Anaerobic metabolism is the gatekeeper for aerobic energy

Model of Energy Metabolism

The following is a description of the model of energy metabolism developed

by Alois Mader. It is not in any textbook despite there being thousands of
books that discuss energy metabolism. Yet it describes a scenario that fits
the data better than any of the theories in the textbooks. The lactate
threshold or maximal lactate steady state is acknowledged but its origins are
said to be a mystery. It is no mystery. It is the result of a few basic forces
playing off against each other producing results that are easy to see and
described by Mader's model.
The basic idea that is missing from current energy metabolic theories is how
the aerobic and anaerobic systems interact. And despite the very large
majority of the energy being delivered from aerobic energy, something else
controls this delivery. This control or, as we express it, a gatekeeping
process is the anaerobic system. An athlete may have a very large aerobic
capacity as indicated by a VO2 max test but he or she may not be able to use
it to the extent they wish. The following is a little more technical than other
things the reader will see on this topic but it explains this gatekeeping effect.

Mader model - Pyruvate/lactate formation at a given effort level depends

on three variables. These three variables are:
1.

VO2 max - this is aerobic capacity or the maximum rate of energy production by the
aerobic system. VO2 max is usually estimated by a device attached to the mouth and nose of an
athlete. The device measures oxygen uptake by athletes as they complete a progressive exercise
test to exhaustion.

2.

VO2 steady state - this is the amount of aerobic energy that is being used during a
sub-maximal steady state exercise. It is usually measured using the same instruments as for VO2
max.

3.

VLamax - this is anaerobic capacity or the maximum rate of energy production by the
glycolytic system. It is sometimes designated by the term Plamax or maximum production of
lactate. In reality this is the maximum rate of production of pyruvate and lactate but since lactate
is what is measured La has been used for this term.
The theory states that VLa (the production of lactate) at any steady state
level is a function of VO2 max, VO2 at that level and VLamax.

VLa = f(VO2 max, VO2 steady state, VLamax)

For example, suppose a runner has the following aerobic and anaerobic
capacities (VO2 max of 60 ml/kg/min and maximum lactate production rate
of .7 mmol/sec/l.)
This chart below shows a lactate/pyruvate production curve based on these
capacities. This is not the typical lactate curve you have seen throughout this
set of modules on endurance sports and the triathlon, even though it is
deceptively similar in shape. The curves you normally see for lactate tests
are measures of lactate levels in the blood, usually plotted against a
measure of speed or power. This is an estimate of lactate production not
lactate levels and it is in the muscle fiber itself. Notice the measures are
different. The left axis is lactate production, not lactate levels. The unit of
lactate production is lactate mmols per minute per liter. It is a rate such as
miles per hour or meters per second. The total lactate production capability
for this athlete is 42 mmol per minute per liter based on the estimated
maximum production level of .7 mmol/sec/l. So this chart indicates that the
athlete will never get close to the maximum production level.
The lower axis is VO2 for the current steady state effort level.

Remember our formula from just above, VLa = f(VO2

max, VO2 steady state, VLamax). The VLa is the
left axis in the chart. The VO2 steady state is the bottom
axis. The VO2 max and VLamax are constants for each
athlete and remain the same for this testing protocol. As
the intensity of the exercise rises and is measured by the
VO2 measured at each stage, the rate of lactate
production will also increase. The red curve measures the
rate of lactate production.
Thus, as the athlete increases in speed and increases his oxygen uptake, the
amount of lactate produced also starts to rise. At first it will rise very slowly
but as the runner increases speed not only will his oxygen uptake increase
but so will the production of lactate. So at very low levels the anaerobic
system that produces the lactate is being used only sparingly but at higher
effort levels, the percentage of energy supplied by anaerobic energy
increases and then reaches a point where it starts to increase very rapidly.
Notice the anaerobic capacity of this athlete is 42 mmol per min per liter
(VLamax of .7 mmol/sec/l x 60 seconds) but on this chart he never gets
close to that capacity as production rates range from less than 1% of
anaerobic capacity to about 7.1% of anaerobic capacity as he approaches
80% of aerobic capacity (48 ml/kg/min).
The next chart compares two athletes with different aerobic capacities but
equal anaerobic capacities. It is similar to the preceding chart except the
new athlete has a VO2 max of 75 ml/kg/l. The lactate/pyruvate production
curve is lower at every steady state VO2. Increasing the VO2 max and
keeping the maximum lactate production rate the same, produces less
lactate.
So the amount of lactate produced by the glycolytic system depends not only
on the strength of the anaerobic system (VLamax) but also on the strength
of the aerobic system. As we pointed out earlier the muscle must choose
how to replenish the ATP and as the aerobic capacity increases it chooses to
replace more of the ATP by aerobic processes at every effort level.

At a steady state of 40 ml/kg/l the athletes with the greater aerobic capacity
(75 ml/kg/l) will produce less than half the lactate of the athlete with the
lower aerobic capacity (60 ml/kg/l)

With athletes that have similar aerobic capacities but different anaerobic
capacities the muscle again will make different choices on how it replaces
the ATP. In the chart below three athletes with different anaerobic capacities
but the same aerobic capacity (60 ml/kg/l) produce substantially different
amounts of lactate.

The athlete with an anaerobic capacity of .1 mmol/s/l will produce very little
lactate until he gets close to VO2 max and then his lactate production will
shoot up dramatically. The athlete with an anaerobic capacity of 1.3
mmol/s/l will produce substantial amounts of lactate even at low effort
levels. So as anaerobic capacity rises or falls the muscle chooses different
systems to replace ATP.
The lower the maximum lactate production rate, the further to the right is
the curve. This shows why marathoners want to have a low VLamax. The
lower it is the less lactate will be produced and the higher percentage of VO 2
max they can run. However, they will not have any speed for acceleration or
speed at the end. Nor would they be very good at 1500 m. Remember our
comparison of the three runners. A runner with a higher VLamax and the
same VO2 max will be faster at 1500 m.

An aside: actually a marathoner will not want a VLamax as low

as .1 mmol/s/l (extremely low) because the body will not
produce enough lactate or pyruvate to fuel aerobic metabolism
by burning carbohydrates and the muscles will have to use fat
as a fuel. This will slow the athlete down, because fat

metabolizes at about half the rate of pyruvate and causes the

athlete to contract the muscles at a slower rate.
The lactate production rates between individuals with a VLamax of 0.1
mmol/s/l and one with 1.3 mmol/s/l is very dramatic. The next chart shows
that the rate of lactate production is 10-14 times greater at a VLamax of 1.3
mmol/s/l vs. a VLamax of 0.1 mmol/s/l for three different steady state
levels.

This dramatic influence of VLamax on lactate levels is not widely discussed in

either the academic literature or in the popular training press. What are the
implications of this for training and for performance? Continue as we discuss
the anaerobic system further and discuss how to train it to help achieve an
optimal performance.

Training to control the

gatekeeper for aerobic energy
Implications for Training and Testing

The implication of the charts in the preceding section is that an athlete will
generate considerably less lactate at lower VLamax rates as well as fewer
hydrogen ions. This means that the muscles will be less acidic and will be
able to contract more freely at higher percentages of VO2 max. For
endurance athletes this is highly desirable as they will be able to race at a

much higher percentage of VO2 max before generating large amounts of

lactate.
Jan Olbrecht has found that it is possible to train these VLamax rates. There
seems to be a genetic maximum and there is probably some lower limit for
each athlete. But it is not uncommon to raise or lower this parameter during
a training season and thus affect lactate production and the corresponding
lactate curves and the performance of an athlete during an event. Coaches
often do this type of training instinctively as they know that certain types of
workouts in certain sequences lead to better performances.
The following three charts provide insight into the differences between the
measures of the aerobic system and the anaerobic system. The important
thing is that a coach or sports scientist cannot take their in-depth
understanding of VO2 max and apply the same assumptions to the anaerobic
system. It is a very different world. First, two charts that illustrate the
conventional wisdom for aerobic capacity.

Source: A physiological comparison of young

and older endurance athletes, G. W. Heath, J.
M. Hagberg, A. A. Ehsani, and J. O. Holloszy,
Journal of Applied Physiology September 1981
vol. 51 no. 3 634-640
Notice that trained is higher than untrained and that younger is higher than
older. Nothing unusual here. Just what one expects. If you train, your VO 2
max will increase but the maximum it can reach declines with age. But here
is a chart we showed earlier on anaerobic capacity. It shows something
entirely different.

Source: Biochemistry for Medical Sciences,

Newsholme, E., Leech, A.,
John Wiley 1983
There is not much published on this concept and that is one reason why no
one pays attention to it but just because it is not a subject of research, it
does not mean that it is not important. It should be a major area of
research. Notice it is the "couch potato" or untrained individual that has a
high anaerobic capacity, just the opposite from aerobic capacity which is
lowest in untrained individuals. So training seems to lower anaerobic
capacity. But that is a flawed conclusion, as only certain types of training
lower it. There is no information here on sprinters but if there were, their
values would be high, much higher than the untrained people in the above
chart. The 100 m and 200 m sprinter would be extremely high and these
people obviously train. Thus, certain types of training lower anaerobic
capacity and other types raise it or keep it high. There are definitely genetic
limits as only a few can become world-class sprinters or at the other end,
world class marathoners or Ironmen.
But what is the proper anaerobic capacity for an athlete? That depends on
the event the athlete is training for and the strength of the aerobic system.
No matter what the event, more aerobic capacity is always better. However,
this is far from true for anaerobic capacity. Anaerobic capacity has to be
adjusted to aerobic capacity and the event.

Some typical training scenarios - For short races it is very common to

manipulate the anaerobic capacity during a normal training season. For
example, swimming is mostly races lasting less than two minutes. During a
training season the coach will always start out with endurance training. As
the important meets approach, the coach will switch to high intensity
workouts (often referred to as quality sets) which have the objective of
raising the anaerobic capacity of the swimmers to make them faster. Since
their races are short, this increase in anaerobic capacity provides the speed
to do well in these short events. But for longer races this increase in
anaerobic capacity would be detrimental. For endurance athletes, anaerobic
capacity should often be lowered, but not always. Some athletes already
have low anaerobic capacities so lowering them any more could be selfdefeating.
The relative strength of the aerobic and anaerobic systems determines
substrate utilization for ATP replacement. This is the key point every
textbook misses and because they miss it they are inadequate on providing
proper training advice. As an athlete goes through the training process these
energy systems will change depending upon the training stimulus and
subsequent adaptation. This means that the proportion of ATP replacement
by each system will change accordingly. This is reflected in the following
three principles of lactate production:

Intensity Principle Lactate production increases as intensity

increases (within each individual athlete).
Aerobic Capacity Principle - As aerobic capacity increases the
utilization of the anaerobic system will be less at every effort level if
nothing else changes. Less lactate will be produced at each effort level.
Anaerobic Capacity Principle As anaerobic capacity
increases the utilization of the aerobic system will be less at every
effort level if nothing else changes. More lactate will be produced at
each effort level. The reverse of this is also true. As the anaerobic
capacity decreases the utilization of the aerobic system will be higher
at every effort level. Less lactate will be produced at each effort level.
One of the important implications of the last principle is that the amount of
the aerobic system an athlete can access during a race is dependent upon
the strength of the anaerobic system. The stronger the anaerobic system,
the lower the percentage of aerobic capacity an athlete will reach at the
maximum lactate steady state. For longer races this is one of the most
important factors affecting performance. Essentially, the anaerobic system

acts as a Gate Keeper for the aerobic system. It determines how much
can get used. An athlete may have a huge aerobic capacity and not be able
to access most of it because of the anaerobic capacity.
Implications for Training

Since training can affect both of these capacities in ways not always
expected, it is useful to continually monitor an athlete to assess whether
training is having the desired effects. The following chart indicates what can
happen to lactate levels when aerobic and anaerobic capacity changes.

The chart can be read as follows. In the upper left hand box where anaerobic
capacity rises and aerobic capacity also rises, lactate production could go up
or down at a specific effort level. An increase in anaerobic capacity will tend
to increase lactate production while and an increase in aerobic capacity will
tend to lower it. So when both of these capacities increase, the net effect
could be either higher or lower lactate production. It could go up or down
depending upon which change had a greater effect.
When aerobic capacity goes up and anaerobic capacity goes down, the
amount of lactate produced is often dramatically less. This is a situation
quite common with swimmers and many other athletes during base training.
However, when a swimmer increases anaerobic capacity training later in the
training cycle it is quite common to see lactate levels rise because aerobic
capacity has essentially topped out for the training period. Thus, the athlete

is in the middle box on the left hand side. For an athlete such as a swimmer
who is competing in short events (1-2 minutes) this is an indication that
they are getting faster as their anaerobic system will be producing energy
more quickly during these short events.
A note on training. Every set and every workout will affect the aerobic
capacity and the anaerobic capacity to some extent. Some more, some less.
Some workouts may affect one capacity more than the other. To reach a
desired balance it may be desirable to train one capacity in the wrong
direction for a short time period and then counter act this effect with training
it in the other direction. The reason is that it may be desirable to get one, for
example aerobic capacity, to a certain level but the best way to do that it to
train the anaerobic capacity either too high or too low for the event.
Subsequent training might be to then adjust the anaerobic capacity,
hopefully without affecting the aerobic capacity. Training over a season is a
continual building to an objective but constantly modifying one or both of
these capacities over time to reach the desired balance.
This section is only a brief part of Alois Mader's model of energy metabolism.
One of the most important contributions of this model is an explanation of
how the anaerobic system affects energy metabolism and training, which
was our emphasis in these three modules (Anaerobic mechanism, anaerobic
gatekeeper, controlling the gatekeeper). For short races such as swimming
the model explains how an athlete can get faster while the lactate curve
remains the same or even moves to the left. It also explains why most of the
training for short events must be aerobic even though the anaerobic system
is the primary source of energy during a short race. For longer events, the
model explains just what causes the maximum lactate steady state and what
percentage of VO2 max an athlete can utilize during distance events such as
the marathon, cycling road races and the triathlon. The model also explains
why elite athletes, especially endurance athletes, are in more danger of
over-training than lower level athletes and thus must be more careful of how
intensely they train.
Some References:
Mader, A. and H. Heck (1986). "A theory of the metabolic origin of
"anaerobic threshold"." International Journal of Sports Medicine 7(Sup):
S45-S65.
Mader, A. (1991). "Evaluation of the endurance performance of marathon
runners and theoretical analysis of test results." Journal of Sports Medicine
and Physical Fitness 31(1): 1-19.

Mader, A. (2003). "Glycolysis and oxidative phosphorylation as a function of

cytosolic phosphorylation state and power output of the muscle cell."
European Journal of Applied Physiology 88(4-5): 317-38.
Hartmann, U., & Mader, A. (1996). The metabolic basis of rowing. In
Rogozkin & R. J. Maughan (Eds.), Current research in sports science (pp.
179-185). New York: Plenum Press.
Mader, A., Hartmann, U., Hollmann, W. (1988). Der Einflu der Ausdauer auf
die 6mintige maximale anaerobe und aerobe Arbeitskapazitt eines
Eliteruderers. S. 62-79. In: Steinacker, J.: Rudern: Sportmedizinische und
sportwissenschaftliche Aspekte. Berlin: Springer.
Mader, A., (1994). Aussagekraft der laktatieistungskurve in kombination mit
anaeroben tests zur bestimmung der stoffwechselkapazitt. In: Clasing, D.,
Weicker, H., Boening, D.: Stellenwert der Laktatbestimmung in der
Leistungsdiagnostik. Stuttgart: G. Fischer.