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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Over the last 4 days I had  5 new MOXY users sending me cvs files  and the fun challenge to  read what I observe and see, how close  my ideas where to reality.
. One of the more interesting topics was  my " speculation" based on observation of  NIRS traces on  what and how the client would possibly   behave.
 One of the behavior influencing  NIRS  information is the respiration.
 Remember the O2 Diss curve  see pic  again as a repetition or refresher.
 Than see  an older  study we did  with NIRS  where we " warmed up.
 Green in this case  is  the tHb  ( now  internationally it is brown.
 Green is now SmO2   for all MOXY users so we  speak the same language when we exchange information.
Color code  internationally for MOXY users.
 Green is  for SmO2
Red  for O2Hb
 Blue for HHb
 brown for tHb

So " warm up to optimal tHb
 Than same  load ( performance  and just played with hyper and hypocapnia. ( hypercapnia was defined as EtCO2   over 45 mmHg  and hypocapnia was defined   for EtCO2  below 25 mmHg.
 The  middle ground was defined as 35 mmHg EtCO2 See reactions and the easiest way to observe is looking at  O2Hb  ( red. as the  info on how oxygenation moved.

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Yes there are studies from  real study sources and I like to show one here.
 This  as a friendly respond to an email I just got with  a simple summary.
 Nice talks but all B.S..  I like more G.S as I   run a goat farm.
 Here a study from outside the farm.
Med Sci Sports Exerc. 2007 Jan;39(1):91-100.

Related trends in locomotor and respiratory muscle oxygenation during exercise.


Laboratory of Human Movement Studies, Faculty of Sports Sciences and Physical Education, Lille University, Lille, France.



We investigated the potential effect of respiratory muscle work on leg muscle oxygenation without artificial intervention in non-endurance-trained young subjects and searched for the range of intensity when this effect could occur.


We simultaneously monitored accessory respiratory and leg muscle oxygenation patterns with near-infrared spectroscopy (NIRS) in 15 healthy young men performing maximal incremental exercise on a cycle ergometer. Pulmonary gas exchange was measured. The respiratory compensation point (RCP) was determined. Oxygenation (RMO2) and blood volume (RMBV) of the serratus anterior (accessory respiratory muscle) and of the vastus lateralis (LegO2 and LegBV) were monitored with NIRS. The breakdown point of accessory respiratory muscle oxygenation (BPRMO2) and the accelerated (BP1LegO2) and attenuated fall (BP2LegO2) in leg muscle oxygenation were detected.


BPRMO2 occurred at approximately 85% .VO2max and was related to RCP (r = 0.88, P < 0.001). BP2LegO2 appeared at approximately 83% .VO2max and was related to RCP (r = 0.57, P < 0.05) and with BPRMO2 (r = 0.64, P = 0.01). From BP2LegO2 to maximal exercise, LegBV was significantly reduced (P < 0.05).


In active subjects exercising at heavy exercise intensities, we observed that the appearance of the accelerated drop in accessory respiratory muscle oxygenation-associated with high ventilatory level-was related with the attenuated fall in leg muscle oxygenation detected with near-infrared spectroscopy. This suggests that the high oxygen requirement of respiratory muscle leads to limited oxygen use by locomotor muscles as demonstrated in endurance-trained subjects. The phenomenon observed was associated with reduced leg blood volume, supporting the occurrence of leg vasoconstriction. These events appeared not only at maximal exercise but onward above the respiratory compensation point.

The pic shows you some ideas and  the regular reader can see, why , when doing an IPAHD ,we  in some  cases can observe a change in SmO2  and  at the same time in tHb   and if we combine this with  RF and TV  from your VO2  datacillection you can see, why we  may in fact look upon a possibility to   talk about limiter and compensator.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Short respond to a discussion and idea exchange I have with a  great coach  S.M.
 Here an answer  and you can  imagine the question.
 Sandy , what many coaches or centers do is, that they buy one Spiro Tiger complete set.
The Spiro tiger has a so called steering unit where the whole electronic is to control the respiratory frequency you like to train the ratio whether you like to go 1;1 meaning same time nits inspiration and same time units expiration or you can go 1:2 till up to 1: 4 or 4:1.
You as well can go free Respiratory frequency.
The second part the steering unit is doing , and that`s where the fundamental difference is to any other so called respiratory training device is the control of your EtCO2 level. The unit will tell you , whether you breath too deep or too shallow for the frequency you choose and the tidal volume you choose.
The TV is given by the bag size you will use for your client.
In a very simple term:
If you run very hard you may move a VE in your VO2 test of 100 liter per min.
The reason why you move 100 L of air is the demand of O2 for the speed you run but as well the demand of getting rid of CO2 to keep your pH and your H + in balance and the CO2 level somewhere between 37 +- 3 mmHg.
Under this `chemical `situation you body is optimal functioning.
If somebody is not able to move this amount of air you have to to stay in a homeostasis you may , if you under breath ( so you only are bale to move 80 liter but for that performance you need top move 100 Liter you will start to collect too much CO2 in your body,This will shift the O2 diss curve to the right side and as such your body on the one side will release more O2 ( as you are not just short of bringing out 20 Liter more air to get rid of CO2 but you as well do not bring 20 L enough air in to have a proper O2 supply you may need.
So the body as a `survival `reaction will help you to maintain the O2 need by releasing more O2 from the blood.
That`s when we see in some cases the SmO2 dropping. Now you see, what we mean with delivery limitation.
On the other side if you over breath you get dizzy , drop in CO2 and shift to the right and much tougher to actually get O2. The reason is a too low pCO2 so the body does release less O2 so more CO2 is produced due to O2 independent production and more H+ and CO2 is created till it is normalized.
Now the Spiro Tiger will control exactly this so the hyper or hypocapnia will not take place. If you do not follow the system it will shut down to protect the client from a too high CO2 or too low CO2.
So basically we can train the respiratory system to move much more air , than you ever can train by going all out. We have top athletes who now use 6 liter bags and bigger and breath 40 - 50 x per minute so we look at VE far above and beyond 300 liter.
Your `classical`literature would not agree with this and argue it is not possible.
Well we do it in our small rural community every day in the morning , when Brian has his ice hockey player for a workout.
Now the Spiro Tiger can be tricked so we can train to tolerate a different CO2 level if we start to play with it and we can combine MOXY to see now how the body reacts..
This is the steering unit.
The client can buy , like he will buy his own running shoe , when he uses your treadmill a so called user set.
That's where the air moves through and mouth piece and bag. He than is responsible for the cleanliness as he owns this and brings it to the training like his shoes and than may have the Spiro tiger like a indoor bike or treadmill , when they do a circuit workout or what ever. See simple PP with explanation.
Hope this makes some sense other wise come back with questions. Many center buy the user sets and than sell it to their clients. Many clients than buy a Spiro Tiger as you can do that at home as you may watch TV or listen music or relax.
You may be injured and can`t go running but you can maintain your respiratory system as well you metabolic CO2 O2 balanced idea.
Not everybody benefits from a Spiro Tiger the same way.
So that is a reason why we assess and now with MOXY everybody can do it. If you combine with VO2 you have an even better info as you see TV and RF development as well as CO2 trends and you see, whether the respiration is already a compensator or whether it is the limiter.
Depending on what it is you design the program. You may work on coordination for your respiration or on the TV or or Frequency or on pH balance and so on or on your core strength.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Sorry , I am behind with some explanations I  have to give to the  many feed backs I am getting in.
 Here one   from last week.
 It is a "IPAHD"  done    on a treadmill  by  our  friend S.M  from the eastern  part of Canada.
 See the pic  and a  shy  try to make  some " Zoning".
 Here   first some  additional points.
  We have   different levels of assessments based on tools you use  and  most likely as well whether you run your  assessment as a hobby , as a  part time coach or as a full time center. See pic 2  . A part of our  MOXY competency center  seminar script .
   So in this case we  look this form a level 1 assessment point of view, but as you can see, there are   still open questions.
 So back to the result.
. 1. We have a result, where we have a person starting if this person started  without warm up just cold Turkey on the treadmill with a very  high SmO2.
This  has some interesting indications.
 We see certain  population  with this very  high start level.
 The interesting part is that  there are 2  " competing groups " showing the same start  picture.
 a)  highly extreme endurance athletes with an incredible mitochondria density and  therefore a very high myoglobin content where the store O2 besides the O2  moving in from  Hb transport as O2Hb.
 Remember NIRS can't make a difference between Mb   and Hb loaded and unloaded.
. B) we  have  another group with a  high SmO2 . People with sever COPD  on O2.
 The interesting part here is, that due to  the fact , that they are on O2  they breathe very shallow  and  fast  and  are  most often CHRS people   Chronic hypocapnic respiratory syndrome people. They  tend to   look like they are very nicely oxygenated, but as soon they try to move they have to give up despite a high SmO2.  The hypocapnia   makes them   the situation   with a O2 Diss curve shift to the left  and they   can't use the O2  despite a high amount  in their body.
 The  additional of O2    and the lack of CO2  production  reduces their respiratory drive  and their diaphragm will get weaker and weaker and interestingly enough loose a lot  of the  as well needed FTF fibers.
 True  we  give them a better feeling  but do we  speed up the atrophy of their respiratory  muscle system ???
 Give somebody who has walking  problem a wheelchair  and your loos the  small ability he had to walk completely.

 So back yo to this test.
 We have a runner  starting with a  high SmO2  and starting just slow enough to  show and additional increase in SmO2. Reaching a very nice and very high clearly demonstrated SmO2  top plateau.
 Than showing  a  drop in SmO2  not extremely strong  and than a stop.
 I am not sure, but I think, that this was not  stopped due to all out   so this person could have gone  most likely  one level more. If it stopped, than due to  some discomfort or what ever reason,.
 Nevertheless even with one  level more the SmO2   would still be super high.
 Indicating , that this person has a utilization problem.
 Which in the first moment  looks like a contradiction.  At the start we argued a great mitochondria density   so  lot's of ability to use O2  , than at the end we argue a flat SmO2  so utilization problem.
  Here the  point.
 2 reasons ( actually more but stay  simple here )   what can cause a utilization problem.
 a)  You may have a great Hb loading ability  due to  great Hb health  but you may have a low mitochondria density  so the incredible delivery you  can  offer to move O2  in  can't be utilized due to the limitation of areas, where you can convert the O2  to energy.
 so  high SmO2   as high loaded  Hb ( O2 Hb )
b) you may have a  very high mitochondria density   ( now  a sub option)

 and you have 
a1) a  good Hb  loaded situation but  you are a very poor respirator meaning you breathe too fast  and too much air for what is needed and you are  always slightly hypocapnic  for the   performance you go, so you can't release O2.
 Simple test. In a  normal  endurance run you should be able to have a decent speed  like marathon race speed and easy be able to breathe 4/ 4. In fact  with a small reduction in speed you should easy be able to breath 6/6 and if you run n the ARI / STEI intensity you should easy be able to run 8/8.
 If you cant' you have some major  respiratory inspiratory  and expiratory deficiency.
 The second option why you may see a very high SmO2  at the end is a  big Mitochondria volumina  so lot's of O2 on MB  but you may  have a low   O2  carrier capacity on your Hb due to anemia. So you    can release  O2 just at the start  little bit as long the O2  diss curve  for Mb is  more to the right than  the Hb  but  as soon you drop your Po2 lower  your Mg  curve will be left form  Hb curve and you can't release  despite a good loaded Mb  and you  do not have a lot  to release from a weak Hb transportation capacity.
 So in this case  I take the risk  of a speculation but to confirm we would need a VO2   information on the respiratory  reaction on TV and RF  and EtCO2.
 This person  may have a  respiratory  limiter  and or an actual  O2 transportation limitation.
 What  can show as a proof is  to do specific respiratory  workouts   during running to create a hypoxic reaction and a high  CO2 level to  stimulate EPO and the hormone  we now all know by now , who helps to release O2  from Hb . See  pic we had many times now  from O2 Dis curve. Remember. at school we always see the O2  diss curve but we never  see the full curve  at the beginning where Mb release O2   better for a short moment than Hb  . This is needed  and you can see why , when you look at SmO2  reaction in an all out sprint.
 The reaction , where we all learned that it is " anaerobic  alacticid ," when it  is in fact  aerobic lacticid."
 Smile  confused ??? 
See  O2 diss curve the way we  get  educated  and than look  at the full picture   at the start of each  load we would do.

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
A  feedback I got here.
  In short " 
"Great ideas  but   most likely a " dream"
  May be true.
 We work  with this idea of respiration as a very important part of  performance since  many many years  back.
 We slowly get  some support.
 Pic  1  a sample out of our  non scientific kitchen where we  cook   hundreds of this samples  to try to understand  .
 Than a  study  form a  more accepted kitchen  with s some  slightly  smaller sample  rates.

Eur J Appl Physiol. 2010 Mar;108(5):913-25. doi: 10.1007/s00421-009-1293-1. Epub 2009 Nov 28.

Effect of hyperventilation and prior heavy exercise on O2 uptake and muscle deoxygenation kinetics during transitions to moderate exercise.


Canadian Centre for Activity and Aging, School of Kinesiology, The University of Western Ontario, Arthur and Sonia Labatt Health Sciences Building, Rm 411C, London, ON, N6A 5B9, Canada.


The effect of hyperventilation-induced hypocapnic alkalosis (HYPO) and prior heavy-intensity exercise (HVY) on pulmonary O(2) uptake (VO(2p)) kinetics were examined in young adults (n = 7) during moderate-intensity exercise (MOD). Subjects completed leg cycling exercise during (1) normal breathing (CON, P(ET)CO(2) approximately 40 mmHg) and (2) controlled hyperventilation (HYPO, P(ET)CO(2) approximately 20 mmHg) throughout the protocol, with each condition repeated on four occasions. The protocol consisted of two MOD transitions (MOD1, MOD2) to 80% estimated lactate threshold with MOD2 preceded by HVY (Delta50%); each transition lasted 6 min and was preceded by 20 W cycling. VO(2p) was measured breath-by-breath and concentration changes in oxy- and deoxy-hemoglobin/myoglobin (Delta[HHb]) of the vastus lateralis muscle were measured by near-infrared spectroscopy. Adjustment of VO(2p) and Delta[HHb] were modeled using a mono-exponential equation by non-linear regression. During MOD1, the phase 2 time constant (tau) for VO(2p)(tauVO(2p)) was greater (P < 0.05) in HYPO (45 +/- 24 s) than CON (28 +/- 17 s). During MOD2, tauVO(2p) was reduced (P < 0.05) in both conditions (HYPO: 24 +/- 7 s, CON: 20 +/- 8 s). The Delta[Hb(TOT)] and Delta[O(2)Hb] were greater (P < 0.05) prior to and throughout MOD2. The Delta[HHb] mean response time was similar in MOD1 and MOD2, and between conditions, however, the MOD1 Delta[HHb] amplitude was greater (P < 0.05) in HYPO compared to CON, with no differences between conditions in MOD2. These findings suggest that the speeding of VO(2p) kinetics after prior HVY in HYPO was related, in part, to an increase in microvascular perfusion.

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