Part 3- THe Physiological Map

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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.

Part 2: Global Change

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Taking a week off. Body needs the recovery. Started having some nagging pain in one of my shins and my IT band about a week ago, so I'm going the cautious route and taking some time off and then get ready for track.

The second part of my training model paper:

Part 2: Global Change

The example above (in part 1) illustrates how to use science to our advantage. In order to do that we have to stop thinking of the singular effects a workout might have and start thinking about the global effects it will have on the athlete. After this is done, then you must think of the effects in the whole training picture. That is the most common mistake that is seen. We tend to look at each individual scientific variable and how we can individually improve them. This can be scene in most running magazines, where there are plenty of articles entitled “How to improve your VO2max” or lactate threshold or buffering capacity. These authors fail to realize that yes that effect might take place but at what consequence. Coaches that are scientifically trained tend to go from using workouts to improve aerobic capacity to VO2max to lactate threshold and then to buffering capacity. They only think of one effect of the workout and ignore the fact that one workout will cause many different adaptations and it is how these adaptations interact over a period of several workouts and an entire training cycle that matters.
The worst offenders of this are books that classify workouts into zones based on physiological parameters. You have VO2max workouts and lactate threshold workouts and all sorts of other cleverly named workouts. These workouts may improve those variables but the other effects are not discussed and the main problem is that many coaches then get the idea that ONLY workouts from that zone will improve that particular variable. They are then astonished when research comes out that sedentary people improved their VO2max by doing anaerobic or sprint workouts. “That can’t be true” they say, but they forget the global effects of a workout. In our example, an untrained person could improve VO2max doing sprint workouts because the FT-b fibers that rarely get used will get worked out and thus improve their aerobic abilities somewhat. However, in a trained effect, this same increase in aerobic capabilities of the FT-b might occur, but the highly trained ST or FT-a fibers will decrease their aerobic capabilities because of the acidosis involved and they are overwhelmed in the workout. This is important: It is possible to improve aerobic capacity in one type of fiber while decreasing it in another during the same workout! That is why analyzing global change is so important.
To reiterate, the key is finding the global effects of a certain workout. Once you know these, then you can organize your training in such a way that the workouts are blended together to produce certain physiological outcomes that lead to better race performance. This is important because workouts and training do not occur in a vacuum. They occur within the context of other workouts, training, and lifestyle issues that surround them. These different aspects affect that particular workout and will be covered later.
Now that we have a different model for analyzing different workouts via their global effects, it is important to understand how to fit that concept into improving race performance. Even if you know the global effects of a workout it does no good unless there is a model present that gives direction on how to improve race times. In essence the model has to provide a physiological map to better performance.

Part 1-What’s wrong with the Traditional Physiology based training model?

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The Physiological Map series:
Part 1-What’s wrong with the Traditional Physiology based training model?
Part 2- Global Change
Part 3- The Physiological Map

For the next couple days/weeks whatever, I'll be posting a very rough draft of a paper I did for school. The basis of the paper is introducing a different way to use science in training runners. Hope it makes sense.
What’s wrong with the Traditional Physiology based model?

Using physiology or science in training distance runners has gotten a bad rap. There seems to be a backlash against coaches who get too scientific and analytical, thus losing touch with the art of coaching. The coach gets scolded for making things too complicated and forgetting that the goal is to improve race times, not VO2max. The point that the ultimate goal is PRs and not improvement in some physiological variable is one that should be ingrained in your mind as a key theme. Because of that, I believe that the traditional “scientific” coaching method deserves the backlash that it gets for the most part.

At this point I expect that you are entirely confused. Why would I make a statement like that when the root of my training philosophy seems to be heavily influenced by physiology? The reason is that the traditional model of using science in training is extremely flawed. This is one of the reasons why there has been little successful crossover of physiologist to coaches. The problem is not with the scientists or coaches, but with the model that they have in their head. The flawed model is not anyone’s fault but rather a reflection on how scientists think and work. Let me give an example to illustrate the point.

When a scientist looks at distance training he has to break it down and see how different training method effect different variables. This is how we get the information on what kind of training seems to increase the lactate threshold or improve buffering capacity. The next step in the process is the coach then looks at this data and comes to the seemingly logical conclusion that if X training improves buffering capacity, then his athletes should do X training or workout to get an improvement in buffering capacity and because buffering capacity is a limiter to certain races, that race time will improve. So the coach goes out and implements this training with his runners and smugly throws around scientific explanations for why his athletes are performing the intervals they are to anybody who will listen, but something goes wrong and his runners do not improve their race times. The coach then becomes perplexed and either reasons that the science was wrong and becomes an anti-physiology coach or he reasons that the athlete did not work hard enough, thus it did not work. If the coach took his athletes to a lab, he most likely would see an increase in buffering capacity. Then he becomes perplexed and thinks the athletes are “weak” runners and not tough enough because the workout obviously accomplished what it was meant to.
The real reason for failure, however, is in the training model, not in the athletes or the coach or the science. Buffering Capacity DID increase as the science said it would, but you have to look at the global effects of a workout, not just a singular effect. The singular effect was an increase in buffering capacity, but there are many other singular effects that the science did not look into or explain and all of these singular effects make up the global effect. It is this global effect that is most important. In our example, the intervals had one singular effect of increasing buffering capacity. If you did research, another effect would probably be a decrease in aerobic capabilities (either aerobic capacity or power) due to the heavy acidosis that the athlete endured to increase buffering capacity. Thus these two effects combined (and any others for the workout) would make the global effect an increase in buffering capacity with a decrease in aerobic capabilities. With this new information we can then more easily use the science and come up with a combination of workouts to get the desired result we want, faster race times. If the athlete was training for a 5k, we would have to counteract this workout with one that increased aerobic capabilities to prevent them from falling. If the athlete was a 400m runner, we would not worry too much about a slight drop in aerobic capabilities as the larger increase in buffering capacity would be more important.


Part 2- Global Change
Part 3- The Physiological Map

On to Club Nats and freezing weather

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11/25/2007
10 with andy, easy, felt bad
The rest of the day was horrible. I came back and thought it was just the cold weather getting me, like yesterday. So I laid underneath some blankets for a while trying to get warm. I then started getting the chills, and took my temperature. It turns out I had a fever of 100 degrees (which is high for me, my normal is in the 96-97 range due to the thyroid thing). As soon as I got up, I started throwing up and dry heaving into the toilet. Turns out I got food poisining, most likely from the Luby's we ate the night before. It was a miserable day.

11/26/2007

6mi easy in the afternoon. Felt better, still not 100%.

11/27/2007
morn-8mi decent pace
aft-6mi easy

11/28/2007
morn-2mi warm up, was supposed to work out during class but professor changed class
aft-9mi at a solid pace (6:10, 5:45-55 middle, 5:40ish last mile)


11/29/2007
6mi of a weird workout.....This one needs a lot of explaining...
2mi w/up, 1600 (4:18.1(63,66,65,63)), 800 jog plus rest, 800(57,29,29- 1:55.4), 200 jog, 200 (28.0), 2mi c/d- different workout than I planned.

The original intention was to do 3x1600, progressive starting at low 4:30s and progressing to mid 4:20's. I've been on this kick of running by feel, so I decided that was what I would do. I'd take the splits but not look at them until near the end of the rep. Obviously, by seeing the first mile you can tell my brilliant ingrained pacing skills (they are actually good at 60sec pace....just not so ingrained at slower paces). So after the 1600, I decided doing 3x1600 would be stupid, so I decided to do 2x1600, w/ 800 jog. Since I was 63 the first lap the first 1600, I decided I'd go until 800 without looking at my splits then try and hammer home the last 800. So I take off and was feeling good. Right before the 400m, I thought I was a little fast, so I decided to check the 400m and it was 57. When I saw that, I hit the brakes and thought about how long this 1600 was going to be now because I'm retarded. So at 480m I decided to screw it and run a hard 800m to get a last good anaerobic stimulus. So I went from slowing down to trying to change gears. I ended up running 1:55 low then grabbed the knees for a second and jogged 200m and did a 200m kick in. Overall, it was a very good workout. It felt great to be able to run 1:55 without any problems after a decent 1600m. It got me excited for track.

aft-7 easy

11/30/2007
morn-8mi recovery
aft-8mi solid pace, fast first 3mi, steady 2mi, fast last 3mi- fast was probably sub 5:45.

12/1/2007
morn-13mi easy + 10x100m w/ 2 easy, 1 good


12/2/2007
morn-10mi easy + 10x100m w/ 2 easy, 1 good


12/3/2007
morn-7.5mi decent pace
aft-5.5 1mi w/up, 2.1mi loop (10:00, 4:41 at mile), 3min rest, 1mi (4:23), 1.5mi c/d

Last hard workout before Club Nats. It's supposed to be freaking cold (it's in Ohio, duh.) and may be wet so it will be a fun one. I felt like I needed a longer sustained workout to get me ready since last weeks workout was short and fast. So I went with 2.1mi, 1mi. It was done on my 2.1mi loop that is mostly grass with 800m of concrete. I waited until the sun went down a little to cool things off. It was upper 40's, but the wind was blowing hard and with the lack of sun it felt colder. To further accentuate the cold, I went shirtless with short shorts.

The idea was to get used to not being warmed up while running at a fast sustained pace. To accomplish this I went with a short warm up of only 7min followed by a minute or two of light stretching and I ommitted the strides from the normal warm up. The result was that I spent the first part of the 2.1mi getting warmed up. To further simulate this idea, I ran the first minute or so like I was getting out for a race, then settled in. The only split I have on the course is the first mile, which I hit in 4:41. The 2.1mi I felt like I was cruising and was tempted to just finish off the 5k since it would have been pretty fast, but decided that wouldn't be the best idea. Instead I took my 3 minutes of standing recovery and then ran the last mile like I would the last part of the race.

Overall, it was a very productive workout and it felt real easy and comfortable. Good sign of things to come this weekend!
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