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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Here 2  studies from friends  form the USA  east  and west coast. The reason why they are interesting is the discussion on the darkness of skin color  and whether  MOXY  ( NIRS) in this cases  may have a problem  to be used.
 Both cases  are  dark skin.
 The fist case is a very nice  regular  dark ( very dark skin . Here the  data   just looking at SmO2.. there where 2  activities done we will look closer later.
smo2  all.jpg 
This SmO2 trends are very common   and you can see in the  so called  more " aerobic load  the 5 min bike we have  a possible more O2 independent involvement or  lets' say a less  ability to use O2  compared to the  so called " anaerobic" load, where we  use much more O2 ?????

Now this next  picture is a  dark skin athletes   great  athlete  and we will show the  full case with some critical thoughts .
 Here just the full data  we go sent to us  form the MOXY
smo2  frye.jpg

Now  when we go though this cases  any comment is NEVER  a critic  but an open thinking  why I may use  another option or  idea.
BUT it is a critical thinking towards what I did over  40 years  with being a  strong believer  35 years back on lactate threshold  and   a big  believer in VO2 max  as this is  all what we did  at that time  and it was  new great   but   we where limited on the technology  we used  compared  what we  could do this days.

So if you like to move into this phase of MOXY use  stay tune d and  come  back with questions  otherwise  you may loose  many   information's very relevant to MOXY  or NIRS use in general.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
I like to start with this case study  below.
smo2  frye.jpg 
Again, this is NOT a critic on the group , who sent us  this information. In fact it is a BIG thank YOU
 to open share the information with us.
Any  of my comments have as well be taken with a  carefully critical approach, so we all can learn  and get better.
 The simple goal is  to  find a way of closing the gap between the isolated  scientific  exercise physiological approach, which is super interesting but often without  any practical application for the coach in the field or even worse , for a thinking athlete.

Above case.:
 What information  do I  have:
1. Raw data  and above is the graph of the SmO2  from the moment they started the MOXY to the moment  where they stopped the data collection.
2. Top motocross athlete  with a dark skin ( so question of the  reaction of the SmO2)  can MOXY SmO2  drop  properly or is there a ' Matrix" we can apply?
3. Assessment on a stationary bike with a 4 min step test ( hmmm or  5 min not sure anymore) and a 1 min break in between each  of the steps.
Increase of 40 watt  after each step  plus 1 min rest section.

Problem. ( Discussion)
a)  we have no  clear  start point  in the data collection  and no clear endpoint.
b ) we have no start load ( watt) information nor do we have the amount of steps  he did.
c) we have no other bio marker like HR  ,RF, and so on.

 This is great as we have simply MOXY data with some hints.
 This makes it great to see how  much  we can or can not read out of the SmO2  and tHb trend.
Risk : We  can be very  wrong, which is great as well as this will sent us back  to  study more  and learn to understand the information better.

Answers  / interpretation and discussion on this case:

1. Matrix  and  skin color.
 A:  we are not yet  completely sure.
 As you can see in the beginning of this tread, we show to cases, one  from the east coast with a   5 min pedal workout  hard  and   some wall squatting hard  with a friend  who has a very   nice  dark    ( very dark )   skin color  and during our visit    and  with his own testing we have no  indication in his case at all, that his  skin  situation  actually influenced  the SmO2  and tHb trend.
We had last weekend in Las Vegas  live demos during the expo  and had a very  smart person there,  nice dark skin  great  biceps workout  live  and a very  " normal"  often seen  SmO2  trend without  any indication that the trend would be different than on a  less dark skin.
  I t may be  somewhat a  less extreme trend  but it is  still the same trend.
 I do not believe  we can make  any Matrix  or calculation but I am sure somebody will find a  formula  for a Ph.D  to show it in a study.
 Do we need  it ??? is it useful,  can we trust it ????

2.Open questions:
This assessment was one as mentioned on a MOTO cross racer. It was a  " classical" wattage stationary bike test.
How many  world class  cyclists  are getting tested on a motocross bike ????

The muscular load on a stationary bike is basically all concentric muscle work.
 The  actual load on a motocross bike on the leg  for sure is  basically all  or nearly all eccentric muscle load ????
What do we know  from this athletes on physiological load on the MOTO cross bike ???
 What   limitation does he has on the MOTO  and what compensation  may he use  to survive a  race ???
 No information what's how ever.
  So we  test him on a stationary bike.
 We get a result and we will know  after this  bike test, what his limitation and his compensation will be on a stationary bike.
 Based on this test (  we will show it  later) we can  make  a stationary bike specific  "zoning"  and we will be able to design a specific individual  training program for this athlete  to improve on the stationary bike his  next test result.
 We will be  happy  he may be happy   but we may see no  or even a  worse result on the MOTO in the next races.
Question: What is the point  to test him in a very different sport and improve him in a very different sport , when his  goal is to  actually be a better  MOTO racer ?
So before I shoe you the potential result  from the  stationary bike test here a suggestion

A )  A Motocross racer  has to be tested on a  MOTO cross bike in his sport.
 So you   take 2 - 3 MOXY's ( much cheaper than a wattage trainer and no even mention a VO2  equipment )  and you apply the MOXY on   motocross specific   extreme loaded muscles  plus on a muscle ( if that exists )  where the load  may be minimal in motocross.
 Or in short test severe involved muscles  and  test one relative  little involved muscle.
 The involved muscle give direct local limitation  and compensation feedback.
 The less involved muscles  will give feedback on the systemic load in this sport.
Once we have this  real  sport specific result  we  can design if we like a motocross specific  assessment but we for sure can design motocross specific   circuits  and workouts to address the  weakest link  of this athlete.

What we try to say.
 With MOXY you now can test sport specific  and you may give up a treadmill and a stationary bike.
 Again not many  runners like to bet tested on a rowing ergo meter. ????

 So  with this ideas  I will in the next thread show  , what I may be able to read out of the  raw datas  from the csv file we got  from this assessment. I like to ask the above question in  2 pictures  as a summary.

Is it smart to test this guy here moto.jpg 

in this sport here ? road bike.png or should we test this  guy  here
  in this sport ? moto.jpg

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Okay so let's focus on the data we have  from this case (Motocross  athlete assessed on a stationary bike.).
What can we do ?
 We  can explain  and make an interpretation of the data  and the physiological reactions this athletes  had  during a step test on a stationary  bike.
 We  can not :  give a training program  for this athlete he can use  for motocross training nor can we  assess his potential limitation  and compensation  option  during a motocross  race or  workout.
We  can give him individual training intensities  so he will improve his   cycling ability  and will show up next time with a better stationary bike test.
BUT  this will no show  up  as well as a  for sure improved performance in his sport.

Below the total overview  once more.
smo2  frye.jpg  First step:
 We know he did a  4/1 step test 4 min load 1 min complete rest.
 We know he did  40 watt increase.
 The most  centers are afraid  to start very low  wattage. But even if he started  low  with 80 watt  and he increased  by 40 watt  and we take 6 - 10 steps  he would have done :
 6 steps  80 + 5 steps  to 280 watt which s not a bad load  for a non cyclist  with a low body weight.
 if  he  would have done 10 steps  so 80 + 360  he  would have pushed 440 watt which would be a top  world class  cyclists. So we can look in the graph for a pattern  with 6 - 10 clear trends in SmO2.
Here what we  would speculate. explan pp.jpg

So let's focus on the red section , where we see a clear pattern of load  and deload.

smo2  actual test frye.jpg  This would suggest  7 loads  with increase in load. Last load  was not complete.
 7 x 40 watt = 280 watt  and a  start wattage of  somewhere perhaps  of 100 watt +-.
 Indicating a  end load of 340 +-   a step perhaps, which is  an excellent   performance in wattage.
 Now  SmO2 is not always optimal, as it may not show   perfect the load de load.
 A great add on is to use the tHb  which gives  an immediate indication of  change in blood flow  or  Volume.
 Let's see.
thb smo2 test frye.jpg

You can see, that for sure in the lower intensities  where SmO2  is high ( very high ) the change in blood  flow  /volume is a better indicator  as  even in low intensities we  will have the initial muscle compression tHb outflow followed by a decompression to settle in   of tHb ( increase in tHb)
 In this case we  can as well nicely show, why we  not like 1 - 3 min step length  even in low intensities.
 Look at the tHb trend  and whether we  actually reach a physiological homeostasis  and  whether  after 3 min we really  have reached  an optimal respond or whether it keeps it going . Same can be observed in the higher intensities in both SmO2  as well as tHb.
 What we learn:
 if we assess cardio vascular  as well as respiratory  and metabolic endurance information we have to have long enough steps to give the physiological system a chance to see, whether they  still could compensate  for a occurring limitation. Any classical 3 min step test misses this points  and  the result is forced  on the body  as a    time restrain test rather than a physiological respond test.
 Next up   we will look closer  in this test.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Okay, here my speculation +- 1 step.
 It looks to me that this was the actual 4 min/ 1 min step test  section in the whole MOXY data collection.
You can see the " baseline of tHb  and SmO2  at the start if the test  and you can see the surprising nice return to baseline at the end of the test in both parameters.
 What is interesting is the fact, that we  actually go back to baseline. This is an indication  in many cases, that the test  was really not a load pushing anything out of balance. This does not mean that it was not hard, but it means, that he  quite , when it was somewhat uncomfortable and  he  had no  limitation reached  resp  he  did not  call for  any compensation.
We  may have a HR info somewhere  and it would be fun to watch, whether  he simply only    has a higher HR  at the end  and no return to baseline in that parameter?

 1. Look at the very high baseline SmO2. We do not know, whether  tHb is  individually high as well as  we  have no absolute numbers  for tHb.
 SmO2 . This high  baseline is not very common  at a real resting baseline.
 So we know  from the full data collection, that he moved  a lot around prior to the start here so he actually increase  SmO2  due to this  activity  and as  well may have increased his tHb.
 Higher HR  and so  on. What was his  " baseline " HR  at the start of the test. Speculation:
 He  may have had the "order" to  " warm up"  and he did this in  or on his own feeling but with the warm up we  started  already to loose a lot of  needed information for a future training program.

a)  tHb trend  from rest gives us some  " capillarisation " feedback.
 b) trend in SmO2  gives us some feedback to  find the ARI ( active recovery intensity )
a + b  will support our decisions.
 As well the fact, that we have a " return " to baseline at the end of the test  rather indicates, that he  was NOT  resting baseline at the start of the test.
 Here  an example from our South African group  with a 5 min  step test  without  rest in between steps.

smo2  thanjpg

You can see the  actual baseline followed by an expected increase in tHb ( blood flow) and an increase in SmO2  as more O2  is delivered  than needed.
 You as well see the reaction at the end of this test  with  a clear increase in athlete baseline  and as well the same  situation in SmO2.
 This  athlete  had a respiratory limitation  based on the end trend reaction we  can see.
 What we do not know in a  step test even with 5 min is,  at what intensity he started to get to the respiratory limitation and where he  started to compensate  and with what  option  to sustain a few more   step increases..
 When we us  a  idea like 5 min  step length 1 min  rest we  create after each step the situation we  in a  full step test only create  at the end of a  test.
 Meaning we create an information on SmO2  and tHb  by  suddenly (  at the stop   / end of the test )  have no " demand " of O2  from the working muscles.
, we have immediately a change in muscle compression to   zero ( as long it is not the limiter )  but we have still a full ongoing delivery system activity  ( HR  + SV  plus RF  plus TV plus )
 Some  mechanical reactions  are  instantly ( compression due to muscle contraction )  so tHb  will increase immediately if  muscle contraction is gone.
 Resp  tHb  will drop immediately if the muscle contraction created a venous  or  perhaps a arterial occlusion ( pooling ).
 What will have a lag time is CO2 stimulus.
 hypercapnia   will increase tHb  but  slow down SmO2 recovery.
 Hypocapnia  will   reduce the tHb increase  due to vasoconstriction..
 Many more simple  info's  e  will learn to add to see the full picture. Back to our case.
  a) look SmO2 in the first  few steps ???? difficult to know , whether he simply reached  an optimal O2  situation  as we  just have a plateau so we do not know, whether he is  stable in  delivery    and utilization or he is  simply  on its optimal  O2  stage. Therefor we miss ARI  and STEI  trend for zoning.
  BUT : we have some small help from the tHb trend.
 Look what  it tells us:
  tHb is a sign of blood volume  trend will show  when we start a load  an initial drop :
 Muscular compression and therefor  blood outflow .
 Followed if the load is not above  a certain limitation a  decompression trend   with an increase in tHb back to base line but  most often above baseline, as HR will be higher  and therefor CO  as well which   helps to increase  blood flow in the working area..
 So tHb gives us a hint, where we    have as well most lily a higher SmO2 intake than utilization.
 Summary : step 1.
 Where would you place ARI  and where would you start  STEI.
 Why ??
 Give it a break  and  lets' go to the next step tomorrow.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
So let's go  first back to a  step test  we showed  above. It is a 5 min step test sent to us  from South Africa.
The discussion  at that time with this group was to show them, that, if you decide  to  do a step test fro cardiovascular,  and respiratory information you have to have a step length form at least 5 min  do get any decent physiological feedback.
 The " classical" 3 min step test  just simple  do not allow the physiological system to show their potential reactions as limiter  and or as compensator.
look  at this 5 min step test  . Each 5 min duration is in the grid  so you can see, that the critical time  before we  see a change is  pretty much in the middle of the step.

A a 5 min.jpg

Now  as you can see in the above test we have a nice  initial section of increase in tHb  and  in SmO2.
 IF you let  your client " warm up "  uncontrolled  or with  any protocol  but not  observed  you loose a lot of very interesting information of the structural or functional reactions of you client. Therefor you may miss information  crucial for a individual success full training  plan.

In short:
tHb is a  great indicator  of blood flow / volume  and as such as well an indicator of the capillary situation of your client.

 A client with a  big capillary bed  and or a great capillary reaction will show a  much different tHb trend  than a  beginner or a client with some  vascular problems .

This is not new  at all.
 Here a nice  help  from a web site  and if you read  and than use the idea of MOXY  and ThB  you can give yourself  the answer.


Exercise as a Challenge to Homeostasis

Strenuous exercise is a severe test of homeostasis. Oxygen consumption and carbon dioxide production can increase to 10 times normal, mostly due to increased oxygen demand by the muscles (Shepard, 1999). If we were insects, oxygen could diffuse directly to tissues via the tracheal tubes. But because we depend on our circulatory system to deliver oxygen to our tissues, this large increase in gas exchange is a circulatory system story. Blood flow to exercising muscles increases from about 1 L/min at rest to over 20 L/min (Guyton, 1985). This tremendous increase in flow is called exercise hyperemia. Exercise hyperemia comes about mainly because the muscle capillary beds (normally about 20-25% open) all open up. This dramatic change is caused by local adaptation (do you remember what that is?). While resting muscles are high in oxygen and low in carbon dioxide, most precapillary sphincters are contracted. However, when the muscle starts consuming oxygen, the precapillary sphincters open, and blood surges into all the muscle capillaries.

On the other hand, a poorly-conditioned, sedentary person might only be able to increase his oxygen consumption 3 times (rather than 10 times in the trained athlete), mainly because of a circulatory system that can't carry as much blood to the muscles (Laughlin, 1999).
Delivery limitation our input

This tremendous increase in oxygen consumption and carbon dioxide production has dramatic consequences for the circulatory system. Heart rate can triple. Mainly because of an increase in heart rate, cardiac output increases by 5 times, or up to 7 times in the trained athlete (Shepard, 1999; Laughlin, 1999). Mostly, this increase is caused by increased venous return, which in turn in caused by decreased resistance in the muscle capillaries, and the fact that working muscles are squeezing the veins and increasing the velocity of blood moving through them (Laughlin, 1999). Pulmonary ventilation increases 10-20 times. "
If pulmonary ventilation ( VE ) is increasing  over  increase in TV  and RF  than we have a great improved  return of blood  to the heart so SV is going up.
If we have a respiratory limitation :  so  only RF  goes  up an din some cases TV even  decreases the pump effect is gone  and we will see a drop in SV
 This is another reason why we  can't look at VE only but  we have to look ate VE as RF  x TV  the same as we can't look at CO  only but  at CO  as HR  x SV.

Now if we  run a " classical" step test  and you can see this above we can see, that initial muscle compression due to increase in load  will "overrule" the   vasodilatation due to different reasons.
 At the immediate increase in the next  step ( ;load) we have an immediate increase in muscular compression. In lower intensities  this  muscle compression outflow will after a short phase   be  corrected   back to the needed  muscle tension for the  step load  and as  such we will see a  decompression reaction of tHb. The initial low  HR  for the new load  will be corrected  with an increase in HR  and  if still possible in SV  to adjust the new needed  CO
. This all needs a certain time  an that's where the  at least 5 min step length comes in.
  Now if we instead of loading  more  at each step  get a 1 min complete rest in we  create a very interesting physiological window.
 The sudden step means  we  stop immediately the muscle activity  and as  such the need  or the utilization of   angry  at   that moments.
But we  do not stop immediately the  delivery systems like the  cardiac  out put 9 HR  and SV )  or the pulmonary   respiratory  activity VE   = RF  and TV
 This systems  have a lag time. As  such we  will have  a still strong delivery  but no utilization or lower utilization.
 This creates    with the one minute rest  an overshoot in SmO2    and a reaction in tHb.

 Based on the level of overshoot  and the reaction of tHb  we  can make a lot  of  conclusion on different  physiological systems reaction.
 So we really look at least if not more on the trends in the rest  period  an the start phase top the next step.
 Why should we repeat the same load again.
  If we  just make a 1 min stop like in this case we discuss we do not create a homeostasis  disruption as we do not go back to the same load but we simply wend a  load , where we  may or may not have reach a homeostasis.

 I like to    activate your brain a little bit her  for the weekend.
 Below the  closer observations   at the  stop section of out  assessment ideas.
 look at trend in tHb  one is  at the  lower intensity  of the assessment and one is  at the end phase of the assessment. If you look and think you can see, the answer on what started to limit many physiological reactions.
Last. Physical  stimuli react immediate, physiological  reflex / feedback  reactions  have a lag time.
 tHb  can show this nicely.
 Example. A  muscular  contraction compression shows  up  immediate .  a vascular reaction  vasoconstriction or dilatation due to enzyme  or ot34hr stimuli has a lag time and will show up slower but will maintain the effect  for longer.

hutch start watt bias.jpg 
hutch bias clsoe.jpg 

 Not the performance  as such ( watt . speed  and so on ) but the physiological reactions give us the  needed information  to design an individual training program.

 Today  " bio feedback trend  and market:
 Hexo skin ,  catapult,   and all the increasing available   acceleromteres   are great but  of minimal information  for  intensity control, as long we do not know how the    values    are  supported by  energy delivery and demand.

 Using SEMG  or   accelerometer,  testing for  distance run in a tennis game  and  for  ball contact during a soccer game  are great information, but  we need additional feed backs on  who this  distance  was cover in the view of  energy delivery  and demand ( SmO2 trend ) as well as on delivery  and option in blood flow tHb trend.
 Ice hockey player  who goes all out  ( tHb  different ) than a  player, who paces himself ( tHb trend.
 Difference is the   recovery   and delivery  as in one case  we have a local  limitation   in the other case  with have a systematic involvement.We will show soon a case study in that direction. so stay tuned.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Here a fun comparison of trends.
 2 world class athletes . 
here a MOTO cross racer we discuss the case here.
thb smo2 test frye.jpg 
and here a world class downhill ski athlete

gi leg thb smo2.jpg

Look at the SmO2 trend.
 Ask the question how   skiing  and MOTO may have  or may not have a similar load on quadriceps.

MOTO was a 4/1 load
 Ski as  our idea of 5/1/5 load
 Look att difference in tHb  : was it different start with  and without  " warm up "

Here a load of a  cyclist  and look what  sport specific ability may do  for SmO2.
 So Moto and skier should be assess in their sport  and we can  than discuss SmO2  and values of cross training
Courtesy South Africa  5/1/5  top cyclists
Mark clinet thb  smo2.jpg

 How would this cyclists SmO2 been  on a MOTO cross  or in a downhill ski load ?

 We may just simply have to go back to 1967  when this was all not available  but some critical brains at least challenged the VO2  max idea. Over and over again DAL MONTE  and not sport specific ability to use O2  as an optimal fuel.
 How in this " antique " case would have the SmO2 trend Kajak VO2.jpg

Over and over again Dal MOTE 1967 how would have a SmO2 trend  be in this above cases.
 He was so far  ahead of his time.


Development Team Member
Posts: 369

I have three open questions from this case study thread

(1) Jeurg made the following comment : "tHb trend from rest gives us insight into capillarisation." I assume that this means that if the capillary bed is well developed, there will be a more immediate and steeper drop than if the capillary bed was less developed because it requires a greater amount of blood to "fill" greater number of capiliaries (of course, muscular compression and lack of delivery at this point are what cause the drop - but i am trying to establish why the drop might look different for well capillarised athlete."

(2) Jeurg posted the following image of 5 min step test (no breaks) and noted this athlete had a respiratory limitation. I am not sure how this conclusion is being reached. Is it the reactions of the Sm02 and tHb at time 3000, that are being used to make this deduction? i.e. immediate rise of tHb and perhaps, although difficult to see to confrim, a slight lag in Sm02 recovery? 

5 min step.jpg

3 - The following graph below of a cyclist 5-1-5 test was shown, but with no comments on the case. Any thoughts on the analysis of the case? There is no heart rate or accompanying information, but perhaps the following?:

  • We see the flat plateau at low Sm02 at higher loads - discussed in another thread on the forum
  • tHb and Sm02 overshoot up to about 2100, probably indicative of no problem with delivery within these early loads.
  • Within loads, tHb increases strongly throughout - i.e. muscle compression being overcome by increase in CO, and vasodilation or both.
  • Sm02 and tHb on rest start to fall from about 2400. For Sm02 this could represent a shift in the dissociation curve to the right, but is the tHb reaction consistent with this? Within the load, it is possibly consistent as the build up of C02 would increase vasodilation and therefore tHb, but what about on rest? With an increase in vasodilation we would perhaps expect higher tHb recoveries at these higher loads.
  • A build-up of tHB during load could also hint towards a venous occlusion, but the tHb still looks like a reasonably sharp increase on rest (we would expect a drop or slow tHb recovery).
  • There might be a respiratory metaboreflex here - a moxy on other non-priority muscle would have been useful here to confirm?

I appreciate any insights other more experienced readers can offer, so that i can understand this better.


Development Team Member
Posts: 1,501
Really nice  thoughts  and  yes let's see, whether  we get some feedback  from the different MOXY  centers.
 I will sent you my thoughts   in connection  with  your   e mails question. Metaboreflex, versus  respiratory  muscle weakness). Thanks for bringing back   some older  sections as it is fun to read  it myself again and see how I would now  explain  it different, seeing , where many people struggle  and just using NIRS  and not combining it  with  classical feedback on lactate and VO2  even though they still have some  important  roles to play.

Development Team Member
Posts: 369
Thanks Jeurg. Looking forward to the email feedback. As stated i am trying to work through all the cases to gain a deeper understanding from what is already available on the forum. On many of these older cases, i actually find them easier to follow because a lot of them discuss the basics (e.g. why we incorporate rest periods etc).
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