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juergfeldmann

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 #1 
I like to  thank Seboo for his  great  feedbacks here on  the respiratory experiment.
 It may perhaps lead  to a deeper open discussion in the topic  of respiration and physiological workouts.
As well  to  a more critical view on publication on respiration and the  overall confusion we often see in terminology.
 So  (I  like to start some  common language  at least to be used on the forum here  so we talk  about  the  same ideas  and therefore reactions.

I like Juerg idea about a common language, I think will be nice to try to standardize a bit more what is shown on the post, so anyone can understand more easier

Now  here a  start in connection with  what   we may need to know  in case we sue  respiration  and NIRS  for interpretations  as well to show , that VO2   results in a  mask  at the mouth  may  give some very different  interpretations  to the reality which takes place in the body. ( Sorry  Vo2  users but  please come back  to argue, I will use  30 years  of  ideas    from my VO2 testing times  and I still use  it, but  with some more open  eyes  and mind. )

The " definitions'    I like to introduce  are not   based on my ideas but  from  my training  in pulmonary therapy  and respiratory therapy  at the university hospitals in Bern and   Zuerich. I  than used the same definition as  it is  used in these fields  as a teacher  at  the  same hospital and now use it  here in this small town in  the physiological introduction class for the  grade 10 - 12 students and we use it  world  wide  for people  working  with Spiro Tiger  and  for  Spiro Tiger  competency centers.
Now  that does not mean , that there is  always   space  for change  and or improvement.

 Basic  idea.
In a  what ever  is called homeostatic  respiratory  situation  we name the  stage  NORM  or Normo.

So  as  we sit here  we in most cases  will have a balanced  CO2  level  with a  certain acceptable range and depending on  school and  ideas it  is  36 mmHg  EtCO2  +-

So  if  I test fast my one here now  with a  capno meter  I have  ...... wait  will take about  45- 60 seconds  and really better  would be  even somewhat longer to balance . out.

Okay  39 - 40 mmHg  EtCO2.
 My  SpO2  96 %
and my  respiration rate  was  5 / min.


Now   +-  this  would  be called  NORMO  capnic.
Now  I  increase my respiration now  to 15 / min  and  for sure a  deeper  tidal volume (  air  breath  breath ) I will do this  for   1 min.
Okay a  very short moment as I started  to breath  faster and deeper   EtCO2  moved  up  to 43  and then immediately dropped  and dropped and after 1 min I was  at  20 mmHg  EtCO2. ( A little bit  fuzzy feeling )SpO2   was  at 99 %

Now  this  situation now is called  HYPO  capnic  so low  CO2  situation (  at least  at the mouth test area.)

Okay now  I will breath  very slow  and deep. I will do 1 breath every 2 mn  for  6 min  os  3  breath  .
Okay. First  during the  time my  SpO2  dropped  to 86  %. EtCO2  after 2 min   at the mouth  was 44 mmHg after 4 min second  breath out  48 mmHg  and  at the end   54 mmHg.

This  situation  at least  at the mouth  piece  is now called  HYPER  Capnia   high in CO2
Summary.
 Basic  so called normal  CO2  will be called  NORMO
If  we have more  CO2  than NORM   we use  the term hyper  so  above the norm. If  we are  below  NORM  we sue the  term hypo.

 Now in respiration this is used  for other situations as well.

Now let's  stay  with our  example  from above.

In the  hypercapnic experiment we had  as well a  drop in SpO2  86  % (  the  O2  % in the arterial  blood.)
 Now  look the picture  below as a  simple  info on SpO2  levels  depending on altitude.

Altitude and PO2.jpg 



Now  I am sitting here on  +- 800 m above sea level   but it could be  +- 100 - 2200 m  as  sea level is not  optimal  for the info but rather  the barometric pressure   today.


So  NORMOXIC  would be  possible  97 +- % SpO2

 
Now  if  I am in altitude  and  86  %  of SpO2  we  would name this a  hypoxic  situation.
Now  if  I go now in my  workout  room  and use  my oxygenator  and   push it  to 30 %  O2  and   take it  to my  face mask  I would  create  a hyperoxic  situation( SpO2  will not  show this )

Summary:
Again we have a current norm  and  when  we  add more  O2  to it  we  go towards  hyperoxic  and if  we  reduce  from the norm we   name it hypoxic

Now  in both of the above  examples  the NORM is  where we  have no  actual clinical  reactions  or  symptoms. .
 
As oon we go of  the NORM we   have a homeostasis  disruption and will have   initially some functional reaction and if  we  survive  them we  may see some structural  changes  or  adaptations.

I hope so  far so good ?????
 Now  another common exampel is body temperature.
 NORM temperature  is  36.5  +-

If  you  see  40  degrees celsius  you are  ?????????  termic,
 If  you see 35 . 5  you are  ?????? termic .
 So  again hyper  or hypo as in  compares  to the NORM  situation.


Now  if  I  do  no activity  I may breath a  VE  of 10 l / min.
 Now here is where  many   even great papers  start to confuse us.
 This is a graph  from a  post  I think  from Daniele.


queslaty  VE  and VO2.jpg


T
he feedback  of  information  based  on VE is    with a very limited value  and often   creates   wrong conclusions. We will perhaps  depending in the interest  discuss this much deeper on here.
  So   here just in short.
 VE  is measured  at the mouth. But between mouth  and  actual  gas exchange area  and  creation  of  CO2  and exchange of  O2 is a  so called  dead space  so  apart of the  outside  world  we forget  and or not see. We  may do some more experiments  to show  what is missing. Now  I had   a  in depth  discussion with  one or the   authors  but    of no   end result  as  they   where looking for a  device  for   hyperventilation training. Again we may go there but the Spiro Tiger is exactly the opposite  or at least  not  even close to hyperventilation. it is a  NORMOcapnic  Hyperpnea

Hyperpnea or hyperpnoea is increased depth and rate of breathing.[1] It may be physiologic—as when required to meet metabolic demand of body tissues (for example, during or after exercise, or when the body lacks oxygen at high altitude or as a result of anemia)—or it may be pathologic, as when sepsis is severe.

Now here we  go.
 Normal breathing.  You can  normal breath   with 60 RF  or  5  RF  as  normal means  the   ventilation needed  to stay in a homeostasis  like normocapnic.
  So  if  you breath more than normal in the  needed  situation  you will be   hyperventilating  and if you breathe than needed  you will hypoventilate.
 
Now  out if  what ever reasons in sport  physiology we have many  who change this idea.  Example.
 You run a  800 m all out  and  youwill increase VE as good a possible.
 But   towards the end  you may simply not have the capacity of VE  to maintain  homeostasis  and you may in fact  increase CO2 in your body. Another hard  push here. It is not  at all as we leaned  by wasserman  et all  due to   uffer of lactic  acid  and bicarbonate  releasing CO2  [wink] Forget  this  to  deep for the moment. The fact is  you will  have  a  inability  to release   enough  air  and with it enough CO2. You will have to much CO2  and you will be   ?????? capnic.
 ( This will shift  the O2  diss curve to the ????? ) You see this live  with NIRS    where  how and why .?
 But  VO2  mask  shows  what   and why. Same  question to lactate in the finger  sample.
Now  the run is over  and the  runner is  starting to breath even harder now . Why ?
 Is  he  hyperventilating  or is  he  even  still hypo ventilating   as the need  for a normal ventilation is not reached  yet  to maintain  and restore a homeostasis.?

 What  would be in that situation a  normal VE ? Now in case he keeps  that   high VE  flow  going  despite  the fact   he  successfully  balance  back to a needed  homeostasis  what  would we now have ???

 To close this  up  there is one   term  which is  needed to understand  as it will show up  again , when we look the  VE  graph  and show   why it is  of minimal value. 

Tachypnea is sometimes distinguished from hyperpnea when tachypnea is meant as rapid and shallow breaths, whereas hyperpnea is meant as rapid and deep breaths. This distinction is not always followed; the words can be synonymous.[1] Similarly, some speakers maintain a distinction between hyperpnea and hyperventilation, whereby in hyperpnea, the increased breathing rate is desirable as it meets the metabolic needs of the body, but in hyperventilation, the rate of ventilation is inappropriate for the body's needs. The resulting decrease in CO2concentration results in the typical symptoms of light-headedness, tingling in peripheries, visual disturbances etc., whereas in hyperpnea in the contradistinguished sense, there are generally no such symptoms. This distinction, too, is not invariably followed.

 Experiment:
You have somebody  who is breathing a  VE  of  30 l / min at rest. B Normal need  for this person would be  10 l / min. We  therefor  assume  that he or she is  ?????? ventilation.
 Meaning   that  CO2  will be ????

First  aid  you take a  paper bag   and why ? 
  Now that's  where  tachypnea comes in.
 If  you  have a person panicking  and  hyper ventilating   we have an increase in CO2  but as well a  very overshooting  VE  and  expiration of  CO2  so  hypocapnic  due to hyperventilation ( SpO2  ?  NIRS  SmO2  ???? )  Why

Now  we have  another person  panicking as well  but reaction with tachypnea. Very shallow  breathing  500 ml TV  and   very  activated  due to stress so high CO2  production.   Paper bag ??????

Person 1  hyperventilating.

 VE  30l/min   RF 20 TV  1.5L dead space  250 ml  so  dead space   volume L / min ????

Person 2  tachypnea  and hypoventilation

VE  30  RF 40  TV  ????? dead  space  250 ml  so   deadspace /  min  ????  What  does  this  mean in O 2 intake  and in CO2  out put ????

 Next up  we take  Sebos  great  graph  here a  preview  for you to start thinking.

sebo closer look.jpg 

juergfeldmann

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 #2 
let's  start  with Sebos  experiment  and just look first lap  1 closer.
 Now  the beauty is   you see it live  and there is some section you  can only see live  but not  when we look now  the graph  and Sebo  can jump in  to  give his  live feedback  as in some cases it is very individual.

sebo closer look.jpg 

1. look the first  2 min " normal  breathing  normal ventilation as  the body will create  to be in a " homeostasis . look  at the  base line  I made  and see, when he  is back in this  " normal base line   situation.
  Yes  when he was breathing normal again  but wwe have one  more  " normal " in between  where we have a different " baseline "  later  on what we  have to look for on thsi  situation.
 so lap  1  and look   normal breathing followed  by holding breath.
We  can assume that  holding breath is  more towards  hypoventilation ???  just a very extreme  form of  hypoventilation so much less than  NORM
So  what  do we see in a VO2  mask or  mouth piece feedback on  VO2  and VCO2 ???
What  do we see in NIRS?
SmO2  drops.  Is it  dropping immediately  when he holds  breath . We  do not know   with exception we have it timed  when he  holds  and than we can see when it starts  to  drop. Now  Sebo  was very successful    with holding breath long enough to possibly see o it as he holds  breath . You may see that nothing happens   and   just as you have to breathe you may see a drop  delayed   from SmO2. Lots  of different  options you  can see.   Why  does  it  drop.?
Where is  the O2  disscurve moving to ?
 What  would happen if  he had  on MOXY on an arm and one on a leg  and  is  sitting and doing the  same experiment. ?
  Why  do we see what we  will see ?
 Now  let's  say  he is doing the same  experiment but he is  walking   around in the room. One MOXY on a leg and one on an arm. What  do we see now ?
 Give it  some thought and move to lap  2  and look carefull base line  and what happens  during this  experiment.
What will you see in lap 2  in a VO2  feedback on VO2  and  VCO2  ?
  what is real  NIRS  or  the  mouth feedback  when you do it feel it  and  see  the  values.
 Same  question after a  400 m  run  when we took lactate. What was the value  after  the  400m  and what  was the value  after  5 or  10 min you tested. Where did  you felt  ready to go  with the low  after  run 400m value  or  after the  10 min  18 mmol lactate value ?
lactate post.jpg 

Now  if  you look at lap 2  think in terms of hyperventilation and or  hyperpnoea. How  long  was he  actually  hypoventilation  and using    a high  VE  ( Hyperpnoea )  to compensate  and   when  did  he shifted into hyperventilation and therefore   started  to get  hypocapnic, which than creates what  kind of a reaction  due to O2  diss curve shift  to the  ??????
 Now  this answer  will help  you to understand how  you can create a  hypoxic  hypercapnic  workout to  stimulate  what ? And this without  any tools  just physiological  knowledge  and acceptance  of  the  terms and how  they  show up  and a   live feedback  from any decent NIRS  device. There are  now  actual national teams out  there doing just that and  one  did even a nice publication  from their work with   hypercapnic  hypoxia workouts. Hint  when does  sebo   would have to start holding his breath again to avoid ??????

 


DanieleM

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 #3 
Quote:
The fact is  you will  have  a  inability  to release   enough  air  and with it enough CO2. You will have to much CO2  and you will be   ?????? capnic.
 ( This will shift  the O2  diss curve to the ????? ) You see this live  with NIRS    where  how and why .?
 But  VO2  mask  shows  what   and why. Same  question to lactate in the finger  sample.
Now  the run is over  and the  runner is  starting to breath even harder now . Why ?
 Is  he  hyperventilating  or is  he  even  still hypo ventilating   as the need  for a normal ventilation is not reached  yet  to maintain  and restore a homeostasis.?

 What  would be in that situation a  normal VE ? Now in case he keeps  that   high VE  flow  going  despite  the fact   he  successfully  balance  back to a needed  homeostasis  what  would we now have ???

Let's start with these.
CO2 accumulation is an hypercapnic situation and will shift the dissociation curve to right. 
At NIRS level: SmO2 drop
VO2 should increase due to the above reason (more oxygen released/consumed to/by the muscles) and pH would decrease. 

End of high intensity exercise. Extreme need to ventilate to release the excess CO2 and restore homeostasis.


juergfeldmann

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 #4 
hmm Daniele  you are too fast. Would agree  with all but one I would  argue .

But  VO2  mask  shows  what   and why.

VO2 should increase due to the above reason (more oxygen released/consumed to/by the muscles) and pH would decrease. 

In a  VO2  mask if  you hold  breath  what  would you  see.  ( RF  TV    so VE  and VO2)

So  as we hold  breath SmO2  drops  as a sign of  still use of  O2.
 In the VO2 mask  as  you hold breath you see   ????
 Now  as you start breathing again  SmO2  will go ?????
   indicating more supply  than demand    but a  short moment  with a time delay  what will you see in a VO2  mask in  case of O2  and CO2  reaction ?

Here   a  small experiment  for VO2  user. : Increase dead space  by 1 l  so take a  1 liter tube  like  a  snorkel  and than bretah  with a  TV  of  1 liter. What will we see in VO2  feedback on  O2  and CO2.



juergfeldmann

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 #5 
Now  next hint to seboos  lap 2.
 Look what he  did.
 Now   remember he was doing  nothing as activity just sitting.
 So  what is a resting respiratory   assessment value  for  VE in sitting. What is a   +-  respiratory  rate  and therefor what is a resting TV.
. Now  look what he did  so  how  did VE  RF  and TV  changed  and how long or how many breath  does it need  to  turn  around   the air.
 Than look at a  top  cross county skier  all out  VE  ??/ how much  what RF  and what  TV.
 Or  look at a  world  class  ice hockey player  when he  come s form the ice  out  to the bench . He will  have a VE if trained properly  of  250 L  +  and a  TV  of 5 - 6 L  so RF  ?  So  a huge turn around but  never close  to   what  seboo is doing  with 1 breath compared  to the total VE.
ryinc

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 #6 
Juerg, thanks for this whole post. Still trying to get my head around it all.

From the last post:

As i understand it the V02 mask measures, VE x (O2%in-02%out) factor. So if you hold your breath, i would imagine RF goes down, so VE would go down (assuming TV stayed the same). The O2%out might reduce, but if the impact of the VE reduction in the VO2 formula is bigger V02 would still fall?

In the experiment of 1l tube. I would imagine TV increases (assume RF stays the same) so VE goes up. But dead space increases. So "O2%in" stays the same "02% out" increases and (O2% in - O2% out) probably reduces? So one part of the v02 equation reduces, the other increases but my overall guess is that measured V02 increases, even though true oxygen consumption stays the same?
juergfeldmann

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 #7 
hmm sometimes  we  may overthink  answers.
  In a VO2  equipment at the mask.
 If  you hold your breath the   equipment   measures nothing  so no TV  no  RF  no VE  no VO2, as there is   zero no air flow  so flow meter  stops..
. There is than a very different  situation when you start to blow out  the air.
 That's where it is fun  to see the difference between   intramuscular  NIRS  feedback    and  actual indirect feedback  from a  mouth piece.
. Here  a  small experiment  for VO2  user . Again increase the dead  space  by one liter . breath a    below one liter TV  with any frequency  and see  what  CO2  and  O2   tell you  at the mouth piece  over  time so do it for  about 1  - 2 min.
 Thna  remove the dead space  and  breath  the same.
 Than   change  respiration lo0cation  form   abdominal  to apical  and look the changes in  FeO2  %  and  FeCO2  % . For the advanced   people  test  blood values   for RQ  and compare  to the calculate RER  values.
Than ask  yourself   once you see this  factual results of  RQ  compared  to RER under load in a  step test    how we  can sell the idea of  fat  and  carb  m utilization by using  RER  + RQ ??? Good     story impressive  show   but how much are real facts. ?
juergfeldmann

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 #8 
n the experiment of 1l tube. I would imagine TV increases.
 If  you keep the same TV  as before  the one liter  tube. TV is the  same.
 You increase  dead space and as  such  the  ratio  of  exchange  ratio of  O2 in and CO2  out.

So  if  we increase dead space    we change the  CO2  out put  and the  O2 intake  and as  such  the   option of a   more  hypercapnic  situation. This may stimulate the RF in many cases  so   VE  goes up  due to  RF  but we hope VE may go up as well as TV  may increase.
 Now in a  situation  where somebody may  move  at a  " max lass"  or FTP  ro what we  use balanced intensity  to  deoxy intensity  and the reason    for a limitation is  respiration, than any change in dead space  due to position or   respiratory location change  from  abdominal  to  apical can change the   normo capnic  situation to a  hypercapnic  situation.  The result  for performance is ?  The feedback on the NIRS   is ???  will show  soem more  small experiments  in that direction   during activities.
.
juergfeldmann

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 #9 
Now  we  may b ready to look   once more  at the    question  on  lactate  and SmO2 trend  and the  answer I   like to give   to Craig's  feedback.

Experiment:
Yo   run or bile or  row  or ski a intensity  you  may  believe it is  " MAX Lass' or  FTP  or  critical power  30  or what ever you believe you are  stable  for   at east  20 min in performance  at least. The classical MAX lass steady state  would be  16 min ? now body really knows  why 16 min  we just learned it.
 Now   you take   lactate after  8 min  and after  16 min  and  you suppose to be +-  minimal  change in the lactate reading. Physiologically we  would  argue that the lactate production and the lactate  consumption is balanced.
 Now  lets  assume any  number  as  nearly any  values  are possible.   even above  4 mmol  .
 3.8  as an assumption.
 Now  yo keep the same performance going   and you  try to  breath hypercapnic  or hypoventilaition . ( now  you know what  that means  for  us.)  you  do hypoventilation  so you  ventilate less  air  in and out  as  actually needed  to maintain a   homeostasis. .
 So    you may perhaps  at the  MAX lass   to stay  there  ventilate 75 +- l/min.
 You achieve this  with a  TV  of  2.5  l per breath  so 30 RF .
Now you  keep the TV  and you reduce  the  RF  to 15 . Therefor  you  will be far below the needed  CO2  release  and   O2 intake. If  you have no  VO  equipment  or  flow meter  you can do it  simply by   count  the breath per steps  and reduce  the  RF   to  half . So  you may breath in  on 2 step in and 2  steps out  now  keep  same  speed and breath 4  steps  in and 4  steps  out    or  even better 6  steps in and  6  steps  out. Now   keep running  and  if you can sustain 8 min  take a  sample ( lactate  [wink]  and  if  you can  go longer as it is  you max lass  speed  take another sample  at  16 min.
 What will  most likely happen is, that despite the  same speed   you can not sustain it   when you educe  the VE.
 Why. You accumulate  CO2  and  so on.
 Now  if  CO2  goes up  our  O2  discurve  shifts  to the right  and you will be able to release  O2  easier  as it is needed but you will reduce the ability to load it in the lungs so SpO2  will  drop .( hypoxic  hypercapnic )
  Now  at the beginning, as  long you see in NIRS  SmO2  dropping  despite the fact  that it is getting harder  you will see that lactate  actually  drops  as well.  You release    O2  despite the fact that you load  anymore optimal  and  the release of  O2  paired  with lactate as an  energy source will keep you going somewhat longer as it is more efficient in an O2  supply limitation to take lactate as  the fuel  source  and CrP  than  glucose    but  for sure not fat.

Now  if  you do the  opposite   you  breath hyperventilation.  than  O2 Diss curve shifts  to ???? so make it  harder  to release  O2  and you  have  SpO2  high but O2 is  NOT bio available  and  SmO2  will increase  but  lactate  as well despite the optical feedback  that you actually have  enough O2 .

 NOW  there is one situation, where   you will not be able  to hyperventilate  when there is   what system  pushing  the limit and is the reason  for the  MAX LASS intensity?  That is  in the classical  school  here we   see LT  and VT   at  the same performance level but only  in this case. 
 We may see the  deflection of your  VE  or  VCO2      at the same level but we can keep going  as   the  respiration  is  either the limitation hre or it could be the compensator. In both  cases VE  may  deflect  forma  linear situation but in the limiter  case, VE  goes  up  but  only  as RF  goes up and TV  stays  or even is   dropping  so CO   retention  and hyper capnia .
 If  respiration is the compensator you see VE   up  as RF may  stay or go up and TV  goes  up as well . Why is  this different 
  100 L VE  RF  25  TV  4  dead space  %  or  250ml   ???  ventilated  air  with exchange  of O2 and  CO2   = 
 100 L VE  RF  50  TV 2 dead space still 250  but  ?????
 Now  why   all this matters  or  why   we  over many years   and still often not care  about this .
 Because we    create training intensity based on performance  and not based  on physiological stimulation.
 Try  to sit back and  think  what you could  achieve  when going much  slower  so lower  performance but start manipulating  one or the other idea. What  could you stimulate     ?
Why are high intenity  zones   very   bad  to  create  a targeted  stimulation.
sebo2000

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 #10 
This is super interesting post, I'm away till Friday and can't really process this fully.

Comments about RF and TV are super interesting and make sense, but I have to figure out how to apply them in real life race situation, how to make "the best out of my breathing" [smile]




juergfeldmann

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 #11 
you will get there.
 Hint. Do I need  O2  ( utilization )  now   at that moment in a  race or  do I  have the   time o reload  to Hb  and  Mb. 
Think  in sports  like tennis  or    ice hockey or  other game  sports.
 or in MTB  when you have  inclines or downhill sections.

Than  depending on the   sport or  activity  we look , whether we  actually can deliver the O2  or whether we  have a   moment   delivery problem  due  to occlusion situation. Or  can  we  deload  CO2  or  do we  have an outflow situation. That's  why we use NIRS in  competition to assess. 
 Take an example in figure  skating  where we can see, whether the athlete  can afford  a  triple  combination as we may see  after the first  jump  an occlusion building up  and   there is now  way  that over the next 15 - 20 seconds  the body  can handle  two more all out  contraction due to lack of  energy  supply  and  deloading.
 So in the short term  we can change the  choreography  in the long term  we can  try  to create  the athletic  ability  for h  this options.

 Now  in the race or    competition  you aim for the  best efficiency . In the training  you aim for the   biggest inefficiency  to make a  simple cookbook  rule.
.Example. In the    competition  you like to have  an optimal  outflow for example  so you  can  balance  H +  and  Cr.P  recovery.
  To  train this    you  do in the workout  the  opposite  you try  to reduce  outflow  to  up regulate  the  H +    situation  for example.

 So  you  try to hyperventilate  so you are  hypocapnic before  the  triple combination. Where in the    workout   you  hold  your breath so you hypoventilate so you  are hypercapnic . 
This only if  you   try to stimulate your metabolic idea. If  you  do technical  jumps  you     do the same  as in a  competition so you have a  perfect muscle  coordination.  On   the screen  you see this very easy  and  live  so  you can pace  your skater  in between the jumps perfectly  so  you  do not create unnecessary  crashes  and pain. If  you  ue an upper body   placement  and legs  you as well see, when  your  delivery system  start to get pushed  to the limit  and  you   get a longer  recovery in  before  you do a  athletic  element. In the mean time  you may work on   stride combination or of   dance  elements  rather than  doing to any  jumps  where we see the muscles  and the energy supply is not yet  ready to go  again.

juergfeldmann

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 #12 
sebo closer look.jpg

Now  lets  got  to  Lap 2  reaction.
In Lap 1  we had a  resting  NIRS level and  respiration followed by a holding breath. The holding breath accumulated  CO2  and as  such we  saw a  shift in O2 disscurve  reaction to the right  and SmO2   started  to  drop.
 Seboo  was able to hold  about   80 seconds.
 Now  I do NOT know Sebbos  RRA  resting respiratory assessment so I use   as an example some numbers from  another person.

 Resting respiratory frequency  when doing nothing.   8 +- 2/ min
TV 680 +- 20 ml  per breath So  VE  +-  5.5  L/min
 so  he  was  reducing in  80  seconds  +- 7.2  +- L/min

 Minimal  activity  did  not  produced a lot  of CO2  moving  from the blood into the lungs ,where it got  trapped..
Now in Lap 2 Seboo did  deep and fast breathing

So not  sure  how deep and how  fast.  So  example  from the above  person.

Deep   breathing he   moves a  TV  of  3.8 l  an fast    where he can maintain he  3.8  l TV  is  35 - 40  breath per min.

Question. S  we know he did  just sitting so minimal of CO2  production from blood to lungs  during the deep and fast breathing.
So how many breath did Seboo  had  most likely to do to get ride of the accumulated  CO2  from the  80 seconds  holding.

Now look Lap 2  reaction. What will happen, when he  is now getting rid of the CO2  but he keeps breathing deep  and hard  for somewhat longer than actually needed to achieve  a  homeostasis.?
 Try to explain the SmO2 reaction in Lap 2. Now start thing ahead to Lap 3. 
What happens when you look at EtCO2  with a capnometer or you try to be aware of how  you bretah . What tendency do you see often , when  thinking how you breath versus you simply breath as you sleep. ?



juergfeldmann

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 #13 
Okay  we are  still in Lap 2. 
Questions: How many  deep  breath  may we need  to  balance  the  hypercapnia  from holding breath.
 Now what is happening if  we keep  going despite  we  reached  CO2  balance ?
How  would SmO2  look  like.

Then we  go  to lap 3 .
 What happened  there  and than   Lap 4. So  if  we  do nothing just sitting,  and  we breathe fast and shallow  to  try to  reach what  reaction.
 How  shallow  do we have to be  to  create  despriet a  high frequency a hypoventilation. and than we  have  the  problem  produced  with the  paper  bag  hyperventilation versus  hypoventilation.


juergfeldmann

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 #14 
Now  an add on  from a very interesting email discussion  with a tennis  coach. Now  the  location of ventilation  in the lungs  is not  just a  problem in   tennis but in many sports.
 So here the  pic  again  where  you can see hwo   respiration  and the location of  air flow  will have a direct impact on  the CO2  balance. 

gas exchnage.jpg 

Now  if  you have a  capno meter or a  VO2  equipment  with  CO2  sensor  or  you use  a  spiro tiger  combined  with a SpO2  sensor  or  you do it under load at  MAX Lass  for  old  school users  and you  have a  patient  and or athlete who is respiratory  trained and can choose the    location  very  clearly  you can see   live how much  this can change O2  and CO2  reactions.   And  with it performance. If  we  do not   understand  and  recognize  this    physiological  reactions  we often have no  answers for  very different performance losses.
 So in our  tennis  discussion  you can   test  this in a  training session  over a certain amount  of back hand repeats.
 Here  to give a  small inside   idea  on what we are discussing  for  the general reader  and  you will easy see  why and what we look  for.

wawr back hand.jpg



Djoco both haded.jpg 

2
 backhand  shots  with  very different  techniques.
  Now    respiration is one  part of the question and to go back  for MOXY  placement  in  Stan's  case.

1. leg  quadriceps  or gluteus  max.
 
 2. Intercostal 7 / 8

3. Rhomboid right side
 Look at  spiral  muscle sling. Now  you can see  technical deterioration  when you see the loss in  reaction through this  sling.  Very often it starts intercostal  .

Now  this  will as well answer  the  question I  got  from  some rowing coaches.  3  moxys  and  you  then  can as well see  what kind  of  technique  you like  to   teach and what kind of  coordination your  rower is actually doing.

here the answer .

three styles.jpg 




 

juergfeldmann

Development Team Member
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Posts: 1,501
 #15 
Thanks  and good  critical feedback  from a  tennis  coach I like to share   here.

1.yes  OR no  WE  CAN NOT TEST  THE RHOMBOID  ACTIVITIES  WITH  moxy  AS WE AS WELL WILL HAVE  NO CLEAR RESULT  WITH  semg ON RHOMBOID.


 
Bad  explanation  from my  side  as so often and great feedback. You place  the SEMG or  MOXY on the  location , where we know  the  Rhomboid is  but in reality  you  fix  it on the horizontal trapzius  section and will have the reaction of that  muscle  in NIRS  and  SEMG. the   action is  similar  hnw   true  not completely  that great as  the rhomboid  action. So below a picture  from an old   seminar  handout  I made 30 years  back  for  SEMG  electrode  placements at the  university hospital school of  physiotherapy in Bern Switzerland for Physiotherapy  and sport.
 In many, but not all cases  MOXY  placement  can follow these guides.

tennis  placement.jpg 

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