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Juerg Feldmann

Fortiori Design LLC
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 #16 
Thanks for this great feedback.
 @ small ideas or thoughts to start.
1. NIRS opens many questions, when using it the way we use it in practical applications.
 . Our goal is to  get a world wide group together as we are well underway to see many interesting situations. Now the next step may be to have a full  IPAHD test done ( we need to change this name, as IPAD  may get into some discussion here  . smile )
 Now interesting would be to see an IPAHD upper body  test and  one on the lower body and assess, what limits  upper body and what limits lower body. Have an athlete with incredible deoxygenation in the upper body and one with no deoxygenation in the upper body and see, what the difference is.
 We have  ( Brian ) identified 2 types of ice hockey player as well and we  like to find out  what caused one or the other way how the  oxy or de-oxygenate . We will show soon this pictures as well as Brina has now an incredible big numbers of ice hockey specific test done. So stay tuned.
  Short announcement.
 We are in the process in Switzerland to  open a center, where we  would collect  all  test information's and data's and have a central software program so people testing  the way we like can sent their data's in and have a very fast and easy way of getting  an overview and overlap from all the  information you goatherd with Physioflow, NIRS, VO2  and more.
 The  betaversion is running and  it has as so often ongoing adjustments in that process but it is here to grow.
 Individual athletes  and centers  can all  come together sent their info in and get a printout with answers  and often answers with more questions.
 This way we can in a very short time collect hundreds of information's including training interventions and  will get much faster a  better picture of what kind of stimuli create what kind of a reaction in what  type of  people.
 Hope this makes sense.
. For groups and people interested in this direction contact me under :
 Factquestions@hotmail.com
 or andrifeldmann@hotmail.com.
 All study group people already have a drop box input options to sent  all their test in as so many do now. Thanks for the great support and we all look forward to have many many MOXY users out there  contributing in real live to our  many questions.
HallvardN

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Posts: 16
 #17 
Hey!
I'm back with some interesting results from the case study with the female skiers unable to desaturate to more than 80-90 % SmO2. We have tried to test different forms of occlusion, breathing and local muscular work. The results has been quite surprising. 

Maximal desaturation lower body:
Normal running/skiing: 75 %
Squats(local muscular work): 73 % 
Squats with 200 mmHg occlusion: 70 % 
Walking with occlusion: 53 %

Maximal desaturation upper body:
Normal skiing/double poling: 80 %
Local muscular endurance work(repeated triceps-press): 20 %
Local muscular endurance work with 200 mmHg occlusion: 10 %

With different breathing interventions where we tried to make her breath fast and slow we have had no noticable results, but we have not tried IHT-like interventions where we drop the O2 sat down to 90%+- yet so could still be some different reactions here.

So here are multiple questions. Why is she unable to desaturate during double poling with normal blood flow and even stranger, why is she unable do desaturate more than 53 % during lower body work with complete arterial occlusion? For the lower body the general trend seems to be that harder muscle work makes the desaturation ability worse and we see a massive Thb increase when she is increasing her stride length or increasing the incline with normal blood flow. 

So the question for us is what to do to stimulate her to use more of the available oxygen? During activity the heart and respiratory system seems to compensate even at very low intensity, like 110-120 heart rate for this athlete with a maximum heart rate of 190. Could this athlete make a relative hypoxia with going even slower, like hiking or similar or is perhaps  training with occlusion an idea for her to make a hypoxic state that she doesn''t reach during normal training, even at very high intensities?

Would be very glad for some input on this case. Happy summer!



Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #18 
Wowww this is great  information. It shows 2 main  points.
 
 1.There is no cookbook approach in sport testing nor in training.
 2. We know very little and once we start digging we know even less.
 So no wonder ideas like 220 - age have many great followers . Or FTP ideas or maximal VO2  and than taking a %   of it to plan training's.
 No questions asked as there are no questions available.
 In short I have to get my head around this incredible info. What I need is :
 The cvs moxy data's.
 The VO2 data's if you have with RF and TV and if possible the EtCO2 values.
  The physio flow info.
 We than can send them to our headquarter in Switzerland ( and see in a simple form , when we overlap the info  on what  changes when.
 The beauty of this info is.
 We have to learn to think an combine  the information  with the different physiological systems.
 When using  only VO2  or only Physio flow or only NIRS we may very easy get to a wrong conclusion.
 When combining we may get some trends and directions.
 True we may get no conclusion but we can start training  her in a very specific way we think may create a reaction and than test and retest as it is easy and fast and pain free, when using MOXY.  Give me some time on this one and   I may have some thoughts an hints but unlikely   the truth or gospel , .
 Just really happy  from all the stuff you guys do and  I hope we can expand on that in the future to learn all together more .
 I am really interested to see the occlusion moxy data's as raw data's. We did some test yesterday where we used Rhomerts idea on  compression due to muscle load to see how that would look like.
 Look at the picture , no comment yet as we work through a set of tests to see, whether it is  in any person or just on this one.
Here just a thought.
 a) occlusion . It is that we bind of  blood flow.
 I try to explain that to my patient this way.
 You have a garden hose and you clamp it off suddenly on one specif point .
 Now you have behind and before the occlusion some reactions.. What  will you see before the   clamp in the water level. What will you see behind the clamp.
 What happens just before you have an arterial occlusion.
 Now if you do nothing with the arm you occlude you have a relative clear picture.
 If you work  with an occlusion you add something I call  compression to it .
 The  place where the moxy sits is as well where the compression takes place.
  Or with the garden hose.
 You use a  3 m long board and you stand on the board, which is on the hose, that is compression and that's' what happens. when you work out. Now you combine a compression with  an occlusion  and we may have to rethink a lot more from the reaction. as  with the occlusion we have a stable tHb but with the compression we may change the tHb again and as such we may move blood  away from the area the moxy may try to measure it. Just a  fast thought but no answer at all. Think about the difference between normal socks with an elastic which really are "occlusion" socks , versus compression socks.
 Think about compression in a big picture on a calf muscle.

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HallvardN

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 #19 
Thank you so much for the info. Here is a printout from an occlusion workout, walking with heavy incline from the female xc athlete. What is interesting is the massive drop in Thb at Vastus Lateralis during occlusion which was set at 200+mmHg during this workout. The occlusion was set high up on the thigh with distance to the Moxy to not interfere with the results. We tried to do the occlusion process fast, but had some good tries and some really bad ones. Still tired in my hand from pumping up these occlusion, think I have to invest in an electrical pump or something :) 

So this opens up some new questions about how this athlete react to restricted blood flow. Where does the blood go? To a different muscle layer, a different muscle or some other solution I haven't thought of? Could the lactate shuttles make some muscles or even muscles layers compensate for others during an hypoxic challenge?  It could perhaps be an idea to put the Moxy on other lower body muscles like Gastrocnemius to see if this is a general trend or if other muscles are stealing the blood and compensating for the weak Vastus Lateralis.  

One more question, that has perhaps been answered on this forum before, but are pretty crucial for this analysis, which muscle depth does the Moxy measure muscle oxygen at? 

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Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #20 

Thanks will look at closer over the weekend, as the curves look very familiar.
One of the first questions we had, when we created the same reactions a few years back was:
Definition of occlusion and more important: Expected reactions in theory on occlusion.
As mentioned in the reply before, it is crucial to forget the picture we have form scientific test, where we create an occlusion without any activity behind the occlusion.
Here the questions.
1. If I create an occlusion than I have two possible occlusions.
a) Always first a venous occlusion followed by , if enough pressure is applied ,an arterial occlusion. See the two classical pictures. See att one of the main problem is the speed of the application of an occlusion.
A normal BP cuff is simply too slow so you will have always some left over as the pressure increases from a Venous occlusion followed by an arterial occlusion.

See 3 tests done by three different groups and only one achieved a proper result. The one from Andri Feldmann (Msc University Bern) in his work. If you look close enough you can see which one it is. Now when studying occlusion, than we look at trend in tHb as indirect information on possible blood flow under certain conditions.
If we create or apply pressure for a venous occlusion than we have still intake in the occluded area over the arterial system on blood so tHb will increase.
If we have zero activity in the tested area we still have a certain amount of O2 use but less O2 use than we get O2 in. So O2Hb will increase as a sign of more intakes, than use of O2.
But we as well will still have a resting muscle activity, using O2 and developing therefor HHb  so HHb will increase .
 Now if we apply more pressure, than we stop not just outflow in the tested area, but as well inflow. So the blood volume and with it the tHb in the tested area will not change anymore.
In case of a rapid arterial occlusion application the tHb will barely change, just simply will stay stable. In case of a too slow application of the occlusion tHb will first increase somewhat and than will stay stable.
In case of an " inactive" occlusion application we simply only have the resting O2 demand of the cells in the occluded area and as such , depending on the O2 demand will see a drop in O2 Hb ( red ) due to O2 needs ) and therefore an increase in HHb due to increase of deoxygenated red blood cells. the discussion here is open on how far we can drop O2Hb. Can it go to zero and if yes what is the risk of it. Does the body defend pO2 and how good an how long and if we would reach pO2 of zero what would happen. ? The other open questions we have is the fact, that we not only have information on haemoglobin loading or deloading of O2, but as well of the myoglobin level. So drop in O2 always can be a drop of O2 on Hb and O2 on Mb..
Now so far this is what we may expect on occlusion under resting conditions.
The situations changes rapidly, if we do the same test and apply an occlusion under different conditions,.
a) Immediately after a heavy workout. What changes is the situation of the applied or produced EPOC. Now we have an occlusion but as well a possible much higher resting O2 demand.
So you will see a very different picture.
Than b) apply an occlusion and at the same time keep the muscle activated like we have in the test above.
Now we have again a new interesting task on hand,
1. An actual occlusion would keep tHb stable?
So what we see is not an occlusion or:
it is an occlusion with a compression.
What does that mean?
As we create an occlusion we stop tHb increase or decrease and it suppose to be stable
. Now under activity we most often will not create an occlusion but a compression. See tHb reactions . on the many IPAHR picture we showed here already..
The initial start of a bike (pedal stroke) always creates a muscular compression in the tested area and therefore we will see a drop in tHb.

 

Now the question could be. – If we push down initially we will see a drop in tHb but on a lower intensity we will see a decompression, where tHb will increase again.

 Now when we make a compression due to a position we may see an increase in tHb due to a short term venous compression??? So what would we expect during a pedal stroke tHb dropping when we push from 12 – 6.00 or tHb increasing when we pull from 6 to 12.00.

 I moved that questions many months back to some cycling experts and the answers I got back from some had many speculations involved but none was actually close to what we actually see, when looking much closer. The rest did not had any opinion, despite writing and giving lot’s of “expert advices “

 The most interesting findings we made here is, that the actual bike fitting situation can exactly reverse the tHb picture due to the change in position. . The question than arrives, what may be the better position physiologically.MOXY / NIRS in fact may change  the way we may fit sport equipment and may increase the idea, that physiological factors may be sometimes  as much important  as physical factors like aerodynamic . Again possible a compromise or a closer look on durations of the activity will make some different decisions out o these ideas.

 Here 2 pics from 2 world class athletes during a IPAHR. Of a cycling 360 degree movement. You can actually see the RPM they had during this load.

 
\ Now depending on the intensity of the pedal stroke we will see a “decompression” phase to adjust ( create a homeostasis of the needed power we have to apply to maintain the wattage load we have put on). This means that in the decompression phase tHb will increase.
This could make or create confusion with the situation that we could argue: tHb increase is a sign of a venous occlusion. Here are some of the tricky and fun parts of the interpretations of the MOXY ( NIRS ) data’s and that's where we work since over 5 years to get a hand on.( and still  working on it)

Now if we go back to the information’s we have and results from our great example from Norway.

a) An actual occlusion will show a stable tHb. So the drop in tHb would be a compression during an occlusion.

 Meaning, that under the moxy (test areas)  due to the activity the muscles created a mechanical compression, reducing therefore the  blood volume  (tHb ).

 Now due to the fact, that in the distal section of the occlusion the tHb (blood volume will stay stable, the question will arise on where the blood volume is pushed to, when the tHb under the MOXY ( test area is reduced  due to the compression of the muscles???

So what we did, once we had teh same open question as we have here a few years back (Have to find the data’s as I often move them somewhere and than forget where.

  I used  for example different sites on the muscle ( Vastus  lateralis , medialis  hamstrings group but as well  gastrocnemius , to see, whether I would have  a decrease in one area tHb drop and an increase in another area tHb  does up during an occlusion.

 The easier way to do it is on your arm. Make an art. occlusion proximal of the short biceps head.

 Than make an activity, where you try to only involve forearm muscles and not biceps or visa versa.

 Have one test unit on biceps and one on the finger flexor muscle groups.

. The result is super interesting.

 Questions.

 This type of test could be named hybrid.

 Why. We have in vitro and in vivo tests.

 Now people thinking in terms of existence of a central governor may easy understand, why one testing idea or scientific approach lacks one main  issue.

 The feedback loop from and to the working muscles, and therefore the influence of the Central governor.

. So here what I did before I started to see, that the central governor or for us the ECGM (extended central governor idea may have some interesting truth. It is exactly what the Norwegian group is doing.

Create an occlusion and than an activity in the occluded area. Here the thoughts and you may find teh answers .

 Hybrid between in vitro and in vivo.

 In the occluded body part  we will still have a metabolic reaction like increase in CO2   decrease in O2   *( o2 Hb change and HHb change, but as well an increase in H + for example).

 The problem or the beauty is, that we have no interference with new blood coming n so the tHb would or will stay stable. The muscle activities may shift blood from one area to the other but in any case O2 will drop ( O2HB will drop ) and HHb will increase.

 The question is, whether the blood moving in and out of the contracted area is changing O2 content and how due to compression and decompression.

 When we look what a compression makes on the venous blood vessels and what may happened in the arteriole than there are many speculations possible.

 The fact remains, that we still have a connection to the CG.

 The problem is, that the change in CO2 for example or in H + for example may give a feedback to the CG to increase respiratory activity.  Now if that happens, the problem is, that the increased activity will not change the situation in the occluded area due to the  problem of occlusion. So we have an in vivo in vitro situation. An area who not reacts to the CG and a CG who reacts to the reactions in this  area.

 Hmmm does that make sense in Swenglish. ???

If   and only if. The CG or ECGM  is working , than we should see an increase in respiratory activity despite the fact, that there is no connection in blood circulation to the occluded area.

 The CG respond (increase in respiration can’t solve or try to compensate in the occluded area as CO2  and with it H +  is not able to be balanced.

. Now the increase locally on CO2  and as well of H + will shift the O2 diss curve and we would expect a further drop in O2 Hb than we often see.

 Why is that not happening.

. On the other side we can take lactate on that side and have by the same load a very different picture.

 The main problem with lactate is, that we cannot occlude long enough to see the actual real lactate value as it still lags behind.

 What we can see is a relative high SmO2 value in many cases as we see in this group.

 The reaction we see is very similar as we have here and it may give us some very interesting answers on the fibre constellation of an athlete.

 Think why.

 Summary.

 The occlusion activity  experiment shows  for us an interesting key to the  idea of the ECGM and hwy  there is a very dangerous  idea to make conclusion  from  in vitro  to in vivo experiments and visa versa as the CG may have  changed result very strongly if the  reactions created by the CG could have made or create an influence on the metabolic reaction in the tested area. 

Last but not least a small brain workout.
 Last pic is a pedal stoke inside view at a load of 300 watt. Think occlusion , compression and blood  volume shift. 
Your ideas now for the weekend.

 

 

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HallvardN

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Posts: 16
 #21 
Thank you for so much for great info here. So interesting stuff with how we can use occlusions to see how the muscles react without having the influence of the central governor with increased blood flow, breathing etc. In all of the testing we have done we have seen that the subjects has the ability to desaturate more with full occlusion than without during heavy or moderate loading. This points heavily to the influence of a central governor to protect central organs during free blood flow or alternatively that the increased muscles oxygenation during maximal free flow is a result of increased blood flow due to other reasons than hypoxia, for example low pH and increased need for H+ transport. 

We have done a little bit more testing during occlusion on this athlete. This time we have done the same protocol with walking on inclined treadmill and the moxy at different muscle groups. The first desaturations you see is from the placement on Vastus Lateralis as before, the second last one is from hamstring placement and the last is a Gastrocnemius measurment. This results are really interesting.

The Vastus Lateralis has a trend of dropping Thb and general high Smo2.
The Hamstring muscle has a trend of increasing Thb and relatively low Smo2.
The Gastrocnemius has a initial rise and drop in Thb and a pretty low Smo2.

Okay, I start the guess time here:
To me this looks like a situation where the most active muscle groups are shuttling the blood to less active muscle groups during restricted blood flow in this athlete. From a couple of other athletes we have tested this(just with the standard Vastus Lateralis placement) the trend is more like what we see during a resting arterial occlusion with flat Thb. This athlete seems to for some reason make the more inactive muscles compensate during occlusion, perhaps with letting the main muscles work oxygen independent and the less active muscles work more oxygen dependent. This could possibly explain how this athlete can compete at a pretty high level despite a terrible ability to desaturate in the main muscles. 

So what are the training ideas we have by now?
Very low intensity training at a level where the other muscles groups or the central organs compensate at a minimum level.
Training with occlusion to force the main muscles to desaturate. 
Another crazy possibility is to do some kind of approach where you fatigue some of the compensating muscle groups, to force the main muscles to do the work, even in a situation with restricted blood flow, from occlusion or some form of metaboreflex. 

Think we have a better idea about her reactions now, so the question now is how to go from here. The training ideas are starting to get pretty messy now, but that's what is most fun :)

Cheers!


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Juerg Feldmann

Fortiori Design LLC
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 #22 
This is great and confirms what I did  since a while  , just  I thought I am crazy with this infos and results.
 Here a question to help me out.
 Can you indicate +- numbers, where you changed  to what as you can see 5 drops of SmO2 in the  picture.
 Here perhaps so we can see very fast in the future on what we talk about.
 Color code suggestion.
  Red for O2Hb
 Blue for HHb
 Green for SmO2
  Brown ( we had yellow but bad on white background )  for tHb
 and purple  for people using HbDiff from other equipment which measures TSI % to compare..
 Or any other color suggestion is accepted. Just time with so many more people  starting to use MOXY , that we have an international code so we  will  learn to see very fast how and what is going on..
 There  is  really an interesting connection between  readings  under occlusion and   without occlusion. And the  trends  seem to look towards a very crucial integration of the CG , when  we assess not just  one bio marker like VO2  or Lactate or SmO2 but for sure when looking at different reactions from the different systems.
 We did a s series of one leg squatting. Reason . 2 legs   so we have 2 test  with one person and can compare basically like we would have twins.
 There seems to be  a very interesting connection between for example respiration reaction under occlusion  and without occlusion. but we need many more test as we only have about  16 samples so we will be back here once we have about 100 test done to be sure we have a trend or we have no trend at all just individual reactions.
HallvardN

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Posts: 16
 #23 
Sorry for the confusion with colors. Will use the standardized ones next time. Here is a picture with some clarification. The picture is from the same session with 5 walks with 200 mmHg occlusion to fatigue. The three first one is done with Vastus Lateralis placement, one with hamstring placement and the last one with Gastrocnemius placement. This is marked at the picture. 

Hope this make sense!

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Juerg Feldmann

Fortiori Design LLC
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 #24 

First no sorry needed you guys  do an incredible job.  In fact changing color  will make  us think more on what we look at   but  for  regular readers it may make reading easier if you are not used to the trends .
 So here my questions back.
 a) If I understand properly  all 5 sets  ( 3 x  vastus lateralis   walk followed by hamstrings  walk and  cal walk where done at the situation, where you had  an occlusion somewhere ( where ) on the leg.
 If yes.
  question one.
  An occlusion as discussed would show no  change in tHb  from the beginning to the end.
 What we see here is  in all  three  muscle groups changes in tHb.
 Assuming we had a good occlusion than we have  to  think , that the tHb ( bloodvolume  change has to be done by shifting blood from one area to another area.
 due to compression in one area  and a possible decompression in an other area.
  This could be logically done by antagonistic muscle activities.

 What your great  cases show is, that when using  NIRS under occlusion we still have a change during activity in tHb due to compression.
 Now here a closer view on the three cases.
 look at trends in tHb () brown ) and SmO2 green.
 Question 2. Take  a look at the lateralis trend. See that SmO2 is basically the same but with a very different tHb reaction.
 Question 3. Black full line versus doted black line.
 Can you tell me, where  you stop the  activity . Will explain later  why.
, as the increase in SmO2  and tHb can have 2  options on why.
. Can you figure out what I mean.
 Last but not least.
 IN 1 week we will set up a discussion group and board with  MOXY users  hopefully   with you guys on board, where we internally start to discuss options for trainings and how we  go about  the changes due to training.  
 So here the three closer looks  plus the  picture with the question. This question on where you stopped will be interesting for all three muscle groups as well the new model you guys will soon get will have a marker options so we have it much easier to look at the trends and reactions.  

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Juerg Feldmann

Fortiori Design LLC
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 #25 
We try to get some more  experiments in  the next few days . We run for the moment a whole set of tests daily and will go through the data's and show it on here.
 Here a small hint. Look at the vastus lateralis tHb reaction.
 So the question is here, what and why does tHb change, when we have an occlusion proximal of the tested area. ?
 Take a direction  of the difference between occlusion and compression. We did some isometric compression tests and will show you the  sometimes surprising results.
 As well we have no  reviewed over 100 of tests and seem to have 2 very distinct  type of reactions of athletes  in an IPAHR.
 Will show you the picture , as this will be one of the first steps to see, why do we have this difference and what is the strength and the weakness of this athletes with this so different reactions.
 Than we look at real sport performance and  what they did to create this incredible different reaction. Once we  have some answers here we may be able to work on the  training ideas and see, whether we can change the athlete by  maintaining the strength and work on what we may consider weakness.  The launching of the MOXY  next month will give us a  much bigger opportunity to have keen MOXY users involved in this developments.
HallvardN

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 #26 
Okay, thank you so much for feedback. I have been gone for a little while, running a training camp for kids in the norwegian mountains, but is back online. Check out video, norwegian kids are crazy. Smile



Back to the case. I have made double lines and between these there are occlusion. I was a little bit to quick last time as I see the blood volume trend was a little bit different than I wrote down. To clarify: 

The test is done with occlusions 200-250 mmHg high up on the thighs. It consists of 5 occlusion walking intervals to voluntary fatigue. The red lines marks where we have moved the Moxy to different muscle groups. 

From what I see now the theory about less active muscles compensate for Vastus Lateralis is perhaps not to good as I see now that for example the hamstring has a flat and not increasing blood volume trend during occlusion so I keep on trying a new one(I'm interested to hear Juergs response to this). Could it be that the mechanical compression due to muscle contraction forces the blood away from the measured layer in the working muscles during walking with compression? What if the muscle needs a higher blood pressure to counteract the effect of the mechanical compression and when we block this possibility we see a decreasing Thb in the working muscle? Would be nice if Roger could give us a little bit of information about the Moxy measuring depth to make my guessing a tiny bit more accurate


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Roger

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 #27 
Hi Hallvard,

On the Moxy measuring depth issue...  The Moxy algorithm assumes that the tissue is made of of layers of epidermis, dermis, fat, and muscle. It's designed to have maximum sensitivity to the muscle layer and minimal sensitivity to the skin and fat layers. This works well up to about 12 mm of skin and fat. Beyond that, the sensitivity to the muscle layer is reduced so the readings are going to be more affected by the shallower layers.
Juerg Feldmann

Fortiori Design LLC
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 #28 
Hallvard, can you sent me the cvs file as I like to do some additional closer looks to  see the interesting trend.
 There are some question.
 Under occlusion we have  no change in blood volume anymore ( theoretically  but that's when we make a test where we create an occlusion and do not work active ( or real active)  in case like yours we add as mentioned before a additional question.
Stable blood volume in the leg but possible change in volume due to compression. Now under compression we can first see an outflow of tHb , followed by a decompression or, and that's where it is interesting  a reach of a compression pressure, which creates a venous occlusion level and therefor we may see an increase in tHb due to that. This than from the trend looks similar like a decompression situation but when we look closer at the  O2Hb trend and HHb trend we  have some more clues.
 The interesting part is to look at the reaction of the cardiac system and the respiratory system
The really interesting part is, that we "cut" of  the circulatory  system from the rest of the body but we  may still have feedbacks from CO2 / H + and other metabolic accumulations. Now fun is to see, whether the central governor still creates an accordingly reaction  due to the stimuli , withy the  problem ,m that the actions may not help to solve the problem.
 Example H + and CO2 accumulation  - increase of RF to try to balance CO2 ( pH )  but as there is no escapee of the metabolites it  does not help . In fact we have to look ,whether it actually may increase the stimuli to try to get a reaction . So many more questions here and  we will have lot's of fun , once the MOXY is circulating worldwide to  people like we have here on the forum.
 This is the strange question I have  . Hallvard create a study , where we may have an  in vivo and a kind of in Vitro reaction at the same time.?????
HallvardN

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 #29 
Interesting! Here is a new picture and csv file of the same case study done another time and a little bit better to make it a little bit easier to read. Same format: occlusions 220 mmHg+ on the upper thigh and the Moxy at three different placements during walking with incline. 

Perhaps we could try to put on the Physioflow and Bioharness and look at what is happening at respiratory/cardiac level as there might be a central action involved. We will look into it!

Attached Images
Click image for larger version - Name: Screen_Shot_2013-08-13_at_3.31.16_PM.png, Views: 23, Size: 107.76 KB 

 
Attached Files
csv Britz_perfectocclusion.csv (7.15 KB, 17 views)

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