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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
I have for the moment a university student  ( Human kinetic) here for some work experience. We did  many hours of  MOXY and other physiological assessment.We may show more of his work on here as we go along. ) Nick McLean )
 Today's task was.
 Does a change in respiration by the same or more or less the same cardiac load (  stable HR) may change the trend in SmO2 and tHb.
 The  hypothesis was:
 A change from hypercapnic breathing to hypocapnic breathing may change  SmO2  as well as tHb.
  We know that hypo or hypercapnia can change vascular reactions and as such a " forced"  hyper or hypocapnia may   change O2 Diss curve as well as  vascular reaction.
 Walk with a HR of 85 +-. Than 5 min respiration with 6  steps inspiration followed by 6 steps expiration
 Than 5 min 5/5 and 5 min 4/4  and down to 1/1. Here the  picture for your discussion.

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Here another fun study.  Goal was.
 a) repeatable data's  with MOXY.
 b) influence on respiration on SmO2 and performance.
 In very short. We did a strength exercise  with 2 options. Respiratory intervention and no intervention.
 Task was to go to   subjective failure.
  As you can see in this case he was able to do only a short  time  meaning 8 resps and he had to quite.
 In the other test he was able to do the same exercise 32 times.
 Question now, Why , what happened and what was the  reactions after the load.
  So much to think about for our student and  as it looks outside the BOX. Small test to see what we learn this days  at a university and how critical  do students learn to think or is it all about  marks and repeating what we have to repeat to pass.
 This kid is  beautifully and very critical  and understand the concept of critical thinking without making conclusions too fast. Here for all of us to give it some thoughts.
 Strength training  and MOXY is the  issue here.

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Here another case study from our  University student .
 Goal was to demonstrate the relative term of hypoxia.
 Resp. the idea, that Hypoxia is more a question of bio availability of oxygen rather than the actual lack of O2 alone.
 We did two specific  works. Here one of them the other one we can show later, as he writes an academic paper for his university.
 1. Goal was to create a "hypoxic " situation by  moving the SpO2  down below 90 %.
 Than assess the reaction of the SmO2 and see,  whether a hypoxia  SpO2 of 90 % and less, which is an altitude  of around 2800 m and + would have an influence ion the bioavailablity of  Oxygen by looking at the SmO2 reaction, when  moving with an SpO2 of  98 % versus  below 90 %..
2. Create a situation , where we would  work with a EtCO2 level of 25 +- and normocapnic and hypercapnic of 50 +
 Here the result and you make your own conclusion based on the result.
 The green is as usual the SmO2 values. Start and finish are given . Load is always the same  power.  normocapnic was around 37 as a start load. The initial drop in SmO2 is  compression ( of the muscle on the    vascular system and therefor  a venous outflow followed by the usual decompression phase due to the relative  low  load.
 The second peak is a rest before same load was started and the  normal outflow followed by the picture under hypercapnia an than short  stop last peak with an outflow and a  decompression and the picture you see.
 There is a very specific lactate trend when doing this 2  respiratory intervention.
What would you expect under hyper and what under hypocapnia . What is the tricky part when just looking at SmO2 alone with out  using the other systems reactions. ?
 Same as always. Lactate alone , VO2  alone and so on is not of a lot of value , when we not look at the  full team involved.

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Here a repeat work from Nick. Strength workout with same weight ( load) to exhaustion.
 One with a specific intervention to stop the body from extracting  ( getting rid of H + ) see the incredible difference.
 In both cases, as long the body is able to use O2 we have the identical load ability  but than you can see the forced end due to the forced inability to get rid of  H + ( CO2). so no chance to sustain O2 independent energy supply due to the interference of most likely H +  and the ATP  Mg ( H + )  reactions ) ( Lennartz et all ) Have fun to look at the picture.
 It is  an incredible nice information for us now to show and see the change in performance in  Ice hockey player, if they are able to get rid of CO2  ( H + ) and as such can much longer use O2 independent energy supply.  On Tuesday we will start testing the first really big group on ICE with Brian Kozak to test the limitation of the groups we can assess in a short time.
 We now run a "golden standard " of a IPAHR protocol on ICE and will shift this idea over to europe as well so we have all centers using the same idea so we can gather data and learn from them.
 I will show some of the results as we go along.
 It is basically a replacement of a "Wingate" test by using performance ( time or wattage ) but by integrating the  physiological information of the fact , that we may have to same physical loads ( Watt and Speed or time ) on 2 athletes but a very different way how the use energy to create this result. So really to see the difference between 300 watt and 300 watt by looking at SmO2  use as well as tHb trend.
 The combination of both will tell us, whether  one athlete has a more superior O2 independent ability 9 old idea of anaerobic power ) versus aerobic power and at the same time we  can see, whether it is an actual strength limitation due to the reaction of the tHb.
Here the great picture and you can see with the first one how incredible repeatable SmO2  ( de-oxygenation is with the MOXY. We knew , that this is possible since many years but  it is great to see, that a equipment many thousand of dollars cheaper can actually do what we could do with great perfect  expensive research graded equipment.

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
I owe you some more info  to the post on the three respiratory version ( second post on here.
 Look at tehSmO2 trend and make some spontaneous  conclusion.
 Now look at the lactate trend reactions we had there.
 Remember, that lactate  is NOT a sign of O2 deficit at all it can be but in many cases lactate can show up without being in an anaerobe situation at all.
 In this study the load ( wattage and RPM ) where  through out the test  always the same so no change in actual O2  ( energy need from the leg point of view.
 In the  first set the lactate was planned to be in an around 2 --3 mmol and stable.   > This was the case so we had lactate  circulating in the system.
 The second phase where SmO2 drops the lactate dropped as well down to 1.9 the lowest at the end of the stage.
 The third set was  than an increase in lactate to 4 . 1 at the highest level.
 Now it is up to you to come to some type of  ideas or  "conclusions "

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