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sandor

Development Team Member
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Posts: 61
 #31 
or worse, now i see, it may not be asthma, but actual exercise induced hyperventilation!
http://www.ncbi.nlm.nih.gov/pubmed/10400486


Exercise-induced hyperventilation: a pseudoasthma syndrome.
Hammo AH, Weinberger MM.

Abstract

BACKGROUND:
Exercise-induced asthma is common and generally responds well to an inhaled beta2 agonist.

OBJECTIVE:
We examined the physiologic changes in airflow and gas exchange that occurred during standardized treadmill exercise in patients previously diagnosed with exercise-induced asthma whose histories appeared atypical or where conventional treatment, including an inhaled beta2 agonist, was ineffective.

METHODS:
During a 1-year period 32 patients, aged 8 to 18, met these criteria. All had been previously diagnosed as having exercise-induced asthma. Exercise consisted of treadmill running at a time when the patients had received no inhaled beta2 agonist, cromolyn, or nedocromil for at least 4 hours. Spirometry was done before and at 2, 5, 10, and 15 minutes after exercise; oxygen saturation was monitored by pulse oximetry; and end-tidal CO2 was monitored with nasal cannula.

RESULTS:
Despite their previous diagnoses of exercise-induced asthma, 11 patients who described chest tightness during exercise had decreases in FEV1 less than 15% with all but one of those less than 10% (mean decrease 5.6%) but demonstrated decreases in end-tidal CO2 greater than in all of the other 21 patients (mean 23.2 versus 9.8%, P < .01). Only 4 patients had unequivocal evidence for bronchospasm with cough and wheezing accompanying chest tightness in association with decreases in FEV1 from 18 to 22%. Seventeen patients had neither their symptoms reproduced nor physiologic abnormalities.

CONCLUSIONS:
These data show that chest discomfort perceived as dyspnea during vigorous exercise may be associated with hypocapnia from hyperventilation without bronchospasm in children and adolescents previously misdiagnosed and treated as having exercise-induced asthma.





juergfeldmann

Development Team Member
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Posts: 1,501
 #32 
Sandor  , wwoww thanks so much  for this replay  as it  gives me a perfect   opportunity to  show  the fundamental  changes in exercise  physiological testing. I originally had a   whole sets  of  graphs  from rowing ready to  explain the data's  you sent  in  comparison to some world  class rowers  I  have the  fortune  to support  with some ideas and suggestions.

So  here  what I will try  as I have  approximately  50 mails  who all will benefit  from this  section here.
 My original hope  was, that VO2   classical  believers  would actually trigger his   discussion but  as so often it works  out differently.
  Here   what I hope to get done on the weekend.
 I  gently  but  clearly  will show  and disagree with the   abstract  and the  full study  you  use to back up the  idea of an exercise  induced  hyperventilation  during    workouts.
 I will try to make the  case, that the equipment  and  data collections they used  move  the  conclusion in a very different direction, than  what we see when  we  combine  VO2  (EtCO2 )  but we never  would use  EtCO2  alone  as it is  only a small help  as we need to know  the  reactions intracellular or  in the blood  so  to start out  look what EtCO2 means, where it is it tested  and is  EtCO2  really under activity  =  PaCO2  and PA  co2. Is  RQ under  activity  like  a   harder workout  really  RER.
Why does RQ definition  for  fat  and glucose between   0.7  AND 1.0?  But  RER  is often above  1.0 ?

We have  to  accept the limitation in EtCO2  and FeO2  % in  VO2 test equipment when compared to   the actual  location  we look  with NIRS (  same  for lactate   lovers)

EtCO2  and FeO2 %  are tested   at the mouth or  nose  level as  an indirect,  delayed feedback on  gas exchange  from the muscular level plus  some  dead space interference in between.  
Than because it was the  at the time bets  and easiest  way  to test we simple  equaled  EtCO2 =  PaCO2 ???

The interesting  time will be soon here, where thanks  to COSMED  Italy  we now  have more people  doing  what we do since  years  comparing live   directly  mask or nose  gas   values  with actual  changes  intramuscular with  NIRS or  actual  blood gas  analyzing  with sampling blood.
 So the new VO2  equipment  from Cosmed   can be combined with MOXY. ( And the above study  could be reviewed  again  with data's  from different  places  and not just  EtCO2   at the  mouth level.

 We will have  for classical VO2 user  some  sleepless  nights ahead if we  not start thinking  in a combination and accept the fact that classical VO2 is a  team summary  of what happens  in different teams members  and will confuse  many initially (as  it did  it to us )

 Here  to start very short.
 The time lag in  EtCO2 values    compared  to the  SmO2  reaction and tHB trend  will be the  topic  of discussion.
 
 You will have a very low EtCO2 depending on  respiration ( TV,  RF  and dead space and respiratory pattern    like ratio of inspiration to expiration time )

 But you may see a  very  fast drop in SmO2  due  to a very high  intramuscular  PaCO2. But a very low EtCO2  at the mask  level . Why ?

 Than you may have  a very high EtCO2  but an increase in SmO2.   Why ?

 Very similar  to lactate dynamic   combined  with SmO2  trends.

  A  drop in SmO2   ( fast  drop )  may not show  up as an increase in  lactate in a test sample but we may have  an increase in SmO2   and  than an increase in  lactate ????
Hope you see where we  go with this.


Now  start to read  carefully the pdf file not the abstract  from Sandors used  research.

I used that  exact study  about  4  years  ago  with my  grade  11/ 12 student  to show  the relative  risk off  using  studies  blindly  even if  pear review if the data collection    misses  certain  crucial reactions.
  Here what you search in the study.as it is a  interesting    section  where they contradict their own  conclusion.

 1. Hyper ventilation as per definition will reduce   CO2 pH  up . these creates a  left shift of the  O2  disscurve . which  increases affinity  of O2.  and SpO2  will go up. Look  for :


Mean decreases in O2 saturation and end-tidal CO2 in those patients were similar to that seen in the

four patients who experienced wheezing and coughing in association with

chest tightness

What causes  O2  sat  SpO2  as they  tested it  to  drop ? Or in other words where  does the O2  diss curve  has to  shift to  have the affinity  to create the drop in SpO2 ?

 If  this  may be the  case  what  happens there  to  CO2   and pH  if the O2  disscurve  shifts
 to get this  affinity reaction ?  How  can the  CO2  concentration in the moth  test  influence  the  O2  diss  curve in the body.

 Here a practical  experiment the  grade  11/ 12 student  had  to  do.


1. Hold  your breath. test  MOXY  reaction in the   biceps  and  quadriceps  as you hold  the breath.
 Describe be  what  you see and  why.

2. Repeat the  experiment  but   measure the EtCO2    as soon you have to give up holding your breath . What do you see e and  why ?

3. Repeat  the test but breath  shallow (  using  only  dead space  TV. So  you will have to v create a  RF  of  3o / 40  / 50  . Look at the live  EtCO2  values  and  live SmO2 values  , what do you see  and why ?

4. What   do e expect   when testing  PaCO2 in the blood as the names  suggest  and the DEtCO2  with the capnometer  you use.
 . What is the conclusion  form this basic  experiment ?   follow  up  discussion we had.




  a)  how  will a biased  close  look on O2Hb and HHb look  when we  have a  delayed  EtCO2  reaction.

Draw a  hypothetical  tHb  O2Hb  and HHb trend.
 
 b)  explain  the below values  and meaning  and  why   they support the O2Hb  and HHb  reaction of the   squatting exercise ?

2  loads  4  and 34  RF.jpg 

What  causes  the lack of  re saturation O2Hb trend  in the  left  activity compared  to the  right.

 The above  data's  are  courtesy  to   Per Lundstrome  form the   seminar  we  had  at the Red Bull  research center in Santa Monica California.


juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #33 
Only  2  responses  ( mails  )  so far. so like to give  some more   hints.
. Definition  of dead space.
 What influences  dead  space  at rest and what  during a  load ?
- If we look  at  EtCO2 in combination  with  SpO2  than we have  always  if we  test during a load  look as well at VE  ( l/Min  and how VE is  created  over RF  and TV. Here three examples  for  a real situation  .
 VE  ( l/Min is  90 l/min)
 VE  90  Athlete  1:  RF 30 / min 
                    A  2 :  45 / min
                   A  3  :  60 / min  TV   ? dead space  % ?
 Here  result  from 3  rowers  sent to us  from a  USA  test center  which  starts to combine VO 2 and  MOXY. ( The head coach  doing this assessment is  from Europe )


Below  three athletes   and you see the graph of  Respiratory  frequency  development during a  VO2  max  test
rf all 3.jpg 

Now  below  the same  athletes  same test  .  Tidal volume reaction

tv all 3.jpg 


now  how  could  this  affect  the  EtCO2    and the  PaCO2 ?  here the  CO2  ( EtCO2  trend  of  all three  below

co2.jpg 


Now  if  we look  how  the  CO2  and O2  reacted  taken one  out of the three  see below.


o2  co2.jpg


Which  of  the  above 3  atheist  is this  O2  CO2  reaction  what TV  and what RF ?

The  result  will be a  very   low  EtCO2 O2  diss curve  shift to the  left  ????
 Hmm  where is  the  CO2  ???  so   O2  disscurve  shift  to the right ???

If it is a   exercise  induced  " hyper ventilation " than we  have  O2  disscurve  to the ???  and SpO2  would be  ????
 Now  here the study   graph  where they   concluded  it is  an exercise induced hyper ventilation.

below  graph  from the  study

et  co2  and SpO2.jpg 

You can see EtCO2  drops   so  "conclusion " hyper ventilation which  would mean  O2  disscurve  to the left  see below  because if  EtCO2  low  due to  systemic  low  CO2  than PaCO2  will be low  as well. If this is the case we have an easy  way  to  " glue "  O2   so SpO2  will go up. This is the reason  why fetal  Hb  can take on  O2  as the mothers  O22  disscurve  is  more on the right so  easy  give up  and O2  and  fetal  Hb  easy pick up  as more on the left.02 diss curve 2.jpg

2.jpg


Now  to proof that the EtCO2 is really  due to hyper ventilation  they   have to show  the  respiratory reaction so VE  TV  RF as  shown  above  plus  as well use    PaCO2  blood test  to  see, whether their  conclusion is   true.. I  can not see any of the  back ups in the study.
 So  if  SpO2  drops  than we  may have a  O2  disscurve  to the  right  so harder  too pick up O2  in the lungs to the blood but easier  to use  O22   from the blood to the cell.
 
Question . How  can we use MOXY now  here, if  we can not afford  an I start or a  blood testing blood  gas  option.
 What  would we see in   SmO2 reaction  and what would we see in tHb  reaction  when we suddenly stop  the load  so  CO  and VE  are up but no  demand  anymore of  O2  or better less demand of  O2  and no muscle  compression influence on tHb ? 
Summary . Their  explanation paired  with their graph  indicate  a  drop in EtCO2  due  to respiratory    reasons  rather than a  hyper ventilation  as  EtCO2  down in  the mouth  area but  SpO2   down  as well in the  blood )   Hyper ventilation would  create a  low ETCO2  and  a low  PaCO2  and  a  increase and high SpO2. Hyperpnea but  hyper capnia  in the   muscle will create a low EtCO2  / a high PaCO2  which can not escape   due to the respiratory limitation  and will  therefore  shift to the right the O2  disscurve  so   back up  for this over a  drop in SpO2  (  hypoxia  hypercapnia )  and  the  next back up will come over  MOXY trend of  tHb  and SmO2  .  how is that trend looking ?  or  best blood gas  support.

When we  talk in  respiration on this issue  we have either a  hyper ventilation, which  can be voluntary  or   a  reaction ins certain situation   or we have a  exercise   create  hyper pnea

voluntarry  hyper peno  and hyper ventilation.jpg 

Why is  this  interesting.
 Well  for ay  coaches  who may  earlier or later start to  use  physiological stimulation over   performance  created  stimulation ,as you may  like to know  what you   create  or   like  to stimulate  you have to understand  how respiration,  cardiac  reactions, blood flow  and  delivery/ utilization  actually influence each other  daily,  no matter  what  %  of a training zones you believe in. . Physiological training  means I  apply  a  specific  stimulation in a  very specific load   so I  can decide  the reaction I like to archive.

Andrew

Study Participant
Registered:
Posts: 45
 #34 
I am hoping the new equipment we are bringing to market will help this discussion along, by CLEARLY indicating breath rates and tidal volumes, as well as adding information on VO2. Please feel free to have a look at our short video, and imagine how easy it will be to assess respiratory factors with the vo2 Master. Even more exciting for those reading this forum will be the implications of using live respiratory feedback in TEACHING athletes to breathe better, much like we used to do with the simple Bioharness, but now, improved data and simple app to help with analysis.
http://www.vo2master.com
Jiri Dostal

Development Team Member
Registered:
Posts: 51
 #35 
Hi Andy, great work! Something, that I was looking forward to have for a long time :-)
Could you just explain littble bit about the technology? How do you measure flow and FeO2 and, and how do you calculate other measures. Thanks!  
Jiri
Andrew

Study Participant
Registered:
Posts: 45
 #36 
The technology is a pantented process for measuring volumes that is not much different than some of the lab-based desktop vo2 monitoring devices. We were able to eliminate the moving parts, and incorporate the oxygen sensor into the small mouthpiece. From the flow volume measurements and FeO2 data, it is simply a matter of calculating the difference between the inspired oxygen content and the expired content to yield the volume of oxygen consumed. The big leap forward was removing the wires and cables, which we were able to accomplish with the help of a very smart engineer. We are just producing our Version 2 at the moment, with testing starting again in the next few weeks. We hope to have Juerg's feedback from a unit we will send him in August, once we clean up a few challenges and improve the accuracy, which currently sits at 2-3% different from pan-based equipment. However, I am confident that some of that perceived error is actually on the lab unit, which samples continuous air flow through a long tube, with the inherent error that occurs with that method. Our unit has a much higher sampling rate, located much closer to the source, who'd I believe will yield more accurate and more reliable values.
If you see the website, you will see we are taking pre-orders, at a price of only $999, which means you can purchase a unit for about the same cost as it currently takes to pay for two vo2 max tests at a "testing centre".
I will try to post csv data from a 5-1-5 this weekend, along with Moxy data to show changes due to training from this spring. I will look forward to feedback, and comments, but mainly am excited to see how the VO2 data can help with the discussions and training ideas Juerg is bringing to this great group.
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