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I like to start as promised this  thread  to  discuss or debate somewhat deeper than just to show how we  can  collect  MOXY/NIRS  data's  and what we  can  read out  or may be able to read out.

There  are  some  very specific    point  who motivate me to take this  intriguing  topic  on here.
 As  most regular readers  know  by now, that I am not  able to make cook book  or  recommendation as a  general recommendation, as I  do not believe we are abele to get this  right. The problem  we  create is, that  many out there  see, that NIRS  could be a great additional tool  to make  some differences  form what we  do  , taking %  of  something )  and  replace it  with  some more individual  feedbacks.
 What  they all ask us  in many discussions  and e mails is a very simple  to understand  concept.
 We  than  try to deliver  that  and show a  "  zoning " idea  including   where we see the  potential current  assessed  limiter  and or compensator.
 Now the problems  start on  two  fronts.
 a)  the coaches  are than not happy as they like to k now  more into details  where  and how we  find this limiters  and compensators.
 So  they  do not like the  approach  we all accept  with  an y critic  the  %  cookbook  we all sue    whether we  believe in VO2  max  LT  or  FTP  or what ever. We  get the result than we  take a  calculator  and  get the zoning  without  any  critical  discussion  or  questions. Now when we  offer the same approach we immediatly get  the accepted  and  well taken  critical question, that  they like to know  how we  made this  conclusion.
 ??? double standard  ?>???
 Than  as soon  we   offer or  try  to show  how the different physiological system  may interact  we have the problem , that  many  of  the current believes  are getting  a  critical  review  and  that's  where we often than get stuck.

 So I hope on here to  get  people interested in  some  intriguing ideas  and    we try to back them up  as  good as we  can to  engage in a debate here and come back  with questions but  we may not  always  have the answers.
  So here  3   motivator  to start this thread.
  1. Sandy  and Rachel  foremost  as they give me  the  chance to use outside information to show  weakness and strength  of  NIRS  assessment  combine d with as much other ideas we  can get  and or afford.

2. Ruud.  with this  section here.


I know that these things are scattered around the forum and if you look closely you will see there often is this kind of structure. But given my own experience (almost a year now) it is sometimes hard to find that structure. Not a critic, but just to help.

and  by 


Based on the information, you posted, thinking out loud I think the answers are:

  • If you wanted to get more O2 from the lungs to blood, in effect you want the disscurve to shift left, which increases O2 affinity/stickiness. One way to do this would be to reduce C02 which (in theory) can be achieved by breathing intensely (i.e. opposite of holding your breath)
  • If you wanted to get more O2 from the blood to the cell, in effect you want the disscurve to shift right, which reduces O2 affinity/stickiness. One way to this would be to increase CO2 which (in theory) can be achieved by holding breath for longer

Unfortunately don’t have Moxy yet, to try the experiments above. Again, if the answers above are correct, then I am confused about the case of top endurance athlete (and for which Rachel's picture is similar according to her) where SmO2 values are persistently high implying that transfer of O2 from lungs to blood is good, but transfer from blood to muscle cells not as good (as this would imply CO2 too low, not CO2 too high). 

and this section here

Can you or Jeurg ( or anybody else) elaborate on some further ideas on the types of training and tools that you would use in instances of other limiters. The intention is not to create a "cook book" as Jeurg would state it but i am trying to understand some practical examples of how one might say train cardiac system without stressing respiratory or muscles. Or train, muscle strength without stressing other systems. Or more generally train utilisation without stressing delivery, or train delivery without stressing utilisation?

 So the next thread  I  try to start to get  directly into this point using Rachel's  assessment information.


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Posts: 1,501
Rachel's  overall  assessment   first.

smo2  hr  all.jpg 
In the first  overview  or  first glance  when looking at this  data.
- 50 +-  %  resting SmO 2 with  an incredible fast increase to a very high level  and than minimal change  even  at the end where Rachel  for sure worked  hard   perhaps  even very hard.  and  we have some confirmation based on her  HR  at the last stages.
Just or  fun  short   feedback on HR   at  480  time  marker we have  an interesting    step  and perhaps starts  where Sandy decided to make a different step as it may otherwise go  far to long  to get her  to the end  of the assessment. ?
- SmO2 trend in a first  spontaneous    thought.

 a)  This looks   like we often see, when we  have a  non or minimal involved  muscle  included in the assessment. So  great  delivery  and no  real  demand of  O2  and  only  depending on systemic  limitation we  will see a  change towards  the end  with a  drop in tHb  and SmO2. This we still have to look  at.
 Now   vastus  lateralis  in  ultra long distance runners are very efficient in striding and have a very small activation  on  vastus lateralis and even less, if they are heel striker.Mount a MOXY  at  gluteaus  maximus  and  see  whether this is a  runner with more work  from hip  rather than  from a  load in knee extension and very  minimal eccentric  quadriceps  activity. 
b) incredible  good  delivery  so  great   cardiac  out put  and good  respiration
c)  not  great  feedback  due to positioning  and so on.
 But  for  this we simply  add the needed  thB  anyway.
  So below  a closer look  at  SmO2  and tHb  of the full assessment length

 The thB  shows  a very nice   great  trend  where we see  1 min stops  and new  starts  to the loads. So good data collection  and what we see is real
close  thb  and smo2  all.jpg  Now here   the first  feedback needed to see how we look at this info.
tHb trend. ( not absolute numbers  or not a specify  value  just trend. 
  Question :  
What reactions or  activities s will influence tHb.
 I try her  to start with the first few basic  reactions we may see   to keep it on a level we all can use  as coaches  and athletes. I may  miss some  but that is okay  and   question will come up. 

1. Start or resting tHb in the one minute  calibration  time  is  an indication of the current blood flow  or blood volume in the   area  where we fixed a MOXY
Main reason  why  tHb increases in a   start phase is :  vasodilatation effect  due to alarm phase.
- Increased  blood flow due to increase in cardiac output. So both will indicate  an increase in blood flow.  and a third one  is  an increase in capillary  blood flow ( will be a  hard discussion later )
 Against  an increase in tHB  or blood flow is the mechanical  compression  due to a  muscle contraction.
Now  mechanical  reactions are  now  . systemic  reactions often have  lag  time.
 So  look  at the start  ' tHb  drop  due to mechanical  overrule of the current  blood flow. Now in her case we  can  nicely follow this. every time she stops  and start. / mechanical compression , followed  by  a  decompression  and increase in tHb  due to  a great  or  good  blood flow  caused  by the cardiac output  and  any additional vasodilatation effect.
Now this  in these graph  for sure till about  420  . Than we  have some questions  for a  close look , whether the  small dip in tHb  before stop is a  occlusion  outflow  or a  reaction due to jumping of the treadmill.We  will get to that later.
 Y Think  already  how we  would separate  a  jump  reaction versus  an occlusion outflow ? What we see as well  is that at rest tHb  goes steady  up and up till to the last  2 steps  where we have during the load  a  drop in thB  as well no additional increase in tHb  at rest. Indication. CO  and vasodilatation  in the load  are now overruled   form forces  who   do not allow  anymore  as good of a blood flow. In simple  ideas  2  option.
 1  mechanical  so immediate  to see when we  go closer  or systemic  as a vasoconstriction due to different reactions. This  are the  tow simple  basic  ideas you look .
1  immediate  so mechanical  most often, versus delayed  so system  reason.  So let's make a  short stop here to digest this   but   not before  we look one  real good point

Unfortunately don’t have Moxy yet, to try the experiments above. Again, if the answers above are correct, then I am confused about the case of top endurance athlete (and for which Rachel's picture is similar according to her) where SmO2 values are persistently high implying that transfer of O2 from lungs to blood is good, but transfer from blood to muscle cells not as good (as this would imply CO2 too low, not CO2 too high). 

The  interesting  and great  section of this is
  where SmO2 values are persistently high implying that transfer of O2 from lungs to blood is good, but transfer from blood to muscle cells not as good

First part is  absolutely  understandable. We have a great  cardiac output  as well   in the   most section of the assessment a  good respiratory  action so great loading    fro lungs  to the blood . Indications  would be as well a  simple  SpO2  sensor..
If   Ryinc  and Rachel sent me on my email their  home addresses I will sent you a free SpO2  sensor  a thank you for  your   open debate here.

So far so good great delivery  till perhaps  some slight  problems  toward the last to  loads.

 but transfer from blood to muscle cells not as good

Well we do not know that based on what we see.
 What we k now is that she is running  so   it seems she uses  nicely  O2  form blood to cell  but she  simply delivers  much more than  she needs or  at least till to the last  2  loads  so we  do not get a situation, where she needs  to use a  great utilization   because  there is less  supply  than what she needs.  Let's  try in different words.
 Delivery means  we deliver blood  to the needed area  and hopefully this blood is saturated  with O2. There are different reason why this  may be not optimal  and one of the more common once in sport is  the not optimal loading of  IO2  from the lungs to the blood  due  to the O2  disscurve. The first place to see this is the SpO2  sensors.  Now  we may or may not see a  reaction in the  mussel.  If the O2  we  nevertheless  still delivery is  more or  balance d at what we need  for the current activity , than SmO2  will not react.
 If  we  have an activity who needs a certain amount  of O2  and due to   either natural  or manipulation of the O2  disscurve we  can not load  as much we  will see  d drop in SmO2. So utilization kick  in  which is now   more than delivery.
 If  utilization I less  than delivery  we have always a high SmO2   but that does not mean  we do not utilize  we just  can not see it as  easy. Now  in some sports like perhaps ultra long  distance  running  we  hope to see the  drop in SmO2  very very late in the assessment as  we  hoe  we have  as much a possible a  great delivery to  always keep utilization happy. A  drop indicates  that the " end " is coming a you   use more  O2  than you can delivery  and that is not what you aim  for in endurance  sport > ( exceptions   )  for all cyclists. In  many  for sure  very high performance sport the   tactic  is  taking over. Remember M  Farahs'  5000 m  run. Here we need  as  goo as  delivery as possible  so  he  has  always  more O2  than  he needs  and  at the end  we need  an optimal utilization. meaning he  can accept the feeling of a  steady dropping SmO2  to very low levels. Same in cycling, where we  may need  to close  a gap  or stay  in the group  at the end of  a hill otherwise the draft is gone. So in this cases you would like to see a long increase in  high SmO2  but as well at t the end the ability to dig in and use  as much O2  as possible  Utilization. On the other side  in ice hockey we know we  will create a delivery problem  so we need the ability to  deoxygenate utilize  as  fast as  accepted  but as well need the ability  to reload  as fats as possible,  So in Rachel's  case  we  have a great delivery  and  by the end  speed in here  assessment we  start to drop out of balance  with  delivery  and go  towards  a g higher use  than delivery.
 I sit good that she  can not  utilize  very low. Yes  and now. If  she is  on a level  where mainly finishing the distance is the goal  and improving her personal  best , than we  not really have to see a very low  desaturation ability  as this would give a  few  seconds or min  at the end  versus  many minutes  when we  work on increasing the  balanced  SmO22  situation. When is it  more important? If in her races  there is a some tactical games to stay or split a group  or  in an end  sprint.

 So  what we look is  in an assessment, what  creates really this  shift  form  okay  O2  delivery and utilization to a  change of  a higher rO2  use than delivery.  Summary.
This is really what we  did  all along over  all this years. Looking  for this magic  Threshold  , where  O2  delivery and  O2  utilization is  just balanced  and where it  moves  towards  more O2  use ( Anaerobic )  and therefor there is a time limit  how long we  are able to do this. Now that  section  when we reach  higher use than delivery  is the section, where a  better    working utilization allows  you  to use more  and therefore longer  O22  so you may win the end sprint  as you need O2  for  sufficient ATP  maintenance  and energy  supply .  So next up will be exactly that can we find  with the data we have the reason why Rachel got out of  O2  supply  an demand balance  and what  physiological system or reason created this. That would be  at least on the day of her assessment the limiter  and perhaps we  can find out  how she  tried  to  compensate  for the last few  load  s  and with what system  could she do that. This  would be the compensator.  So    please jump in , where  I lost you or may have not a good explanation.


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Posts: 168

Juerg, quick question. Since the O2 drop follows the decreasing tHb trend, how can I, and others, determine situations like at end of Rachel's 5/1/5 are ACTUALLY increasing O2 utilization and NOT more or less another sign of decreased supply ? 



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Posts: 1,501
Fred , well not  surprising  for me  that this great question comes  from your side .
 It is in fact  a  question to ask.
 If  we look  SmO2  as  an indication of  either  : 
a) oversupply  or less demand than supply , than we have   normally an increase in SmO2. like we  can assume  a the start.
b)  if we  have a balanced   supply  and demand  we  can  see  a  flat SmO2  on all different levels  so  with a  value  of  85 +-  but as well with a value  of perhaps  30 +-. Similar  to  lactate user    and MAXLASS    where we  can have a stable  lactate by  2.4  or  by  6.2  and so in. It is the situation, where we  do not know  how much we produce and how  much  we  reuse there  as well.  So in SmO2  trends  we  may  go   very hard  and  have a  delayed  delivery  so  SmO2  drops  down  and than we may just  get into a balanced  supply  and demand    so we  may stay on that relative low  value.
c)  we  use more  or demand more than we  can supply O2  drops.

So  the question    Fred has :
increasing O2 utilization and NOT more or less another sign of decreased supply ? .

We  may assume that when we go harder  we may  ask  foo a higher utilization in a  step test  as we increase the demand to maintain ATP levels. So  we  can  relative  safely assume  the utilization may increase.
 BUT not always   because we  may in fact have a local limitation  and we may shift  to other not  assessed  muscle groups  to maintain or increase performance. So in this case  we   do not increase demand  but  may try to hang on  what we  have  so same  utilization  and  often same performance or  muscle contraction so  SmO2  will get flat. If we  have a reduction in motor units and push the same we often see in this muscle a occlusion trend.

 But we in fact  can have  an increase in utilization  but as well a  decrease in supply.
 Example  SV  drop,  example increase n  muscle  higher compression  so less  flow  which leads  than to  decrease in SV  as a feedback.
  Now if the contraction is  really very high w e may actually  start an occlusion trend  so tHb  will go up  and we see the feedback  when we  release  ( occlusion outflow ). if  we increase  but only compression  so we   will reduce  back flow   and therefor SV  we see that as well when we stop  as  cardiac output is a   systemic  reaction  so we  have a decompression  which will  in the rest increase  tHb  but we  have a delayed   SV reaction whci9h means the tHb in the rest will not  peak up  to  the  levels before. In Rachel's  case  we  have this in the last 2  rest  look how  tHb always over shuts the previous  rest tHb  level in the last  2  last one  we miss  due   to  stop of data collection w have a trend of a maximal tHb . The above can be one reason   and or we reach a  capillary  maximal  ability of blood flow or volume.
  Now  decrease in supply  could as well be  due to a respiratory   limitation   as we may change  to a  much higher RF  but  ass we have a limitation in VE  we  may  reduce  therefore TV. So we have a much higher %  of  dead space  air  we move  and we will create a hypercapnic situation. Now  again this would be a  systemic  reaction  so delay  at the moment we stop.
 The reaction to expect . SmO22 drops  despite  the fact  that we stop the O2  disscurve still  for  awhile on the right side so  take O2  but hard  to  load in THb  no  muscle contraction and this  is  supported  by  high CO2  vasodilatation so fats  and  overshoot  of tHb  at the rest stage.

Now this  sounds all great in theory  but  can MOXY / NIRS really back this up.
 That's  where we used  physio flow ( check  CO  reactions, SEMG  check  recruitment   trend, Check lactate  ( not sure  why anymore )  but we thought we need lactate as a feedback .so lots  of  poking  with minimal  information. Cheeked  VO2  reactions including  CO2 and than   compared the  reactions of  all the above with NIRS trends  and NIRS trend in different  depth  when we use  Portamon and MOXY
Now many feed backs will show up in the extremity as we  can afford O2  reduction  easy in this area  and far before we  get into  O2 sully  problems in vital systems. Even nicer is  to follow this idea in  non-involved muscles.  So you see   what we have to  do . We have to  check the last  few  steps  and see, what may change  at the 1 min rest  and reload   level. Now  it is  your   task  to  tell yourself  or  discuss  on here what you see.
   So below  the   last  levels and you see the time markers  so the last  4  steps  or  lauds. first  3  and  4  last.
last  3  and  4 dieetc  chnage.jpg 
So  what do you see in reactions  ?

 Now   the next  picture  is the  next  tow  loads  last loads  at the 1 min rest and reload situation  second last step  reaction

second last  step  delay  thb  smo2.jpg 
And below  last step reaction
last  step  delay  thb  smo2.jpg 
  Now  allow  me  one  simple question  to all Wattage user  and Lactate threshold   defender  and VO2  max  calculator.
 I used  all of this ideas ,but please tell me  where and how  you found  anything even  remotely close to what we  can  see  with NIRS. Than compare the price  you pay  for   any of the equipment  we  all used  and  what  did you really physiologically  achieved in the direction of   individual   findings  in your client.
. For  me it is fascinating  after  all this years  to get involved in debates  with   all this  classical  ideas  and even more fascinating is the  level  of  aggression  I often    get  when debating this issues  now. Most interesting is  than the next  step. The step , where  people see the potential value  they can ad to their  assessment ideas. ( BUT than they find a LIMITER like    for ample  respiration or    right cardiac  ventricular    limitation. So  they suddenly  actually have the  reason of  stagnation or    loss of performance  but now .  How  to train that    now as we  know the limitation. In the pats no  problem with that  you open your cookbook  you take your calculator  and you load  by xt  %  and the discussion is over. If  you progress  you   are happy but if  not ???
 So the question is   why do we have this discussion and why  do we not  embrasse this potential and   work on it. What it needs is  some time commitment to  get into the thought  process  and  as many regular readers proof  to me it is possible . Look at  great feedbacks  form Daniele  and many mails  I am getting daily. True it is  far  from perfect  but it  may be a step in a new  direction in individual  quality  coaching. Chef  versus  franchise  all over again.  Fred  an  all  thanks  for   giving me a  chance to think loud  here.


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Posts: 15
I'm loving this feedback.  I keep rereading and trying to extract as much as I can.  And Sandy is doing a fabulous job helping to explain it to me as well.  Thanks for sharing all this Juerg.  It's very fascinating.  I gave my moxy to Sandy today so she could grab the data for me so as soon as she can or as soon as she sends it to me I'll post the file from my Co2 run.


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Posts: 1,501
That  sounds  nice  and  if  Sandy  can sent the csv  files  than I  can take some of the work of  from her  and we  can look at here together. Hope to be back later today  an show  some close ideas on the  last few  pictures   form you  with the  indication  of what that all means.
  Sounds  fun  and crazy when we  talk  about a  CO2  run  does it.
 Different way how define   training goals and    specificity. We  can run a with a  fixed  HR  or a  fixed performance  but  do we know  what we  may trigger , of we  can make  as you shows  easy  and nicely  a  specific  idea  and target  and than  go back and see, whether it triggers a change  and if  yes is it the change  we  have planned  for   or not. In any case, if we  know  what we  stimulated  and  how we   stimulated  the  idea  , than we  know  that the  result  I  form this no matter  whether it is  what we were  hoping  for or  not  but w e have an outcome  feedback   in physiological reactions. If it improves  performance that is great  if it is a step we have to  do  to built upon  this  and  we have no performance improvement  yet that is great as well as we may have  expected it. One of the most intriguing  reactions in that direction is the needed increase in vascularisation  before we  can se an increase in  mitochondria density.  So   we ma have to accept  a  non increase in performance as we may need first  a proper structural  change  to build upon this. Therefor n panic  when we see  we increase capillarisation  and it is  now a  question o time  before we  see performance improvement.

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Posts: 65
Rachel CO2 run 090115.PNG 
Here is the graph of Rachel's CO2 run, Juerg I have sent the file to you through email.  Rachel warmed up completely which is not hard as it has been 37 degrees and almost 100% humidity here.  She then ran all out holding her breath for as long as she could.  The goal was then to recover to the same blood flow (tHb) as reaching pre-interval SmO2 is never a problem.  Rachel discontinued intervals (after 3) when breathing became hard to regulate.  The dip in blood flow you see after the 3rd interval is her climbing a bridge.

During Rachel's assessment the following happened:
-she jumped off the treadmill to grab a water bottle
-I put the SpO2 monitor on her at interval 3 (it was 95), interval 4 (it was 89) and then at interval 5 where it read 95 again. (?? assuming this has to do with her compensator)
-Rachel is a light heel striker however she has VERY little quad involvement when running which we have been working to change.


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Posts: 15
Did some experimenting with my moxy on my run today.  I normally wear it on my quad but Juerg suggested (which Sandy already confirmed) that I don't run with my quads and perhaps a different placement might show other info.  I started with it on my glutes (glute med) for the first half of my run and didn't see much difference than when I wear it on my quad.  For the second half of my run Sandy suggested we try my hamstring, and volia I finally saw desaturation and it came with not too much effort.  Sandy will post and send the csv files to Juerg sometime today.

Another intriguing thing happened through discussing the fact that I am clearly using my hamstrings.  I have very, very tight calves ALL.THE.TIME and Sandy said that its probably the result of running with my hamstrings and it following through down the line.  My hamstrings never bother me but she was showing me a hamstring specific stretch.  When I tried the stretch I apparently created an occlusion and quickly desaturated from 89 to 77 and my blood flow decreased.  

So, what does this all mean.... thoughts?

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Posts: 349

First Jeurg, thanks for following up on this case study. Rachel (and Sandy) thanks for sharing the data and permission to discuss it.

You asked a number of questions that i would like to try have a go at answering - remember no/limited experience in assessment so might be completely wrong!

Think  already  how we  would separate  a  jump  reaction versus  an occlusion outflow ?

I would expect that in an occlusion outflow, bloodflow would slowly increase (due to pooling), At the same time, Smo2 would most likely start decreasing as a trend because deoxygenated blood is not escaping. Then at the point where load is removed - blood flow would suddenly increase due to occlusion being released and because deoxygenated blood is now released, Sm02 would increase reasonably quickly.

On a jump reaction. I would expect that there might be a more sudden blood flow impact. Due to immediate muscle compression, blood flow would probably fall and then as muscle decompresses it would rise again. Similarly Sm02 would probably drop at the point of jump, but then rise quickly again as utilisation falls away.

Now Rachel's case
In relation to the last few loads that you put up
Comparing the 3rd/4th last loads vs the last loads, the key differences to me seem to be:
1. tHb decreasing in the last loads, but not in the loads before. 
2. In the last loads, on rest tHb increases immediately, but there is a lag to Sm02 recovery - it actually continues to fall slightly after the load is removed.

Now on number 1 above (thb decreasing in last loads) 
As you explained, there seem to be two possibilities - either an immediate mechanical reaction or a slower systemic type of reaction. To me in this instance it does not look immediate, it looks like a trend - so it seems to be a systemic reaction?

On number 2 (lag Smo2 recovery)
- First we know load has been removed. 
- It is possible that Smo2 keeps falling because muscle has not relaxed and therefore utilisation does not fall away completely. However, to me this seems unlikely given that we know thb does increase immediately.
- So what other options, for Sm02 slow recovery
-Reduced cardiac output - does not seem likely given that tHb increases immediately when load removed.
- So that leads to the respiratory problem possibility that Rachel/Sandy Jeurg highlighted? Would the correct interpretation be here that Rachel's diss curve has shifted to the right because CO2 too high so more difficult to transfer 02 into blood, and takes some time after load removed to recover? (also noting that the last graph Sandy posted also seems to show a fall in Sm02 and slow recovery when holding breath = CO2 increase). 

Interested to hear, if this is completely incorrect?


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Posts: 15
Ref my last reply (#8).  

I was watching the new "intro to muscle oxygen monitoring" videos last night and there was one part where Jeurg discusses muscle contraction and creating an occlusion but in the context of strength training.  

My question is are you creating that same contraction when doing a stretch (it wasn't an extreme hamstring stretch, I felt it but it wasn't painful) and why would this happen?  

I have been having what probably is compression syndrome issues with my calves where my feet get tingly/go numb after running for awhile.  My calves are super tight and I am having lots of trouble getting them to release.  Can I use the Moxy to help and figure out what is happening in this situation?

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Great   info  Rachel.
 1. I will explain in short here the  tHb reaction in connection  with  compression.

1a)  compression due to outside influence.
 Occlusion workouts    is  the most extreme  option  where we  can create a  arterial occlusion IN this case tHb  doe snot react  as w have no inflow  and no outflow but just  what is in the occluded area.. Ope  who choose this strength training idea  would benefit  from using  MOXY as in many cases we sse  muscle  actual be damaged  due to a too long  occlusion time.

Now different   situation  for  occlusion trends.
 . or better blood flow restriction. I will   later show this step by step in  your  assessment  so it may be even easier to understand it there.
 As well as we  will use in your case tHb as a guide  as well for your   live  workouts.  Now here in very simple wording.
  You have a  blood vessel  or  blood vessels. You have to  type  of   vessels Arterial  or venous  flow.
 In stupid simple terms  the arterial vessels  have a higher  quality  and are very elastic  and therefor you need more pressure before you inlfcunce the lumen in this pipes. The venous  vessels are  less  quality in the way of elasticity  and therefore  less pressure needed  to  start restriction flow there. ( That's  why you have   an upper  and lower  Blood pressure  to read  out.  so   you  start  muscle contraction you create  pressure  form outside   and tHB will drop. The reaction often is a CO increase and if the pressure  from you heart is  higher than the compression tHB  will go back up again.
 You push harder  so  CO  can not overrule the compression  and tHB  will  keep dropping. If  the pressure exceeds a  certain  mmHG  you start to reduce  the outflow  (veneous occlusion trend  and more  blood comes in than can go out  and tHB goes up  occlusion pooling. The  most  pooling is when  venoeus system is  completely compressed.  If you keep increasing pressure you start  to reach an arterial c occlusion and tHB  stops  going up.
 If you release a bit  you have again inflow  and no outflow  so tHb goes up. If  you increase  alot  than you have  again an outflow  and THb  will actually drop as  an occlusion outflow  reaction.

 Now think what happens if you do a certain  type of stretching and what is the result of it?
 Will be back on these interesting conflicting habits  later. Stretching to the limit or the limit of stretching in sport. A  long lasting an ongoing disucssion based often on myth than actual facts.

Development Team Member
Posts: 65
Here is Rachel's Saturday run.
Rachel Run 090515.PNG 
Closer look at the second half of run where we placed it on the hamstring.
Rachel Hamstring only 090515.PNG 
Followed on Sunday with a short hamstring run (easy pace) and a leisurely group bike ride broken n two parts.
Rachel Wagner Run bike bike 090615.PNG   


Development Team Member
Posts: 1,501
Sandy  great work  as usual. Again  can you sent the csv  files  and  we  can go even deeper into the discussion. As  we  can see  short hand  vastus lateralis  is a  minimal involved muscle  but we  can still use this for the limiter  compensator  ideas  but  the  other info here much nicer  for  " zoning"  or what ever we like to call it. Greta great work  and I will dig in to  get  Rachel ideas together with you into a  deeper discussion. Cheers Juerg

Development Team Member
Posts: 34
Hi Jeurg,

I know this is not a physiology class, but I am trying to understand something.

You say:
"In stupid simple terms the arterial vessels have a higher quality and are very elastic and therefor you need more pressure before you inlfcunce the lumen in this pipes. The venous vessels are less quality in the way of elasticity and therefore less pressure needed to start restriction flow there. (That's why you have an upper and lower Blood pressure to read out. so you start muscle contraction you create  pressure form outside and tHB will drop. The reaction often is a CO increase and if the pressure from you heart is higher than the compression tHB will go back up again."

What I understand from a bit of reading and from your description:
Arteries are more compliant (more flexible).
Arteries will allow for higher rate of blood flow because they are better able to expand to accomodate increased internal pressure, so under normal conditions they can accommodate higher flow rate.

Veins are less compliant (less flexible).
Veins will not allow for as much blood flow because they do not expand as well (the restriction flow you talk about).


Soft latex tube = Artery.
PVC tube = Vein.

Occlusion occurs when for instance:
External muscle contraction applies pressure to the artery or vein.

What I would expect to see:
Arteries normally allow for higher THb rate of flow because they can expand to allow for higher volume, but are more susceptible to occlusion because they compress more easily.
Veins normally allow for less Thb to flow because they do not expand well, but will be less susceptible to occlusion because they do not compress as quickly.

What I don't understand:
Arteries deform easier to allow blood flow, so why should they not also compress more easily when external (muscular) pressure is applied?
Why are veins not more resistant to EXTERNAL compression/occlusion if they are more "rigid"?


Development Team Member
Posts: 1,501
Here is a nice  to read link and look mainly on the properties  on the  bottom  ( structural  difference ) rather than the functional difference. )

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