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MTF Carter

Development Team Member
Posts: 27
Hey everybody. Just wanted to put up my 2 tests from last week we did here at MTF with Clint and Roger.  I noticed when I increased my respiration rate it helped but as you can see it only goes so far. haha


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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Carter, beautifully info and great to show the reason, we  I like IPAHD versus Mypahd.
 The first  3 o=pictures as you can see is a classical step test done as we always did.
As you can see we have an information we can assume,:
 HR will go up  nicely but no clear info where it  may find a " new " current performance related homeostasis.
SV will  go up and here we can see three versions. Up ( small overshoot ) and plateau.
 steady up till to the end of the test.
 Up short plateau and drop at the end.
Therefor HR x SV will create an accordingly picture . For Starters  that's what we use  from Physioflow  SV, HR and therefor CO as the result of it.
 In advanced users we add EF %  and LVET to it as they are  calculated ( EF %   from EDV to SV ) ) but LVET is measured as the left ventricular ejection time.
 This time we multiply with the HR and create something we call CCT ( cardiac contraction time ) This is  just  in short here an interesting trend we see, when comparing  top athletes with starter fitness people.
 CCT is the time  in seconds per minute  where the cardiac muscles itself does not get oxygen due to the contraction to push blood out.
 ( More later as we advance.)
Respiratory info from a step test.
 VE  will be the result of RF x TV.  Here we see  most often RF trending up.
  and in some cases going up and than plateaus.
 Rarely do we see a drop in RF at the end of a test.
 TV has different trends. Either steady up, or   first increase  followed by a plateau and than a drop.. In some cases  a short increase  than a steady slowly drop.
CO2 and FeO2  all different versions  and if you look carefully than you see the  CO2  and  O2 are very directly linked to respiration TV and RF and as such easy to  show the  link by " manipulating " the RF or TV.  There is a lag time of 30 - 60 seconds on the read out if you do that.

Most interesting is the fact, that it  strongly depends on the equipment you use.
 If you do not believe this, use your VO2 equipment and make one test  at rest or under load with a face mask so you can breath mouth and nose and than make one test with a mouth piece only and closed nose as some equipment do and look the  result.
 You will be surprised on the difference in the  respiratory numbers and therefor on the VO2 information.

 Here we look at  2 information's mainly . SmO2 as the muscle oxygenation   and tHb as an indirect information on blood volume trend. This for the MOXY users.
 For Portamon users we look at TSI % as the tissue oxygensaturation.
 If tHb is stable like in this case here TSI % and  SmO2 have a very equal trend and can easy be compared. They have different absolute values.
 If the tHb   changes ( meaning the blood volume changes due to many different reasons we will address as we go along , than TSI % and SmO2  can go very different.
 What we see is that when the  circulation increases at the surface due to the need of cooling the body TSI %  often increases towards the end of a test , which for many seems not the way it suppose to go. SmO2 clearly decreases as we would expect. Nothing wrong with the " contradiction' as it is no contradiction but a perfect addition when we combine in bigger  professional centers both this information. At the start of a test, where we may see a drop in TSI % in an intensity we would not expect a drop already we see an increase in SmO2 . Same reason. When we compare T1 and T# in Portamon and than combine with SmO2 MOXY we see the  move  from blood from the skin moving towards the muscles. so tHb changes respectively blood volume changes  and as such SmO2 will increase due to more blood in muscles and TSI % decreases due to reduced blood flow in the surface. Again I will show many many test  we did in the last 7 years to show this nice features and the great way to combine in a center both information and  than use MOXY for the client  during his workouts.

Now in a step test we will see like in all above physiological system a stead decline or increase in most values due to the increase in performance.
 Problem" Now we start to speculate, where  what system may actually start to  change as  a compensator or limiter.
  NOW :
 go to Caters IPAHD.
 This is a physiological guided protocol.
 Look at the trends of  each of the above parameters as it is repeated 2 x for 5 min with a 1 min break to see recovery or not recovery  reaction.
 You can very easy identify different reactions.
 Your job:
 Go to the cardiac info. Look at HR and SV  in each double step and CO as suggested above. See  what  stops increasing  ( plateau ) and what tries to compensate  in the same system.
 Than do the same for respiration TV and RF, than look  the same on tHb and SmO2.
 Now you have a beautifully picture of  where the current limitation is and where the second   limitation is  an d who tries to compensate the longest. As Carter mentioned, compensator can only go so long.
 As faster the compensator pushes himself to the limit as less long he can work as a compensator.
 Have fun and try to think  out side the BOX.
 Now you can see why we use IPAHD. I show you how it will look at the end with our software, when you combine all the above  info's from the equipment in one print out version. Here from our Friends from Norway in collaboration with our friends in TICINO ( Italian speaking part of Switzerland.

Look at the lactate trends as well and imagine we would have made a step test instead an IPAHD. what would be the "curve" of the lactate  dynamic ?
 Last hint. Look at the  SmO2 trend in Carter and the Hb Diff in the Portamon in the  att.
 What do you see.
 Here to just add some info. If the tHb changes than we can't use TSI % and SmO2  as a comparison, as TSI %  can move in a very different direction.
 That's why we have some studies questioning this  trend and  have some speculations on it.
 Clint Freezing study on compression stockings  show beautifully the opposite trend in TSI % and SmO2  due to the compression application on the surface.
 Andri has a Case study  with a Finnish world  class athlete  where we had a live audience witnessing the great combination between SmO2 and TSI % when looked upon different options instead of discussing  the 2 equipment as they test different but the same wave length. See explanations  from Roger.
 So in case we see a change in tHb we will use Hb Diff  in Portamon to have a closer ideas on SmO2  or better use MOXY as any center can afford that now.
 Now last but not least. Think BIO watch  HR, RF and SmO2  in combination with performance and you easy can see than when you have an IPAHD from a Center how they can use this info to  show you optimal intensities by daily using your physiological response from the last  training to adjust your  workout. Reason: You do not like every day to overload the LIMITER or to overload  a compensator. If you know where  and when and how this happens  you can  nicely play this in your workouts.
 Problem.  Need some experience but  any coach with years of  using  the " classical" ideas can easy learn and will  easy be able to create a very new and fun workout system  just for you.  Time to go here to work with clients have a great day  .

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Okay Carter and the rest,
 Here lets' go into some more in depth d ideas an discussions.
 1. You can see that the step test does really not give us lot's of info besides , what we know we get tried and some info's go up and some go down.
 Let's start  with  2 areas.
a) Physioflow.
 Step test see att. 1.  Up to 200 watt we had a very nice contact and than there was some problem with 2 electrodes. most likely the  ECG electrodes on either the left side or the right upper chest.
 The HR does not show anymore a good contact. In this cases simply push n one of the 2 and see whether they move back to a good contact and if yes tape it hard down again.
Now look att 2  in the IPAHD and the great connection all the time  with the  Physioflow. Now this has nothing to do with the test protocol  but is  one of the possible  small problems we face when starting to use this equipment.
 What is super interesting in the IPAHD cardiac information :
 look at pres start reaction on SV,  HR  and CO result and how they interact HR up SV down  same CO.
 Than look where it happened  look at  LVET and you see the presstart reaction.
Than look at   the  1 min rest and see, where the  CO or HR does not return anymore to the previous level. No look  at the same moment in the RF section  and at the SmO2.
 At the end of the second  250 watt he tried or did or had to do something. He changed respiration. By 250  you can see it influences the SmO2 by after an initial drop  it increase, meaning , that  he either used less O2  or he  was loading more but deloading less.
 If he used less Than something had to work more efficient.
 Pedal stroke, slower breathing  and less deep.
 If he was loading more  than he would have to  increase RF and TV as well  to get hypocapnic.
 To actually influence this you have to be able to maintain it at least 45 - 60 seconds and if he did that  he was successful  at the end of 250 watt.
  Here speculation but it is fun.
 At the end of  the second 300 he  again has  this interesting reaction  in the respiration but  only short  perhaps  30 - 45 seconds and not good or strong enough to be able to influence the SmO2 values .

 Now last but not least look at the IPAHD moxy info and you nicely can see stable tHb  so often a sign of  optimal   delivery of blood. But you can see no change or flat in the  SmO2   which often means  not a delivery problem, but a metabolic muscular limitation in the ability to use  more O2  despite the availability of  O2. So he  would go " hypoxic " here, as he   still has O2  but it is not bio available. Different situation can lead to that. One is a limitation of mitochondria density or  and a limitation of vascularisation  . Only so much blood vessels and they are fully used.
  At the moment we see this plateaus we can go back and see where is the HR and the CO. is this  slowly  creating a plateau.
 True it could be  a cardiac limitation question.
 Now here some hints.
 If it is a delivery problem we will see most often a drop in tHb as a reaction over the central governor
Now  for people who  do not believe in that idea here another option.
 In caters case you can see  by 300 a plateau in the SmO2  and a  slowly plateau in CO.
 If it would be a Cardiac limitation than you can try :
 let the client sit up an do some additional work  either rout of the seat or with some additional arm motion.
 If it is a cardiac limitation you will try to steel blood  and O2 to the additional working muscles and the  cardiac system will get into trouble. If it is just a leg limitation than the HR will go up and  CO will go up an there is no real additional problem in the legs just more work for the heart.
 The opposite would be  Marshalls " sleeping Giant " reaction 1967 Give it some thoughts and Carter take me apart  with my speculation of respiratory    reactions or perhaps your  manipulation tryouts with respiration at this 2 interesting trend areas.

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