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In the final lecture of this module, we'll
focus on the maximal oxygen uptake, or VO2 max.
The most widely accepted measure of Cardiorespiratory fitness.
VO2 max is really the reflection of the combined abilities
of respiratory and cardiovascular systems to deliver oxygen to contracting muscle.
And of those muscles to consume oxygen. If we look at the relationship
between oxygen uptake and power output, we see this linear relationship.
However, depending on the level of training, the
level of fitness, and indeed the genetic endowment,
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the VO2 max, level is attained at, varying levels.
In sedentary individuals it's relatively low.
The value here, 30, is the,uh VO2 max expressed in
millilitres of oxygen, a kilogram of body mass per minute.
If we look at, normally active individuals, they might
be in the range of the 40s to the 50s.
If we take those individuals and put them on a training program, we can expect
to see an increase of anywhere from 10 to 20% depending on the starting level.
If we look at highly in trained, highly trained endurance athletes, we see very
high values up here in the 70s and 80s and in some cases they're very low 90s.
These very high values probably represent
genetic endowment and very hard physical training.
Both are required to really reach these very high levels.
In cross-sectional studies that have been taken on various
athletic groups, you can see that the VO2 max is
generally higher in those groups where there's a heavy
reliance on the oxidative energy systems and the cardio-respiratory systems.
So in cross-country skiers, in distance runners, speed skaters, these
are not the speed track speed skaters but more the endurance type speed skating.
orienteering and running, cycling very high values in the 70s, 80s.
I think the highest values that's been reported in the literature is 92.
For a very well trained cross country skier.
In the less aerobically dominated events you can see lower values,
and in the untrained values, as I said, 40 to 50.
With a, a period of endurance training, we could expect
an increase in that VO2 max value for non trained individual.
If we think about the factors which determine the VO2 max, most of the
attention is focused on the oxygen delivery,
pathways and in fact is within the muscle.
In recent years its been suggested that such an approach ignores the important
wall of the central nervous system in
driving people to exercise recruiting the muscles.
And there's no question that the brain, has an important role in motivation during
a max test.
Can drive, subjects or athletes to a high level.
But, in terms of limiting the VO2 max, a lot of attention, as I said, is
focused on the oxygen delivery pathway, the respiration,
and the ability to maintain, arterial oxygen saturation.
The central circulation, the maximal cardiac
output, and the oxygen carrying capacity
of the blood. The ability to, distribute, that blood
into the contracting muscles, and finally, the ability of the muscles themselves.
To consume that oxygen, which is going to be determined by the amount of,
the extent, of mitochondria, the oxidated fuels,
and the fibre type, the capillary density.
If you look at the relationship between oxygen delivery, and the oxidative
capacity of the muscles. In small muscle group exercise where the,
the maximal cardiac output is not challenged, the oxygen delivery is so,
more than adequate for the oxidative capacity of those arm muscles.
In contrast, if you look at exercise involving the legs and
a larger muscle mass, and you begin
to approach the maximal limits of cardiac output.
The oxygen delivery is somewhat less than the oxidative
capacity of the muscle, and this implies that during
large muscle mass exercise, it's the oxygen delivery which
is really, right limiting for the maximal oxygen uptake.
And here's the relationship between the VO2 max and oxygen
delivery derived from the earlier slide that I showed you.
redrawn with VO2 max now as the dependent variable and oxygen delivery,
we define oxygen delivery as the arterial oxygen content, times the cardiac output.
And we know that cardiac output is the product of heart rate and stroke volume.
And you can see for those various groups
that were listed earlier, sedentary, active, trained, and
endurance athlete, with an addition group here studied
after a period of bed, bed rest, or de-conditioning.
You can see the relationship between VO2 max and oxygen delivery.
And it's for these, this reason that there's been so much attention
focused on the ability to deliver oxygen, particularly, the arterial oxygen content,
of the the blood that's being delivered to the
contracting muscles, I'll talk about that a little bit later.
We look at the respiratory system, we saw
in the previous lecture, in most healthy people,
exercising at sea level, the arterial oxygen content
is reasonably well maintained, the arterial oxygen saturation.
In some individuals however, as we discussed
you can see this desaturation, and this is what occurred when these subjects were,
breathing in air at 21% oxygen, the normal atmospheric oxygen content.
Clearly if you reduce, the inspired
oxygen, partial pressure for example if you
go to altitude, you see a more pronounced desaturation and that's not surprising.
But what is surprising,
to some, was this desaturation on 21%.
And as I said, the most likely
explanation for this is pulmonary diffusion limitation.
You'd see large increases in cardiac
output, maximal cardiac output after training.
There's relatively little change in the morphology
and the diffusion diffusion characteristics of the lung.
And this reduction in transit time challenges the
ability of the lungs to fully oxygenate the pulmonary blood.
If you increase the oxygen in the inspired gas so that these
subjects are now breathing 26% oxygen, you can say that you prevent the
saturation and you see a slight increase in the VO2 max, so
for some individuals there may be a pulmonary limitation to the VO2 max.
As
I said however, most healthy people exercising at sea level.
The lungs are not thought to be a limiting factor for maximal oxygen uptake.
There is a plateau in oxygen delivery,
and here's the relationship I showed you earlier.
Between oxygen delivery and VO2, and you can
see at the higher intensities here, this levelling off.
And this corresponds
with a levelling off in cardiac output, and the reason that cardiac output levels
off, is that stroke volume has levelled
off or even declines slightly at maximal exercise.
And although heart-rate can increase slightly up to its maximal level, it is
this slight reduction in stroke volume, means
that cardiac output can no longer, increase.
This has the consequence of limiting the
leg blood flow and the leg oxygen delivery.
And it's sought that this is an
important factor in determining the maximal oxygen uptake.
Another experiment that, that's been used to
investigate these is using small muscle group exercise.
So a single-leg exercise where just the
knee extensors, of the lower leg were used.
that two to three kilo of active muscle mass, compared with two-legged cycling,
either incremental exercise or very intense exercise, up to maximal levels.
And you can see, at the,
with the single-leg knee extensor, the
ability to increase cardiac output and maximally
perfuse the small muscle mass, is, is really quite free and is not limited.
In contrast with the, the two-legged cycling,
the increase in cardiac output is somewhat constrained.
If you then look at the increase in leg
blood flow, you can see at the higher intensities
with the larger muscle mass, the inability to maintain
the trajectory of increasing blood flow and a labelling off.
These are some of the data in the
literature that suggest that oxygen delivery as determined
by the maximum pumping capacity of the heart
is an important factor in determining VO2 max.
The central circulation can influence the maximal
cardiac output and the amount of oxygen
that is in the arterial blood that can be delivered to the contracting muscle.
Alterations in blood volume.
have an
, impact on end-diastolic volume, maximal
stroke volume, and therefore maximal cardiac output.
Plasma volume expansion acutely, in untrained subjects,
has been shown to increase the VO2 max.
And similarly, loss of central blood volume and dehydration, reduces
maximal stroke volume, reduces maximal cardiac output.
Over the years there's been some interest in
interventions that aimed at increasing the red cell mass.
Blood doping, which has been involves the removal of a small volume of blood.
Storage in appropriate chemicals, and then rein-fusion, to
increase the blood volume and increase the red
cell mass, has been associated with an increased
in VO2 max, and an increase in exercise performance.
And it has been outlawed by, various sporting authorities.
as a form of, of doping.
Erythropoietin, a hormone released from the kidney
in response to low oxygen levels, stimulates the
production of red cells, and was a popular
chemical used, to try and improve endurance performance.
Similarly, that's been banned. And altitude training,
one of the adaptations to, exposure to altitude is to increase red cell mass.
And all of these factors are designed to
increase the oxygen carrying capacity of the arterial blood.
Especially in well trained subjects who, as part of their training that see
an increase in their blood volume and
a slight reduction in the haemoglobin concentration.
So these other interventions. Have been,
trialed to increase red cell mass on the back of an expanded blood volume.
Increasing cardiac output has to be distributed to the muscles and there is an
association between maximal oxygen uptake and the capillary density of the muscle.
So not surprisingly not only is there an increase in
the maximum cardiac output with training as we saw in
the cardiovascular lecture also an increase in the capillary density
so that the distribution of that cardiac output into the contracting
muscles can be optimized. The diffusing capacity
in the tissues is also important the ability of the oxygen to move from the
red blood cells in the capillary through the distischill fluid into the muscle.
And this is influenced by a number of factors the surface area
of the capillaries, capillary network, the
surface area of the mitochondrial network the
tissue fluid levels the distances.
And all of this is rolled together into
a term known as the diffusion muscle diffusion capacity.
And we know that it does change as a result of exercise training and
contributes significantly to the increase in VO2 max following training.
It's important to understand that all of the, the variables involved in
oxygen transport to contracting skeletal muscle.
And indeed, the abilities, the ability of the muscle to consume
that oxygen all contribute to an oxygen, a maximal oxygen uptake.
And as is, I said at the outset, also
the ability to fully activate and recruit those skeletal muscles.
Here's a an overview of changes in VO2 max that could be predicted to
occur with changes in various parameters.
And they listed here, the cardiac output, the diffusing capacity of the
lung, the diffusing capacity of the
muscle, the haemoglobin concentration, the avoeole ventilation.
All of these factors contribute importantly to maximal oxygen uptake.
On balance however, most of the evidence
suggests that the ability to deliver muscle
to the contracting skeletal muscles, is the most important determinant of VO2 max.