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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
I like to tell you a "story " like we   do with clients to explain a live feedback  during a workout  and how we use  MOXY   for many different live   ideas.

 Case. Live  calibration    load  to prepare  for a vascularisation  workout. We use  4 bio markers.
 3  you can see on the graph.  HR  SmO2  and tHb. Number 4   ( respiration not.)  We  use a bio harness  classical  version so we  can see respiratory wave  form  and RF. Summary for the respiration over the 4 loads.
  RF  load  1  16 - 18.  / load  2 16 - 19  but higher amplitude of  wave form ( What does that mean ? )
 load 3  RF  26 - 28  same amplitude. / load 4  RF  34 - 36  same amplitude..
 A  respiration limitation could be seen at the  end  when we stop  . What  could  hint  towards a respiration limitation in case of tHb  and SmO2. Remember 2 reasons of respiration limitation. 
a ) actual  respiratory weakness  
b )  actual   metaboreflex.indicate a systemic  limitation which  can show up in a non involved  muscle trend  so look at this  on the picture  as well.

peri thb smo2both.jpg
Above you see 4 loads of  10 min duration. The top  peripedal  graph is the  feedback from the quadriceps 
 The bottom is the feedback  from the non  or minimal involved  delta   muscle ( pars  acromialis)
 As usual  green is SmO2 trace  , brown is thB trace  and red is HR  trace.

( hint. look at SmO2  on the delta as well as tHb .  - indication of  systemic  limitation yes or no   ? )
Start  load  1 leg  . 
SmO2   info :  as usual  initial  fast drop in SmO2. Reason. Immediate  demand of O2
. So immediate  utilization.
  it is forced upon this  client   as  he has no other choice  but to use  what he has  as he  not yet can get enough O2  delivered  for what he  needs. This is a typical picture  of a   limitation of delivery    and a   utilization as a compensator. We know the limitation , as HR is still low  and RF is  low as well   so CO  and VE  are not yet  in optimal   ability  to try to   deliver what is needed or what the demand  asks  for..
 Fast  jump to  end  of load 4.
 SmO2  drops  but not even close to  where we are at the start.
 This is  an indication of  good utilization  but   even a better delivery  as HR  and RF  are  very high so VE  and CO  high   as they deliver. In fact they  deliver more  than  actually can be handled  from the  mitochondria   ability.
 So   as we  deliver more   than we  can utilize the SmO2  is  not  as low  as at the start , where we  delivered less than we  actually can utilize.
. So this is   immediately a  red flag of a  client  with   most likely  no delivery limitation  form the systemic   partners but a  limitation in mitochondria density as if he  would have  much more he  could   use more of the delivered  O2  and SmO2  would drop further.
 Now a limitation in utilization can have tow  main reasons.
 a)   low  mitochondria  volumina  and therefor as well a limitation in delivery over  a low capillarisation.
b)  good capillarisation but a functional  current limitation of the  utilization ability  due to some overload  perhaps the day before  with   for example eccentric  loads.
 So  we can have a similar picture in SmO2  form a   weaker  or beginner athletes  with high SmO2    due to over delivery  and under utilization    and a top endurance athlete  with  a  overload d from workout  so  underutilized due to    rebuilding of  " damage "  muscles    but a good  delivery  due to , high  vascularisation.
 ( question ) where will we see the difference  of this  2. Back to load  1  and SmO2.  after an initial drop the delivery system  got  time enough to increase their ability  ( HR  up SV  up  RF  up   or TV  up ) Dilatation  due to activity.
. So we  now over deliver  and   use  less than we  deliver.
 result is  an increase in SmO2. in both  involved  and non involved. Once there is a  decent balanced reached  the  delivery  will settle into a homeostasis. So what do w expect  from HR  and RF ?.
 Now  there  will be a difference between  vasodilatation which is  expected  as soon we  work. tHb is a trend information on this question.
 Many   underestimate the   balance  situation between  CO  and  muscular  contraction compression.
 The above shows  what I mean . Check the reaction from start of tHb  during the 1 min load In one muscle  we should see a  minimal contraction and therefor the CO  will dominate  and create a vasodilatation  due to all the different reasons.
 In the other muscle we  have   a muscle contraction and therefor  compression and we will see  what kind of a trend.
 2 reason  in the leg.
 If  we  have a  start load  with already high %  of maximal strength we   will see a domination of compression so tHb will ????
 If  the load is super easy than we  may  still see a drop in tHb  because the CO is not challenged  enough and we need a higher  load  so CO may react  after all.
 Summary . In the ARI   active recovery intensity  we loo  for   the following   situation.
 All the  needed system  will start up and will start to increase activity  to support a potential higher demand of energy . BUT non of the system is pushed even closer to its  limitation . So we  can play in this ARI  with any kind  of manipulation to train and stimulate any limiter without  risk of  already asking  for help  from compensator,. ARI is used  to  eliminate  work of a compensator  but try to stimulate   a limiter on its own.

  XX the underestimation in  compression   reaction is  coming from an old mistake when looking  at blood flow  and NIRS (tHb.) Some people use a Doppler  at the femoral arteria  and  argue that  blood flow  will go  up as a vasodilatation in the systemic  reaction due to  workout.  Absolutely  true  and nothing wrong with that. But if you  squeeze  your  big toe  you know you reduce blood flow there . Is there a change in the Doppler result in the femoral arteria  ?
 Now  if you make a   venous occlusion  in the popliteal area  on the  same leg you test  with Doppler the flow in the  femoral arteria  will not change, but NIRS feedback in the calf  will.
 So testing blood flow on one place  and concluding just because Doppler is a great tool that  there is  as well evidence  for any other  body part is pushing  some speculation rather than testing with Doppler  at femoral and with another   at the NIRS   placement  under contraction ???? 

Next part  load 2

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Now  summary  what  we can see after. The peripedal  tells us  during  live what is going on  and as a  coach  I may look after the client  sends  me the csv  file. Here how it could look like.

thb smo2  excel l1 - l4.jpg

We  talk for the moment of the reaction in  L1  9 Load  one.
 Dark green and brown is  involved  leg muscle. Light green  and brown is  non or minimal involved  delta  muscle. Smo2  . High demand  of  energy   O2  at start for leg muscle. less  and minimal  for Delta muscle. Drop to limitation at that  stage  of  delivery.
 Delivery picks  up  and now  more delivered than  actually needed  for this   load  so  SmO2 increases  in both.
 tHb Initial drop  due to muscle contraction compression  and weak  counter balance  from CO  and lag time  of  systemic  vasodilatation.
. Than increase in  blood flow in arms  as no or minimal  muscle  activity ( contraction compression  ) and CO  and  vasodilatation overrules  compression.
 In legs  not enough overrule  due to either too high  muscle contraction for the load  or   weak  CO  fro the moment. But as well a potential indication of  lower vascularisation. ( dangerous cook book advice )
  Now  start using the same ideas  already to think ahead   in this terms   in the L2  section.


Development Team Member
Posts: 264
Before moving to L2 I have a question regarding this:
In legs  not enough overrule  due to either too high  muscle contraction for the load  or   weak  CO  fro the moment. But as well a potential indication of  lower vascularisation. ( dangerous cook book advice )

The other indicator SmO2 is increasing over the load, so overall the delivery is more than consumption. What could explain a stable or decreasing tHB in such cases?
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Daniele  sorry I am  slow here. Good point of   the question before we   move to load  2.
 On the other side  the question may come up as well in load  2  when you look tHb  reactions.
 That's  where i lie  to have the involved  and non involved muscle on the same  picture . Here again to  have it handy.
excel thb smo2both.jpg

 Now  here  your  discussion point 
The other indicator SmO2 is increasing over the load, so overall the delivery is more than consumption. 

Yes this is most often the case and that's how we look at  it in practical applications. Now  this comment is not  to  add confusion  but to avoid a  flood  of  email  with  BUT  at the start.
 it s is  always interesting , that when we started    with ideas  people would argue  that it is too complicated  and  now as we  try o make some base line  statements  I get this BUT  mails  and I completely agree.
 BUT: SmO2  can go  up  and it is not  always ( but  let's  say rarely ) a situation, where it is not a  sign  of more delivery than utilization.
  You have to take  tHb into account. There are  situations   where  SmO2  as a  %  of   loaded  Hb  can go up but overall   there may be less O2  in the tested area. tHb  can drop  and SmO2  can go up  but there is less O2  there.
 Why. For all the BUT emails  you have to think  hwy  and how  it happens.
 For all the baseline  users. the statement  from  Daniele is  what we use.

could explain a stable or decreasing tHB in such cases?
Danile  come back if I understood this  question wrong  . Here  I try to give some thoughts  to this.

The change in tHb  has to be looked in the combination of systemic reflex  reactions    so internal  reasons  of  vasodilatation ( tHb goes  up )  and vasoconstriction (tHb  goes down )  and  mechanical  reactions   due to  outside  compression. Body position  or    compression from equipment  or  compression  from muscle contraction tHb  will drop  of may not change  as  internal forces  and out side  reasons  may balance each other out. Fix a MOXY on your biceps  and lift the arm  for  1 min  than d drop the arm  for  1 min an you have some fun reactions  in tHb  and SmO2.
 So  when we look at tHb trends  try to  look what may have caused the trend you see.
 Example. On an indoor trainer  you may see when you start  an initial drop in tHb  due to a  start  needed  hard  push to get the   trainer going  so tHb   drops as a  compression outflow  but as you settle in the load really does not need this amount of  muscle contraction and you will reduce   the muscle contraction (  perhaps  less motor unit recruitment  so  compression releases  and tHb  can increase.Now  if you take HR  into this picture  than you will see that  the  compression decompression reaction may be faster than the increase in HR  but as HR increases  you may see an ongoing increase in tHb  due  to an increase in CO and now the  blood pressure may be stronger than the muscle compression  and tHb increases. If  it is  weaker  than  muscle compression it will drop  and you as well have  the situation, where it may just balance out  each other. Again on a bike this can be   used very very easy.
 You can  create a workout in the STEI  intensity  and you simply change  pedal techniques  from pushing only  to pulling only  an you can see how tHb  will change. You as well can bike free handed  up right    upright  but on handle bar  and than in aero position  an you will see by the same  wattage  a very different tHb  and therefor often SmO2  reaction.
 That's where physiological bike fitting  can come in. You can go into the  crazy aero position sitting on the  front  tub  and see how great or  bad it is  for circulation in your quadriceps  and SmO2  situation.
 Dan Martin lost a   stage in the last years  Vuelta  due  to this  as he  had no power left  in the sprint  when the peleton picked  him up but he was  for  close  to 3 min in this down position so most likley an arterial  occlusion  and a SmO2  and therefor CrP level on his quad  who had no chance to   get loaded in the short  150 - 20o m  he had  left to try to sprint   and win the stage.

aero 2.jpg 


Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Now  let's go back  and look at load  1  and perhaps  add load  2

excel thb smo2both.jpg 

Let's look first L1  and L2  SmO2 trend In L1  a  clear increase in both muscles, as  an indication of more  delivery of  O2  than   used. There are   three " delivery " systems  we may look at.
a) Cardiac  system  with   increase in HR  and increase in SV

Some  people  react    first over increase in HR  followed by SV  and some seem to react  less  with HR  but more  with SV.
 What both need  is a  better return  of blood    back to the heart.
 One part of that return  is  muscle pump  so muscle contraction.
. We see a  drop in tHb  at  the start as a  muscle compression reaction  and we  often in low  loads see a  decompression reaction as the initial    start   reacts with a  far  higher  contraction force than needed  and as  such we  can balance  force  after a  while so we  may see a decompression reaction ..

 You will  easy learn  from the pictures  to  see, what is decompression  and what is vasodilatation as a  part of  a higher CO  overruling the muscle tension.
 Here a picture  where  you easy  can find the decompression section in tHb  and where the increase in HR  and therefor CO  will show up in case it can overrule  muscle  contraction force.
  See  whether you can find the  section in tHb.

J thb smo2.jpg   Small hint.
 Compression decompression are outside mechanical reactions  so they take place  bang as they happened. CO increase  and as  such potential vasodilatation due to higher pressure  have a  lag time  before we  can see them.
  Now below  a picture  from a  compression   situation  followed by a  slow  increase in CO  and  overrule of  muscle compression  and as  soon we let go muscle contractions we see a  decompression situation.
compression decompression vasodiltataion.jpg

Even on here if you look carefully you see a  short influence  of  overshoot compression to a    small decompression phase  before the CO takes  over.
 Now this reactions  can only be seen when we  get rid of   muscle contractions suddenly.
 In our    case  we  discuss this is an ongoing  4  load   steady increases  at   each of the 10 min  so not that great of  an option to see  this reactions  of   tHb   and SmO2  as  when we  get rid of  muscle activity  and have the lag time reaction  of  the   slower systems  ( HR and RF )
 So the  cardiac system is a  good indicator on how we may react.
 So next up  we will look at  L2  and L3   in comparison  to L1  and see, whether the  HR  combined  with tHb  will give us e more feedback. Stay tuned.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Sorry  as usual we got side tracked (actually I got)  in this topic.
 So let's see,whether I am able to make a better overview  on what I like to get  to the  regular readers with this example.
Here to have it fresh.
thb smo2  excel l1 - l4.jpg

SmO2 trend  in L1. (dark is involved muscle, light color is  less or non involved muscle.)
Involved muscle in L1 clear initial drop due  to O2 demand , but very poor delivery.
 =  very nice feedback of a great utilization in case of a bad delivery. This  helps  to get  an initial  information of a clients  ability to utilize under a  bad delivery situation.
 At the start we know , that we have a poor delivery for the initial  1 or 2 minutes, as we start with a very inactive delivery situation.
Non involved muscle.
 Depending on the initial  drag of a bike trainer or some initial balance reactions in running we see a  small drop in SmO2  followed by  a great increase of SmO2 , as we now delivery better and we do not use a lot of O2 in the non involved muscles , so great increase..
Great increase in involved muscle as well, in case we do NOT start too high of  an intensity.
Now tHb  action.
 1. We  all learn , that in case of an activity we will increase  blood flow in the  working muscles, in fact  in all muscles  as the cardiac  output  will increase  plus some vasodilatation reflex  help.
I showed  somewhere  before  a nice picture  of blood volume shift  under activity . Here  just another  way to  show it.

blod distribution.jpg

 Now  here are some  thoughts  and points we often get discussed on.
 One of the points  by critical  observer  we had is:
 Why  would the tHb drop when we know, that  an increase in activity  and as  such an increase in CO  will  create a  systemic vasodilatation. The point they make is that,  that when they use a Doppler  for example at the arteria femoralis , you can clearly proof that  blood flow  and blood volume therefor  suppose to go up everywhere in the leg..
 So their point is, that the "proof" of  an increase in blood flow  at that femoral  artery  suppose to  show therefor a  blood flow increase  at  any point ???

Well if they would use for example the  Doppler  at the knee popliteal area  and  at the femoral area  and they would create  an occlusion above the  popliteal  area , they would see no blood flow in the lower leg under activity, but still a  great  flow in the femoral area.
 I hope I get the point through.
 Yes , an increase in CO  and vasodilatation  help will increase blood flow.
BUT if we add some compression, whether this is  artificially from outside or internally due to muscle contraction ( compression) than we have a  " fight" between the pressure produced  from CO  and    opening due to vasodilatation and the  compression and therefor reduction in blood flow due  to muscle contractions.

 Below is a great example we are discussing
 The blood flow (tHb) in the delta muscle reacts as we all know and expect. Increase in CO ( cardiac output ) as well as  dilatation help  and we  have  an increase in the  tHb reaction.
 We  have no or minimal  " fight "  to sustain , as there is minimal  or no  muscle contraction  in this muscle.
 On the other side in the leg muscle, where we  contract  muscles  we have a  " fight " between the   CO  and vasodilatation  and the compression due to contraction. Now look  further.
 If the statement  from tHb  critics  is true, that we  should  have  ( higher CO as more  blood flow [wink] a steady and great increase in tHb.
 Well we  have that, but again  only  if we get  rid of   competing   counter reactions like muscle compression  or   reflex  vasoconstriction to maintain BP ( blood  pressure ) or reflex  vasoconstriction if the delivery is getting towards a limitation and priority has  to take place.

 Now  at the end of a  test, no matter  what kind  you  have ,let MOXY  run for at least 1 min or better longer without  any activity.
 Why. Because  we  get rid  of the " fighting " situation.
 So people with a decent vascularisation and a decent cardiac out put  will see  an increase in tHb  which will be higher than the  calibration tHb value at the 1 min  rest at the start. Now  all this " story telling " can be observed  easy on the example below.

 Nice  overshoot of tHb in the leg muscle  as a  feedback of a  bigger capillarisation and vasodilatation than at the start.  Interesting is that even in the non involve muscles in this case we have  an increase as we stop.
 Now look very carefully  in the L4  , what do you see as a  trend  coming up in tHb in the non involved  muscle.  So we have here a situation , where this  athlete  just started to reach the limitations of  the compensator  and  has to move to   the last step of  help of delivery by blood volume shift  from non involved   areas  to  involved areas. This takes  place over  vasoconstriction. Now  what we see below is that in L2  the tHb in the legs  is  the " highest and than in L 3  and L4  it drops.
 meaning  , that the muscle compression  ( contraction force  overrules the increase in CO.
 If this is the case we should see a  compensatory reaction  in L3  and L4  and in L1  and L2  not   or minimal  compensation needed. ( training  idea.  a)   work on SV increase  or on  intra  and intermuscular coordination.
 The  easy  feedback or bio marker  for CO is HR.
 The  better option would be having HR  and SV  but again for  practical coaching applications we  have HR.
 Now  HR  will go up  during a stable load  due to different reasons.  and one reason is when  we   have a problem to dramatically increase SV.
 Now if the  tHb  drops  due to   muscle contraction we   start to reduce  some what   back flow  to the heart  and as  such pre load  which   at least makes it much harder  to increase SV. Therefor we have to go to HR. I this is the case we will see that in the HR  reaction . Let's look at the HR reaction in this case. first the   tHb reaction  followed by HR reaction.

 THB  BOTH.jpg 

QUAD  EXPLAIN LIMIT  AND COMP.jpgNow  for the advance  readers.
 You can figure out  where this  athlete  reached a  maximal SV and than he maintained  the SV  and than he  actually dropped the SV  towards the end.
 Now yes I  already see  mails coming in that this never happens  SV  will reach a plateau  and that's it.
 And here  for  extreme  critics  a  case  study  done at the university of Trois Riviere  ( Quebec) with Claude Lavoie  ) many years back.

Claude HR SV CO.jpg

Now  the  critical reader can  follow the load  and with it the lactate reaction after each load. Read very carefully  and you see, why we are not very convinced, that lactate is a good tool to be compared  with NIRS  as the timing on what  and when we see NIRS reactions is  immediately  or  with a very  very short lag time, versus lactate which as a huge  lag time , so that what we see in the  finger  was  perhaps long done  before the  trend  shows  up. Why is  the lactate value  lower  after  a harder load.?

lactate post.jpg


Development Team Member
Posts: 264
Juerg, sorry if I insist but I am still struggling to understand the behaviour of increasing SmO2 with no increase or actually decrease of tHB through the load.
The one below is the graph of the first 2 same loads. In particular in the second load where I see tHB progressively decreasing and SmO2 increasing.
Red is HR, Green SmO2 and brown tHB.
At the first load there is no much reaction on SmO2.
What is interesting is the second load (same wattage as the previous one):
As you wrote in another post, let's assume that after the first minute of the second load, delivery is 100tHB and let's assume that is fully loaded, so 100 O2, SmO2=55% so 55 O2 remaining and 45 O2 utilized.
Towards the end of the load, we can have 90 tHB, SmO2=65% so 58 O2 left and only 32 utilized.
It looks like the oxygen consumption is decreasing through the load ?
At rest tHB is still below the starting value and since HR has increased from 60 to 82/85 I would assume either a lower SV or a vasocostriction.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Juerg, sorry if I insist but I am still struggling to understand the behaviour of increasing SmO2 with no increase or actually decrease of tHB through the load.
The one below is the graph of the first 2 same loads. In particular in the second load where I see tHB progressively decreasing and SmO2 increasing.

Daniele  , no sorry needed  from any side. If it is a sorry , that it is  from my side ,  as if it is not clear  , I am not sure  so lot's of  talk  and noise  and no substance  or I am  not  able  to explain it that it makes a decent sense. I may need  some help  form other readers  as well. So I like to  try again  as far it  makes sense  to me , which still  does not mean I am right. So be careful and great if  you insist, as many do not out  of what ever reasons.

 Now  first a correction if my  answer  gave this impression .

 As you wrote in another post, let's assume that after the first minute of the second load, delivery is 100tHB and let's assume that is fully loaded, so 100 O2, SmO2=55% so 55 O2 remaining and 45 O2 utilized.
Towards the end of the load, we can have 90 tHB, SmO2=65% so 58 O2 left and only 32 utilized.

Woww if I  wrote this than that is terrible  and very very poorly  written.
 Here why:
delivery is 100tHB and let's assume that is fully loaded, so 100 O2, SmO2=55% so 55 O2 remaining and 45 O2 utilized.
If  " delivery"  of tHb is  100 tHb  and  we assume   this tHb is fully loaded so 100 O2  than SmO2  is 100 % If SmO2 is 55 %  than  we have 55 O2Hb "pieces"  and 45 HHb pieces  where as O2Hb is loaded Hb  and HHb  is  deloaded  Hb

 Now  here  we have to be careful. NIRS  and  in specific  MOXY is great  but there  are  clear limitations  and  if we only use MOXY  we still make a lot of speculations.
 If we combine MOXY  with  actual  other feedbacks  like cardiac  hemodynamic, VO2   information , Blood  values  like Hct  and so on we  can reduce the speculations  to  more  actual information. So many of the interesting combinations we show you here  are created  thanks to years  of combinations  with all this equipment. Problem you have to come up  with 100'000 $  +  to have them all  and the idea we  try to give out here is , that  you as  an athlete  or as a coach or as a fitness center can with MOXY  create a much more individual  feedback than what we had   or still do in the past  with  calculators. That is the mina message.
 What we do here is lot's of  fun  and as  many readers  can see it si  really  interesting to see  how many information's  can come up  with  combining the different physiological feedbacks  in one small tool.

Now  back to Daniele's  example.
 Lets' see whether I can summarize it in words.
a) 2  same loads  so same wattage.. 5 min duration 1 min rest.
 So example 150 watt for 5 min   than 1 min rest  possibly  no activity   followed by t another 5min load  same 150 watt.
a1) First  what is interesting is, that by the same watt we see a very different physiological reaction, indicating or  at least  opens the question, whether the same watt ( performance ) is really the same  physiological  load ???
 Now   what answer  would we have to give on this  question.?

b) first load in the example shows a  slightly increase in tHb  and  a  more or less  stable SmO2  %.
Now  tHb is used  as  an indicator of blood volume  or  v blood flow. BUT we assume that . We  assume , that when tHb goes up , meaning all O2Hb  and HHb  together  will be the tHb  that we  most likely  can say , that there is more blood  in the tested area.
Now tHb  does NOT give  us a volume in L  it is  just a  trend without any values.
 Stupid example. If your  total blood volume  ( Plasma  + cells   ) is  10 liter  and we    take a Hct  ( hematocrit)of 50 %  than we have 5 L of  cells.
 Now  again  numbers here  are stupid  and just  for  examples  purposes.
So  this 5 L of cells  are (stupid number) 1000 cells. so tHb  would be 1000.
If  SmO2  now is 60 % than:
 tHb  1000 ,SmO2  60 % :600 cells  are loaded  with O2  O2Hb  and 400   are HHb unloaded.
Now in  load  11 ( 150 watt ) we have a stable SmO2  let's  take it as 50 %
So we know that 60 %  of  the total cell (tb ) will be loaded so in our  number example  from the 1000 tHb 600 are O2Hb ???
 So we may have started  by 10 L  total blood  and  50% Hct. Now  at the end  we  are on 12 l total blood ( we do not know that but  we assume it )  and  we still have  50 %  Hct  so 6 L cells
 so if thee  concentration is the same we have now 1200 cells  
= tHb  1200. SmO2 60 % : 720 cells  are O2Hb / 480 cells  are HHb.. ??

Now  during this  first load we see a  steady increase in tHb. with  stable SmO2 %
so  based on above we have  at the end of the load  despite always loading 150 watt 120  cells more of O2Hb  so  more O2  than at the start.
 This could indicate, that we delivered  more O2  than we  used  and if  we assume we use  all the time  the same O2   we clearly deliver  more than  what we  need . BUT  this is not  reflected in SmO2 . 
 That's  why we need  a  combination of feedback  from tHb  and SmO2 /
 I hope  I can get this idea over  but always room  to  discuss as it is a  very simple  example.
 If  we add now  the HR as  an additional feedback , than you can see that  delivery (CO2) is  nor t that stable . We may have  an initial frequency reaction  followed by a  slightly drop in HR   and one reason could be a increase in SV now as we increase   blood volume we  may create a better preload  and as such can afford  to drop HR  as SV  goes up to maintain a needed  CO.

. Now  hope it makes a little bit more sense.
 I like to add here. tHb  can NOT be used  to make a  diagnosis  of  anemia. Same  problem with SpO2.
 You may have a  100 % SpO2  saturation meaning that all the  Hb in your  finger tip is loaded  with O2. Now you may have a person with 95 % SpO2  .Which one  has more O2.
 We  do not know. As the 100 %  may have 100 tHb  so  100  O2  the 90 %  one  may have 200 tHb  but only 90 %  are loaded  so 180 O2.

 Now  second load .
We have a  tHb  which is dropping. Indicating a  reduction in blood  flow  or volume  or  cells
At the start 12 L  total blood 50 % Hct  6 L  cells  1200 tHb
At the end  10 L total blood 50 % Hct 5 L cells 1000 tHb

Start 1200 tHb  50% SmO2 = 600 O2Hb  and 600 HHb
End  1000 tHb  70 % SmO2 = 700 O2Hb  and 300 HHb
 So we have a drop in blood flow   but an increase in  O2.
 meaning that we  have like in the  first 150 watt load   more O2  at the end than  at the start. How  can this happen.  What  reactions  could create this situation. ? I will try to dig up a n example we made many years back where we created  all theoretical possible  scenarios  of tHb  and SmO2    and than based on this  we tried, whether we  can create  this pictures  with real activity  and it worked  .

Development Team Member
Posts: 264
Juerg, keeping the same numbers of the example:
Now  second load .
We have a  tHb  which is dropping. Indicating a  reduction in blood  flow  or volume  or  cells
At the start 12 L  total blood 50 % Hct  6 L  cells  1200 tHb
At the end  10 L total blood 50 % Hct 5 L cells 1000 tHb

Start 1200 tHb  50% SmO2 = 600 O2Hb  and 600 HHb
End  1000 tHb  70 % SmO2 = 700 O2Hb  and 300 HHb
 So we have a drop in blood flow   but an increase in  O2.

Can we conclude that O2 consumption is lower at the end of the load compared to the start?
Suppose we deliver X%loaded (I did assume X% as 100% before):
at the start it has been  consumed 1200*X%-600
at the end it has been consumed 1000*X%-700

Please let me know if I am wrong.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Daniele, I am not sure whether we  right or  wrong,
 You can see , why I hate METRICS. We  can  manipulate the in all directions  till we  are  right !!!!
This  examples   have one great   info. We have a limitation  in MOXY as well. That's where it is great to bring in some additional simple to use bio markers  to get  more feed backs.
So your  question  which is as well my question:
 Can we conclude that O2 consumption is lower at the end of the load compared to the start?

In this case, where we  know  we are  at the start  I would   conclude  and hope the conclusion is   in the  right direction  YES. I think what we see in both  same loads  really is the same reaction.
 We start  from zero in the first load   and  have a know  poor delivery situation  so we  for sure take   some O2  from the local  supply line  and than    during the load  start to get  the delivery up to seed so  we have more supply   than we need.
 We  can see  this a little bit in the HR trend  when you go back.
 So the initial start  is not  as effective  as   when we are 5 min in , where all settles  somewhat down.
 Than a new  rest  so  an interruption of the bodies attempt  to try to get  back into homeostasis  in this  load  for the first 2  sets.
Again a start  with  some  need  of  local O2  supply but a better delivery  start as you can see  from the HR   reaction ???
 You can see as well in the load  less ( overshoot) of HR  so  possibly  already a  better  involvement of SV.
 Than    we give another 5 min time  for   the physiological systems   and  for blood  supply  into the working  muscles  and  therefor most likely   towards the end a  better supply  with  more efficient  HR  ( CO ) reaction as well a  more efficient  VE  (RF  x TV ) reaction )  Think here alone in mobilization of costo vertebral joints  and  better  ventilation form the apical areas  towards the basal areas, which allows  a much better O2    exchange   in that section. See  optimal  gas exchange in the different sections  of the lungs.)
 For sure better  inter  and  most likely well better intra muscular coordination so  less O  use  alone  form this part of  the O2  demanders.
 If we  use SEMG  in    as well VO2  than you can see  a much  lower SEMG  activity as we   improve  coordination but  as well a lower VO2   by the same load towards the end.

 Now just to make  things more interesting. I  can create this type of a picture . tHb  dropping  and SmO2 increasing  with the exact opposite  information as I just did. Meaning  that we  can create a vasoconstriction  and a  in crease in SmO2  by  creating  a very ineffective O2  bio availability.  How  ? This means  if you have the answer to this  interesting  point you will understand , that we  can create a  hypoxic training units  with a very  low wattage level , if  we  for example  are injured  so not  allowed to push  heavy loads  like  patella  irritation  or  even ITB  problems  but as well other  reasons  where we should not push heavy loads.

Plus next is   that we  can use this  for MCT  1 and MCT 4  stimulation  with a very low load  so e are sue we   use MCT 4  in the  low load  but as well are sure we  create a hypoxic  reaction  and still have a very low  load. Basically I  can stay of 150 wattage  for low  and hard  load  physiological  specific  and  do not have to go 150 watts  350 watts  to create a  heavy  and  low load if the goal is  just physiological stimulation without   strength  involvement  and the risk  of  occlusion involvement.

 Last but not least  this  trend tHb  drop  and SmO2  increase  as well can be created  when we  do  bike fitting  and reach a very specific  position  for a very  specific muscle.
 I  do not like to go closer into that  as we have  with the golden cheetah group a much  more professional  group  who uses  MOXY  for bike fitting  so  I am sure they will share this information with us  and than you can see what I mean. Hope you see  why I  hate to make a simple statement  and conclusion but  there is  so  much interesting reactions o look at that  the MOXY picture  alone is great but has to be taken in  careful context  with other  cheap and easy to gather bio makers.
 HR    as most have HR monitors. RF  as most  can easy  count  and  sometimes in a  indoor situation SpO2  sensors. As you can see using SmO2  alone   is  not always a sure bet  as we have to take tHb into account.
 There are many   interesting mall studies  out there looking  to improve  SmO2  values  and  as soon they have a result  with a higher SmO2  %  they conclude, that what we do is great for performance as  we have a higher SmO2  value .
 Remember   bio availability. We  can see a great increase in SMO2  and  just creating a hypoxic  reaction as e see it is going up. This is one  of our favorite   practical   examples  we run  in our workshops  to   just get  immediately the people into a spirit  of being positive  critical on what   is coming up.
 Is that really  true ?


Development Team Member
Posts: 264
I had fun trying to replicate the same graph [smile]
Two workouts, one with moxy on the VL and one on the not-involved Delta
10minutes steps with approx 25 W increase.
First SmO2
And tHB
it looks like some metaboreflex reaction during last part of step4.
But SmO2 is still very stable on both...

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Hey  that is  fun  great  job.
 Now a question from my  side.
 When  you quit the  workout  is  that a  complete  stop at the end 1  min or more  re-calibration or did  you simply slowed down.
Here my answer to this question.
 look in the case where we discuss look calibration tHb  and SmO 2 at the start  and than  at the  end.
 The  case we  discuss  has a great  vasuclarisation and mitochondria density in that  assessment  and that was the focus  over the last 6 month.
 In the case  you show  I am  not sure   whether  you  started out  with 1 min calibration   and than finished  the same.
 If yes  look the difference.
  Than look the   difference in  tHb  and you made the red  circle  as you already picked  it up.
 The drop in tHb in the non involved muscle indicates  a  deliver limitation from somewhere.
  So you create a vasoconstriction in the non involved muscle  to  re-direct the  blood  flow  to the leg  muscles.
  That means  you  or  who ever did the  ride has  to  try to   maintain the BP  but has not yet a problem  with O2  delivery. So this would indicate  a too  low CO    for the blood vessel systems  which are there  and the   BP  cant be maintain  so  vasocostriction in a  body part , which  at that moment is not essential  for what wever is  asked  from the body  to be done.

Development Team Member
Posts: 264
In both cases I just slowed down to a very easy wattage.
I've added the HR graph.
The spike at the end on workout 1 was a 20 sec all out.
As you can see even in the last part of step 4, HR did not react much

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
hmmm question:
 We  have 2  HR  and  a  delta  and  VL  SmO2 information tHb information.
 Do you mean  you did  2  x  the same  workout  once  a  MOXY on VL and than  one on Delta as you have just one MOXY ? Woww if this was the case incredible   great HR  feedback.  Now I know is  seems  hard  but if you like to get the  most out  of   feedback  always  try to  make a complete  stop to get rid  of complete  muscle action  and  pump effect from the muscle  contraction. Easy  biking has a great  venous  return  effect  so  we  will   loose  the optimal feedback  of  the delivery system  this  way.
 So  one minute is  not  that bad to stop.
. The HR  shows  a  small trend  of starting to  be a compensator . Try the  same  workout  but make somewhat bigger steps    . The example we  discuss is  150 watt 200 watt 250  watt  300 watt.

RF 6 march.jpg

I will show you  on the weekend  how  you use this idea  to  prepare  for  any workout  and than  how  you make an easy fast  check  whether you have reached the optimal intensity   for what ever you plan  to  do. So stay  tuned.

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