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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530

S. M  sends us  some really  nice  and  incredible help full  assessments.
 Here is one  I just   got  to review.
 So what I like to do is  just looking at the  MOXY trends  as we did  and guessing / thinking combination.
 The goal is  that e  can  learn to  " read"  as much out of  this simple  collection of data's  as possible  over time  and when  going back to the  deeper data collection  with  Physio Flow  and VO2  get a confirmation, that we start to be able  to get a  pretty nice   information  and than  get the backup  form the  center data's.
 This way we can use MOXY on our clients. They can do some control test  at home or outside  and sent the info back to the coach and the coach can readjusts if needed the  training program  and  take the client in  perhaps every  so and so many month to do an all out  and all including  assessment  to review  changes in LIMITER  and COMPENSATOR. So here first  SmO2  and HR  data's  from the latest  great  feedback.
Warning !!!! I may be completely off and that is great as well as  we all than  can practice  to try to understand , where theory  and real live info have some open questions. So  here to remember  from the first  researcher :
Pic 1.

Now here  the assessment of this client   in SmO2 trends  and additional HR info. I like to  look   just for fun  the HR info  first in this case.  You can see till 1500 time a not really clear  HR respond  compared  to after 1500 ???
 This   could indicate, that  the  activity  before  1500 was not  really that  high  or not that clear  for the cardiac  system to really  be in  great " working mode ???
 Why ?.
 If we look at the start , we have  a very rapid  increase in SmO2    and a  very rapid  and high  HR.
 Now that would contradict  my  initial statement , that it was not a real challenge  for  the  cardiac system.
 Well Alarm phase   here nicely   and a  jump in HR  but than  despite  an increase in load  till 1500  no real  HR  reaction anymore, as well as  very hard to  optically see, where the 5/1/5  changes take place  ( compare  with the really nice HR  5/1/5  reactions after  1500.
 Speculation  and that's where the center   can go and use physio flow  to see, whether the speculation is real  (unseen real  ) or   the seen is unreal  - Greek start of materialism)
  well this is  what our ideas are all about in physiological testings. Is  what we see VO2  wattage  real  and what is behind ,  what is unseen.
  Mathematical  formulas  are real but  there is a lot of real unseen behind  which  would contradict the mathematical models used in physiology. 
So back to the unclear.  HR   increase till 1500. An initial  HR increase as a reaction  but than followed  with an increase in SV. If  we look later  tHb  than we see , that in clients, where the initial alarm phase  creates a severe drop in tHb  due to the  muscle contraction,  we have a HR reaction as this is the only  way of increasing  CO immediately  an than we see either a  flat tHb  and or an increase in tHb , so  more  volume return  ,which allows a better  pre load  and CO goes up  with  increase in SV   and HR  can even drop or at least   be stable.
. Here as a future side branch .
 When looking over  100dreds  of data's   when we see this  trend like here  you have a  flash  of   thinking
 Muscular  local  limitation.?
  Not optimal vascularisation ,so  compression   and no  rebound, as there is a limited piping system  and it is already  used to the limit  in that particular  motion.
Danger  : We  may get  complaisant  and than  forget to look further . so this is just a loud thinking here, where we may or  may not end up..
 So lets' look SmO2  till 1500. It is  after  an initial  extreme increase a  gradual increase in SmO2 indicating  a steady  higher intake of O2  than what is needed  for the performance.
 Interesting is that incredible  step incline.
 This is not a diagnosis  but you " normally"   will see  in an initial start .  ( Alarm phase ) a drop of SmO2   with  a rebound  and an increase. We do not see this  here.
 This is  strange as it would indicate, that the activity does not  asks  for an initial  release of local O2   deposition( Mb )  and O2  from Hb. ????
2 options we see here often.
 1. Mental  pre reaction:
 People are very exited  and the HR is already up  ( adrenaline )  "pre test"  and they  already   walk or  run or bike in their mind. HR up,  RF  up    and so on.
2. People with a respiratory  problem.
 They start out  and immediately  go over RF  ( like the cardiac  over HR )   but   not optimal depth breathing  so very apical breathing  and limited  diaphragm breathing . This leads  to air exchange  with  a hyperventilation  reaction  causing hypocapnia  at the start of the test.
 So SpO2  will go up  and with it SmO2   but   some limitation there  at the start to release  O2.
 So in this case  it may be fun to see later  whether that could be an issue.
 Respiration as a LIMITER in a later stage   would  show some changes in tHb  due to vasoconstriction. ( metaboreflex )  so we  can see  later  whether this is an issue under load  but could be an issue  here at the start.
 Like HR  this would balance in  about 5 - 10 min  so when we  go back  on HR we see that   by 300 - 600 HR  gets a kind of a "plateau. But we see  on SmO2  that after the first 5  min  and 1 min rest  we actually have a  reduced  increase in SmO2   with a  nearly  gentle  drop. Now this   as we start again  is now a " normal"  reaction of  an initial drop of SmO2  due to the immediate  need of O2  after a start.
 So by 300 - 600 min  respiration seems to  have  started to react accordingly  ( possible  normocapnic  now )_ Now  to make a short break  after this .look  at the  area of 1500 to 1800  ???
 what do you see.
 Something went very different here ????  Drop in SmO2  as a sign of  a delivery  limitation  respectively a much higher demand  of  O2  but as well a clear  increase in HR 
There had to be  a change in activity level  walk , run  and or bike pattern  (out of the saddle, change from  walk to run, change from flat walk to an incline  walk  and so on. ????

The  last pics  are some   base line to some of the points.
 EtCO2    or PACO2  in the different section in the lungs  . So see that  apical ( apex  breathing pattern.) This  can be the case in triathletes  with wet suit  and cold water  and pre race  hyperventilation. So the  great swimming   turns  from a crawl to a  survival breast stroke  due to the  situation, that the O2  Diss curve shifts  to the left. So SmO2   super high  but O2  not bio available. 

Last pic  as  a  "mental"  pre test   reaction with a completely overloaded  HR  .
This is a is a Physio Flow   HR  SV  and therefor  SV x HR = CO.
 Look at the   initial  reactions in the " warm up "   and  look at  HR  and SV  and CO  ( circles.
  That  after the  " warm up"  look at the 3 min step test " Classical VO2 max  test , again  even after  the warm up  a  HR reaction with an overshoot. 
Just  for fun look at the  all out  HR  and the SV at the same time.
 This is a great example of a  cardiac limitation  where SV a actually  collapses  at the all out.

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Okay part 2, lets look the section of the assessment  where we have the  circle 1800 we have  5 min  before that (1500 the  clear  drop in SmO2. ( delivery problem  or limitation)  but as we can see  in the following step with the same load  she is able  to  " refuel"  so more O2  is coming in, than is used ?

 Remember  an increase in SmO2  can  indicate  this idea  and or  it coupled be a  situation, where we  reduce the  O2 bio availability to to a shift of the O2  Diss curve to the left . Respiratory  problem  with  hypocapnia..
 Now  if it is the first option :
 reoxygenation after  an initial  Alarm phase reaction due to  an  abrupt change in the activity , than we  would see  an increase in SmO2   together with an increase in tHb  as the load  is  now accepted  and  more  blood is getting back in  as the initial contraction  to start the change is not needed anymore.
If the second is the case ( hypocapnia [wink] we would have  with it a  circulatory  vasoconstriction  and tHb  would be same or lower   compared to same previous load.
 So now let's look just  at that   step the tHb  trend. See pic 2 see  tHb  at the step 1500 - 1800 where we  assume that there was a sever change in muscle activity , asking  to start out with more O2  than can be delivered  and as well a higher  compression situation  so  lower tHb.
 than  1800 - 2100  and increase in SmO2  (same load)  and an increase of tHb  decompression and back to a more efficient  load  after the initial " shock ( alarm phase)
 There is the point , that an increase in tHb  could indicate  a start of a venous   outflow reduction   towards  a venous occlusion. What does not fit into that possibility is the fact, that SmO2  is increasing as  this would be very rare . But as a second  indication, that it is unlikely  a venous occlusion trend is the fact, that in the 2 follow up  steps   where the load is higher  this  does not appear  anymore , but  with a higher load   we would expect a  higher chance of  now an occlusion to occur..
 Next up what  do wee see after that  change in activity what ever it was ??
Stay tuned.

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Okay just got a feedback  on the " theory " of mental  stress  and alarm phase.
 :Yes you have different options to react in the  fight and flight  situation
see pic  1. Walter Cannon & Hans Selye .
How  do we  simply  can test that  with what we have:
CO  = HR x SV  with  Physio Flow  ( for advanced users  you can add the info  on MVO2  here   = O2  use   from the cardiac muscle )  as well as  CCT  = cardiac contraction time as the result of  HR  x LVET  ( left ventricular  contraction time, which is  an additional  option  in  performance sport to compensate   for a better  CO over the ability  to  extract more O2   from the  coronary  blood circulation
 oxygenation trend  and as such  an indirect  info on a-v O2  difference , which is the other  part of the Fick equation  ( VO2  = CO * a-v O2 Diff.)
 Here we use MOXY  ( NIRS ) as you can see in all this threads.
 Reaction of ventilation  VE = RF  x TV   is taken  from VO2  testing equipment.
This is actually the only  direct information we have  from VO2 testing  as it is over the flow meter. All other readings have a time lag   and  do not reflect  a direct information   on what is going on. That's why we have the problem of using  the VO2 information  of gas exchange in higher intensity as a RQ = RER reading. ( But it is used ) 
 d) muscle activity and change in   motor units  recruitment patterns  is tested over a SEMG.
 e) blood circulation  and change in vasuclarisation is tested  with NIRS   when we can take different penetration depth, but as well ( not yet  completely sure  ) with MOXY  over  a certain trend reaction  ( still working on it )  Now here another  example of an overshoot  due to an Alarm phase  ( Hans Selye  G.A.S ) look at HR  and in this case even  SV  at the start of the assessment

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
so to get one step further. after the clear drop in SmO2 and the clear increase in HR we have  or can assume , that there was a  very different effort done. Example  could be standing up in the saddle, changing incline in a walk test or changing from waling to running. So the next same performance step is a beautiful example  , why 3 min classical test would miss this. Given enough time after an alarm phase can show ,hat the physiological system can adjust if you are  close  at a LIMITERB / compensator  performance.
than we have in this case an intensity with still a good delivery system delivering  still more than needed
than we have to more steps  with same performance. Drop   in SmO2  but really  minimal.
  with this high SmO2  we  can easy say that there is no delivery limitation in the first place but rather a utilization problem..2 possibilities
1. Respiration  and hypocapnia (  RF  and TV  (VE ) would help us here  from a Hypocapnia point of view
or  respiration problem from a volume point of view The  trend in tHb  can unfortunately support both.
2. A muscular limitation  with vascularisation  and mitochondria density.
If you have no VO2  data access for VE /RF  and EtCO2  you can let the client do  a workout n form of a test by starting the  jog section  and let the speed be the same  but play with respiration 3/3 4/4 5/5 6/6 for 5 min each step. so you can see  the reaction there.
Fortunately in both cases  you will do  nearly the same workouts  to improve.
 a) utilization workouts over  involvement of respiration in the STEI trainings  and
b ) using the respiration to create a hypoxic  interval workout.
The vascularisation  ( angiogenesis [wink] has to  main " believer"
 a) mechanical share forces
b)  hormonal  / chemical  reasons
For a  we  either  go  an intensity with the  highest tHb  to have a  good SV and lots. of blood flow
or  for the second  idea we  play with respiration to create a hypoxia  ( Create some lactate production as one precursor  of angiogenesis as well as EPO   created  from intermitted hypoxia.)
this is up to the coach to decide   what  he  or she  likes to do.

Development Team Member
Posts: 65
This is very cool and I can see why normally you wouldn't want to mix modalities ie: walking then running during testing because of the questions it raises however in this case it has been helpful as that is what this client does and can't figure out why it's so hard to run and why she can't improve her running.  Very helpful!
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
S.M. thanks for your  nice feedback. S.M. is   well underway to be a MOXY expert  and  we will start to  sent people  who mail me  form this part of the country   to her for assessments.
 I  would like to  show  some thoughts  in this case  on how I ( which is not always a good idea )   would approach this person  fro some workouts  with the 2 areas  we identified  as potential limitations. So , if S.M.   agrees we can do that on here  ( no pressure )  but I for sure will sent you the ideas. It is up to you.

 Second  :
 I like to  thanks the  MOXY users  who sent their  private clients  tests  to eukholdings@gmail  for  interpretations, as this is possibly for the moment the  fastest  and best way to learn  on how to use  and make your interpretation.
 You can contact  euk  and they will sent you info on options   and prices  for interpretation.
. It is  not just a print  I can tell you, but  as deep as a discussion can go to the different cases.
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Here  2  examples  from S.M.  
 Cook book  so  always  questions left  n how to make it taste better.
 Pic  1  and 2 
  Example  from S.M.  for possibly an endurance athlete with good utilization    but delivery problem

Pic  3  and 4    from S.M  client  with   a  extreme utilization problem     but good delivery system.
 Possibly a beginner  or somebody who trains  very   different  with little success  of progress, as  she  has  no ability  to use O2  properly.  Mitochondria density problem   paired with  respiratory limitation.

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530

I like to go  once more into more details  as  many readers   start to see the direction we  go.
 In a physiological system, there is  normally never  one  single system, who  will decide  over    live and death. There are many different back up systems  who  may try to really keep us alive.
 Meaning that  if we reach  somewhere a .limitation    other systems  may try to compensate  for it.  In the short term  this would create some functional reactions, if it goes over a long tie, where a system  may have to compensate it can lead  to structural changes   and they may not always be  beneficial.
. Example right cardiac  overload  due to respiratory   limitation ( smoking )  So when we look at the   reactions during a workout or test we have to keep this in mind.
 If  we  look just on  max  information like Max HR and Max VO2  and Max  lactate  and max Wattage, we miss the point  that this max is the result of a team work.  Maximal result of a team is  when limitation and compensation work optimal in a team  so you do not  needed one start but many great players  working for each other.
 So when we look at  VO2   in the classical term  we have.
 VO2 = CO ( HR x SV)  x  a- v O2 difference  )  a  for arterial  and v for venous . So  a  drop in SmO2  will indicate a  bigger a- v Difference  as more O2  is used  than with a higher   SmO2.  Both   parts CO and a-v O2 difference are   interlinked  with each other  see pic  1  and pic  2

What we can see In this "classical" ideas  is the start of  accepting  that  respiration may be a part of a team  and  now with MOXy we can even show how  respiration c an directly  and fats change  the a- v O2  Difference.
 Every new MOXY user  shall try  to  manipulate respiration.
 Now here the   trick.
 If you choose an intensity, where   you do not reach a limitation of any system  you can much easier  use  any manipulation for  any system to see how the body reacts.
 If you choose an intensity, where you reach one  systems limitation, than  other system s will start to compensate  and push themselves  as well to a limitation.
 In this intensities it is much   harder to get a reaction, as  your time  is limited on how  long you can use the already  active  and under  pressure  compensator  to  play even more .
 In the 2  examples  from S.M  above  we have  2  very specific  situation.
 One shows  a limitation in the ability to actually use  and  attract the available  O2  to be a part of the energy supply.
 This   person  may have  always somewhat  difficulties with her muscles  as she   from the beginning will try to find O2  independent energy sources to  fulfill the energy demand. She may always have   pain n her legs if she is a  runner or walker.
.  The VO2 in this case depends  n the delivery    of CO  and very little of the ability  to use  O2   once it is delivered.
  It is a picture  we  see often with beginners  with a limited mitochondria  and capilarrisation structure.
 We can see that when comparing  left and Right side   after  an injury like  ACL repair , who one one side the ability  to  de-oxygenate  is getting worse     compared to the other side.  pic  3  left  ACL repair  after  4 month. Not optimal rehab done  as   we often  do  not look at the "inner " changes but simply at the   volume " diameter of the muscle.

So here  what we look for the o=coming week:
  If:  we  can  sue  both  sides  of the VO2  equation   for increasing VO2  peak  than we should  be able  in one and the same person to create the   2 results we have from S.M  in one person.
  Once  by attracting the  CO  to work  harder    but  avoiding   O2  from  getting released  from Hb  and once by   working hard to  improve  O2  release  from Hb   but reducing  CO.
  Sounds  like an adventure  stay tuned  and I show you    studies  we did  exactly that     manipulating   cardiac  and respiration so one  works  well the  other   is limitation and vice versa  and this in one  and the same person  to have   either a utilization problem  or a delivery problem.
 If we can do that than e can use this a specific  workouts  to stimulate one or the other resp  to load  or  unload  one or the other system.

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Here is a stupid  loud thinking   summary on the limiter and compensator I use  with some of the high school students  here to r try to get the idea across. Any changes  are welcome.  And last  our view  n VO2   as it  moves  towards a team approach
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
One of the questions was coming up:
 The person  with this incredible high SmO2  values  even at the end of an assessment. What  can be done  or what  is the  reason for that.
. One  part of the observation, the inability  to actually use O2  ( bio availability )  despite   enough O2    in the working area . ( Hb and Mb )  can be caused    due to a  respiratory limitation.
 . In cases like this  we normally  do something called RRA ( resting respiratory assessment)
 It is a concept  we developed many years back  and   allows us to use a VO2  equipment  to actually assess the respiration  at rest  and  how and whether we already have a  problem  with gas exchange  (   capnia ) at rest.
 The following pics  will show you an assessment I just did a few days back , where we had a very similar situation.
 Exercise intolerance with  very fast   uncomfortable feeling in the working muscles  and tightness. The  assessment  showed   on the NIRS  a similar picture like we showed on here. The RRA  showed a CHRS  ( chronic hypocapnic respiratory syndrome  already  at rest  and during the night with a shift of the O2  Diss curve chronically to the right  and the inability to  extract  O2  easy.
 Side effects  are  sleeping apnea as well a  weight gain  despite controlled  nutritional intervention ,but the inability  to use O2  for optimal FFA  at rest.
 Training plan. Respiratory training during walking  and at home  with the goal to   bring  her into normo capnia as well as   hyper capnia  to learn the feeling     so  there is no panic if  during exercises  she  may go towards hypercapnia.
 Than  re-test and see after  6 weeks whether   her body functionally  starts  to accept normocpanic     respiration. Here the pic  for your info. in the number scale you see Norm for this age group and gender  and  first test  are the actual result. so you can see how a CHRS  will show up   with what  data  out side the NORM.

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Now  if we look  S.M's  client  with the interesting high SmO2  %  and the   limitation of actually  using the available  O2  we  have to look at  2  main options.
1. Structural limitation of   blood vessels  and  mitochondria   density.
 2. Functional limitation due to respiratory  limitation.
  It  does not look as  structural limitation in the  respiration but  at a  functional limitation in the balance  of  CO2  :
 If we go from the  possibility , that we have 1  as well as  2   than we can use  training options  to stimmulate   function as well as  structural  ideas.
 To   stimulate   angiogensis  ( building of new  blood vessels [wink] we have  different  directions  and theories.
  One  of the theories  is   mechanical  origin.
 So in this specific  case. S.M  can try to  do    intensities, in the STEI     are   so we have  the ability  to use  compensator  over longer time. If we go into  FEI   or  for sure HII  we have no chance to use compensator  over a long  enough time as they  have to compensate  and not have the ability  to be overloaded.
  So in this case  respiratory games  with  for example  4 steps  in  4  steps out    and increase to  5/5  6/6  and   more and more up  and steady look  with  MOXY whether we see a  deoxygenation trend  during the 5 min   with respiratory manipulation and   than   back to " normal " respiration.  I like to show you here some case studies  from far back.  One of the  many   response  I get on mails  is, that all sounds interesting but:
 Well than I get "classical" papers sent   to read.  I  am  in an age  , her classical papers  where the gospel.
  So   when ever we show  some point's on here we can back it up  otherwise  we will tell you : We do not know. So just  actual  facts  here  very little theories.
 Here  2 pics  you can get your head wrapped around.
 Influence of  respiration on cardiac hemodynamic  as well as  influence  of respiration on oxygenation trend.
 If you combine  both you can see   why and how we use tHb  in MOXY assessment  to combine the different reactions  with each other.
 Here in  very simple  terms  (  exceptions  are always  possible )
  Hypo capnia  ( low  EtCO2 30  and below  will create   an increase in SpO 2 and SmO2   and a drop in tHb   as it  triggers vasoconstriction in the peripheral   circulation.
 Hyper capnia  5- +- EtCO2  will do the opposite   drops  SmO2  and  creates a vasodilatation.
  So  in connection with cardiac hemodynamic  we  will see  and increase in tHb    reaction an increase in SV  and  if at the same load a  drop in HR.  as well as a drop in SVR ( systemic  vascular Resistance  )as a part of the vasodilatation. For the specialist   LVET often  drops    and therefor  as well CCT.
  Why. Not sure  why ?

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Development Team Member
Posts: 168
Juerg, hi, and thanks for the nice info sharing--your assessment charts are awesome.

I do work forward with many folks presenting with these similar respiratory situations. I find the walking / running respiratory games are key, and also using the SpiroTiger Smart while viewing up on the big screen via the viewer software is quite helpful. In particular, the live graph on the right side of the screen showing the ratio of inspiration : expiration. My sense is the hypocapnic folks at RRA, breath at 30-40 percent inspiration and 60-70 percent expiration. When using SpiroTiger Smart, I coach them towards balance of 50 percent inspiration : expiration to begin with. This creates a challenging RMET workout for them, and many move towards hypercapnia.

With MOXY, I'm now moving into watching the reactions of this general SpiroTiger workout via the SmO2 changes and the individual benefits.
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Fred  , what can I say,
 You are far above and beyond  the  "classical" coaching ideas  and  wow  no question where I will sent   people from your are  to get  help.
 I will send you a n excel sheet   where you  can see  the  RRA  and you can try it out  and we  can improve it as we go  forward.
  Cheers Juerg

Development Team Member
Posts: 168
Thx, Juerg. I appreciate your sharing the RRA template, no doubt an enormous amount of time and energy to develop this tool. I look forward to reviewing this and anticipate it will add incredible ideas.
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