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400H.png 400m Hurdler with a year of training under his belt.

I am new to the assessment process and interpreting the results.  Figured I would post to get an experienced opinion. 

Step increments were 6.0, 6.5, 6.9, 7.5, 8.0, 8.5, 9.0 MPH 

Attached Files
csv 400hRVL.csv (280.56 KB, 14 views)


Development Team Member
Posts: 1,501
first never trust  Experts   so  take it  with a   careful view  and add you experience  to it. Before  I  will look  very closely here  my take  form my time  as a  Track and field  coach in Switzerland  with the biggest  track  club  at that time  STB ( stadt Tunrverein Bern ). My    friend  at that time  and involved in some crazy ideas we had  with the club.  ( Wild  Thomas)  was  Swiss  champion  and a  top 400 m hurdler.
 Now  with MOXY in our hands  my  first assessment really would be a 400 m  race  with one MOXY on the quadriceps , one on a hamstrings  and one on  a shoulder muscles  most like  delta  acromial  part. Than assess   tape  with a Video  and   overlap MOXY data  and video  and  start looking  at technical changes  and  what happened.
 There is a  great Spanish  system out  there WIMU  who allows this live  with MOXY feedback  as you see the video  . Than we  have a real live feedback on energy  reactions    including  delivery  and utilization feedback  sport specific  and now  we can set  up specific   limiter workouts.
Than    your 5 min step test will help  for some  workouts  but as well a classical interval workout  you may  do like 200  or  300 m reps  so  loads in the time frame  +-  30 seconds.  with  recovery in between  similar like we  do with a  ice hockey players RIP. What I would look  in the workout is  a  set  where you go  flat  and one where you add hurdles  so we see, whether the   run over the  hurdle  changes the way  we  delivery or  limit delivery.  It sounds like a lot of  work but really it  takes  a few minutes to mount the MOXY's  and than  to download. Sent  me the MOXY  csv  file and your  email so we  just look at for you    private  as it is a very private  idea  you have here.
 Thanks  so much for  checking in  and I hope we  can  get you some interesting ideas.
 Remember. We  assess not test  so any  workout you do is an assessment  and we  can after a few  workouts see , what the stimulate or  may not stimulate.
 HR  is great but not really needed in the  short RIP  assessments. What you track anyway is the times  as a part of performance. And  what we need if possible is  RF  after  the loads so simply count  if you have no tools  for this RF. And last but not least  a  simple tool  for  SpO2  so an SpO2  sensor.
 If you mail  me your  addresses I will sponsor  you one  and send you one  . My  email Will be  back later with a  frist  look at your ddata collections  and thanks  again  for  the  feedback  from  your field  of  expertise.

Development Team Member
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Juts short before bed time  super interesting. He  did as it looks a 5 min step test  with 1 min rest  and he added  three  harder  loads  at the end . I will go though both  and  do  some speculations as I have no clue  what he exactly  did  so I may run wild  and wrong but that is the fun part.
 Here just to show  where I am going to look at .

 1. overall SmO2  HR
smo2 hr  all.jpg

Some interesting  drops in SmO2  just before  recovery. so lets  than look at tHb  and SmO2
all thb smo2.jpg 

Hmm even more interesting  and  will talk later look at  first two  1 min rest  and than the rest of it.
 so will need a closer look and than  I will look the lasts three loads.

after  step test  all 3  loads  thb smo2.jpg 
one  data  drop out  but  otherwise  perfect  so no effect on what we look.

The  question  here I try to answer is  duration of the three loads  which where equal loads  but the question will be  30 seconds  versus  45  seconds in a    fast   rushed look  at this. Or  respiration versus muscular  limitation. Last  just for  fun to thro w  out. 5 min step assessment    and the three loads in a biased  view  as a fast  idea on delivery  versus  utilization  what can you see.

bias all.jpg 


Development Team Member
Posts: 5
He was jumping off the treadmill so that could be why he had the sharp drops and corresponding Thb before recovery.  

On the last "5 min" segment he only lasted 4 mins.  Then on the 30 sec all out efforts he completed 30s (15% incline, 12MPH) - 24sec (15% incline, 12MPH) - 27 secs (15% incline, 11MPH).  

From my observations it was a respiratory limitation and a poor delivery on the last 3 hard loads. 

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Posts: 1,501
ha ha  thanks  for the feedback  too bad  you  told  this already as I have all prepared  to  read out  what you just  used  so I will nevertheless show you how  I reached this  conclusions  based on MOXY only. Thanks  so much  and more feedback  on your email is  already underway. Will be back with graphs  and picture's  to show   the reader, how  even with not being there we  can read  what you did  or what happened. Cheers  for now.

Development Team Member
Posts: 1,501
Here  I am back  with some  fun ( at least for me ) interpretations  form this great data collection. Let's
 start in the overall view  many  software  now can  show.

Below is the total  data collection. so  clearly the 5 min step test  followed  by 3  additional loads.

smo2 hr  all.jpg   just get used  to look and  think loud.
1.SmO2  trend. Low  start  SmO2 with 55  %  ( good  or bad  ?  non of both  just him  and  by looking at one  single assessment we  have no real feedback. The starting SmO2 is  great to use, once you collect a  set of  data  to get a +-  individual level   and than you can see  over time as in many other bio markers  what is a  " recovered' Level"  and  how  resting SmO2 looks like after  certain loads  and  when  certain systems  my  not be recovered.
 This is great  to combine  with HRV  and  resting respiratory assessments. and    as well with phase  angle  for cell  membrane recovery situation  for people using bio impedance. For  juts MOXY users: You will find  a  nice trend  information and   you often can  already  at the start of another workout  tell   that the athlete or you are recovered  or not.
In tis case interesting: in the 1 min recovery  no  actual overshoot  compared  to  resting base line   SmO2  ????
 So  have to see why.?
 Can he over shoot . Well thanks to the  game he  added  after the step test we  have the answer : Yes
So  my  question than is: Why  does  he not overshoot in the 5 min step test? What is different  between the 1 min rets in the  5 min step test  and the  3  x  loads  after the step test.?
2.  SmO2  desaturation level.
During the 5 min load  he  roughly de saturates down  to 25  % .
 Now  he has this interesting dips just before the 1 min break so this  has to be looked  at  much closer  and  for sure in combination  with blood flow feedback  so tHb.
What you  can assume is, that the three loads  after the step test  where most likely a much higher intensity  shorter  for sure but much   higher performance.
 Classically they  where  anaerobe  alacticid.
 MOXY feedback would  let is  argue , that  in this higher intensity  he   used a higher  %  of  O2  so  lot's  of O2  involved  for te  short duration  of the load.
 (  Loud  thinking. Are  the HIT   workouts, which at least show in 6  to 12  weeks  studies( great  studies  by Gibala  et all University of  western  Ontario, great   and better O2    reactions  after 2 - 3 weeks  of 30 seconds  all out  compared  to LSD. The latest  study  I  saw  at the ASCM  poster session was a  study with the same idea  but  over 12 weeks.
 Initial  changes  in a  few weeks  where clearly better for  HIT  versus  endurance. The 12 week study  showed a much less difference   and in fact  very close  to the same result   of HIT  and LSD  after 12 weeks. So  function  limitation  and    when doing longer  structural adaptation ? )  , that they improve  O2  use  at least or even better  than  long slow endurance  perhaps because  30 seconds  is not  anaerobe  but  a lot  of O2 involved  so great function  stimulation  for O2  utilization.

So  in practical terms.
 If  we have  athletes  with a great performance but a  relative " weak desaturation ability  like down  to 55  or  even  not  as low.
 In this cases  a  functional  aerobe  training  may  give  for them a  big boost in the short term  for a race  or  important  event.
 If  the athlete  already   desaturate  down  to 10  and lower the  so called  HIT will most liley  see less effect.
 Again  responder  and nonresponders on  Peaking  workouts. ?????

 400 m hurdler . This  can be one  great feedback on  whether hard  " workouts    will have a benefit  or  a  risk.
  In middle distance  races  trainings  with a high metabolic  created  acidosis   have  high risk  of stress fracture. (  showed the study on Ca  release  on the forum a while back )  so better work on technique  and respiration  and maintain the desaturation ability over a  respiratory acidosis  workout.

 Actually a great way  for injured athletes  to keep the O2  utilization on the  great level  without  having to push  high intensities  during the recovery of their  injury.

So back  to  the all out  3  sets
  So  they actually stimulate  O2  utilization much more aggressive than  LSD. ???
 Now  functional stimulation over Alarm phase  re  showing a much faster  change  as it is a functional change  and that's;  what the HIT research  shows. The question than is  whether this functional stimulation  over time  may or may not   lead  to a structural change. So  function utilization improvement  for  example  due  to H +  situation,   temperature, pH  change, CO2    situation  and last but not least  on DPG  hormone  for the right shift of the O2  disscurve.
 Now  how long  doe s this  functional changes  last, versus  a  structural  adaptation  with  higher mitochondria density  , higher capillarisation  and so on.

So both  ideas  stimulate  O2  utilization  but with different  reactions over  time. ????

 Now  back  and a change in graph  to  look at  the step test closer  and the three lauds  in separate  graphs.

step test  thb  smo2 only.jpg

Step test only  SmO2  and tHb.
 Most interesting is the  drop in tHb   at the rest period  or  at leads it looks like 
- is it a  CO  limitation  so BP  correction. Very very  unlikely  so  it has to be something " reducing"blood flow  during the rest. Now look very careful . look at  resting  base line  thB  what can you see ??

Now  is  Blood flow  really reduced ?.  yes or no. If  yes  why , if  no  why not. If it is reduced  what  would trigger a reduction?  If it is NOT reduced   what triggers  the drop. ?

Now  lets look it  very close in different section of the step test.
start closer look.jpg 

Now let's  go closer super close look at  slow start.jpg 
We got  a hint in the  feedback  above. Try  to  mimic  what happens   in this phase  of the step test  and explain . Here just for  fun a  closer look at this in the middle  section of the step test.

close  rest middle  section.jpg 

 explain   for your selves.


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Posts: 1,501
Now here some  brain gymnsatique  before bedtime. Hnmm how  do you increase blood flow in the brain ???

Now  here the overall vie w and  I like you to look mainly a  simple  point base line tHb.
thb smo2  30 av all.jpg

Now look the last  step in the step  test  and keep the overall picture in  your  mind.
end of test.jpg 
What  do you see.
 What causes this  and  when we look  at I fitness  question on Limiter   than there  are  two options  for this situation . What are  they ?
  Now  to help a little bit look at the three  follow up loads  and the SmO 2 and tHb  reaction. The question on duration  is   for me  30 seconds load  versus 45  seconds  load  and I will show to morrow  why  we would pick the 30 second load. ( Ha ha  true  he told  us that  but I show  you  why  I would pick  most likely  30 seconds  form the MOXY data's. here  to show the three loads.

after  step test  all 3  loads  thb smo2.jpg 
so both the  5  min step test  as well as the three all out  show  a lot of physiological feedbacks  but  for me  more important in this  discipline 400 m hurdle is the economy  of the muscle contraction  where he has a  strength  but the strength is  as well the weakness. He  works   when he runs  he  does not  flow.


Development Team Member
Posts: 5
Since you mentioned HRV.  I took a HRV measurement using the Omegawave before the assessment.  

RMSSD was in "his" normal range. RMSSDH.jpg His aerobic measurement below (Amplitude Frequency Analysis of ECG) has been trending low. 

AerobicH.jpg  It looks like each step he was creating an occlusion. This is why Thb drops during rest. 

I am thinking out loud but can this give me a hint to fiber type?

Also I attached cvs data from his delt as well.

Attached Files
csv 400hLD.csv (266.88 KB, 10 views)


Development Team Member
Posts: 1,501
Aaron  thank so much  for your  feedback  will be back on this  later.
 Here just a good morning  brain stretch.
 Well if  we  talk about stretching . I use NIRS  to control the quality of stretching. Why is this help full and what  can it tell us ?

Now  here  where  or  what I look in the three loads  after the step test.
 The question you see is  simple.
 30 seconds versos 45  second loads  discussion  and why I think it may be  30 seconds  and what caused the   question  for 4455 seconds.
  Here the three graphs I  made  to get my brain organised  in this    question.

Firt slook  at HR  and SmO2

last  all out  HR  smo2.jpg 
Now  we know  HR  has a lag  time  so ????

 Than  I look  the  tow  options  of  MOXY trend  which end  up as  about  30 second  load  or  45  second "load" first 45 second  below

45 sec load.jpg

now below  30 second  load ?
30 sec load.jpg 
Now  much smarter  is ( but this is  fun )  to know  as you are there  what the  load time is  and than you immediately  know   why we have  what kind  of  after  NIRS feedback reaction. If  we  do not known  like in this case  it is fascinating to see, whether we  can track down  what may  have happened.
  Here  an internal feedback  to Aarons  from Andri.
 It is  fun to read as it is in English  despite  coming  form Switzerland.
 Andri is the leading  NIRS  specialist really in the world  as he combines  all the fun tools  we  always discuss  and pushes it to the limit. He  did  one  of the first  real  bigger  critical masters in NIRS  at the university in Bern and runs  the European  section  form Switzerland  under the name SWINCO  ( Swiss innovation company )

Here  to enjoy  a hint  for the above  explanations

Just to make a quick point about EIAH, because I do think this is an underestimated problem in interval or high intensity sports.


The problem with EIAH is that we consider this a problem in aerobic exercise and traditionally thinking then would say it is only a problem for endurance sports and not for so called anaerobic sports like Hurdles. However, it is now very clear that all activity levels are highly aerobic (nicely shown by NIRS and Moxy), and that there really is no anaerobic. This means EIAH is a problem for all athletes because shows a limitation in O2 supply at the arterial level. How do we address this? Well many researchers are very conservative and say that we are not quite sure how to address this problem and multiple mechanisms play a role in EIAH. This is of course very possible, but not very satisfying for a coach and not a very practical answers. Therefore we have to make the most logical step forward and keep adjusting as science comes in in order to make progress rather than endlessly waiting for the perfect answer (which never arrives).


On this note:


inadequate compensatory hyperventilation (arterial PCO2 >35 Torr) commonly contribute to EIAH, as do acid- and temperature-induced shifts in O2 dissociation at any given arterial PO2 . (Dempsey et al.)


This is the point Juerg was making and in my opinion the most logical first step to addressing EIAH in athletes. You need to make sure the muscles of the respiratory system have the ability to maintain compensatory hyperventilation without fatiguing. In other words EIAH needs respiratory training.








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Posts: 264
Some considerations regarding this very interesting case.

First one is just regarding the timescale of the graph, which seems to be 0,5s tick (5minutes step correspond to 600).

Step test.
1. Is it possible that this specific tHB trend during the resting period is due to the "jumping off the treadmill" creating a venous occlusion trend?
2. As already mentioned, SmO2 is kind of flat at around 25%. The reaction is on HR and tHB which increases during the last loads. So as highlighted by Juerg few times, even if SmO2 is flat it is not an homeohastasis state.

All Out Loads.
Same considerations regarding the time scale and the durations has been 30-24-27 seconds (as per Davis statement).
So, if I am not wrong, the first load should be like that:
It looks like there is a venous occlusion trend in the first part. Perhaps due to high incline (15%) and very strong contractions?


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Nice discussion  and    Daniele's  thoughts  are pretty much  what  we  can go through. Will be back later  on the  5 min step test  and  why I had  similar  thoughts  on   the 3  hard loads  with the graph  Daniele  shows looking  at the tHb  reaction  and the graph  I showed  with a   shorter  30 second    duration.
 I  will try  today to show you , where  we have some   laces  to  debate  and   that's  where it is nice  to  have the actual time of the load  and than the actual  physiological reaction. Small possible hint.
 If  I  stop by  30 seconds   than that  means as  so often a physical stop   so speed  wattage load  stops. Does  that means  , that   we as well stop physiologically ?
 The  whole discussion in  the classical  O2  deficit is  build on this notion, that  what we  see physically  and on   indirect   equipment's  is  what happens . We  know  by now that this is often not the case. There is no deficit  as a deficit  means  you have to go below  0.  there is no pay  back at the end  of a VO2  test  of  O2  , there is a  delay of  physiological  systemic  reacting  like the respiration  has to settle  down  as it may  still work  somewhat to  create a H +  or CO2  balance , The cardiac system  may still be some what active  as it has to support the  respiratory  system  and so on. So that's'  why the change  to EPOC  extended    or what ever  period  of  oxygen consumption. Not  due pay  back a  deficit  but  as  the body is  in a higher activity level than resting level to  re set  for the  homeostasis  at rest.  So here some points  I  went  through.
 a) it seems a  occlusion  reaction in the load  so tHb   going up  more likely due to occlusion than  due to   super great  CO.
b) that  creates  an outflow  limitation  so we  have somewhat   some problem to get rid  of  H +  and  for surer of  CO2. In the short term that is  not a  bad situation  as  an all out load is  a planned delivery  limitation  so we  can not  hope  for too much O2  delivery. But we may have  a lot  locally. So how  can I  get to this  or  how  can I utilize  it better.
 Well O2  diss curve  shift as a  natural   help . So  we  can  desaturate  lower  due to less O2  sticky ness.
 Now  how  can I  avoid  the  collapse  of the blood vessels  due to  muscle tension if  CO  is not very helpful. Ah gain a short term survival  compensator is the vasodilatation effect  of the   high CO2   level.
 Now  I have to  quit  either because  30 seconds  was the plan  or the body  runs  out  of optimal O2  supply  even  form the local area. So  protection feedback  to avoid    dangerous  drop of  ATP  different    security  systems  . H + inhibits    ATP  splitting  and   CG  reduction  of motor unit recruitment  so peripheral  and  central  protection  do  avoid  ATP  collapse..

 Now  let's  assume this  possibility  exists. Now  you  plan to stop by  30 seconds. So bang you stop.  Not really  and  as you  physically  stop  you still  have a  high CO2 level so  we get rid  of muscle contraction  and have a  somewhat  okay CO. So before  we may have the  outflow of occlusion we  still may have the vasodilatation effect  of  CO2  and the now  somewhat   pressure  of CO  without  muscle contraction  force. So  O2  is  still less sticky  SmO2  will  for a  short moment still drop tHb  still increase, till the  reaction runs out of   option  and the occlusion  reactions  takes now  over ???

 Ho  do you  "proof  " this.  a) SEMG  is  still somewhat activated  but  immediately less.  CO is  slightly  up ( Physio flow )   CO2 level clear  p   ( Capnometer )  and it takes  about  15  - 30 seconds    depending on the athletes  respiratory  training   to balance this out so  an increase in SmO2  will have  a  delay. When we train  respiration   than we see this delay is  much much  shorter.
 Which opens the question, whether the  CP  recovery is therefore  much faster  as well   Top respiratory trained team athletes  can recover  CO2  reaction  in 5 - 10 seconds  as they are able to ventilate  short term 300 +  L  VE. More  idea later


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Posts: 264
I took the freedom to show the 3 hard loads at the end of the assessment, based on SmO2 graph (start to drop) and timing of the loads (30/24/27).
In all the loads SmO2 "struggles" to recover with a further drop in load 2 and 3 when the load is over.
This could be a sign of a large shift on O2 Diss Curve to the right during the load and weak respiratory.
One final thought/question about tHB.
The increase in tHB could be due to both an initial venous occlusion and, later, to a large CO increase during the load (HR in these cases goes from "rest" values of 140/150 to almost max, 180 in this specific case)?


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Daniele  that is  fun  and yes   see,  above  the options  we had  without  knowing the  actual loading time  and the discussion  I  made  with  myself. As you can see you got  a similar  or the same  end result   once we  look at the time.  1  Look HR  and SmO2  and you can see that the  SmO2  great drop  would not fit  with  HR. But  what do we know  about  HR  and SmO2 in reaction time. Normally  HR  has a lag  time  as  it is a part of  the delivery.
 No2  if  SmO2  changes  due  to demand it has a  small   lag time but  much less than  HR. SmO2  can have a lag time if  it  is  like HR  a part  of a  systemic  reaction. So  a high CO2  value  will take  some  time  to get balanced. 
   Here a  cook book  a sit  is individual  and depends  on the   ability  and   performance level of  respiratory  muscles and  whether we  train them accordingly  or  let  them  develop as we  go. It is  a good    indication on timing.


When you look  carefully  and  the closer look shows it nicely  than you can see that the first  hard  set  we  really hard  till he hit the end  of tHb  increase  as  a  indication of a venous occlusion  and  a great  hard  muscular  contraction. But he did not  keep or was not able to keep this up  so he   released  some of the tension  and  we see the immediate    occlusion outflow  even  during the time  load. The  reduction in muscular  activity  immediately  reduced the demand of  O2  so SmO2    as well did not  dropped  perfect.
 Now  careful . This is   as we  assume  he did this  in this muscle.
 To know whether this is the case we  need  performance ( yes )  and he may  have simply  shifted  to  other muscle groups  to maintain  performance  and here he  was    able to maintain a  certain level  but not more.  Now this  opens  a  many century old  discussion  and I will  bring it up here.
 In short  there  where  great studies  done  who looked  at   the " timing " of  STF  and FTF  type  fibers  when going  hard  and harder.
 In a  short summary. You use  first in lower intensity  all  fibers  and than  as you  go longer  but  decent intensity  you seem  to move  to STF  if you keep  going harder  to FTF  but   and there is the interesting open  question. In all out  intensities they  saw  again an increase in STF  fibers.  The  answer. No answer  but   the question  why. 

Now  Clint  had  a great  section , where he  showed  a  nice  steady  drop in SmO2  as we see in the three loads  than a  " hesitation  " of SmO2  and  than moving into  a  nearly  flat  section  and this   sometimes  despite  they still go hard.
 The  argumentation and they seem  to made some studies  was, that despite the   stop in SmO2  drop  they  where able  to maintain performance  and even  got  faster.
 The  explanation was that they  at the end  started  to  recruit  mainly  FTF  fibers  and therefore  there  was  no  need    of O2.  Here  tow things we observed .
 a)  if  we added  SEMG  we never had  an increase in SEMG  activity  form the moment we  had  a  flattening  SmO2.
 Now  we  may have missed  but when ever  SmO2  stopped nicely  dropping  we  had  a  flat  but   most often as well a drop in SEMG.  I use this  very often acoustically  as I  load the SEMG  for acoustic  signal  so as   more  fibers  you recruit  as louder and  as more stable the  beep. If  you start  to release  tension  your  beep  is  less intense  and  has interruptions. So the  " hesitation "  of SmO2  drop   is most often  together  with the hesitation of a  constant  beep.

 Now  what we as well had, that the   drop in SEMG  did not  interfered  with the  at the moment power out put  or performance.
 BUT    once we  added   more than one  muscel  to the testing  so we added  for example in a  squatting   gluel  muscel  and  rectus  to it , than  we could see, that yes the suatting still took place  but with a  slightly different muscel activation  so  for example less    knee  angle  but  mor ehip flexion. This  is  nicely  to be seen in speedskating  all out  loads  where the   nicee  sittying  position for a greta push of  changes in a  same height  of the head  but   bum goes  up  and legs  are much less bend  and tyey  for a  shot moment  can maintin  spped ( but  a end is  close.

 The  second interesting  part  on the notion, that  FTF  will kick in towards the end is the dilemma  that we  argue  ( old  school ) that in an  all out  load  FTF  anyway  work  form the beginning as it is  anaerobe. So how  would a  fiber  who  just pushed ATP  and Cr. P  to its  lowest  level  be able  to  again  kick in  at the end  of  this all  load.
. The  other question  is  again. If  we believe the  newer  research  who  shows   some interesting super early integration  of  O2  to  maintain  ATP   than we  have  at least to ask the question.
 Is the ATP  we  use in STF  fibers   produced  or maintain  differently than the ATP used in FTF  fibers.?  We  will   most likely hit that discussion  on  why we have  a  difference in  SmO2  drop in STF  and FTF  fibers,  and which one has a bigger  drop  in SmO2 levels , The so called  aerobic  fiber  or the  so  called  anaerobic  fiber.
 Once  you start looking  at this level  you will be  really confused.
 When looking  at  FTF  STF  scoliosis  fibers  you will be surprised  off the outcome. If looking  at  Break point s of  calf  muscles    which   some  argue  are high on STF  fibers  compared  with  quadriceps,  than  why  do we see a  earlier  break point in  quadriceps  SmO2  trend  than in calf  muscles. A big interesting observation, when we look that  equipment's  are used on calf muscles  to find a  lactate threshold.  The future  is  very  fascinating once people start using  NIRS in all this  fields  and for us  it will be great to see whether we  get  confirmations  and if not  why not in many of the games  we did   over the last 15 +-  years  really  daily.
 I  just today  did  some fun assessment on a  calf  muscle  1  year  after  an Achilles  tendon rupture. SEMG  paired  with NIRS.
 Tomorrow  I will do  an assessment  for  an insurance company  for  return  to work   court  case  and I   use MOXY  to show  that there was a  problem  at the moment   somebody gave a good to go based on optical  visual  quadriceps  look  rather than on  actual  physical  and physiological ability.

 Now the  last  two of the tree  loads  . Well  Daniele  has the answer.  It is a  lag time  after the load  of SmO2 increase.  CO2  to high  so hypercapnic  and this  creates a  great  vasodilatation  so  despite  a  stop of  muscle contraction  where we  would expect  a  drop immediately  of tHb  as an  occlusion outflow  the  CO2  level paired  with CO  level  did  overrule  a  short moment the  thB  drop . but look it is a  systemic  reaction so mechanically  we  see a " try " out of a  drop  than the short  overrule  ( look at gas  exchange  timing )  before this was balance d or close  to balanced  and than we  have to  expected  occlusion outflow.
 So yes  respiratory    reason here  for this reaction.
 You  can see  Daniele  is the expert  by now  and  great observation  and great discussion points.

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