Corinne Magoon
Kinesiology 323
Spring 2014
VO2max Lab Write-up
VO2 max is a measure of the body’s maximal capacity to transport and utilize oxygen during
prolonged exercise and represents the point at which an increase in workload does not result in
an increase in VO2 (Powers 76). During exercise, the demand for ATP in the working skeletal
muscle leads to an increased demand for oxygen, ultimately leading to increased respiratory and
cardiovascular output. By measuring the ratio of oxygen to carbon dioxide in the air inhaled
compared to that of the sample exhaled, it is possible to calculate approximately how much
oxygen was used in the body for aerobic energy production; therefore, oxygen consumption can
be used as an index for aerobic ATP production (Powers 69).
During prolonged exercise VO2 increases linearly in relation to workload until VO2max is reached
(Powers 76). Because VO2 is dependent on cardiac output and the difference between arterial
and venous blood concentrations of oxygen, it is considered a good indicator of overall
cardiovascular and respiratory fitness (Powers 76, Lab ). Trained athletes generally have a higher
VO2max than an untrained individual because aerobic ATP production begins earlier during
exercise (Powers 70).
In order to understand the concept of VO2max more clearly, on February 6, 2014, as a group of
eight students, we measured a 65.9 kilogram subject’s VO2max while running using the Bruce
Treadmill Test Protocol on a motor-driven treadmill. The subject ran through five stages of the
Bruce Treadmill Test Protocol, with each increase in stage resulting in a higher speed and incline
than the previous stage. Two group members adjusted the speed and incline of the treadmill at
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the beginning of each stage. A subject monitor was available to manage the mouth piece and
make sure the subject was comfortable. One group member acted as a heart rate monitor to give
heart rate measurements at each stage. Three group members worked together to collect gas
samples and take measurements from the metabolic cart.
A Rudolph one-way breathing valve was used with gas bags and a 120 liter Collins spirometer to
collect gas samples of exhaled oxygen and carbon dioxide; samples were analyzed using a
Parvomedics metabolic cart at the end of each sampling session. Prior to beginning exercise a
one-minute resting gas sample was collected while the subject was seated to determine a base
VO2. In order to obtain the most accurate measure of oxygen consumption, the subject was
allowed to reach steady state before each sample. We took one minute air samples during the
final minute of each of the first three stages, and in order to avoid overfilling the Collins, a thirty
second sample was taken during the final thirty seconds of the fourth and fifth three-minute
stages.
The ambient temperature of the lab was twenty three degrees Celsius and the barometric pressure
was 756 mmHg. Due to the fact that the air we measured from the Collins contained moisture,
we used a KSTPD conversion factor of 0.89 to find the volume of air exhaled at standard
temperature and pressure without the partial pressure of water in the air. After converting the
VESTPS of 96.7 L/min to a VESTPD of 86.1 L/min we are able to calculate the subject’s VO2max by
finding the product of VESTPD and the ratio of oxygen and carbon dioxide in inhaled and exhaled
air.
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1. VO2 (y axis) against Bruce Protocol Stage on treadmill. VO2max was 0.12 L/min at rest
and increased to 0.30, 1.43, 2.45, 2.95, and 3.33 L/min for stages one through five respectively.
3.50
VO2 Vs Stage
3.00
VO2 (L/min)
2.50
2.00
1.50
1.00
0.50
0.00
0
0.5
1
1.5
2
2.5
3
3.5
4
4.5
5
Stage
2. HR (y axis) against Stage. The subject’s resting heart rate was measured at 65 and rose
steadily to 108, 134, 173, 178, and 188 bpm for stages one through five respectively.
200
Heart Rate vs Stage
180
160
Heart Rate
140
120
100
80
60
40
20
0
0
0.5
1
1.5
2
2.5
Stage
3
3.5
4
4.5
5
4
3. RER vs Stage. RER was 0.56 at rest and increased to 0.58, 0.67, 0.79, 0.87, 1.01
VCO2/VO2 in stages one through five respectively.
1.20
RER vs Stage
1.00
RER
0.80
0.60
0.40
0.20
0.00
0
0.5
1
1.5
2
2.5
3
3.5
4
4.5
Stage
4. VO2 vs HR. As heart rate increases, VO2max increases as well in a linear fashion.
5
5
3.50
VO2 vs Heart Rate
3.00
VO2
2.50
2.00
1.50
1.00
0.50
0.00
0
20
40
60
80
100
120
140
160
180
200
Heart Rate
5. CHO ox & fat ox vs stage. Fat oxidation increased through the third stage and began to
decrease; carbohydrate oxidation increased consistently throughout the five stages.
5.00
Substrate Oxidation Vs. Stage
Substrate ox (g/min)
4.00
3.00
CHOox
2.00
Fat ox
1.00
0.00
0
-1.00
1
2
3
4
5
Stage
6. %CHO & %fat vs stage. Fat oxidation was 100% in the first stage and decreased steadily
throughout the five stages. Carbohydrate did the opposite, and increased as the five stages
progressed.
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120
% Subrate Oxidation vs Stage
% Substrate Oxidized
100
80
60
% Carbohydrate
40
% Fat
20
0
0
1
-20
2
3
4
5
Stage
Discussion
1. At lower workloads VO2 is linearly related to workload. Do these results imply a causal
relationship between VO2 and work?
There is a causal relationship between workload and VO2 in that an increase in workload
leads to an increase in VO2 until the point of volitional fatigue. As workload increases,
the mitochondria of the working skeletal muscle must produce more ATP. An increase in
aerobic ATP production during prolonged exercise requires an increase in oxygen
delivery to the muscle via the cardiovascular system. With VO2 being dependent on
cardiac output as well as the difference between arterial and venous oxygen
concentration, increased oxygen delivery and utilization increases VO2 (Lecture 33).
2. Discuss the physiological significance of the leveling off of VO2, while workload
continues to increase.
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Each stage in the Bruce protocol is at a higher speed and incline than the previous stage;
with this increase in intensity, the workload and amount of energy required of the body
increases as well. As the working muscles require larger amounts of ATP to continue the
action, the cardiovascular system is required to move more oxygen to the working
muscles to maintain ATP production in the mitochondria. If the subject was able to run
through another stage, we might see the VO2 max reach a plateau, because the
cardiovascular system has reached its capacity for oxygen transport. An increase in
workload will result in an increase in VO2 up to a certain point, but there is a volume at
which oxygen transport and utilization cannot be increased any higher; at this point we
see VO2max plateau while workload may increase.
3. Given the graph, what causes R to increase rapidly at point A?
Respiratory exchange ratio measures the ratio of volume of carbon dioxide output to the
volume of oxygen used (Powers 79). Due to the fact that fat and carbohydrates require
different amounts of oxygen to be oxidized, RER is often used to estimate what substrate
the muscles are using to produce ATP. Because fat oxidation requires more oxygen than
carbohydrate oxidation, a higher RER would represent more carbohydrate oxidation than
fat oxidation (Powers 79).
4. Describe the relationship between heart rate and workload. Why does the heart respond
this way?
VO2 max is dependent on cardiac output, which is dependent on both stroke volume and
heart rate. As the demand for ATP in the working muscle increases, the demand for
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oxygen transportation by the cardiovascular system increases as well. As more oxygen
needs to be delivered to the working muscle, the cardiovascular system increases both
stroke volume and heart rate to deliver a large amount of blood. The Frank-Starling law
states that an increase in end diastolic blood volume leads to stretching of cardiac muscle
fibers causing the muscles of the heart to contract harder, as a result increasing stroke
volume (Frank-Starling Relationship).
5. Why does the absolute amount of CHO and fat change w/ increasing exercise intensity?
Why does the percent contribution of each substrate change w/ increasing exercise
intensity?
During the first few minutes of exercise, the majority of ATP is produced by anaerobic
metabolism, oxidizing primarily fat. Prolonged exercise brings about increased blood
levels of epinephrine, which subsequently increases phosphorylase activity (Powers 80)
causing breakdown of muscle glycogen and increased lactate production. Due to the
increased availability of muscle glycogen, the body transitions from oxidizing fat to
producing ATP primarily by oxidizing carbohydrate. As it requires more oxygen to
metabolize fat than it does to metabolize carbohydrates, it becomes more efficient to use
oxygen for carbohydrate metabolism during prolonged exercise. Prolonged exercise may
also require a large number of fast-twitch muscle fibers, which metabolize carbohydrates
more efficiently than fats due to their lack of lipolytic enzymes.
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Resources:
Dr. Azevedo. Exercise Physiology Lecture Notes Spring 2014.
Exercise Physiology Lab Manual, Spring 2014.
Powers, Howley. Exercise Physiology: Theory and Application to Fitness and
Performance, 8th edition. McGraw Hill, 2012.
R. Moss, D. Fitzsimons. Frank-Starling Relationship: Long on Importance, Short on
Mechanism. American Heart Association; Circulation Research, 2002; 90:11-13.