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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
This is  an amazing  site  and worth while to  spent  some time on it. They are pushing the limit in an incredible way on  adding metrics into the training.
It is as well a great site to see how fundamentally different ideas  can be  , when looking at ideas of  changing performance, but how most likely , when both ideas are opening up  towards  each other , the combination could be an extreme game changer.
Using physiological clean ideas and wattage ideas in Pro cycling could change a lot of  ideas  we have about cycling. Instead  of using plasma expanders artificially, we could use  natural options. Problem ,the wattage  at the stage of stimulation would be very different than when I inject them or use  gases for inhalation, to change delivery options  and so on. One of the interesting parts is, that when I talk with top cycling coaches and tell them , that the athlete has a SV limitation?. They  have limited, if any idea, what that means in  combination with using %  of  FTP power Training.
 There are some cook book guidelines for SV  workouts , but any critical coaches who  looked at this  loads in combination  with  for example Physio flow and NIRS could find very easy, that it  can work  but  not  has to work  and it can be  far of  SV  stimulation in some cases  due to different limitations  at different days   or in general. We  showed different examples  on this forum with SV  drop from the university of Trois Riviere live case testing.
In fact  many  coaches  now accept  that we  can find limitations  but than have for the moment some problems  on how to apply the current %  FTP  system into the findings.
 Now  here an incredible  summary to enjoy.
   When you read this though you can see how the different ideas may have developed.

 I am coming  from a physiological back ground  working with people   in rehab  and  world  class athletes with one single idea in mind :
  Health. So the  first  and single  biggest concern is to  find out , what is limiting   further   performance   and  improvements and who, because of this limitation, may  have to compensate if I simply push  hard  and therefor  always  overload the limiter  and always need the help  from a  compensator
 I use  an example  from a  rehab client.
 Limitation : Respiration due to the fact that he worked in a mine. So COPD  developed  due to  smoke  and dust.
 This creates a  specific overload  of his respiration with asking 2  system to try to help  in cases  of harder performance demand to compensate. In short   he will  ask the cardiac systems  and  a part of the buffer system ( Kidney's  to step in ). Long  story  short  summary. He  can end  up  with cardiac  and  kidney function  problems  due to a chronic   overload d of his respiratory  system..
 Classically  we will treat  now his cardiac  and   kidney  systems  and forget  to   try to work  on improvement ,if possible of  his COPD.

  In sport we may have a  capillarisation limitation  in combination with a   mitochondrial density limitation. So pushing hard  , as we have a  utilization limit  , will create a  high demand on  CO2  release  and we always  will overload respiration as a compensator  and   the limiter will be  barely challenged. The SV will be  reduced   due to  preload limitation and a such we always challenge  CO over HR ( frequency )  and less likely over   muscular  development

Our  idea is  to find  limiters and than develop intensities , where we could  use  wattage in certain sports, or  speed, is the idea. So we think, that it is the physiological ability of  an athlete  who  will show up in a certain  ability to push  wattage  or performance.

This is not new  and  pushed the use  of lactate as a bio marker into  question, when lactate is  combined  with a  performance number.
   Example below 2  athletes  same " aerobic " capacity , but different storage ability  of glycogen.
 So three step tests in a  row  with  in between loads  at  LT  2.  You can see how the  energy  storage  as well influenced  a part at least of the CO,  the HR  level , and a  such end time  and  as  well   maximal performance result. Using MOXY in this  test idea  will show you nicely how energy storage  will change the reactions  and trends  between lactate  and oxygenation information. We did   some similar  studies  with this idea  as LBP  was  used , to show  how   trend information's  are better to use  to avoid interference with  nutritional changes. Now  with NIRS we have  even better feed backs. and live
  Simple reason.
: we look directly  at  O2  ( oxygenation  trends   and not over  indirect  reactions)
 A  strange  part  for us  is  to understand , as we  can do that now, looking directly  at O2  reactions,  why we  would use  lactate to find out , whether you are  Aerobic  or  " anaerobic' .  A lactate number  does not tell you this  at all. You can have a reading of  4 mmol in your finger, but  go perfectly aerob  at that moment.  You can have a 1.6  in your finger  and really   sit deep in an  oxygen independent load.
 You can have a Max lass  at a  3.6  +-   blood lactate concentration  and next time by  2 .9  or  4.2  but in all three cases  you are perfect in balance.
  With   MOXY  you have  : 
1. increase in SmO2 , which means  you have a great aerobic  support  and a  low , but existing  O2 independent  activity as well.   so aerob.

2. You  can have a flat  SmO2 ,  so you are  a kind of in a Max Lass, but you  do not  have  a number  just a flat SmO2   and  a flat  tHb  and you know you are  supporting the energy demand over O2  just okay  but have a higher O2 independent help  as well ,so border line  but stable aerobic.

3. Than you have a dropping SmO2 , so you  know , too low  delivery  of  O2  than  would be needed  ,  so   " anaerobic "   big help  from O2  independent   and still but reduced  O2  dependent  help.
 The word  itself   , aerob  and anaerobe,  actually tell us  exactly what we see now  in  real live  feed backs with MOXY.
 So why to go back  and use a great idea  but it is  not a  feedback on O2   but an indirect  speculation of  what O2  may   do or  whether we  are  aerob or  " anaerobe"
 Single lactate numbers tell nothing other, than what we find  for the moment in lactate concentration in the  blood.  They do NOT tell in what  energy production stage  we  are  at the moment of  sampling.

glucogen speicher.jpg 

  I think it is  not the performance  who can make that decisions ,how physiological systems  have to work. It  is the ability of a  physiological system  , who will   create the   performance we see.

 Than we have the   other world  you can read  below, where we see  actual  daily changes  in performance,  but we  may  only have limited if  any feedback , why this  happens.
  We  do not know, whether today the muscle strength, due to the load from yesterday  may create  an occlusion reaction and therefor the duration to  push CP is very different as I reduce  outflow  and therefor  have an other limitation for the duration , than when    in 2  days my respiration may be the limitation as  I   have a fatigued   respiratory muscle  from the training  I did yesterday,  so   I have a problem to  get rid  of  CO2  now   but because I have  a high CO2 I have  a higher tHb  and  a better  SV  and I  can have  a lower HR  and again a different duration I  can  sustain  on CP.
 So  using time  and estimation is a  fascinating model  but as you can see, and I am very biased,  I am not  that concerned  on  time  or power , but much more on  what  I  stimulate  and stress and the  time and power will be depending on the physiological limitation  and not the other way.

 Power and time   are not deciding  what  your physiological  systems  have to do. Your physiological system will determine the power  and time you can push  . 
So    over time  when  we  open  both   directions and combine this,   we  are the real winner in a  huge  step forward in  rehabilitation and  sport , as  power  is  the best  way to see objective changes  . Now if you know  how you achieved  this   power improvement  you  are the real winner as you direct and control the progress over information and physiological  feed backs  rather than over calculations  and speculations.

 Enjoy the read  and  think through  what I  tried  to explain  when looking at the info

" Determining CP + W' correctly for use in the W'bal model 
11 posts by 5 authors
Page 1
Nathan Townsend
8 Apr
Recently I've made several posts outlining why W'bal goes negative if you use FTP instead of CP in the model.  This occurs mainly because FTP underestimates CP.
In most cyclists (excluding elite and pros), CP lies in the range 20-30MMP.  So you simply do a TT in this duration range, and I recommend this as a doublecheck of your CP, but it does not give you the value of W'.  For that you need to conduct short TTs also.
I do not recommend the 3min AOT test because during the last 30sec of this test you are still recruiting type IIx fibres.  These fibres are fatigued but they still produce some force. Therefore, the potential to overestimate CP exists (especially for well trained cyclists) because this essentially violates the concept of CP, which is that type IIx fibres are not being recruited.  Secondly, getting access to the lab equipment is difficult to perform this test.
The recommended "gold standard" to estimate CP is to conduct 3-5 time to exhaustion tests as constant power in the range 2-15min.  Again, the problem with this is that not everyone has access to a cycle ergometer that has a constant power mode.  Secondly, TTe tests are notoriously variable due to psychological factors.  At the point of exhaustion, if I were to offer you $10,000 to continue for another 30 s. I reckon you'd give it a red hot go.
A practical field method has been validated in a couple of studies (see links below).  These use standard self-paced TTs instead of TTe tests over the same duration. There are some important points to consider though when conducting self-paced TTs. 
1.  Most important is that the TT is done as evenly paced as possible. Going out too hard could cause premature fatigue, whereas going out too easily might lead to some W' being left in the tank at the end  (ie: you do not attain VO2max)
2. The key to estimating CP properly is that we want the shortest and longest duration which elicits VO2max.  2min might just not be long enough in all cases, so I would recommend 2.5 or 3min to be sure.  Anything over 15min (if evenly paced) begins to approach the maximum duration that humans can sustain which elicits VO2max ie: a TTe test lasting >20-25min will not induce VO2max.  Task failure occurs in combination with other reasons such as increased central fatigue, that are less present at shorter durations.  So to be safe, I believe it is wise to cap the long end at around 15min.  For this reason also it should be obvious that the 3/20min test has the potential to underestimate CP.
3. The durations should be evenly spaced.  Thus duration of 3,8,14min would be preferable to 2,5,15min for example.
Lastly, a small modification that I believe could be used to prevent an underestimation of W' by a conservative pacing error, is simply to commence your "end spurt" about 30sec earlier than you otherwise normally would.  If at the end of the TT, the power is still rising and especically if it is above the average power, this would indicate that you have W' left in the tank (thus inducing a small underestimation).  However if the power is decreasing at the end, and it is below average power, then it implies you've expended virtually all that you can.   If the pacing is done very evenly though, we do not expect a large end spurt to occur anyway.
If you have 3-5 tests in the range 3-15min you can then model CP + W' using several methods including the nonlinear 2p model which does a hyperbolic curve fit, or the 2p linear models with fit a linear regression to either power vs 1/time (s), or work vs time (s).   You could do all three models and take the average.
Another reason why the 3/20min test is potentially problematic is because you are restricted to the linear models only.  In this case the 3min test has a large effect on the value of CP.  This makes a little sense physiologically, but can be a misinterpretation of the data.  For example, lets say we have two cyclists: A: 3MMP = 450; 20MMP = 300, and B: 3MMP = 400; 20MMP = 300.  In this case, cyclist A will have a lower CP by about 10W despite the fact the highly aerobic 20MMP test result is the same in both.  Cyclist A will also have a much larger W' in order to compensate.   This is a valid explanation, however the exact same results could occur if cyclist A had a higher CP, and only a marginally higher W'.  This problem starts to get ironed out if you use the nonlinear hyperbolic model and especially if you use 4 or 5 evenly spaced TTs to fit the data.
So there you go.  In a single training session you could go find a decent bit of road where you can hammer out a 14-15min TT, then do all three tests with an approx 30min recovery gap in between.  You could then go an do a 25MMP to doublecheck the CP value or even include in the average of the other CP model estimates.  For standard interval sessions  conducted under similar environmental conditions as the test method of CP+W', you should find that exhaustion will occur when W'bal = 0 +/- 1.5 kJ.  It's not perfect though and Phil's paper using short intervals and recoveries (20s on / 10sec off) revealed a larger error in W'bal at fatigue.

Validity and reliability of critical power fieldtesting.


High agreement between laboratory and field estimates of critical power in cycling.


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