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Juerg Feldmann

Fortiori Design LLC
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 #1 
I like to show you here a very practical example of a client I tested 2 days ago and today just now finished  with him to explain, how he can use this information.
 I as well explained him ( Biased ) that once we have a MOXY his quality of training will be even better.
 So this will be a start of looking at tests with a classical 3 min step test better  but this  ( MyPAHD) will  lead to the UrPAHD as the sub group of our IPAHD idea.
 Goal is in simple term.
 ECGM  extended central governor model.
 A combination of current research from great people combined in a simple  idea of assessment.
 We look where what system  fails to provide further  help to an overall performance.
 The weakest ( not  to confuse with sick ) system  " fails" first but potentially strong system may be able to compensate.
 So here as a repetition the idea of Limiter and compensator  as att 1.
Att 2 is a simple inside view  in the ECGM idea ( you build up your own words top it .
  Att 3  the word document is the personal taring program  for this client with explanation how his body works and individual  " intensities. and bio markers. I will than try  depending on questions who may come in to show, what and how I explain this client what we do it and why we do it and why he will come back in a few weeks to do a Your pahd  respectively the new protocol and  I show you how we designer this protocol based on the My PAHD. Or in simple words we  have no secrets on what and how we do it , Just simply cooking with water  but as well critically looking at current ideas of the old model.
 It is a short answer to a Blog Roger set up just  now on Noakes CGM and as  he writes nicely :
 Why do we still use the classical model.
 Because there is no alternative idea out there.
 Here it is  a 20 year long development  showing on this Website and opening it up to critical discussion and debate. We do no attack anything people do , we simple ask :
 Could we  improve upon the existing ideas and how  ?

Juerg Feldmann

Fortiori Design LLC
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 #2 
Suggestion.
 If you like to follow the discussion on the word document here print the pages out and have it with you  when you follow the discussion and make notes. Basically a Webinar (with a mixed content but this gives the  most interesting combination. 
 Unseen real and unreal seen ?

Juerg Feldmann

Fortiori Design LLC
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 #3 
Okay here the first questions we can work together.
 Below  you have 2 tests. First one is a running  3 min step test.
 the second one is a bike 3 min step test.
 I will  during our discussion tell you where we made mistakes and why  the bike test is not optimal and therefor has to thrown out of the study data collection. But first some information.
 Look at the  2 TRACES again.
 Yellow is the tHb ( total hemoglobin  ) and it is used  in  many cases to take it as  an information on blood volume or blood flow in the tested area.
 So an increase in tHb indicates in most cases ( there are  as usual some exceptions )  an increase in blood flow.
 Now there are a few  situations in a step test, where blood flow may  drop  towards the end.
 I like to just use one example for the moment .
 R. Dempseys Metaboreflex. Meaning a respiratory limitation may in fact create over the ECGM a vasoconstriction.
  A nice  article  has the title " Breathless legs"
 Att three shows the reaction of the metaboreflex and how we use NIRS to  combine this information with respiratory information.

Purple is the trend of SmO2 and in this case here it is the Hb Diff used with a NIRS Portamon equipment.
 An increase in purple indicates, that more O2 is supplied to the working area, than is used. A flat purple line indicates that O2 delivery and O2  use is in a balanced situation and a drop in purple indicates , that we reached an intensity where more O2 is used as can be delivered.


  Now your fun  task is to see, whether you can make some clear " Zoning" in this 3 min test and where would you put a vertical line down if you  would have to make the interpretation. Remember you are  at the game live. 
 Again picture 1 Run test.
 Picture 2  bike test.
 picture 3  respiratory metaboreflex. 

To see , whether we agree in the ZONING go on the Gale word document and you can see some ideas there.
 Now wait. This is NOT how we think we can use MOXY best. The key is to find  something we call homeostasis and than disrupt this and  try again.
 That is what we will name than  UrPAHD and is a part of the IPAHD idea.
  So last but not least a UrPAHD  assessment to   show you the end stage of how to use MOXY and than the  step is to show you how we can use a MOXY watch when working out for endurance and  how to use it for individual strength exercises or interval planning.

Picture 4 is a IPAHD dome in Switzerland with some of our  friends from Norway

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Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #4 
Zoning is a terrible word, as  there is no zoning but individual physiological reactions, who tell as more on the metabolic demand. That's why you do not see the word Zoning  but intensities in our ideas.

Hmmm I am a little bit disappointed on the respond on suggestions on change in MOXY /NIRS information.
So lets' make it much much easier.
Here see the att on the printout from the same test but taking VO2 instead of oxygenation reaction in the muscle.
Indirect info reading the report the next day.

Here you go  .
Take page 5 on our word document Gale. You see there HR and performance and VO2 in the yellow graph.
 Now see here it is super easy to make a ZONING.
 You take the  highest value of HR and the highest value of VO2 and the highest value of watt. This equals 100 % and now you need a calculator and you have  all the zoning you like to "sell " to you client.
 Nobody really cares whether  70 % is really always 70 % intensity  in every client you have.
 
 No physiological information but the end of the test information.


Okay give it another try  and remember nobody can really be wrong.

Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #5 
let's pour some more oil into the fire.
Juerg Feldmann

Fortiori Design LLC
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 #6 
Now here a much smarter summary than my one above. The title should have been IPAHD and IPAHR from a Dummie

How does a foundational myth become sacred scientific dogma?

The case of A.V. Hill and the anaerobiosis controversy

Part 1

by Tim Noakes

Introduction

The basis of the scientific method is the development of intellectual models, the predictions of which are then subjected to scientific evaluation. Indeed the real value of these models is the predictions they make. Whether or not these models are ‘true’ is not crucial since it is only through the testing of their predictions that their fraudulence can be exposed. As Nobel Laureate A.V. Hill wrote in 1965:

I have long believed, and am still inclined to believe, that all theories of muscle contraction are wrong. But they have been very useful in stimulating new research. In fact, many of the best theories are self destructive, by provoking fresh inquiry and leading to new facts which they cannot explain. The only useless theories are those that cannot be tested and can explain everything (362–3).

Thus the crux of such models is the attempt to refute or falsify their predictions. Successful refutation forces revision of each model; the revised model persists as the ‘truth’ until its predictions are, in turn, refuted. Thus any scientific model should persist for only as long as it resists refutation. This form of science, however, is not always popular; we are usually rather too keen to confirm that the theories of our founding scientific heroes are, naturally, correct. This latter approach seems to be particularly prevalent in the exercise sciences. But when we adopt this deferential approach we risk becoming a tribe of scientific marionettes. Most certainly we betray the efforts of our scientific founders who would much prefer that we disprove and hence perfect their imperfect theories.

My special interest in the exercise sciences has focused on an understanding of the factors that limit exercise performance especially during high intensity exercise of short duration. The most popular current explanation is that the cardiovascular system has a limited capacity to supply oxygen to the active muscles, especially during maximal exercise. As a result, skeletal muscle oxygen demand outstrips supply, causing the development of skeletal muscle hypoxia (reduced oxygen concentration) or even anaerobiosis (absence of oxygen) during vigorous exercise. This hypoxia stimulates the onset of lactic acid (lactate) production as the exercising muscles begin to produce an increasing proportion of their energy from those ‘anaerobic’ metabolic pathways, capable of producing energy even in the absence of oxygen. The most effective such pathway is the incomplete breakdown of the main skeletal muscle carbohydrate store, glycogen, to lactic acid (lactate). Accordingly this model predicts that the most important factor determining exercise performance is the body’s capacity to transport and utilize oxygen and that fatigue results when the maximal capacity for oxygen transport is exceeded. As a consequence, it is argued that the most important effect of any intervention that alters exercise performance, be it exercise training, nutritional interventions, drug use or disease, is to change oxygen delivery to, and oxygen utilization by the active muscles during exercise. Thus it is believed that the common consequence of all the physiological, biochemical and functional adaptations that enhance exercise performance is to reduce skeletal muscle hypoxia or anaerobiosis during exercise.

The historical basis for this model is the original research of Nobel Laureate from the Universities of Manchester and London, Archibald Vivian Hill, which has survived in the classic theory that oxygen consumption ‘plateaus’ during progressive exercise to exhaustion, proving the development of skeletal muscle anaerobiosis (Hill 1925; Hill and Lupton 1923; Hill et al. 1924a, 1924b). But I contend that Hill’s quite simple research methods failed to establish the existence of the ‘plateau phenomenon’ during exercise so that I argue that this core component of his historical model remains unproven (Noakes 1988, 1991, 1997, 1998; Noakes et al. 2001). Furthermore, definitive evidence that skeletal muscle anaerobiosis ever develops during exercise in humans and that this anaerobiosis initiates lactate production and its accumulation in blood, is not currently available (Mole et al. 1999; Richardson et al. 1998; Saltin 1989). As is appropriate, my contentions have been vigorously refuted (Bassett and Howley 1997, 2000; Bergh et al. 2000; Ekblom 2000; Wagner 2000).

In this process I realized that this historical physiological model has become what Waller terms a ‘Foundation Myth’ (Waller 2002) and, as a consequence, has escaped modern disinterested, intellectual scrutiny. The reasons for this serve as a warning of the fallibility of scientists and the current scientific methods under which we labour.

The writer Salman Rushdie, who spent many years in seclusion when his life was threatened because of his heretical views, has said: ‘The journey creates us. We become the frontiers we cross’. My personal intellectual journey did not begin as a scientist but as a medical doctor training in a small city, far distant from the historical axis of academic excellence in Europe and North America, in a country that at that time was ruled by a repressive dictatorship that discouraged free thought. I was fortunate for the exposure to those frontiers. It is here that I begin the story.

Lessons from a medical training

The first great lesson of medicine is to teach one’s supreme level of personal stupidity. Indeed there is a collective level of medical ignorance, so brilliantly described by Dr Lewis Thomas (1985: 10):

The greatest single achievement of science in this most scientifically productive of centuries is the discovery that we are profoundly ignorant. … I wish there were some formal courses in medical school on medical ignorance; textbooks as well, although they would have to be very heavy volumes. We have a long way to go.

Indeed, the beauty of the Textbooks of Ignorance would be their accuracy. I am reminded of these quotations whenever a scientist expounds the ignorance of absolute certainty. Regardless of any appearance of individual brilliance, we are each profoundly ignorant. And never more so than when we are absolutely certain of our most brilliant opinions.

This distinctive characteristic of modern medicine to challenge the truth (Le Fanu 1999), explains the intellectual paradox captured in the classic quotation attributed to a former Dean of Harvard, Dr Sydney Burwell by G.W. Pickering (1956: 14), himself formerly Professor of Medicine at the University of London and a protagonist in one of the classic medical arguments of the twentieth century (Swales 1985): ‘My students are dismayed when I say to them, ‘‘Half of what you are taught as medical students will in 10 years have been shown to be wrong. And the trouble is, none of your teachers know which half’’’.

The second great advantage of my medical education was that it included nothing about the exercise sciences, other than that which I taught myself. Learning in this way has important disadvantages, but one unique advantage is the avoidance of indoctrination, which is the tendency towards a stubborn, if subconscious, acceptance of a specific scientific mindset or prejudice that we acquire from our venerated tutors whom we assume to be intellectually infallible (Waller 2002). This could perhaps be termed the Tyranny of the Founder Effect.

It is an effect for which the exercise sciences are especially susceptible since the profession is still very young and a relatively small band of famous founders including A.V. Hill in Britain, David Dill in the United States of America, Cyril Wyndham in South Africa, Wolder Hollman in Germany, Erling Asmussen, Erik Hohwu Christensen, Marius Nielsen and August Krogh in Copenhagen, P.O. Astrand and Bengt Saltin in Stockholm, and R. Margaria in Italy, have bequeathed an inordinately influential legacy. Indeed the second generation of scientists trained by those giants are only now approaching retirement age. Thus it is likely that the global teaching in the exercise sciences still reflects the powerful influence of those remarkable founding scientists.

My point is that a crucial outcome of our scientific training conditions us to accept only a limited sample of all the possible truths. Further we are more likely to accept those ‘truths’ that we learned from the giants who educated us and, in particular, their ‘foundation myths’ (Waller 2002). So ignorance of the historic precursors to that which is the presently considered ‘truth’ or received wisdom, can be a formidable attribute. For it allows the freedom to consider any intellectual possibility
Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #7 
here an interesting summary of some great articles. It shows ,that our idea of Intensity versus zoning  we try to postulate since over 20 years is picking up some other brains as well.
 Our alternative as questioned at the end of this interesting article is IPAHD  physiological assessment coupled with performance information on an individual base rather than a mathematical formula.

http://www.scienceofrunning.com/2012/06/physiological-model-of-training-why-it.html

Physiological Model of Training- Why it and "zone training" are outdated

Physiological vs connection model.(This is going to be a long one…heads up…..)
                I hate zone training.  It’s a pet peeve of mine.  I hate the idea and the concept behind it.  But so many coaches out there use it, and in actuality we all tend to classify workouts into different zones.  I’ve wrestled with trying to explain my hatred for zone training and what I’d call the alternative method for a while, but it’s a difficult thing to wrap your head around.  I knew I hated it, but I couldn’t effectively explain why to outsiders.  I’d dance around the why’s but never had a satisfactory answer.  Part of the reason was I didn’t have a simple way to explain the alternative.  I could throw a bunch of information and examples to describe it, but there was no easy descriptor. Before getting into what the alternative is, lets look at what exactly the physiological model is and how we got there.
Defining a model:
                The physiological model of training is one that relies on the premise that there are a few big physiological parameters that govern performance.  The big ones mentioned in research and the literature are VO2max, Running Economy (RE), Lactate Threshold (LT), and sometimes lactate tolerance or anaerobic capacity/tolerance depending on publication.  The idea is that these four things combine to create performance.
The central premise of the physiological model is that IF we improve one of these parameters, then performance improves.  But how does this relate to training?  The model takes another step and says that there are certain intensities or zones that will improve X parameter.So the full model really states that IF we do X training, Y parameter will improve and thus performance improves.If this was a logic class it would look something like this:  X->Y= P
Sounds reasonable right?  Well, hold your horses…


Strict adherence:

Before fully diving into what’s wrong with this model, it’s important to fully understand it so that it doesn’t look like I’m creating a straw man argument.  As with anything there isn’t one strict concept of the physiological model, but instead many slight variations covering the spectrum.  I’d like to give an example of that and show the limits of a normal physiological model. 

Not meaning to pick on Dr. Jack Daniels, but his updates between his 1st and 2nd edition of the book Daniels’ Running Formula perfectly illustrate this.  In his first edition, he outlined what have now become the classic zones used in many programs.  What’s interesting, and what is typical of a strict physiological model system, is that in between these zones were what’s referred to as “no man’s land” training. 

 
In his book he defines this no man’s land zones as:
“No man’s land of training. Training intensities that fall into ‘No man’s land,’ are either too easy or too hard to reap the benefits you want. You are not, as may sometimes be assumed, achieving the purpose of training the two systems on either side of the chosen intensity. What you are doing might be termed, “Quality-junk” training. At the least, it is training aimed at accomplishing an unidentifiable purpose. Always have a purpose for every training session; ask yourself the following questions: ‘What system do I hope to improve by doing this workout ‘and ‘What am I really trying to accomplish?”

This is what I’d call a strict adherence.  If you train too fast or too slow of the zone it’s “junk” because it isn’t targeting the special zone which should target some parameter.  This sounds good, but the issue is that training doesn’t occur in isolation and as we will soon find out those training zones don’t even attack those parameters terribly well.  It’s missing the central point of training, that it is a stimulus.  Yes different stimuli will result in different results, but everything is a stimulus to a degree.  If you are too fast or too slow, it doesn’t negate the adaptations, it just changes them slightly.  Secondly, you have to remember that this thinking is with the model behind it.  There is no purpose for the “no man’s land” zone training IN THIS MODEL.  How accurate that is depends on how well the model reflects what is actually going on.  Because every model has holes and doesn’t perfectly reflect what is going on.  In this case, the model fails to accurately reflect what’s going on as we shall soon see.

What is interesting (and very astute of Daniels) is that in his 2nd edition of the book he takes what I’d call a more loose interpretation of the model.  Why?  Because he expands his LT/tempo section of the book to say that unlike in the first edition, tempos can be slower and longer than the LT zone and still get great benefits.   

Now that we get what the model is, what’s wrong with it?

(The above section might come across as harsh to Daniels but that isn’t my intention.  Instead I think it’s cool that Daniels realized the potential of other zones of training and amended his thoughts.  A smart coach!)

 

What’s wrong with the model?

As a quick reminder the physiological model relies on the following logic:

1.       There are certain parameters that define performance.

2.       Training each one of these parameters improve performance.

3.       To train these parameters you work at X intensity.

Hopefully you’ve noticed a few holes in this logic.  Let’s go through them.

First, those big parameters don’t really do a wonderful job correlating with individual performance.  Yes, some studies show strong correlation to a mixture of them, but you can’t really separate out good runners from great runners. Research shows that combining the big 3 of RE, VO2max, and LT explains around 70% of the variation in performance (Di Prampero, 1986). So, good, but not great? Vo2max in particular does a relatively poor job. You can check my fallacy of VO2max article if you want more details.  For now I’ll briefly quote one relevant section:

Showing the separation of VO2max and performance, the Vollaard et al. study found that the change in VO2max was not related to the change in time trial performance (2009).  Studies demonstrate improved performances without changes in VO2max (Daniels et al. 1978). Also, studies show that VO2max can improve without changes in performance, which is seen in a study by Smith et al. that showed improvements in VO2max by 5.0% without an improvement in performance over either 3,000m or 5,000m (2003).    In addition, in looking at long term changes in performance in elite athletes, changes in performance occur without subsequent changes in VO2max.”

As far as the other parameters, yes they all correlate to performance to a degree when looking at groups.  So that is valid.  The question is do changes in these parameters correlate with improvements in performance?  The answer is it depends.  In several studies you’ll see an increase in LT, RE, or VO2max as well as an increase in performance.  In others,  like those mentioned above with VO2max you’ll find no change despite an improved parameter.  Another quick example is a study by Vollaard et al (2009) that found that RE and VO2 changes didn’t explain performance improvements, or in their words: This study demonstrates that improvements in high-intensity aerobic performance in humans are not related to altered maximal oxygen transport capacity”

 

Similarly, with lactate threshold.  An increase in threshold is sometimes tied to a decrease in performance as demonstrated in the world by Jan Olbrecht.  This is usually a result of the lactate threshold increasing while anaerobic ability is decreasing.  For more on this concept see Jan’s work.

 

Which brings us to the point of training not occuring in isolation.  We can’t independently try and improve these parameters in all runners and expect performance to increase.  There’s an interaction between the training  types.  For instance, there’s a strong back and forth tug of war battle between LT work and the so called lactate tolerance work. This interaction effect is somewhat addressed by periodization, but when training is thought of in isolation such as do X and improve Y parameter, it’s often lost. 

So, not surprisingly, we start with a somewhat decent premise and get a bit shakier as we move away from it.  But where things really fall apart is in the next step, which is the most important because it translates lab work to the real world, which is what we are all concerned with anyways.

Training zones don’t really work?

Perhaps most importantly then, the training zones don’t really correspond with improving the parameters.  And even if they do to a degree, there are multiple ways to improve the parameter.  Let’s  look at these zones individually to get an idea.

VO2max

In this new quest to improve VO2max, it was first ASSUMED that training at VO2max was the best way to improve it.  The logic was simple.  Spend as much time at maximal oxygen consumption as possible and it has to increase right?  Sounds logical enough…So the next step was figuring out what paces would elicit VO2max.

Why do we train at roughly 3k pace to improve VO2max?  Well, we got to that point because a bunch of researchers took on the challenge to see what was the slowest speed which would maintain VO2max for a relatively prolonged time.  Depending on what research article you  look at, it generally came out to be something that lasts roughly 7-10 minutes.  Or about the time it takes to run a 3k.  Therefore, 3k pace became VO2max pace.  Yes, running faster than that elicits VO2max too, but it’s not the slowest speed.  We had the intensity.  Onto the next step.

A bunch of researchers did more studies seeing different intervals that would allow you to spend the most time at VO2max during the workout.  That’s where we get Billat’s famous 30-30 workout and a slew of others.  After this we had our optimal interval speeds, lengths, and recovery.

So it was all set.  Do these workouts at X speed with this recovery and you are set.  The problem?

Well the research didn’t exactly back up the idea that to improve VO2max (even if it mattered much…) we should do that.  I could go on and on but a nice little review of training to improve VO2max by Midgley (2006) sums it up nicely:

“Training intensities of 40–50% V˙ O2max can increase V˙ O2max substantially in untrained individuals. The minimum training intensity that elicits the enhancement of V˙ O2max is highly dependent on the initial V˙ O2max, however, and well trained distance runners probably need to train at relative high percentages of V˙ O2max to elicit further increments. Some authors have suggested that training at 70–80% V˙ O2max is optimal. Many studies have investigated the maximum amount of time runners can maintain 95–100% V˙ O2max with the assertion that this intensity is optimal in enhancing V˙ O2max. Presently, there have been no well controlled training studies to support this premise.”


So there we go.  We don’t know if that is the best intensity or not to increase VO2max.  Tons of research, but no clue.

 

I also like one of their other statements:

Synergistic and interference effects between optimised training protocols designed to target specific physiological performance determinants and the influence of individuality then need tobe established before sports scientists can make recommendations to runners and running coaches,with a high level of confidence, on components of  an effective training programme.”

 

Individuality.  Interaction.  IMPORTANT.

So what we’re left with is a magical zone that we’re not sure if it even attacks what it’s supposed to attack (and if that even matters?)

What does this kind of thinking get us? Well, a quick example is certain studies came out a long time ago that said after 50-60mpw amount of mileage, VO2max doesn’t improve, so why would we run more mileage if that’s true since VO2max is the be all end all (Berg, 2003).This isolationist approach neglected the complexity of performance so we ended up with a bunch of coaches thinking you don’t need to run much mileage…whoops.

LT:

The lactate threshold is one of my favorite topics as I like to do lactate testing, but in the Jan Olbrecht inspired way, not the traditional way.  I’ve covered that in my blog elsewhere, but there are some important lessons from that distinction.  For instance, the actual threshold itself is influenced by factors besides “aerobic” ability.  So the anaerobic side or lactate production side influences it too.  So it’s entirely possible to get an improved LT curve while actually decreasing in aerobic capabilities (if the anaerobic capacity is decreased…).  So once again interaction is key, but what about training at LT to improve LT, and thus performance.

Well if we look at the research, training at LT CAN improve LT. That’s good to know. But so does training at various other paces.  Once again there is no magic training zone.  In fact if we look at the one study on well trained runners, if they increased their training volume at near LT by 103%, it didn’t do anything to the actual threshold (Lehmann et al. 1991).

In other studies, with recreational runners, you saw big increases in LT after 2-3 months of training at threshold and then no further improvement in LT afterwards with continued training.  What this tells me is if they wanted to keep improving the threshold, the stimulus had to change.  They had to do some work above LT,  some mixed intervals, aerobic intervals, or alternations. Whatever they chose, the stimulus had to change

In a review on training to improve threshold, Midgley et al. (2007) stated:

In summary, we found only one study that investigated the effects of an increase in the volume of

vLT or vLT training on the lactate threshold of distance runners.[25] This study reported no significant

increase in the lactate threshold. Several training studies have reported a significant increase in

the lactate threshold of distance runners in response to the inclusion of supra-vLT training velocities,[15,29,39] although these findings have not been consistent.[34,36]”

 

Once again, we’re looking at, ya training at LT improves it, but so does a lot of other stuff. And it depends on the type of athlete on how best it’s done. 

Running Economy
But what about Running economy? Run fast and you get more economical? That’s the magic zone to improve RE, right?  Well, sorta.  If you look at research, again depending on the group studied, running fast, at VO2max, and at LT have all improved economy in various studies.  Wait, so has weight lifting, plyometrics, whole body vibration, altitude, training in the heat and on and on (Berg 2003,Foster 2007). Obviously some improve it more than others, but the point is that like with all the other parameters, there are numerous ways to improve them.  It’s not some magical zone that best targets it.

Ignoring whether or not RE is actually a good measure (that’s a topic for another time), it seems silly to assign one zone to improve this, when truthfully people are still arguing over what the heck improves it.

The point of this little tirade is to not say that training at these intensities is bad.  It’s good.  The point is that by sticking to this strict zoning concept we ignore both the individuality of the athlete and of the training response.  In this system it assumes that an LT run does the same thing regardless of whether the athlete is a fast twitch runner or Slow twitch.  While, we know that the effect can be vastly different because there physiology is different.  Same goes with VO2max training or any of the other zones.

Nail in the coffin:

For my final nail in the coffin for why the model sucks, let’s look at a training study on sedentary people that had them all train at 70%VO2max.  So they all trained at the same exact “zone”.  What happened? Let’s check out the data (from Vollaard et al. 2009):

 

What happened was simple.  A ton of different individual reactions to the same exact training load and training zone.  All the way from big picture changes like performance , VO2max, and VE all the way down to enzymatic changes.  There was a whole lot going on and a wide variety of responses.  What this tells me is that stimulus matters.  For some people the same training “zone” will give a different stimulus. 
The same was found in a more recent study of untrained individuals. They followed them for a prolonged period and had them do all exercise at 60% HR reserve.  What happened? Well a big variation in improvements in the big variables even though they were all training at the same intensity and volume (see full study here: http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0838.2010.01139.x/full)

While you might say this was with untrained individuals so what's the point, I'd counter that with untrained individuals you'd expect almost anything to work! I mean you're going from nothing to something, so the fact that there's a huge variation is interesting.
And finally, if we want to go all the way down to the genetic level, here's what happens to people again all training at the same intensity.  Look at the variation in high responders versus low responders for a whole slew of different genes: http://jap.physiology.org/content/110/1/46/T2.expansion.html


Why do we do this?

The answer is simple.  In Daniel Kahnemann’s book Thinking Fast and Slow he describes essentially how human’s think.  In there he talks about the concept of how when we get a difficult question, we often times replace it with an easier question and answer that.  It’s subconscious so we don’t know we are doing that.  But that’s essentially what we’ve done here.

We have a difficult question: How to improve the complex notion of performance?

And we’ve replaced it with “How do we improve these parameters?”

The second question is much easier to grasp our heads around then the first.  It’s fine to simplify and reduce, but in this case we have to ask if the second question really answers the first.  My contention is that it doesn’t.

How’d we get here? The story version:

Back in the day, coaching was almost purely trial and error.  You learned from those who had come before you and tried your own manipulations.  If something worked, it stuck for a while.  The great coaches quickly were emulated until the next new idea or phase took over.  The classic example is Arthur Lydiard experimenting on himself in terms of mileage before assigning training to his illustrious crew.  Trial and error works.  It just takes some time and occasionally a lot of error.

That got us most of the way towards modern training concepts, but something happened starting in the late 70’s, early 1980s and continued through the 1990’s.  Exercise Science actually became a more defined field with actual research on performance.  We began to be able to readily measure parameters like VO2max, lactate, etc. on well trained runners.  Furthermore, we began to conceptualize what may effect performance.  This was the rise of the VO2max paradigm.  All those cool results that showed our best had really high VO2max started coming out and for those athletes who didn’t have crazy high VO2max values, the concept of RE was developed and explained the rest.  Soon portable lactate analyzers came about and we could measure that evil fatigue component called lactate.  More testing, more variables.

                Fast forward a little bit and we have the big 3 of VO2max, LT, and RE and then a few other variables that were occasionally thrown in to determine performance. This got translated to the intrepid coaches looking for an edge.  It was the beginning of the age of Science.  It was cool to make things sciency, and it offered a world of possibilities.  Everyone was looking for the next edge, so science became that.

                That’s when it got translated into the coaching world.  With Coe and Martin’s book in the 1980’s, Daniels’ Oxygen power following, and many others it became the thing to do.  The promise of explaining performance in a neat formula AND being able to make training almost a mathematical model was too tempting to pass up.

The model is thus part of our human notion to want to compartmentalize, our need for structure, and our seeing Science as the next ultimate step to sole all of our problems.  The models basic foundation and premise are broken though.
Done rambling, so what?

It’s not that the workouts are bad. It’s not that we shouldn’t run at threshold or 3k pace or faster.  It’s that the model is bad.  The model is broken.  And if you strictly follow the model, you miss out on a bunch of sweet stimuli that need to be touched on.  You also loose the ones thing that is essential to coaching, creativity.  Instead, it becomes a plug and play system that discourages creativity and innovation.
Hopefully through this rambling mess you get a few things. If all fails, I hope it gets you to step back, think, and question.

 But what the heck do we do about it, if I make this claim that the model is broken? After all I can't just sit here and tear something down without suggesting an alternative.


He is  so right so our alternative is IPAHD  individual physiological assessment of homeostasis disruption
My PAHD and UrPAHD .  the  tool you need most is the ability to assess the O2 trend  and  dynamic at the scenes of activity .
 In one word NIRS and MOXY combined with all what we learned in the past, combine and think it through . It is not broken it just has to be put together in a new way. That's where we start here.
 
Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #8 
Look at  thread no 3 in this page.
 You see some MyPAHD pictures.
 MyPAHD is an assessment you can do in the future at home. You need only a performance info watt or speed and a MOXY watch.
 You sent this info to your coach or center or you use it on your own.
 Goal see the trend in oxygenation.
Designe  your individual physiological assessment protocol based on the MyPAHD.
 See here below the PP.
In our study we look at the values of all existing physiological data collection and see, which one may give us the best information ( Not based on mathematic.
With the study we hope to have 50 - 100 3 min My PAHD's so we can really look at the values and whether we all here on this forum .would suggest the same +- steps for the UrPAHD
Below is an example.
 MyPAHD  and where I would see trends in the MOXY info.
 Than the suggestion where we will assess KOS in anUrPAHD.
 Right is a UrPAHD from Switzerland and the study group there done with a world class MTB athlete.
 They did not yet an initial MyPAHD and therefor sometimes the steps may not be enough or not optimal but this is still agreat test.
See lactate values in the UrPAHD and you will detect a very interesting trend


Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #9 
Here another new MyPAHD
Your brain work.
 Look at  Alarm phase / Adaptation phase and homeostasis disruption.
Look at simple and spontaneous , where you see trend (changes). Now this is the simple example how a coach would get information ( physiological intake form ) remember the " reset your physiological bio marker clock.
 When there is big shifts of this trends ( sen by overlapping 2 follow up My PAHD) than it may be time to do a full UrPAHD with your coach , where  more parameters are assessed  to see  where and who is limiter now and  possibly compensator.
 To design the UrPAHD you now take the MyPAHD.
 So let's try , whether you can design the new individual UrPAHD protocol from this My PAHD.
 Goal . Try to get 4  steps  to load in the Ur PAHD. So look for 3 - 5 clear trends in the Graph. Take the letter, which is a  load ( wattage and you  have the area of interest for the steps you will try to see, whether you create a homeostasis  or a disruption and you do this for all parameters you use..
 The first picture is the MyPAHD.
 1. Look at yellow Blood volume first  make the areas of interest and assign a load. First step is 60 watt and  than 20 watt up each time.
2. Look at purple which is the trend of SmO2. Same here design the changes in trend.
 Note it on here as watt loads .Ask your self . Where do  I see increase in tHb ( yellow blood flow)
Where do I see a plateau in tHb  and where does it start to drop.
Same for purple.
You will see 3 -5 areas you would like to load  but long enough to see  or give the physiological systems a chance to try to move after the initial ALARMPHASE into a homeostasis, than disrupt and repeat and go on to the next step and repeat.
 5/1/5 5 min load 1 min rest 5  same load and so on.

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