According to the Peripheral fatigue model and the Cardiovascular/anaerobic model:

Fatigue is the result of physiological failure, causing the athlete to stop or to slow
down. Failure can be anywhere in the system – it might be failure to supply
enough oxygen to the muscles, failure to keep lactate, phosphate or hydrogen ion
levels down, a depletion of glycogen, or failure to lose heat, causing the body
temperature to rise too high. Once this “failure point” is reached, exercise must slow
down, or stop altogether. The key point is that fatigue is a “limit,” and it lies in the
muscles or the complete inability of the brain to activate muscle.

Performance and fatigue are regulated to prevent the potentially harmful limits
from being reached. The brain regulates the body specifically to protect against that
damage. At the same time, it’s trying to balance protection with the athletes’ desire to
perform well, and that produces a constant balance between two potentially
conflicting goals. Thus, performance is regulated, not determined, by the
physiology. Many world-class endurance athletes use the pacing strategy (faster
start, slowing in the middle, with an endspurt to finish) as a part of this regulation.
The pacing strategy is the OUTPUT component of a very complex
physiological system. During pacing, the work is done by the muscles, which are
stimulated by the brain. When athletes slow down, there are only two possible
causes: Either the muscle is fatigued (the peripherial model), or less muscle is being
activated. But in order to produce this conscious decision to modify the OUTPUT,
a wide range of INPUTS (e.g. heat, altitude) needs to be considered. To put this
into a sporting example, an athlete who maintains a 4min/km pace during a 10km
race at sea-level and in cool temperatures won’t be able maintain the same pace at
1) high altitudes or 2) in 35 degrees with 60% humidity.
COMPARE AND CONTRAST HEAT TRAINING TO ALTITUDE TRAINING HERE

Athletes need to adapt a different pacing strategy in different conditions. Physiology

textbooks tell athletes slow down because of anaerobiosis, oxygen debt, lactate
accumulation. But in most cases the body decides to slow down based on a
sensation that it is hotter or that the air is thinner. The set of inputs and outputs must
be interpreted, co-ordinated and responded to, creating a homeostatic loop,
which maintains the internal “balance” of the body. This can also be called the
Central Governor model, developed by Prof Tim Noakes. The Central Governor
model is highly controversial, lies at the opposite of “textbook” model(s) for fatigue.
Fatigue and the limits to performance are NOT simply mental barriers, they
never beat physiology, even if mental strength and willpower are key factors in
winning.

Further, fatigue as explained by leaky calcium channels, that lower the contractile
capacity of the muscle. This suggests that fatigue is a result of some change in the
muscle. The “endspurt” shows clearly that previous inactive muscle fibres are used.
It is known that muscle is not 100% active during a 10km race. In fact, even when
athletes do their best to exert maximal force for 5 seconds, there is evidence that
they still keep some “reserve” capacity. It is also known that because if someone is
doing a maximal 5 second contraction, and their muscles get stimulated using an
electric current, the force can go up, so clearly what the person thought was
“everything” was actually still sub-maximal! So a reserve is a universal feature of
any voluntary effort, regardless of how hard they try. The “endspurt” is the result
of an increase in muscle activation, controlled by the brain in response to numerous
INPUTS during exercise. It occurs because the finish line is approaching, and the
physiological changes are no longer deemed harmful or potentially limiting to
continuing exercise. The reserve can thus be activated!
Heat is the best example of a “homeostatic failure” model compared to a model for
Central Governor, because it changes the INPUTS. According to the “Peripheral”
model, fatigue in the heat is the result of a failure to keep the body temperature
down. When the body temperature rises, it causes fatigue because the overheated
brain is less capable of activating muscle to keep exercise going (Savard et al.,
1988).

Once the body temperature hits 40 degrees, the athlete:

1. Stops exercise – fatigue co-incides with this “limiting” temperature, hence the
name “critical core temperature hypothesis for fatigue in the heat”
2. Activates less muscle – muscle must be stimulated to contract, and what
Nybo and Nielsen showed is that the activation of muscle by the “hot” brain is
lower than that by the “cool” brain after exercise
3. Has altered brain function – they measured brain waves during exercise and
found that certain waves are altered, which suggests “reduced arousal” levels.

Thus, exercise is impaired in the heat because the body temperature rises until
it reaches limiting values. At this point, the brain fails to activate the required
muscle, and the athlete can no longer continue exercise.

CRITICAL POINT
However, what is key to realise is that these studies have failed to recognise that
during any form of exercise, it is possible to slow down long before you
stop! In other words, because these studies force people to exercise at a fixed
power output until exhaustion, the conclusion they make is that fatigue is caused by
some “failure”. They then extend this finding to say that “impaired performance” is
caused by the same thing, when in fact, they don’t measure what happens BEFORE
the limiting temperature is reached!

The alternative model is that performance is regulated well before the limiting

temperature is reached. For this to be true, it would require that the athlete slow
down at sub-maximal body temperatures (Marino and Cheung provides evidence for
this).
Thus, the athlete should start slowing down even though the body temperature
is not different from that in the cool condition. As a result of slowing down, the
athlete would be producing less heat, and so the fall in work rate will ultimately
produce body temperatures that are not different to those measured in the cool
conditions! In otherwords, you don’t slow down BECAUSE you are hot, you slow
down in order to prevent yourself from getting hot!

The “Peripheral” model of fatigue model shows the following:

1. Muscle contraction during exercise is responsible for producing changes,
including biochemical ones (leaky channels, fall in pH, lactate, phosphates
etc), as well as changes to the cardiovascular system, energy system
(glycogen is depleted and blood glucose falls), and thermoregulatory (body
temperature rises, as discussed).
2. These changes DIRECTLY inhibit exercise, either by:
o Causing the muscle to lose its force generating ability. This is the
theory for lactate, phosphates, oxygen supply (the “anaerobic” limit to
exercise) and calcium ions; or
o By acting on the brain to force the muscle activation levels down. This
is the case with high body temperatures.

The key to this model is that failure is responsible for fatigue. Something has

gone “wrong”, either with oxygen delivery, biochemistry, blood supply, or body
temperature, and this has impaired the athlete’s ability to exercise at the same pace,
so they slow down.
The INPUTS are provided by the heart, liver (or energy supply), body temperature or
rate of heat storage, biochemistry and the brain itself (e.g. memory,
experience/training, social factors). These INPUTS provide what is called afferent
feedback to the brain, informing it of the situation. In response, the brain
integrates all this information, then evaluates it in the context of the exercise bout
before enforcing some output on the system. The end result of this process is the
OUTPUT – the activation or the inhibition of muscle. This is responsible for
controlling the force output of the muscles, and hence the pacing strategy.