Part 3- THe Physiological Map

Part 3-The Physiological Map
The particular model that I suggest is based on the ideas of Jan Olbrecht. Using his ideas and research, we can come up with a simplified way of looking at what physiological aspects govern performance. The challenge of putting such a model together is that we do NOT know everything about how the body works and performs. We have a better understanding now then ever before but the picture is far from complete.

To illustrate this point, you can look at the evolution of what causes fatigue. Originally it was thought to be a result of lactic acid build up or oxygen debt. This theory was then disproved and new ones emerged. The current idea is that lactate is an indirect marker of fatigue because it is the hydrogen ions that come from it that is a major cause of fatigue. But this still does not tell the entire picture. The body is so complex that there are many other sites that could be the weak link and cause fatigue. Some of these include central fatigue of the motor cortex and/or spinal cord, E-C coupling failure, reduced Calcium release, impaired cross-bridge cycling of actin and myosin, and a host of other theories. If we include all of these theories in our model, the model would do us no good because it would be too complex. We do not have the time or even the know how to sit down and figure out how every workout impacts all of these aspects.
The solution is to take what most consider the biggest or most likely cause of fatigue and let that be our primary model. The other things that do not fit directly into the model can then be “spiced” in the training system periodically to see the effects. In this case we can then see how those items affect the elements in our training model. For example, if we read research that shows that certain workouts will prevent central fatigue, then we can experiment and do those workouts and see what the outcome is to the aspects of our model (i.e. the aerobic and anaerobic capacities and powers).

The physiological map below is a simple representation of what takes place in our body when running a race. It is not all inclusive for the reasons discussed in the last chapter. It is simply used to give us a guide to be able to look at and see how different workouts affect it.

(sorry for the crappyness of the picture)

Before discussing the above model it is important to note once again that lactate does not directly cause fatigue. However, we use lactate because it can be easily measured; therefore we know more about it and what happens to it during exercise. In addition, while lactate does not directly cause fatigue, it is indirectly linked to it. It has been shown that an increase in lactate corresponds to several of the factors involved in fatigue. Most noticeably, as lactate increase, pH decreases. This is caused by the increase in Hydrogen ions that come with lactate. Thus in the model used, if we can decrease the amount of lactate, then that means less pH drop and fatigue.
Pyruvate is one of the products of glycolsis. For the purpose of our model we will ignore the steps that precede it and show how to get from a carbohydrate down to pyruvate. Remember that we are looking for a model to use in training and not a fully comprehensive explanation of the systems in our body. We will leave the complexity to the scientists.
Once Pyruvate is produced, for our purposes, it has two options. It can be converted into lactate or it can be converted into acetyl-CoA and transported into the mitochondria. In the mitochondria it will enter the Krebs cycle and eventually result in aerobically produced ATP. The muscle lactate then can either stay in the muscle, causing a decrease in pH (because of the H+), go into the blood stream, thus becoming blood lactate, go into the interstitial space, or be transported to adjacent muscles. When the lactate is in the blood, it can either stay there or be transported to other muscle fibers or to various organs, most importantly the liver.
Now that we have this model, what does it mean and how do we use it? The example on the right of the chart demonstrates this. We look at the things that affect the race and that we can train. Starting at the top of the diagram, the first thing that can be affected is pyruvate production. From this point forward, I will refer to maximum pyruvate production as Anaerobic Capacity. Aerobic Capacity can be seen in the amount of pyruvate that is taken up by the mitochondria and lead to aerobic energy. In our example, the aerobic capacity is 5 units.
Looking at these two capacities, it can be seen how the model works in diagnosing training. In order to increase energy available we can increase the Anaerobic Capacity. That will allow the athlete to produce more pyruvate. However if the aerobic capacity stays the same, then this means more lactate will be produced at that effort level. If we increase the aerobic capacity, then we can see that more of that pyruvate is shuttled into the mitochondria resulting in aerobic energy increase and less lactate at the given effort. Using this model, then lactate is an interaction of both the anaerobic capacity and aerobic capacity, not just the aerobic capabilities which is widely recognized as the only source in traditional training models. That deserves repeating because it is so important:
The amount of lactate is a result of both the anaerobic capacity and the aerobic capacity.
The amount of pyruvate that is converted to lactate depends on the enzyme concentration in that muscle and how much the mitochondria can handle. Slow twitch muscles will have a higher concentration of enzymes that convert pyruvate to acetyl-CoA, while fast twitch fibers have a higher concentration of enzymes that convert pyruvate to lactate. Because the concentration of enzymes is highly correlated with the aerobic capacity of the muscle fiber, we simplify this and tie it into the aerobic capacity.
One more thing that we can look at is where muscle lactate goes. As can be seen, it can go on to be blood lactate or can be reconverted to pyruvate, transported to adjacent muscles or into interstitial space. While this is not a main part of the model, small training effects can increase the amount of muscle lactate that is gotten out of the muscle by one of the above mentioned methods. This is important because if the lactate (and therefore H+) can be expunged from the muscle, then the pH will not drop as quickly and fatigue will be delayed. To get the muscle lactate to be blood lactate depends on two main things. The first is the diffusion gradient, which is the difference between the amount in the muscle and the amount in the blood. The greater the difference, the easier the lactate flows from the muscle to the blood. When blood lactate gets higher and the diffusion gradient decreases then the body provides a little assistance by the way of lactate transporters. These are the Monocarboxylate transporters (MCT’s) and are numbered 1,2,3,4, etc. (more are being discovered everyday). The different kinds of these MCTs have specific purposes. Some have been shown to transport lactate into the muscle (MCT-1) while some have been shown to push lactate out of the muscle (MCT-4). The research on these is relatively new so there is still limited information on how to train to increase either of these. However, we can make educated guesses at this point using the data that is available. Lighter Aerobic and higher intensity work has been shown to increase MCT-1 concentration, while MCT-4 concentration has been shown to increase by more intense work but not low intensity aerobic work. However, the picture is far from complete, thus these only play a minor role in our model. It would not surprise me that in the future; these will play a more prominent role.
As lactate increase, pH decreases. This is caused by the increase in Hydrogen ions that come with lactate. Thus in the model used, if we can decrease the amount of lactate, then that means less pH drop and fatigue. It is thus the amount of lactate in the model that represents fatigue. To use an example on how this applies to the model, let’s use the map above. If the amount of lactate in the muscle is three units per minute and total fatigue occurs when you reach 9 units then the athlete will reach failure at 3 minutes. The pace of the athlete can be seen by how much energy is produced. We started with 10 units of pyruvate. The Aerobic energy contribution can be seen as the number of units in the aerobic capacity, so in this example, 5. The Anaerobic energy contribution can be seen as the amount of units in the muscle lactate part, in this example, 5. Thus the athlete is producing 5 units of aerobic energy and 5 units of anaerobic energy per minute. This is a vast simplification of the real life physiological mechanisms of energy production, but remember it is the model that we are concerned with. Also, aerobic energy is more than anaerobic energy in our example. This is because in real life, the anaerobic pathway produces roughly 2 or so ATP, while the aerobic pathway produces over 30. The total energy reflects how fast the pace can be. So if we increase the total energy to 12 total units, then the athlete can run x faster. So the goal would be to increase the amount of energy while keeping the fatigue length (3 minutes) the same to run faster over 3 minutes.
Lactate Tolerance, or in this model the total lactate that can be withstood (in the above example 9 total units), is a factor that I have not touched on yet. In our model Lactate Tolerance is covered by Anaerobic Power, which is explained in depth next.

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