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:

Breaths of air are taken everyday to sustain basal cellular metabolism

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

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

cardiovascular variables. At the start of the experiment, heart rate, blood

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

contained a significance between resting MAP and peak MAP within the same
population. Another unpaired t-test was done to verify any correlation of the
absolute (no negative numbers) change in MAP between the two populations.
Both data variables were tested against the increasing work rate.
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. Both the
linear regression line and the R2 value were drawn and calculated using
Excel.
Results:
The means of peak oxygen consumption (VO2 peak) between the smoking
and non-smoking population are 2.980.84 and 2.8450.95, respectively.
The t-value of the unpaired t-test is 0.36, which correlates with a p-value of
0.72. The analysis shows that the two groups are not significantly different.

3.5
3
2.5
2
Peak VO2 Consumption

1.5
1
0.5
0
Smoker

Non-Smoker

Image 1: The bar graph shows peak oxygen consumption between the
smoker and non-smoking populations.
The mean of heart rate within the smoking populations MAP at rest is
103.213.07, and the t-value of the paired t-test within the smoking group is
0.44, which correlates to a p-value of 0.79. The analysis shows that there is
not a significant change in resting and peak MAP within the smoker group.
The mean of the heart within the non-smoking populations MAP at
peak is 106.815.24, and the t-value of the paired t-test within the nonsmoking group was 2.104, which correlates to a p-value of .049. The analysis
shows that there is a significant difference between resting and peak MAP in
the non-smoking group.

The mean of the difference within heart rate of the smoker and nonsmoker are 10.11The unpaired t-test comparing the absolute change in MAP
between the two populations had a t-value of 1.54 and a p-value of .1409.
The analysis shows that there is no significance of absolute change in MAP
between the two populations.
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. 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 second
joint bar graph in the middle displays rest and peak MAP values to the left
and right respectively within the non-smoker population.

200
180
Smoker

R
R =
= 0.87
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

25

20

15
Mean Arterial Pressure (mmHg)
10

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.
Heart rate was analyzed using linear regression analysis. Both the
smoker and non-smoking mean heart rates were plotted against the
corresponding work rate. The graph has corresponding trend line to each
population. The smoker population has an R2 value of 0.84986, and the nonsmoking population has an R2 value of 0.87061. The closer the value is to 1,
the more correlated the two variables are.

Image 3: The image displays both trend lines for each of the populations,
correlating heart rate with increasing work rate.

R = 0.1

Smoker

Linear (Smoker)

Non-Smoker

Partial Alveolar Pressure of O2

Linear (Non-Smoker)

Linear (Non-Smoker)

50

Linear (Non-Smoker)

100

150

200

250

300

Work rate (watts)

Partial alveolar pressure of oxygen was analyzed using linear regression

analysis. Both the smoker and non-smoking mean pressures were plotted
against the corresponding work rate. The graph has corresponding trend line
to each population. The smoker population has an R2 value of 0.09873, and
the non-smoking population has an R2 value of 0.9873 The closer the value is
to 1, the more correlated the two variables are.

Image 4: The image displays both trend lines for each of the populations,
correlating partial alveolar pressure of oxygen with increasing work rate.

Discussion:
The results show a variety of difference statistical analysis and
conclusions. There is a significant correlation between the changes in resting
MAP and peak MAP because the p-value is .048, which is less than .05. The
linear regression analysis in heart rate shows an R2 value of 0.84986 and
0.87061 for the smoking and non-smoking group, respectively. All other
results are not significantly different because they had p values that were
greater than .05 and R2 values that were not close to 1.
There are a variety of confounding factors within the experiment that
contribute to the results. Since the sample size is 24, the population sizes of
the groups are relatively small, and in order to arrive at more meaningful
statistical conclusions, a large sample size could be used in future
experiments. Also, during the test, human error was a large confounding
factor. Although the subjects had read the instructions before the
experiment, the actual use of the instruments was not practiced. For
example, if the spirometer mask were not sealed tightly, expired gases
would have yielded a lower value, and affected the variables in the results.
Subject number 1082 in the smoker group had a decreasing tidal volume as
work rate increased, and assuming that this individual have normal

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

has lifelong effects on lung volumes (Loganayaki, 1-2), 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, 2) and that smokers should generally have a decreased ability of
both cardiovascular and pulmonary systems (Nikodemowicz), the data of the
experiment showed that VO2 peak, heart rate, and partial alveolar pressure
of O2 are not affected by 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.

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25

20

15
Mean Arterial Pressure (mmHg)
10

0
1Absolute change in MAP in smokers and non-smokers