to maintain a cycling rate of 80 RPM for one minute. a spirometer connected to a computer constantly measured the percentages of exhaled oxygen and carbon dioxide throughout all intensity levels. Various instruments and methods were used to record and collect the physiological data. In order to statistically analyze the oxygen consumption and blood pressure data. The paired t-test was done to statistically evaluate if there .cardiovascular variables. Blood pressures was taken at the end and start of each intensity level with a blood pressure monitor that gave diastolic and systolic pressures. the biker was instructed to do perform a cool down to slowly bring back the physiological levels to rest. heart rate. t-tests were used. At the start of the experiment. the biker would continue for another minute on the next bike level intensity. and if exhaustion were not reached. An unpaired t-test was done to evaluate the difference of peak oxygen consumption between the two populations. At the end of the experiment. and in addition. mean arterial pressure was later calculated using known equations. respiratory rates. bike level intensity was increased incrementally by one level.

Since heart rate and the partial alveolar pressure of oxygen were continuously taken. linear regression analysis was done to evaluate the correlation between work rate and the two physiological variables.98±0. Results: The means of peak oxygen consumption (VO2 peak) between the smoking and non-smoking population are 2.845±0. .84 and 2. respectively.36. Both the linear regression line and the R2 value were drawn and calculated using Excel. Both data variables were tested against the increasing work rate. The t-value of the unpaired t-test is 0. Another unpaired t-test was done to verify any correlation of the absolute (no negative numbers) change in MAP between the two populations. which correlates with a p-value of 0.72. The analysis shows that the two groups are not significantly different.95.contained a significance between resting MAP and peak MAP within the same population.

and the t-value of the paired t-test within the nonsmoking group was 2.3.5 0 Smoker Non-Smoker Image 1: The bar graph shows peak oxygen consumption between the smoker and non-smoking populations.2±13. which correlates to a p-value of 0.07. .5 1 0.79.24. The analysis shows that there is not a significant change in resting and peak MAP within the smoker group. The mean of heart rate within the smoking population’s MAP at rest is 103.5 3 2.5 2 Peak VO2 Consumption 1. The analysis shows that there is a significant difference between resting and peak MAP in the non-smoking group.049.44. and the t-value of the paired t-test within the smoking group is 0.8±15. The mean of the heart within the non-smoking population’s MAP at peak is 106. which correlates to a p-value of .104.

The first joint bar graph to the left displays rest and peak MAP values to the left and right respectively within the smoker population.The mean of the difference within heart rate of the smoker and nonsmoker are 10.54 and a p-value of . . 140 120 100 80 Mean Arterial Pressure(mmHg) 60 40 20 0 Smoker MAP Rest and Peak Image 2: The bar graph displays MAP values compared against two criteria.11The unpaired t-test comparing the absolute change in MAP between the two populations had a t-value of 1. The second joint bar graph in the middle displays rest and peak MAP values to the left and right respectively within the non-smoker population. The analysis shows that there is no significance of absolute change in MAP between the two populations.1409.

200 180 Smoker R² R² = = 0.85 Linear (Smoker) 160 Linear (Smoker) 140 120 Linear (Smoker) 100 Heart Rate (BPM) 80 60 Linear (Non-Smoker) 40 Linear (Smoker) Non-Smoker Linear (Non-Smoker) Linear (Non-Smoker) 20 Linear (Non-Smoker) 0 0 50 100 150 200 Work rate (watts) 250 300 .87 0.

and the nonsmoking population has an R2 value of 0.25 20 15 Mean Arterial Pressure (mmHg) 10 5 0 1Absolute change in MAP in smokers and non-smokers Image 3: The joint bar graph displays the absolute change in MAP between rest and peak for smokers and non-smokers to the left and right respectively.87061. The graph has corresponding trend line to each population.84986. the more correlated the two variables are. The smoker population has an R2 value of 0. The closer the value is to 1. Heart rate was analyzed using linear regression analysis. Both the smoker and non-smoking mean heart rates were plotted against the corresponding work rate. .

correlating heart rate with increasing work rate. Both the smoker and non-smoking mean pressures were plotted against the corresponding work rate. the more correlated the two variables are.Image 3: The image displays both trend lines for each of the populations.1 Smoker Linear (Smoker) Non-Smoker Partial Alveolar Pressure of O2 Linear (Non-Smoker) Linear (Non-Smoker) 0 50 Linear (Non-Smoker) 100 150 200 250 300 Work rate (watts) Partial alveolar pressure of oxygen was analyzed using linear regression analysis. and the non-smoking population has an R2 value of 0. . The graph has corresponding trend line to each population.09873. R² = 0.9873 The closer the value is to 1. The smoker population has an R2 value of 0.

87061 for the smoking and non-smoking group. Since the sample size is 24. Subject number 1082 in the smoker group had a decreasing tidal volume as work rate increased. For example. Also.05. if the spirometer mask were not sealed tightly. which is less than . and affected the variables in the results. the population sizes of the groups are relatively small. All other results are not significantly different because they had p values that were greater than . during the test. human error was a large confounding factor. There are a variety of confounding factors within the experiment that contribute to the results. The linear regression analysis in heart rate shows an R2 value of 0. a large sample size could be used in future experiments.84986 and 0. correlating partial alveolar pressure of oxygen with increasing work rate. the actual use of the instruments was not practiced. respectively.05 and R2 values that were not close to 1. and assuming that this individual have normal . Although the subjects had read the instructions before the experiment. and in order to arrive at more meaningful statistical conclusions.048.Image 4: The image displays both trend lines for each of the populations. There is a significant correlation between the changes in resting MAP and peak MAP because the p-value is . expired gases would have yielded a lower value. Discussion: The results show a variety of difference statistical analysis and conclusions.

it binds onto hemoglobin carrying oxygen. Outlier analysis was not used to eliminate data points.1-3). 10% COHb causes no symptoms. This carbon monoxide complexed with the hemoglobin is called carboxyhemoglobin (James. 1). Just as a pulse oximeter measures O2 saturation. 1).physiological responses. measurements of VO2 peak on the same individual would need to be taken before and after chronic smoking. and renders it physiologically useless. the Department of Physiology at Rajah Muthiah Medical College in Chidambaram. the journal of cardiovascular pharmacology reported symptoms of elevating carboxyhemoglobin saturation(COHb). and once the odorless gas enters the bloodstream. The hemoglobin loses the ability to carry oxygen to the cells in the body. some of the data was flawed. the inhalation of carbon monoxide from smoking should cause a decrease in V O2 peak within the same person. Furthermore. India reports an inverse relationship between the lasting effects carboxyhemoglobin saturation and forced expiratory lung volumes (Wier. Carbon monoxide is a byproduct of a combustion reaction of smoking. but anything higher than 50% COHb is certain death. Several primary sources report the effects of carbon monoxide from smoking on cardiorespiratory variables. In order to set up this experiment. (Radiff. Since VO2 peak depends on the expired oxygen gas levels. and all of the data points were analyzed and represented in the lab report. Because the University of California Berkeley claims that smoking .

There is a significant correlation between differences of resting MAP to peak MAP in the non-smoking group. even though vasodilation is one of the major factors in stabilizing MAP. heart rate. 2) and that smokers should generally have a decreased ability of both cardiovascular and pulmonary systems (Nikodemowicz). the individual would need to be a non-smoker and become a chronic smoker. . Although there are many scientific articles claiming that smokers should have increased sensitivity toward blood pressures during stress (Blackburn. and partial alveolar pressure of O2 are not affected by smoking. the data of the experiment showed that VO2 peak.has lifelong effects on lung volumes (Loganayaki. 1-2).

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25 20 15 Mean Arterial Pressure (mmHg) 10 5 0 1Absolute change in MAP in smokers and non-smokers .