Flexibility Training (Stretching)

Introduction

Flexibility training or stretching is a conditioning factor that comes closer to mythology than sport science. What we see going on as stretching is often nothing more than an organized act of controlled contortion. We stretch because someone tells us we have to, everyone is doing it so no one stops to ask why, when and how. Newer studies are starting to question more and more the effects of stretching. The following theory, anatomical and physiological information will give you a beginning critical base for understanding stretching.

Anatomy and Flexibility

Passive body structures - joints
- ligaments

Active body structures - muscles including tendons

Flexibility is dependent on many factors which may we may or may not be able to change.

- Age: We lose flexibility with age
- Gender: Women are generally more flexible than men
- Genetics: Shape of joints and bones, muscle tension, hormone levels, muscle fiber type.
- Time of day
- Temperature
- Fitness level and type of sport or work
- Psyche (stressed or relaxed)

We need to distinguish between normal mobility, hyper mobility and hypo mobility.

Normal Mobility


Hyper Mobility


Hypo Mobility


With regard to the norm, it is important to keep in mind that there are individual differences in body type, etc., so there should always be an assessment of the individual athlete and the demands of his/her sport before designing any kind of stretching program. (For example, a gymnast needs to be hyper flexible for his/her sport but for the runner it has been proven that running economy suffers it the athlete is hyper flexible.)

Muscular Imbalance (MIB) and Muscular Dysharmony (MDH)

To be able to stand upright with a good relaxed posture and to look smooth and coordinated during running or any other activity, we need to have a muscle system that works optimally and economically together.

MIB describes an imbalance in the horizontal plane, that is, an imbalance between opposing muscles. For example, the hamstrings are the muscles that bend the knee and the quadriceps are the muscles that extend the knee. These muscles need to have a similar tension and strength to maintain a balance. Such opposing muscles are termed Agonist and Antagonist. While you bend your knee the hamstrings are the agonist muscles and the quadriceps are the antagonist muscles. Another example would be the abdominal and the back muscles. Muscular Imbalance may be developed by improper training. For example, strength training that is focused on developing the abdominal muscles (6 pack) while ignoring the back muscles. This situation may be aggravated by bad posture (sitting all day in a slouched position will tend to shorten the abdominal muscles and stretch the back muscles) or by repetitive work with overload of first the muscle and later the actual joint. The continuously overstretched muscles of the lower back will lose tension and therefore the ability to protect and move the back properly. At the same time, the trained abdominals will shorten and will often change in metabolic activity (too high tension causes oxygen deficit and change of fiber type). These changes will eventually lead to loss of performance and injuries.

MDH describes an imbalance in the vertical plane (a weakness in a muscle chain). Such an imbalance is developed after an injury requiring a cast, where one muscle in a chain loses its strength. The purpose of rehabilitation is to eliminate injuries due to such MDH and an athlete should never go back into competition until rehabilitation is complete. Returning to competition too early can initiate a cycle of re-injury until the problem becomes chronic.

Both MIB and MDH will show up as:

A Performance Loss
B Tension Change (muscle length)

Performance loss can occur due to an imbalance at the knee as in the above example. A shortened antagonist does not allow the agonist to develop the full strength for motion because it uses much of its strength to overcome the resistance of the antagonist. For example, shortened hamstrings will not allow the quadriceps to develop full power for kicking a ball.

The overuse of a muscle can produce a change in the muscle’s metabolic activity. A too high tension will reduce blood flow which will reduce the amount of oxygen supplied to the muscle. This changes the work time of the muscle (anaerobic activity) which may finally even change the fibers doing the work. For example, the back muscles of a rower has STF fibers but constant overuse will increase the muscle tension and therefore reduce the oxygen supply for these muscles, promoting a switch to the use of FTF fibers. This may completely change this athlete’s performance without anyone realizing why!

These changes in performance (strength) or muscle length may be Functional or Structural.

Functional Change from Stretching


The sarcomere is the basic contractile unit of a muscle.


Structural Change from Stretching



A: Normal physiological muscle length
B: Structural shortening of the muscle (decrease in the number of sarcomeres)
C: Structural lengthening of the muscle (increase in the number of sarcomeres)

Summary

To produce an effective training plan it is necessary to assess each athlete and design a program appropriate for the individual not a whole group. This applies to flexibility as well as to endurance and strength. Before beginning on a stretching program we have to be sure that the muscle we stretch really has one of the above problems. It may be that an antagonist is too weak, requiring strengthening, rather than stretching the agonist.

Before beginning on a stretching program and even before testing muscle length it is important to make an anatomical assessment of body symmetry. (Leg length, joint symmetry, etc.)

Once we decide to stretch we have to plan how often and the appropriate technique for each individual athlete. As with all conditioning factors, we have to re-assess over time whether the athlete is making the desired progress and adjust the program accordingly.


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Lactate: the bad the ugly or the real underachiever? by Juerg Feldmann

Part I:

Working in this field for over a quarter of a century I had the pleasure to get inside views on all different ideas and attempts to use lactate in sport and other related fields. We were influenced by the basic works of Fletcher and Hopkins (1907) and finally got the real answer with the Nobel prize of Meyerhofer and Hill. They actually never were able to prove but rather proposed the first part of the aerobic/anaerobic model, which is still the dominant model for many types of training ideas and testing theories.

In short, as lactate was a chemical substance easy to test, lot's of theories started to use lactate as the reason for different "limitations" which took place during exercise. Lactate is and was blamed for:
- Fatigue (what ever this may mean)
- Muscle cramps and Side stitches
- Post exercise muscle soreness
- Oxygen deficit and possibly some more ideas.

Every day and in every TV sport session the journalist and often the retired champion from the particular sport will blame "lactic acid" for the performance drop or some type of reaction we can see on a hard working athlete.

The original thinking was clear:
As soon the oxygen supply was dropping or was getting low the body would, as a negative byproduct, start to produce lactic acid, which then would produce the above possibilities. So as less O2 would be available as more lactic acid the body would produce and the goal of so many different training ideas was to be able to either avoid lactic acid production or at least try to "tolerate" more lactic acid. Even the sport nutritional supplement industry would come up with drinks and supplements, which would avoid or reduce the build up of lactic acid.

In the mean time there are some interesting questions in this direction and it started already in the early 1980's, when we did "lactate testing" at the altitude center in St. Moritz. We had coaches like Dietmar Millonig's brother, who started to use lactate more in a way of assessing trends than the classical very popular way of Mader: 2 and 4 mmol/l lactate as aerobic or anaerobic thresholds.

Other ideas surfaced like Conconi test, and I remember still our first attempt with metronomes and drums to pace the athletes around the field. We developed the first Casio pacers to make it easier and as usual we were sure that was the way to go. Already at that time there were some researchers lonely in the desert asking critical questions but got pushed under the table. Some of these questions are still out there but with some answers and some nice small practical demonstrations:

Muscles are able to release lactate, even without exercising. (Connett et al circa 1984). This was clear as the question that lactate was or may be not only be a part of anaerobic conditions in the muscles, but was getting used by other means.

The same group around Connett and later Gayeski as well as the famous Saltin suggested that there is no proof or evidence, that muscles would go anaerobic during intense exercise and not even in all out workouts. In fact there are researchers out there showing that the O2 situation in an all out working muscles may be actually higher than in a lower intensity.

The next question or discussion was the fact that there is or seems to be no lactic acid in the human body at all, but rather lactate in combination with sodium. Why and where was this "misconception" coming in, for lactate to be the bad guy. Well the main reason was that under a gradual increase of workload there was an increase of lactate to be measured in the system, and in cases where the athletes were really at the end of their "ability" the lactate measured in the system was always very high.

Once the athlete started to feel better the lactate levels normally would drop. So no wonder there was an easy conclusion to make about the influence of lactate to any of the limitation in performance. Now if we would have tested in a graduated step test instead of lactate, blood sugar we may have given the bad name perhaps to this blood sugar.

Now these days the ideas have turned, but are still not fully accepted. Well remember it took the Catholic Church till 2003 before they accepted Galileo Galilei's idea that the world is round and not the center of the universe. So we are doing not too badly in this field, but it will still take some years to come to understand what the major shift (the new paradigm) on lactate will do in the world of coaching and testing. As well as the incredible large number of PhD's which were done under the "old" ideas and conclusions drawn and published out of this research. We as coaches and small field researchers have to rethink and reorganize in a better way, how we set training zones and applications to it as well as "justification" and explanations to certain training ideas like "lactate tolerance training" and so on.

I would like to close this inital part with a summary of questions and "statements" to open a discussion:

Summary:

1. There is no lactiac acid but rather the form of lactate sodium in the body.

2. There is no anaerobic situation in healthy all out working muscles even in the hardest part of the workout or step test.

3. There is no conclusive evidence, which may suggest, that the muscles become anaerobic during hard workouts and that there is therefore something called lactate threshold or anaerobic threshold.

4. There is nothing like a sudden increase in lactate existing much rather a very nice smooth exponential increase. Therefore, there is nothing to find as an anaerobic threshold nor a ventilatory threshold. In fact based on some research from Brooks et al (Berkeley, California) and Dubouchaud, lactate may be produced and used in the muscle as one of the key products and even may be the main reason why we can sustain certain higher intensity exercise thanks to it's existence. Lactate may be one of the most important "fuels" in the body and can be shuttled around to be used in areas which are in high demand of energy.

Conclusion:

If this is all a new direction, then we know, that at the moment when we can measure lactate in the blood and see a trend in lactate accumulation, we know that metabolically there is a heavy demand for Glucose and on the production of ATP as an oxygen dependent energy production. A decline (trend) in lactate in the system will give us the indication that for the moment there is a need for energy but the intensity in which we move is on a level where we can produce this energy demand oxygen dependent but need a very efficient fuel source, which in this case is lactate.

This thinking brought us to the believe, that we should distance ourselves from terminology like lactate threshold, anaerobic threshold and the classical terminologies. So Herb and I decided to name our trend situation we produce with FaCT testing as LBP for Lactate Balance Point. Meaning exactly this: Lactate in balance on any given level, meaning we have no clear trend at that moment in increasing of lactate levels nor decreasing, or at least a very small change as it is a physiological process.

So for us, as we developed and still are developing better ideas of assessing performance changes, we decided that there is only a trend idea working, rather than absolute numbers. With this in mind we had to overcome the fact that we would be the two lonely guys in the north foolish enough to believe that we don't want to work with anaerobic and aerobic but with completely different ideas of zones. To be not too far off the existing world we slowly integrated these ideas in our small concept. Now 15 years later we are surprised that more and more people actually start independently from us to form similar ideas, or like in the case of a German PhD candidate take our idea and simply change the name. The fact that his work was accepted was nice for us, as we see that there is some "truth" behind our crazy ideas.

In Switzerland the idea has a kind of a rebirth with different Centers looking at it, thanks to a PhD candidate with a respected name, who sells it as a new concept. We have one big advantage: thanks to my bad English I produce own names like LBP and so on and it is fun to see this LBP showing up in more and more papers all over and nobody really knows where it comes from. We see people using LBP as the place where the body moves from aerobic to anaerobic.

Here simply what LBP is:

It is the area (not really point) and we may have to change actually LBP perhaps to LBZ (Lactate Balance Zone) where the increase for demand of glucose to cover the energy demand in the muscle is so high that the product lactate can't be utilized in the working muscle and will be released or transported (MCT I idea) into the blood stream to be used in other muscles and organs like heart, liver, respiratory muscles and so on.

The nice thing with this situation is that some researchers believe that in the step of releasing or transporting the lactate out of the "overloaded" area the lactate may as well take an H+ with it and therefore help to try to buffer the increasing acidic situation to survive somewhat longer. So these groups believe that lactate may be the product of, but not the cause of muscle contractions.

In the next few days I will show some basic field tests we did over the last 20 years where we believe they show this idea of a positive lactate and take the old ideas apart. Stay tuned as we will go through a full FaCT test with a very simple language to explain why and how we do the steps and we may use the numbers from Gary as an example of what was going on in his test and how we can use the physiology to run FaCT very simply and anywhere. You will see why at the beginning there is no need for a very specific protocol, but the need to think and react during testing. This alone is very bad because who likes to think during a test and who likes to make a decision to change something during a test?

I remember the look on the person in a University during a test we did with a top Canadian athlete, when we decided during the test at the start that he had to go to the washroom. I said OK we just go back to where we stopped and there is no problem. Ha Ha, and even worse was at the moment where we demanded the ability to prolong the step at the same level for a few more minutes to see the trend better. Ha Ha, there was no way to do that because the programmed computer was just not set for that. I am sure when we left the University they were more than happy that we would go back and disappear into the bush. The only problem was that the information and intensity we got for the athlete from the university were just simply impossible to do, but there are rules and regulations. (Smile) Have fun and stay tuned for some more practical ideas and crazy thoughts.

Juerg

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Functional and Structural Training. By Juerg Feldmann

I had a very nice mail with the clear straight forward question:
"How do I explain functional and structural adaptation in combination with the ECGM (extended central governor model)".

Okay here is a short try:
I will use VO2 max as one of the examples to explain how I see functional and structural training and the limitation. VO2 max (if we are able to measure it) is the maximum volume of oxygen that the body consumes during intense exercise. That means we have to use a whole body exercise to be able to come close to or perhaps reach VO2 max. That is the reason why in sports like cross country skiing we see often higher VO2 max levels than in kayaking. If you test a cross country skier in his sport and in kayaking, he will reach a much higher VO2 in cross country skiing than in kayaking. A beginner in any sport will increase his VO2 relatively quickly in the beginning because with improved technique and balance he can incorporate more muscles for the workout. Therefore, we see at the beginning an increase in VO2 not because there is a change in anything other than the ability to use more muscles, which are already here. Now, because they are a part of the workout they use as well O2 to produce energy.

So to go back to the beginning, to have a high VO2 we need 2 main systems.

1. An outside system, let's name it delivery system, which has to deliver O2 from the outside world to the working muscles. Airways, lungs, movement from the lungs to the blood, O2 transportation in the blood, red blood cells reaching muscle cells which can use this O2.

2. Motors (mitochondria) which can carry out the energy production with oxygen. (If they run into problem with oxygen dependent energy production we can measure that in the blood stream with lactate accumulation, as a trend information of more and more involvement of an oxygen independent energy production in the working muscles).

So based on the 2 points above we need:

a) A good functioning air delivery system to bring the Oxygen into the body and over to the blood (respiratory system) but as well, the CO2 out from the blood into the outside world.

b) A very big and efficient pump to deliver the oxygen loaded blood to the muscles, so they can "suck" it up and use it for energy production.

c) Mitochondria rich muscles, so that they have the ability to use the delivered O2 efficiently.

So the basic question is:
What is the limitation of the VO2 now? Oxygen delivery or oxygen utilization? That's where lot's of people start to discuss and even in the exercise physiology world there is still some discussion here. I like to explain perhaps why.

The ECGM will clearly state that it is always the O2 delivery which will be at the end the limitation of VO2. There are possibly very easy tests you can do, like 1 leg biking. The VO2 will be very low even though you have to stop. That means the limitation was not in this case the delivery, but the utilization in the single leg. So there was not a problem for the heart to deliver enough blood flow to this small portion of working muscles.

Now, if we add a much bigger portion of the muscle mass the heart just simply cannot deliver enough high blood flow to all the "users" and maintain a sufficient blood pressure in the vital organs (brain, heart, respiratory system). The body controlled over some hemodynamic processes controlled by the brain, just simply will not send enough blood to the extremity muscles, so that it will not compromise the blood pressure and oxygen situation in the vital organs.

To control this the brain has some specific ideas; decrease muscle fiber recruitment, produce some vasoconstriction to name two popular ones. There is again a very easy test where it can be shown that it is easy to improve performance if you use a small muscle group in order that the Vital organs will not be a limitation. One leg endurance can be improved by 200-300% but you have a problem to see a change in VO2 max if you test in an overall cycling test.

Now here comes the functional and structural part into the picture.
In a beginner or young athlete, the extremity system (utilization) is not very well trained. Now if delivery is the limitation then we have the problem that oxygen rich blood reaches very well trained muscles. The bigger the capillary network and mitochondria density in these muscles, the more O2 will be extracted from the blood and therefore the O2 difference between arterial blood and venous blood is bigger. Resp., we see less O2 coming out in the expiration air. There is only so much O2 being delivered (limited by O2 inspiration and moving onto the red blood cells and by the amount of red blood cells).

If in a highly trained endurance athlete the capillary density and the mitochondria density is extremely well developed. That will create a problem of not enough O2 for everybody. Now with the ECGM the brain will kick in to protect the vital organs with adequate O2 saturation and will not deliver O2 in the extremity. This very clear system shows why in top athletes respiration and red blood cells are limiting factors together with the heart. If the heart is the limitation, that's just it. If the respiratory system is a limitation it can be trained because we very often don't do that. If the blood transportation (red blood cells) is a limitation we can inject EPO. This is the easiest way of quickly improving delivery limitation and that's the reason why so many athletes "cheat" with this possibility.

In athletes where the heart is the limitation the O2 delivery will just stop to protect the heart. If it does not do that, then we have a sudden death in sport. (Failure of the ECGM to protect the heart.) So no EPO will help here. If the respiratory system is a limitation, then again EPO will not help. If the transportation of O2 in the blood is a limitation EPO will help.

Now in a beginner all the above will not be pushed to any limitation and the adaptation of extremity muscles is very fast. Therefore, we see in 6-8 weeks a very quick improvement of performance as well as VO2.

A beginner has not very efficient O2 utilization, but can easily improve that.
Training for capillarization
Training for mitochondria density
Training for inter muscular coordination
Training for intra muscular coordination
Training of balance to use less muscle for stabilization and therefore be able to use them for mobilization.

Example: A beginner in skating will use lots of leg muscles, just to keep him upright (stabilization). The same muscles would be needed as well for mobilization (moving forward). Now with this double duty they are not very happy. An improved balance will take the stabilization duty off these mobilization muscles and therefore he moves faster with the same amount of O2 used, but now used for different purposes.

Now I hope you get the picture.
Functional training is doing all of that and will show quick and easy improvement. Structural training may not even have kicked in at that stage. So the key is to design structural training for heart and respiratory system. Improve nutrition for blood system production and blood plasma retention so that at the moment the extremity system is in full swing the delivery system can deliver more and better. This will end up all in the way the heart, the respiratory system and the nutritional situation will play together.

The functional training will move through Hans Selye's Alarm Stage and will help the body in a decent time to use what is already there with some minor adaptation in the extremity systems. Duration is 6-12 weeks in most of these cases. Result after that: stagnation and/or even UPS (under performance syndrome) or negative adaptation.

Problem: If you read 100 threads of exercise physiology papers and you carefully watch the groups which were tested and the duration of the test (6-8 weeks), you can see why so often the hard intense overload groups have a much better result over this time than the less intense groups.

If you take a highly trained group, you will see often very little if any improvement at all in VO2, or any other factor, because there is just no functional adaptation available any more. This is one of the reasons why "peaking" with high intensity workouts towards an important race just does not work. The highly trained athlete has not to "peak" because there is no peak production due to high intensity. The highly trained athlete has to recover to peak. His "fatigue" level is so high that he can't perform. If he can get his fatigue level lower he can perform better. He not will lose performance because it is based on structure, compared with the athlete who has no structure, but everything is built on functional reaction.

Summary:
In the VO2 case delivery, not utilization will be the limitation in well trained people. The key is to find out whether that is the case and where in the delivery is the weakest link; heart, respiratory system, blood situation.

If is is the heart, train so that the respiratory system will challenge the O2 delivery so the heart has to react and keep the extremity muscles on a minimum fire for O2 usage. We use PET (Pulmonary Endurance Training) with specific resistance to do that.

If your respiratory system is the limitation, keep the heart rate down but work your respiratory system as you would go for a 1 hour all out run and don't integrate the extremity muscles. We do that with the SpiroTiger.

If your blood system is the limitation you improve that over a proper nutritional delivery (Maryanne Kelly, NOC California) and a hormonal challenge for EPO with a IHT (intermitent hypoxy) workout with the PET and an integration of O2 sat control.

If the limitation is your extremity muscles, you improve that with specific coordination training and possibly stabilization training. The worst case scenario for dynamic sport is the fitness center equipment. The cheapest and most advanced one is the Swiss ball coordination training. (I remember when we tried 15 years back to make a Swiss ball distributorship in Vancouver, everybody would ask us whether we are nuts. Smile they are right we are nuts, but just 15 years later we would be rich, ha ha.)

Now let's see what goes on with FaCT IRIS and the other nutty stuff we have to offer.

Juerg

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Juerg Feldmann

In some of my upcoming blogs I will be posting some of Juerg Feldmann's insights first published on the Fact Canada Forum.

Juerg is a brilliant guy who (I am proud to say) is my friend and business partner in Fact Canada. I would never have dreamed that the guy to whom I was introduced at a Triathlon training session some 18 years ago would completely change the direction of my future. It just so happened that Juerg and his family's new home was only a short jog from my house so it was natural, with our common interest in endurance sport, we would spend some time training together. It was during these training sessions that our friendship matured and ideas were discussed that eventually led to the formation of Fact Canada Consulting Ltd.

Juerg is a truly amazing fellow with a wealth of knowledge in human performance and exercise physiology. He has a dual education (Switzerland) in Sport and Physiotherapy as well as years of practical experience working with elite athletes and teams in both a coaching and testing role. He currently runs a very successful and popular Physiotherapy Clinic specializing in active rehabilitation.

Although he doesn't carry the "PhD" letters behind his name or work in a university, in my mind he is a true scientist. He doesn't stop at just questioning accepted theories if they don't make sense in his mind. He will research the publications and do practical testing till he thinks he has some answers, often using himself as well as his friends and athletes as the test subjects. He will spend dozens of hours developing case studies that lead to some insight. He will formulate new ideas and test, test, test. If he comes up with revelations that he later finds don't make sense due to some new information he has discovered, he will be the first to say so and go off in the new direction.

Stay tuned and visit our website and Forum for more information.

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New Low Cost Oximeters from FaCT Canada

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Six display modes include all 4 directions and 2 sizes. Large size and bright display for easy reading in all lighting conditions. Uses 2 AA batteries for 30 hours of operation.

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Polar AW200 Activity Watch

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At the heart of the watch is an accelerometer and altimeter that detect even the slightest movement. Data from the sensors is analyzed to distinguish the intensity of the movements and calculate the total energy consumption and burn rate.

The Polar AW200 is a wrist watch based on activity technology. Sensing body movement, the AW200 enables the wearer to develop a better understanding of how much beneficial exercise they are getting. This new activity technology developed by Polar measures not only the quantity but also the quality of the exercise. The information is provided to the wearer in a meaningful and easily quantifiable form (active time, intensity of activity, calories and active steps) which helps motivate and inspire them towards improving the quality of their activity.

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