(This page is pertinent to both lecture and lab. However, as indicated below, the last three sections apply only to lab.)
The figure to the right shows VO2 plotted as a function of power for our seven subjects. Notice first that all of the subjects, regardless of size, expended nearly the same amount of energy for a specific level of work. This is expected with a bicycle ergometer. Cranking the pedal in each case required about the same number of cross-bridge cycles per minute, and thus about the same amount of ATP.
The line in the figure is not derived from our data, but is taken from the standard reference work on exercise tolerance tests. In other words, with different equipment at different locations, the same amount of oxygen is consumed at each watt level on a bicycle ergometer.
If we had measured the subjects walking up stairs or a similar type of work, we would have found that the VO2 was different for individuals of different sizes doing the same exercise.
(Note that our resting energy expenditures vary quite a bit. Mainly this is because points at zero watts were taken both at complete rest and with the subject peddling against zero resistance. But also this because the resting energy expenditure depends on body size. As a result there is a small effect of size on the data.)
Given that all of our subjects gave an excellent effort, the highest VO2 recorded for each individual is close to the VO2max for that individual. And looking at population averages, the numbers are as expected for fit young adults. The actual number is strongly dependent on the size of the individual.
Note that the subjects who did the lactate test can also find their VO2max number by using their maximum watt level to find the corresponding VO2 on the graph.
In this type of protocol, it is typically not possible to see the points reach a plateau. Finer gradations around the VO2max would be required.
The maximal oxygen uptake also depends on a person's genetics and level of training for endurance exercise. For example, looking at the table below (taken from the respiratory system handout) you will see that the VO2max for the world class athletes averaged 5.3 l/min, compared to 3.3 l/min for the college students. Note that the two groups are matched by body size. (They probably averaged about 70 kg or so.) This is important since VO2 max depends proportionately on the size of the individual.
The arterial oxygen content, of course, is proportional to the amount of hemoglobin in the blood. The arterial-venous O2 difference increases when the muscles are able to extract a larger fraction of the oxygen in the blood. This occurs when there are more mitochondria relative to the amount of blood passing through the muscles.
Look down the chart and observe what one factor correlates best with the magnitude of the VO2max.
A recent clinical study with older patients found that VO2max is one of the best predictors of mortality, especially if cardiovascular disease is present.
Now let's focus on the results from one subject (Thursday, 2:30). To the right are the VO2 measurements for this subject, who we will continue analyzing below. (The red line is the same as in the graph above for all lab sections.)
The graph to the right shows the ventilation (Ve) for the subject (again Thursday, 2:30) as a function of watts. Notice that the points follow a linear relationship at lower levels of work. This, of course, is as expected, since proportionately more ventilation is required to deliver more oxygen to the alveoli.
But above about 140 watts there is a change, with ventilation increasing considerably more than expected based on the earlier relationship. As we discussed on the previous page, this is because the subject has passed the lactate threshold (anaerobic threshold), in which lactic acid begins accumulating in the body. This causes a disproportionate increase in breathing through stimulation of the peripheral chemoreceptor. Thus the exhausted subject's PaCO2 is actually lower than at the beginning of the exercise.
The R.Q., which is the ratio of the CO2 exhaled to the O2 consumed, is shown to the right for the same subject as in the graph above of Ve. If a person is burning pure carbohydrate the ratio will be 1.0.
At rest, our subject had an R.Q. of about 0.7. This is within the range expected in a resting person.
In one respect this subject was a little unusual in that she was not hyperventilating a little at rest. This is usually the case as the subject anticipates the upcoming exercise. With hyperventilation, the R.Q. is higher than the actual resting level, because the subject is blowing off more CO2 than expected. This is what we usually observe at rest as the subject is anticipating the exercise. Then as the subject begans to exercise at lower rates, the R.Q. settles down to the expected resting level as physiology rather than anticipation controls the breathing.
But above the lactate threshold we expect the R.Q. to steadily increase as H+ stimulates the peripheral chemoreceptor and as H+ reacts with bicarbonate in the blood to liberate CO2. This is what we see above about 140 watts. The final R.Q. at exhaustion was 1.20, which is about what we would expect for a good effort with lots of lactate produced near the end.
As discussed in the lab manual, the oxygen consumption can be converted directly to kcal/min by multiplying by 4.8 kcal/l O2. One kcal, of course, is equal to one dietary calorie, such as are used on food packages.
Another energy unit is the metabolic equivalent (MET). This is useful, since it takes into account the size of the subject. One MET is defined to be 1.0 kcal/hr per kg. A person expends, for example, about 1.0 MET watching TV.
Inspecting the definition of a MET above, you will see that at 1.0 MET your energy expenditure in kcal/min is equal to your weight in kilograms. For other activities, you find your MET level by multiplying your expenditure at 1.0 MET by the number given for the activity in the table in the lab manual. Approximately what is your expected energy expenditure on a typical day? This converts directly to dietary calories burnt during that day.
Clinical studies looking at the effects of exercise typically express levels of exercise in terms of METs. Other values are given in the table on the second page of the exercise.
You are asked to calculate Ve, VO2, VCO2 and R.Q. in the lab exercise, as described in the lab manual. You are also asked to estimate your daily energy expenditure using the blank table on the last page. For the latter, first select activities from the MET table on the second page that more or less cover what you did on your selected day. Then convert the MET value to kcal/hr using your weight in kilograms. Next fill in how many hours you spent on each activity and then total up the kilocalories for the entire 24 hours.
On the lab practical, a calculation question might begin with a partially completed table from the handout. You might then be asked to fill in another square based on a one or two step calculation. The entire laboratory exercise would be furnished so you could look up constants.
Let's look at how the heart rate changed in a subject (Tuesday: 10:30) as the level of work increased. First, observe that at rest the heart rate is higher than you might expect. This again shows the marked anticipation that is characteristic of both the respiratory and cardiovascular systems. As the work level increases, by necessity the physiology takes over, and the heart rate adjusts to that required by the exercising muscles.
Recall that the amount of oxygen consumed by the subject increases linearly throughout the increasing levels of work. (This indeed is necessary since the subject requires a linearily increasing amount of ATP to turn the pedals.) How is this extra oxygen supplied?
As discussed in lecture, the hemoglobin is basically fully saturated at all levels of work. Indeed, the partial pressure of oxygen in the arterial blood should increase somewhat at the peak of exercise, as discussed on the previous webpage.
Thus, the amount of oxygen per liter of systemic arterial blood is basically unchanged throughout the exercise.
The first way to increase the delivery of oxygen to the muscles is to increase the cardiac output by increasing the heart rate. As the figure shows, the heart rate increases linearily with the work after the initial anticipatory, feedforward effects are surpassed. Thus, the increasing heart rate explains much of the increased delivery of oxygen.
But there are two additional factors that can increase the delivery of oxygen The first is an increased stroke volume. Recall that sympathetic nerves can increase the stroke volume. This indeed may happen at higher levels of work. The second additional factor is by a decreased oxygen content of the mixed venous blood entering the right atrium. At rest, nearly 75% of the oxygen in the arterial blood returns to the heart. But as exercise increases, the PO2 in the exercising muscle decreases and a larger percentage of the oxygen unloads from the hemoglobin. This causes a larger difference in the oxygen content between the arterial and venous blood.
The figure to the right shows data taken from a study in which a catheter was used to sample blood entering the subject's right atrium.
Mathematically, the VO2 is equal to the cardiac output times the difference between the oxygen content of arterial blood (CaO2) and the oxygen content in mixed venous blood entering the right atrium (CvO2). (In the table above, the difference in oxygen contents is refered to as the "art.-ven. O2 diff.")