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Juerg Feldmann

Fortiori Design LLC
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 #1 
Thanks Clint.
 Clint has many toys so he combined data collection  from MOXY as well with Portamon and added a portable wireless K42Bb VO2 equipment to it including a Physioflow for noninvasive cardiac hemodynamic.
 Physioflow   gives us information on many cardiac parameters and what we look for is CO = Cardiac output and HR  and CO = HR x SV ( stroke volume. ) and we as well can look at EF %  ( Ejection fraction % )
So here the game   we try.
 I take only  MOXY info and compare it with  Portamon.
 So  Green on the right side of Portamon T1T2T3  is for TSI %.  on the left side red is O2Hb and blue is HHb  yellow is screwed up on the test  ??? possibly HbDiff and green on that screen is  possibly tHb as it looks.
 So remember on the newer MOXY version we have tHb as well together with SmO2.
 So you see below the MOXY info.  good test but even 60 Watt for this athletes with only 3 min time is a  severe  shock  as you can see no real Alarm Phase  to  give time to open optimal blood vessels  but for sure not to move  much more O2 in.
 This situation is often the case, when start load is already reaching 5) % of VO2 max tested. So  Clint should have VO2  results as well and lets see, whether he is already close to 50 % o the tested max VO2.
 Than as we discussed . MOXY is in the game  live  and VO2 is  the next day. So the circles would suggest a  delay of a respiratory reaction of 4 - 6 min after the change in SmO2 
 IF the respiratory system can compensate and is not LIMITER at that stage,
  You can compare TSI and SmO2  and discuss for yourself  , whether we see the change at the same places  ( Time )  as well  you can see not great due to scale the tHb  change  on the left side. Drop[ in tHb can indicate a limitation of cardiac and or respiratory so we would have to check CO  and SV at the level of tHb drop and as well look at reaction of the respiratory system
 If he can breath very very  fast and good he  will show a low CO2 at the end  and  a high FeO2 % due to great hypocapnic  breathing , but this would create a  fast drop in SmO2 at the end  and we can see that in the MOXY . Question is, whether we have  end CO2  and end FeO2  . FeO2 would go up and CO2  down which would mean O2 Diss curve to the left and great SpO2  and great  deoxygenation so drop of SmO2. See  picture of MyPAHD below and suggestion to Clint for the UrPAHD protocol to get real answers  who the LIMITER is and who the compensator.

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Juerg Feldmann

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 #2 
Thanks Clint , here a suggestion.
 I am not sure, as I have very little actual time information. Here a MOXY result.
 I like to have fun so let's see how much I am off.
 I do not believe, that the test started , when MOXY started. So try when you do tests just push the start button for   store data , when you start the test or 1 min ahead.
 I think the test started , where I drew the line ?????
  Than  he had the steps and I suggest  based on the MOXY trend, where you make the 5/1/5 loads.
 Perhaps I am off. He did not pushed many steps. up to 220 and that one  not finished ????
 so  when you have clients, who can only push 220 watts even 60 watts is most often close and sometimes already above 50 % VO2 as the first step is the biggest homeostasis disruption  and in many cases if this is that  big already we never ever can see an increase in tHb and  SmO2 due to the nature of stress. Overshoot in HR  due to the big load suddenly .
 But  we hope  to see this very different, hone we actually give enough time to the different systems to adjust  or try to go back to a homeostasis after the initial alarm phase  . We will see.  Here my take on this.

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Andri

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 #3 
It would be nice if Clint could quickly fill us in on what the athlete was doing prior to the start of the test, if the test started where Juerg indicated the start. Since the MOXY unit starts monitoring when it is turned on the sync of test data is somewhat tricky. Something to work towards in the future would be a marker or start function on the watch. Anyway back to the last attached image Juerg was looking at. It is clear that as soon as the MOXY unit was turned on whatever the athlete was doing lead to an increase in SmO2 at the beginning of the measuring time, which somewhat stabilized through until later on during the test when a clear decreasing trend is realized (of course there are always up and down fluctuations). The question is what was the athlete doing at the very beginning where a rise in SmO2 is seen to a given max value...was he or she just walking around. The reason behind this question is that with NIRS data that I have seen and tests I have conducted as long as a test begins at a very easy resistance athletes will show an increase in SmO2 at the beginning of a test followed by a plateau and then a decrease. If we just look at the test portion of the attached image (again assuming the test started when Juerg identified a start), no increase would be seen. The increase had already occurred prior to the test start. This begs to question using a warm-up prior to a test, we may be losing physiological information by not identifying potential ¨oxygenating¨ zones by already realizing these zones in a warmup rather than in the test. Just some thoughts.
Juerg Feldmann

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 #4 
Andri great point and here an IPAHD from our Swiss friends . It shows a  real warm up prior to an IPAHD and indicates , what Andri refers to, A loss of  extractable information due to a most randomly designed and based on feeling  warm up of the athlete. . We get really picky  on warming up the  wattage trainers, but interesting ly enough nobody cares abort the " warm up of  an athlete here to enjoy
Juerg Feldmann

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 #5 
Sorry forgot the att.

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Juerg Feldmann

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 #6 
Here some info from our " dream study group" centers. Clint  he has the great lab you  basically can't find anywhere in  the USA. He is the only  noninvasive test lab in the USA with noninvasive cardiac thermodynamic  testing as well as wireless VO2   with K42b as well as  portamon and  MOXY. This is the dream toy box for exercise physi9ological assessments.
  Here now   some inside view   when he  started to ad MOXY for our  study purposes.
  1 perfect  info and 1  perfect in perfect info we need as well to learn how we can use this info to improve. See PP below.

MTF Clint

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 #7 
Juerg/Andri
Sorry for the late response, wanted to keep you guys guessing... actually didn't see the post until now hahaa
First I'll attach the VO2 info from the K4 as a screenshot of the parameters you asked for. Let me know if I missed something or if you guys want to see something different?



Sorry for the issues with the Portamon zeroing out the HbDiff, but I've got the problem straightened out now.. just no way to go back and fix it.
Andri the athlete went from seated to standing as we bias the trace on the Portamon. The initial rise in blood volume was from that.. Juerg seems to be correct in assuming the start time of the MOXY. I've been synchronizing the start time of the two devices so I can go back and use the time from Portamon to measure the intervals on the MOXY data as well.
I think Juerg is also correct in saying the athlete was above 50% VO2 at a very early stage.. So we most likely missed the warm up data at 60w, and instead should have had started at an easier pace. For the record, this athlete is one of the top amateur motocross racers in the country. He's a very strong athlete who can Deadlift 350lbs, and squat about the same.. He also has a 31inch vertical. Despite his strength and talent, his prowess on a bicycle isn't much to speak of. It seems standing up and walking around was enough to get him 'warmed up'. Amazing to think 60w was that big of a shock to his system.. I would have guessed a strong athlete like this would have no problems at this low of a wattage.

Juerg this was the original MOXY protocol of a 60 watt start with 20 watt increase every 3 mins.. No 5/1/5.. so you tell me what you think about limiter/compensator? I also find sometimes a drop in tHb is not only due to respiratory or cardiac weaknesses, but a problem with the muscles. Recruiting too many fibers, as seen by increased SEMG activity. I'll go back and retest the athlete this week with the 5/1/5 protocol, and post the results up on this thread... but feel free to take some guesses??? Anybody can guess here.. the winner will get a brand new Goat!!! (courtesy of Juerg) hahahahaa better get this one right Juerg

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Juerg Feldmann

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 #8 
I LIKE TO GIVE HERE  POSSIBLY A VERY UNEXPECTED ANSWER OR BETTER ASK  OUR READERS FOR  SOME THOUGHTS ON THIS  LOUD THINKING .
VO2 testing and specific VO2 max testing in a lab on a bike is  in the best case scenario a decent way of testing road cyclist on a possible  accurate or relative accurate VO2  max information.
 But that's it.
 Using VO2 max testing on a bike with Icehockey players for example to use the information for any on ice or dry land workouts  with exception on working out on a stationary bike is in the best case scenario great  income for the  center , who is doing the testing  but is of minimal   worth for coaches  and or prediction  of any physiological ideas or information..
 Same in  the case of Clint's guy .
What does that mean.
  If we do physiological testing for the sake of helping the  athletes to get information on how to workout, than we have to develop sport specific ideas and activities.
 So Ice hockey player have to be tested n the ice or a skate mill.
  Kajakers  in the water in a kajak, cross country skiers on skis and so on.
 The fact , that we use VO2 max  per bodyweight and than compare this numbers to  make an assumption on performance is well of  what  would make sense.
 We have many very famous examples who show the absurdity of this idea.
  Lance Armstrong before his first New York marathon (  with or without drugs ) had a VO2 max of 85. Paul Tergat the winner in this marathon had a VO2 max of 85 . The time difference  : close to one  hour.
 The " shocking part is, that his problem   and misconception of VO2 max was discussed many years back in the 1970 in   a sport Congress with an incredible nice work done  by Dal Monte

Dal Monte   " Analysis of physical capacity in sport and methods of functional evaluation int sport symposium Teheran 1974"

P 396 Sportmedizin Arbeits und Trainingsgrundlage Hollmann/ Hettinger  Schattauer Verlag 19080  The picture shows you a summary of this great and simple  study and shows you the questionable idea of using VO2 max to predict performance.
  If VO2 max = performance. than we should be able to turn this around (  Andri Feldmann ) and say well  Performance predict VO2 max.
  Can we really do this or do we think this is absurd.

What is   a possible  suggestion.
 Physiological testing in combination with performance.
 Using a great idea like FTP   but look at the  bio markers   at that performance to calibrate not just the bike but as well the athlete.
 Example  FTP 215 watt, HR at this level 155, RF  34 SmO2 60 +- .
 Now  if you go and warm up you could calibrate yourself and see whether you have this balance in the information.
 You may now have by  215 watt HR of 164 and RF of 39 and SmO2 of 52 +-
 What does this mean. Is your FTP  of 215  really still the same workout ????
 Here first the Dal Monte summary out of Hollmann and Hettinger.

Than some case study  of heat ( temperature influence on performance and physiological values  as well a case study  from us on  nutrition and influence on performance and physiological values.

 The  P versus F  Physiology versus Formula is a respond to the great Blog on the  main  page on this website about  CG and the running and  control by the brain . ( the latest two blog's

 




Juerg Feldmann

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 #9 
As so often here another incredible nice feedback on some internal  case studies going on. Clint as so often pushes the next level of approaches.
 For the regular reader on here.
 The first part of our world wide study with  centers all over the globe is finished. Goal was to see, whether we can use MOXY  and whether we can compare trends and information with high tech so called  "golden  standard " equipment like the Portamon or oxymon.
Our answer is  a clear YES.
 In fact the missing option  we where looking for,  namely to have a feedback for our clients life as they work out on their own in a gym or outside is now solved. MOXY is the biofeedback for direct information on oxygenation.
 It clearly will enhance  any current "classical" testing " for center, who  understandably have  some  harder time to just simply switch from what the successfully do since years to a very different approach.
 The best step is to integrate NIRS/ MOXY into the existing habits and over time  e coaches and test centers will learn to make the best combination and use out of the   older and newer tools we  have now available.
 The  main key is to  try to use this bio markers for the person during a workout.
 The dream of a BIO watch is pretty close to be available.  where a client has RF . HR and SmO2  and can pair this with performance, whether it is wattage , speed stride frequency  and so on.
 The beauty now is that you have instant trend info  so you can react upon the situation, before the  story   is getting printed in the news paper tomorrow.
 Hmmm what does this mean.
  MOXY is  you in the ice hockey arena. you see live what happens , true you do not play but  you are as close as it can get.
 That is MOXY you are there and you  see and you can make your mind ( decision ) based on what you see.
 Lactate VO2 ( indirect gas exchange ) is the reporter  who writes the story at home and you read it the next day. True same game, same outcome but a very different perspective on   how you  feel  and see the game.

Summary.
 MOXY  is the  choice of tools for being there.
 What we all have to learn new now is to understand , how classical  workouts  may have to change or   better  what changed  with our "classical' workouts. Why do we see some athletes respond very well and other athletes not.
 Answer.
 It is the different way the "team member"   cardiac , respiratory and muscular team member interact with each other depending on  their limitation or strength. It ends up all back to where nature works so well. limiter and compensator.
 Here a live game from  Clint's study on the influence of RPM in cycling on the  oxygenation and blood flow trend.
  Have fun as we did this already many years ago. This study was done with 2 NIRS ( portamon )  and we can do the same now with MOXY.  tHb as well as Hb Diff  in Portamon will show the same trend as  in tHb and SmO2 in MOXY.
 A combination for a top center is the dream and we for sue will discuss this more as we go along. Why both measure oxygenation but  with some very unique properties for both and when combined instead of wrong and right  we have actually some info we never thought we would be able to do this noninvasive . Wowww great and fun times a head for coaches and test centers.

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Juerg Feldmann

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 #10 
Try to  keep up with the flood of information coming in now. So here just super small  feed backs to our regular and steady growing group of readers.  RPM.
 An ongoing discussion on what is good and bad  ( High versus  low )
 Most often the discussion ends  like a  " Bible camp' I believe  and you believe.
 Reality is, that we can actually   assess this now. 
 The simple answer is :
 RPM is very individual on what is the most efficient way.
 What we may have to accept is :
 It is not just wattage , who tell us what is efficient.
 It is the  physiological team  who decides, how they work most effective together.
 What dies this means.
 When we look at current research , than we often simply have one or  in the best scenario 2 team members in the picture.
 We  look for example  SEMG and   MOXY ( SmO2 )
  what we forget is, that in many cases a  change in RPM will often change the repository pattern as well and therefor the SmO2 values can be influenced by the respiratory pattern.
 So when we test RPM efficiency we use.
  MOXY / SEMG/PF/ Portamon/ Watt/ VO2 info.
  Here some of the classical ideas but  keep the above  thoughts in mind when  coming to any conclusion like the research groups so often  do.

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MTF Clint

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 #11 
Juerg
I curious to know how you would interpret this info, and work it into the athletes training program.. or race strategy? It's nice to know that we can collect this info, but using it to our advantage is the key. How would you turn this into something usable??
Juerg Feldmann

Fortiori Design LLC
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 #12 
Well Clint works too long already with the fun gadget so he understands the limitation but as well the enrichment in using this tools. We are  in a king of a funny discussion with some really great people from the classical field and age of assessment like VO2 max and lactate. What I experience is, that we often discuss  but do not understand each other what we are talking about.
 The above case studies  from Clint and myself ( not accepted as studies ) show nicely what I am talking about.
That is the reason why I added an accepted university paper to show what I mean.
a) A drop in O2Hb ( red in a high RPM  or an increase in  O2Hb  in a low RPM . I saw and see both , does not help for any single  clear information  nor can we make a conclusion on efficiency of RPM as it is done in the accepted paper..
 Why.
 Because the physiological system is simple not dependent on one single bio marker or parameter..
 What a drop in SmO2  or an increase in SmO2 means is only , that you have under the tested sensor more or less O2 in the muscle ( Moxy ) or Tissue Portamon. That's it.
 Now we have to look how this values change as we add different stimuli to the performance.
 Example in RPM.
 Try to keep fixed wattage  200 watt.
  Now you can start to change different variables like RPM, Body position, Respiratory behavior, Coordination pattern inter muscular. Motion pattern  with different timing and so on.
 All this options can have a direct influence on the trend in SmO2 and O2 Hb.
 This brings us  for short to the other  discussion group I worked last week.  The group who uses VO2 max as an indication of  performance as well  lactate as an indication of metabolic efficiency.
  VO2 max = CO  x a-v O2 Diff.
 Now let's see, whether I can explain it with this section , as more readers  may be for the moment familiar with the Fick  equation.
 So here the challenge.
 IF we believe that VO2 = CO x a-v O2 diff. Than we could argue.

CO =  cardiac information so if I can increase CO  my VO2  should go up. True or false ?
 So if I have  2 people with the same CO and the same a-v O2 diff. than they should have the same VO2 max, as well they  should perform  with the same result ????? perhaps true   or perhaps false?
 Or last try .  2 people same CO ( cardiac output ). Is this muscle using the same amount of VO2 if the CO is  the same  ? True  / false ?
Now if we  bike and we increase RPM and O2Hb drops or SmO2 drops does that mean we extract more O2 from Hb or do we load less O2  to Hb and therefor  we see a drop not because of more use but same use but less delivery ?
 Okay I learned that I   give too many thoughts in one post. So let's stop here and  give you guys some time to think ?
 Same home work. Go on your bike  or jog on the sport in front of your computer.  Bike is easier as  you can control wattage but you can do a short 30 second job aboding real work just change cadence. Now bike 50 - 60  easy wattage   for 30 sec. count your RF and now go to 100 RPM and count your  RF. Do the same with jogging very easy slow and  triple your cadence  and in both cases  count your RF. What do you experience ???



MTF Clint

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 #13 
Thanks Juerg
I saw the response you left Carter on his RPM question in the other thread. That was the answer we were looking for. This response below sounded more like a challenge. Now I'm going to get on my bike and pedal fast but breathe slow so I can throw you off.. while I have a goat tied to my back

Carter is a talented athlete who has some very strong points with his cycling, but some clear weaknesses that he is well aware of. As Geoff described himself to me "I'm more like a diesel engine. Slow but steady and I don't slow down" that is how Carter rides his bike. When he is within range of that 77rpm and comfortable, but able to push others harder than they can handle, he is dangerous. However, if he gets baited into the sprints, and breakaways it can hurt him more than the others. So as you said in your response to him, it all depends on what you like to do..

If the goal is to run like a diesel engine, then my theory as a coach would be to train him that way and enhance the great ability he already has. We could work on fine tuning Cardiac output (stroke volume) by matching the proper respiration rate/tidal volume with a cadence of 77.. or we could try to look at the mechanics of his pedal stroke. And he would most likely get slightly better at what he already does well. OR we could challenge him to run higher rpm's until he becomes equally efficient at 100rpm's as he is now at 77. Then he get's much better in a shorter time... usually hahahahaa

If he wants to improve his weaknesses, I think we could all agree he better push himself in terms of cadence, strength, breathing, etc. When we have things like lactate, power, HR, or NIRS to add to the data we collect live during his workouts, it allows us coaches options in setting goals for the athlete. So instead of just saying 'hey Carter go out there and spin 120rpm for 3 spins around the clock' we could say 'give me 120rpm until SmO2 drops to 20% then rest until it returns to homeostasis of around 70-80% and stabilizes'. Then we repeat it as many times as possible until he can no longer find homeostasis or 20% or 120rpm... That is a workout based off of real live data being collected from the athletes muscles. Not from the wheels of the bike or his heart, but the actual muscles that are putting down that wattage and demanding that O2 from the heart.

Thanks Juerg..Maybe this helps you understand where he is coming from, maybe not. Just thought I'd give you my 2 cents and some background info on Carter to help you answer his question. Carter and I will perform an IPADH and URPADH assessment this week and post the results. Let's move the rest of this discussion over to the question Carter posed to keep it going.
Juerg Feldmann

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 #14 
Clint you are already behind and too late ( see picture.
 This research is already done a few years back. ( Smile)

Okay here some  additional points.
 1. As soon  MOXY is released on the market  I hope to motivate many many  users to sent us information and small case studies in. On here for all to see or directly to myself / Andri or MOXY.
 Basically a reality On line research group world wide.

2. When you read the info carefully you will see in between the lines, that we have at least as many open questions than you readers out there.
 Just because we sound smart does not mean that we are smart.
 What we try to achieve is the real situation we are in since about 10 - 15 years, that with the new technology emerging  we have  some much more open questions to the " classical " ideas of assessing testing and training.
 I am in a discussion with some very  very smart people super great people but it is interesting to see, how hard it is to  try to  get them thinking outside the BOX.
 The immediate drive they all have is to for example see, how  MOXY SMO2 relates to lactate threshold or anaerobic threshold or Ventilatory threshold.
How about looking and start  to seem what we actually can understand and  not immediately  relating it to something.
  It is pretty much the same as we always compare with the so called Golden standard.
  How about the golden standard my change  due to new technology.
 Example   testing for fat .=issue.  So the skin caliper would be the golden standard  and now we look how much off a DEXA is from the caliper.
 Perhaps we have to look how much the caliper is of the DEXA ?????
 Now how about  the same approach or at least and open approach towards  new  and exiting technology.

Once we over come this hurdle we may have a  lot more interesting options ahead of us.
Here another example.
  VO2 max testing is done with 3 min steps.
 This is the Golden standard.
 How about at least asking the question, whether physiological systems may react  in different time slots and one may be able to show the actual reaction in 3 min , another may not  or just started to show reactions.
 ( Functional reaction versus structural integration. )
 You can  react functionally with a very fast response with HR  but than you may have a drop in HR as you start to  use stroke volume to keep the needed cardiac output where it has to be to secure the delivery of Blood  ( O2 ) to the working systems.
 Same may be with respiration. You may react with  RF and than drop this to   get more efficient with TV and reduced RF ???
Can you imagine that this may be possible.
 If yes. what  reaction will this have on indirect information like VO2  and lactate ?

The whole question on the so much  discussed  metabolic efficiency.
 How about the idea, that the ATP production from FFA or Glucose or o2 independent is already super efficient . You may always create the same amount of ATP no matter what you use as the energy source to create ATP.
 What can change is not this efficiency in metabolic behavior but the efficiency on how much O2  you can deliver to   create ATP O2  dependent.
 So it is not a question of  metabolic efficiency but a question of cardiac efficiency, respiratory efficiency , coordination efficiency,  blood transportation efficiency ( vascularisation )    conversion efficiency  due to the  density of mitochondria and so on. If we look at the possibility , that we can have structural changes or functional reactions to try to supply the  needed ATP before the body stops using ATP
 Conett's idea
"

ATP reactions  may be controlled over CG ( central governor)

Connett says feedback inhibition of energy or regulatory system achieves its set point - a match between ATP supply and demand – by decreasing ATP consumption rather than increasing ATP production....body is slowed down via CG.
So if we at least give this some  critical thoughts we may start to rethink some classical ideas.
Here a very nice example  we discuss for the moment. The shift of a lactate  curve  ( classical ) test to the right is considered an improvement of  metabolic efficiency due to the fact, that lactate is later accumulated.
 If we change in a set up  like that the step length from 3  to 5 min than the curve will move to the  left. Is this because we have less  " metabolic efficiency " or is it due to the   set up for the protocol.
 Or in other words. where there some functional reactions or structural integration simply cut off due to the set  up of the protocol. ? Much more to come on this as we move along with MOXY and real live. 9 See this classical lactate test and look on the trend and tell me what you see or think.

Sorry got lost ( not unusual )
 Back to Clint.
 Here a picture from a case study , where Brian and I  tried to keep same wattage and same RPM but only shifted respiratory frequency from  10 min step length.  So we  used a RF of 75 +_ 2  versus a RF of 20 +_ 2 and a  " normal RF ) . The idea was to see how  SmO2 and  tHb  may be affected by RF only.
 We have pictures , where we know we changed RPM ( See Clint's.) But we do not know how  the person changed RF due to the coordination change.
 Summary. I  do not say the RF is the reason of the change in  SmO2 when changing RPM . I say it can be  a reason , why we change . It can be a combination  or a accumulation of RPM  fast and RF fast, which create an even more impressive change.
 So if we maintain a fixed RF  and change RPM we can  see,   what changes. Than add as well RF as a variable and so on. like  body position (  TT position versus goat transporting position and so  on.
 The fun part will be once MOXY is out that  many coaches can  in real life info see, what influences their   action and advice may have on the  trend in SmO2.

Summary >
Try :  1.Bike first with fixed wattage and fixed RPM and play with RF. Choose a  low enough wattage so you can sustain a change in RF but not low enough so there is no need to react locally.
 If you have an IPAHD bike  at the STEI to FEI intensity.
2. Than fix RF and wattage and bike with different RPM
 Than keep fixed wattage and increase RPM and RF and vica versa. Finally change positions from areo position to cruising position  with the different options from above.  Last but not least. the " classical " lactate curve has some 2 distinct sections. What happened there and why  ?

Last but not least.
 There are some very nice interconnections in physiological systems.
  If we look at some " classical" ideas, than we can see, why we like to stick with them and not looking outside the box.
 So think: if you stick  with 220 - age you will have no questions and an easy way to make a program.
If you stick with VO2 max and have a calculator you should have no problems to find proper zoning.
 If you use FTP you need to go once for 1 hour and the rest is straigth forward .
If you use lactate  and  you go with 2 and 4 mmol it is  as well very simple. 
 If you use IPAHD and MOXY you better start breathing hypercpanic  . Why ??? 
 

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