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Andrew

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 #1 
This is a basic question on the functional interpretation of tHb values.
We understand the tHb is a "relative" value, and could be affected by placement and skin thickness etc.
The question we have is: during a 5-1-5 assessment on a number of different athletes, we see a riding trend of tHb during the recovery minute. However, we see dramatically different levels of recovery between these athletes (.55 rise for one athlete....0.5 rise for another). Are these values relative as well? OR are these differences an indication of one athletes superior ability to return or supersede baseline due to cardiovascular situation?
juergfeldmann

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 #2 
Great question,assuming riding trend  was a big  finger  typo  as it may be rising  trend ?  So in some athletes  we see in the  1min rest a much higher  tHb  increase than  with others? Different  options  why.
 Let's assume they all relax  the same in the one minute break.
 
1. But that  could be a reason towards  the end. A  higher  SEMG  activity    and  than a   less relaxation of   SEMG  activity would keep  a  higher resting tension ging  so less tHb increase .
 Now  a   less relaxation ,so higher SEMG ,would mean a  still higher  O2   consumption  so   SmO2  would   be less  shooting up as well.
2. Another part you  can look at is the HR  recovery in the one min rest period on a 5/1  you may miss it  but in a 5/1/5  you have 2  times  the same   load ending  and see, whether the  HR  drops  down to the same recovery level or  whether the second time  you drop less indicating a higher HR  due  to lower SV,  or  due to  higher  demand of the  respiratory system as it may have reached a limitation.
2.1 if   SV  drop   than  we look as well at tHb  lower tHb lower back flow  so possibly  lower  pre load  and  SV  can  drop.
 2.2  if  respiratory  reason.  than RF  up    so  dead space  could be up  so EtCO2  up  therefor tHb  will increase more  due  to CO2  vasodilatation but SmO2  would lag behind  due  to O2  Disscurve shift, so respiration was  limitation.
 If  respiration is  compensator  RF  up   or TV up or both ,  so  no vasodilatation  and normal SmO2   recovery as well and often higher SV so  tHb  could go up. More  CO   more pressure   so  vasodilatation.
 Now  combine the next. If  respiration  tries  to compensate  and can  but CO  can not support te effort,  than the  increase in SV  to increase tHB  could back fire  as  CO  can not support the BP  so  BP  will  win  and we see  despite a great efforts of the respiratory compensation the BP had to be protected  due to   limit in CO.

Now    you can  check this  relative  fast to get some feedback  and better ideas.
 If you see this  during  your  workouts  you can in the next load increase CO  demand. If the  tHb  and SmO2  do not  get  effected  despite  a higher  CO  you can assume that the reaction is  not  from the cardiac limitation.
 Than  you  can  play  with respiration  . If  you  can not afford  to play  with respiration  you may be close  orr have  a limitation in respiration. If you can play  relayive easy  you  again  can ruel respiration out. So  you go  and  do a  few minutes  different  RPM  and see  whether the increase in  RPM  or  decrease will have an effect  and therefor you have some indication  that it is  more a muscular  trend   reaction  you can see.

Summary :
 tHb   reaction in the one min rest  can be traced  down  to 
 CO limitation,   = less tHb increase  still okay SmO2   increase  and in extreme  tHB  drop  due to BPP  protection plus  take  HR  recovery trend  and  trend  during load  for more feedback
Respiratory  limitation.  tHb  will  go  easy  up and over shoot   CO2  vasodilatation  but SmO2  may lag  behind.
 CO  compensation  thB  will shoot  and overshoot  due  to high CO  and  a vasodilatation after   laud  1 min stop.
Check  HR in recovery  as higher SV  will allow  a  better  drop in  recovery  and less   increase in trend during load
Resp  compensator.  tHB  will go up    but not really over shoot  and SmO22  good recovery , but HR  at rest may not  drop as  fats  due to the higher   O23 need in respiration  to allow  compensation.
 Now here than is the combination  what happened  when CO is limit and  resp  compensates  or the opposite.

 If the  above  is  ruled  out  as good as possible  than the    local muscle discussion will come up , muscular strength   and so on.






Andrew

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 #3 
Thank you Juerg for the brilliant response, including the details of the different causes of tHb riSe during the recovery period. the original question was meant to help us understand why the BEST athlete we have ever tested (world class mtb rider) have such a dramatic INCREASE in tHb during recovery, compared to our GOOD athletes, who show a much more blunted response of tHb during recovery. All have been trained with Spiro, and we think we have eliminated respiratory limitation, but will go back to data, and the lab, and confirm. Thank you again for the time.
RS Sport

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 #4 
Juerg, one of the best answers ever! [thumb] I really appreciate it!

One more question. What you suggest for increasing CO demand? You use respiration and RPM separately, so what’s left?
Ruud_G

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 #5 
I think Juerg has a very nice example of a respiration/ RPM workout and effects in his mailbox [wink]
juergfeldmann

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 #6 
Andrew  and the rest of  all  readers.
Sorry  for my  slow  response.
 I  try to pick up today night  and will  make  short  statements  with the  risk  that we create   more  questions, but that is okay as well.

  the original question was meant to help us understand why the BEST athlete we have ever tested (world class mtb rider) have such a dramatic INCREASE in tHb during recovery, compared to our GOOD athletes, who show a much more blunted response of tHb during recovery.

The reason  for my  typical  " political " first answer is ,  that I  do not  like to make a  fixed statement. Reason. I am not  completely sure  about the outcome.
  Here 2  options we see after all this years  who show  up most common  but not  exclusive  as usual.

Top  athletes (wrong, certain people )  with a very high  capillarisation and often but again  not  always high mitochondria density  seem to  show   depending on Limiter a very high response  (  shoot up  of tHb   after a  load  , when we   stop   asking  for O2  from the  loco motor  systems.

Reason. : During load , as usual a  competition occurs  between  vasodilatation to try  to  increase blood flow  and therefor O2  supply,  and the   danger  of  loosing BP  due to  too high  vasodilatation. The steady  fight  can create a different picture.
 let's see whether I can get that  logical  though.

 a)  top athletes, where  the cardiac system is NOT the limiter .
 As  they stop  at the end of a  test or   perhaps interval , they immediately will have a  vasodilatation  due  to lack of muscle contraction force.
 This than  will increase  the  tHb  , in case we have a very highly trained  vascular bed.

b ) a  top athlete  with a similar vascular bed, but a cardiac limitation  will have a different reaction.
 The sudden stop will in fact initially  try to increase tHb ( vasodilatation ) but the huge    vascular bed  will create a BP  risk  and we will have a  BP  protecting  vasoconstriction   at least  for a  certain  time  and depending on how fats the BP  feels  save  we will have a much lower tHb  respond  and in case it takes too long we will so no  real overshoot of tHb  so the  unreal seen  kicks  in and not the  real unseen. In this cases  the incredible good  training plan  to increase  vascularisation  and mitochondria density iss now  a risk  and  any further   performance gain  will  only occur, when we   train the cardiac system in this athlete.  Now  this is a  delivery limitation   and we  have this situation in some sport  nearly epidemically. Rowing  and cross-country skiing   have a classical  way of   improving  the vascular bed  as well mitochondria density.  LSD  80 %  of the  total training hours  are done in this   area. So  we  create a delivery limitation  and the only  way  for many  to improve  further  ( VO2  never  or  barely increases  anymore in this athletes  and in fact may even drop  despite a better performance ( improve  off efficiency ).
So  a little help  of O2  transportation delivery will make a huge  difference. The  money involved  as well as the  pressure  form  you and me  as the public   is not an excuse  but a human weakness  to  just try    once to see how it may work and help.

Here a  NIRS/ MOXY  example  from a top athlete  great  person  but a part of the problem in sport  second last load where we see a  drop in tHb in the  recovery  due to a  cardiac limitation.

D rest end thb smo2.jpg 


So  what I did   was to see,whether I  can  have control over this reaction   I was looking  for  clients  with a know  cardiac limitation. . Than we  loaded the is   clients  with a  step test 5/1/5 into a save  intensity  and once we  had the  first reaction  trend as  the one above  we prepared  two occlusion cuffs  for the  arms. So once we stopped  we   either  woud close the blood flow to the arms or keep it open.
 . Question. What   was the result in either or   and  why ?

Than  there was  another simple  option.
 . Know cardiac limitation but as well known good vascularisation.

I had a  friend good endurance athlete  and he had a   heart  attack. Relative  short    after the incident he was allowed  to go back  to  low  intensity endurance activity.
. BUT
  as soon he  would do  some  activity  and mainly when  after an intense  walk  up a hill he would  walk down  again he  would get very dizzy. There was no answer  form the specialist  and   we looked  at it with Physio flow  and NIRS.

Here what happened . After    up hill walk he increase   his    CO as good as possible  and  opened   his still good vascular bed.
 Now   as soon he walked  downhill  he   dropped his HR  and a such his  CO . but he  still had  his  full capillary bed  open.  so  too weak CO  for all the  option to  move blood  so BP   emergency  and he  therefor had  to   create as soon as possible a  vasoconstriction. So   below the   picture  of  an reaction like that  by  increasing    blood flow  due to activity but low CO  due to  cardiac limitation.

eric biased.jpg 
Above a biased   graph  of a tHb  drop  but perfect   re oxygenation.

 Now  we can  actually get this reaction in one  person. We  can  see in cases, where some muscles  wil react as expected  , some groups  may create a vasoconstriction  to maintain BP  and some may actually  show a   occlusion reaction.

Below  an example sent to us  form a cross-country  erg test.

triceps   ham  quad  thb.jpg 
Which muscle  has a  vasoconstriction,  due to  BP   risk, which one  shows  an  occlusion trend and which muscle  shows an except  trend ?

Now  third  option

b) a  top athlete  with a  similar vascular bed  but a  respiratory limitation. ( actual  low ability to move  a needed VE ). so  CO2 accumulation  and therefor  an additional  vasodilatation effect  besides a   high CO. tHb  will  shoot up  and above start  calibration  tHb . In contrast to the one  with a  good cardiac   pout put  so he  ahs no  risk to loose BP  this one here  will as well show a  high tHb reaction but in contrast to the  cardiac  strong one  a  respiratory limiter will show a relative hesitant  to low   shoot up of  SmO2.
 Why ???

 This  one  was easy to create  by simply creating a  hypercapnia. in   or towards the end.  using a  Spiro tiger  and   creeping up   CO2  to  45 mmHg  than  stop .

Summary.
 Greta  vascular beds  can but have not  to show  up with a  nice  high overshoot in tHB   in the  rest periods.
Certain delivery limitations  can  alter the out come  and may therefor show a different tHB  reaction.

Short  summary of reasons in  pictures.
 All three pictures  are  from Holmbergs study  and Calbet. on cross-country skiers. Often show   but here in a  group  and  I hope  it slowly makes sense, why we have so much fun in looking tHb reactions  at least as  intense  as SmO2 trends.

blood pressure.jpg 


sleeping giant.jpg 

sleeping giant blood flow 2.jpg



Now last but not least  I like to add a  small discussion on here as it is a very common  question I get mailed.
  SmO2    with  MOXY  assessments  can but has not to drop very low    so to levels   down  to +- 5 %. Many argue  this is  NOT possible,.
  1. Make an occlusion  and any NIRS  equipment will show a very low SmO2 in about  5 +-  minutes. This in a  completely rested   position (  minimal  activity just  resting PO2  demand.)
Take  RMR  and look  how  much O2  you may  use in 5 minutes or  how much calories you may burn.
 Than   look what a  high   calorie  burn under veyr high activity.. I hope you get the point.

2. Look at tHB  reaction during a  hard  workout  and you can see occlusion reaction. So  an occlusion test  artificially  is a occlusion  without  muscle compression in the site  of NIRS placement.
  Now an activity will not only create an occlusion like reaction but you add a muscular  compression at the site of  NIRS  so you not only reduce  blood  flow   due to   delivery limitation but as well due to mechanical  constriction.

Now  you add  the 
 

Poiseuille's Law

We mentioned earlier that one of the most important factors influencing blood flow is the size, or radius, of the blood vessel. You recall that radius is a math term that measures the distance from the center of a circle out to its edge. We explain the size-flow relationship through a law, and that law states that blood flow is proportional to the fourth power of the vessel's internal radius. This is known as Poiseuille's Law, which can be pronounced like the words 'pause' and 'wee' put together. It's an equation that is used to determine the flow of any fluid through any tube, so you might want to use its pronunciation to help you remember what the law talks about. For example, if the blood vessel has a small radius, the blood flow will be small, or we might want to think of it as it will 'pause' from its normal flow. If the blood vessel's radius is big, then blood flow will be big; and we say 'wee' when we open the flood gates.

 

The vessels leading to organs and muscles constrict or expand to control blood flow.

In simple terms, what Poiseuille's Law tells us is that if the radius of a blood vessel doubles, like it can with vasodilation, then the flow will increase 16 fold, because 2^4 = 16. The same would be true of a hose nozzle. If you take your hose nozzle and open it twice as big, you could expect the water flow to increase 16 fold. The reverse is also true, if the radius of the vessel is reduced in half vasoconstriction, then the blood flow will reduce by 16 fold. The takeaway learning point here is that it only takes small changes in the size of the artery to give a big change in blood flow.

 

And you can see that  NIRS equipment  " calibrated " with a  Occlusion test  will show a  very low  SmO2 in  cases, where all of the above comes together. This  does NOT mean we have it in the whole body but in muscles  which are heavily used  of  have a reduced   blood flow.

 NOW  > MOXY  is NOT perfect but very realistic .  Strong MOXY believers may argue  we have a +- 5 %   variation. I would tend  even towards  10 +- %  variation. which is in the ballpark  of even  many VO2  equipment's.  Now   critical  voices still, will argue. So  lets'  the real pros  in this  give us  some example  on how  low  SmO2  can drop  or better  the  utilization level   to what O2    content  we may be able to desaturate


In mammalian blood the amount of physically dissolved oxygen is around 0.2 ml O2 per 100 ml blood, while the amount bound to hemoglobin is around 20 ml O2 pr 100 ml blood. In water the amount physically dissolved is around 0.5 ml/100 ml water. The venous O2 content is typical around 6 ml O2 per 100 ml blood.

This gives an extraction of (20-6)/20= 70%. For elite skiers extraction up to 93% can be achieved (Calbet et al. 2005).

 





CraigMahony

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 #7 
So how would you train the athlete with a huge vascular bed but with a cardiac limitation? Or for that matter, anyone with a cardiac limitation?
I am talking about in the field, not in the lab. I know you have said elsewhere that to stimulate O2 delivery you reduce O2 utilization. However, I cannot see how you would specifically target cardiac output.
juergfeldmann

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 #8 
Here  first  a feedback   and I will be  back on the   ( myth  of  zero  SmO2  =  zero  O2   under the  NIRS  equipment.
 It is a   increasing comment we see on  some websites  and blogs  and  does  confuse people.
 Here a short  in behind the scene  work  we do daily  with many mails.  Yours  to enjoy . An Answer  from Andri  ( Swinco Switzerland )

Hi  XYZs

 

I will make some generic comments, and then you can come back with specific examples you are having. Best I find is if you talk out load and analyse what you see and we can give you our opinions and offer examples. How does this sound?

Firstly, when looking at SmO2 it is important to remember what this parameter is telling us, and as Roger points out the value should be looked at with an error bar of 10%, while the trending information up/down is more accurate. So take experience you have with HR and applied it to Moxy. If you say I want to ride with a HR of 150, you don’t think having a HR between 145-155 is a big deal, it’s the same thing. This is the same with Moxy.

SmO2 is a measure of oxygen supply in relationship to oxygen utilization; so the ability of the cardiopulmonary system to uptake and supply O2 and then the muscular systems ability to extract and utilize O2. Low SmO2 values are not uncommon, and I can share with you research papers showing, using various techniques, how SmO2 can drop. People make two basic mistakes when they say, how is it possible for SmO2 to drop to near 0% values, that would kill the cell? Well that would be true if we were measuring PO2, which is the O2 pressure in the cell, but we measure O2 on hemoglobin and myoglobin. PO2 has a critical value that it cannot drop under and this has a direct link to SmO2, but it is not SmO2 that is the critical measure. Secondly, people think that if you have a value of near 0% on your Moxy that you know have no oxygen delivery, this is of course not true. It means you have maximum extraction and utilization. If you measure arterial saturation it would still be >95%. This means that you are supply 95% oxygen and near 95% is being extracted in the muscle, and this continuously. The problem with the decreasing SmO2 trend followed by a very low SmO2 plateau, is that it is highly likely that you have increased and increased O2 utilization to a maximum capacity and now have no more ability to further extract oxygen despite the fact that your muscles could use more and therefore you start to run into problems and in order to maintain performance you have to add more and more O2 independent energy production, and you fatigue. In theory you could have low SmO2 values at a plateau and feel perfectly fine because you found an exact balance (like a MLSS with lactate values of 10). This is not likely but possible.

Because SmO2 is this relationship between supply and utilization, it is important to see what tHb is doing, using tHb as an indirect blood flow index. If you see that blood flow is being impeded and at the same time you see a strong decrease in SmO2 it is likely that this strong decrease in SmO2 is a result of increased utilization combined with decreased supply. So when you have these very fast drops in SmO2 in sprints, it is often the result of low supply due to delayed response of the cardiopulmonary system and at the same time immediate strong increase in utilization. And if this utilization capacity is high, in well trained athletes, SmO2 drops very quickly. This means during sprints, a well trained athlete moves very quickly into a duration where there is an increasing contribution of O2 independent energy sources, and as a coach we need to ask if we want this or not; what is the goal of the training.

Again, I hope this helps initially, and spurs more questions.

hourerg

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 #9 
So how would you train the athlete with a huge vascular bed but with a cardiac limitation? Or for that matter, anyone with a cardiac limitation?
I am talking about in the field, not in the lab. I know you have said elsewhere that to stimulate O2 delivery you reduce O2 utilization. However, I cannot see how you would specifically target cardiac output.

Craig, great question and I look forward to getting an answer from the brains. I'm guessing the answer will either be by blood flow restriction via artificial compression or by training hypoxic.

That being said, I wonder if we should also be creating a greater demand. For example, have the cyclist train on an old Schwinn Airdyne. So instead of the heart just having to deliver a large amount of blood to the legs, now it also has to deliver to the upper body as well.

CraigMahony

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 #10 
hourerg

my understanding from this forum was that blood flow restriction reduced delivery so the training stimulus was increased utilization, ie to enable a greater extraction of the available O2 from the blood by increasing mitochondria, etc. If so, this would not help cardiac output training. Maybe I have misunderstood.
juergfeldmann

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 #11 
nice  discussion    and this is than the art of  coaching.
 We  do not like on that forum  to interfere with the coaches ideas on how to work  out. There are many   cook books in   different sports  , who  tell  what intensity, based on VO2 max  and or on FTP   will stimulate SV  development  and  as such possibly cardiac out put.

What we hope on this forum is  to  show you the different  options to use  NIRS/MOXY  and how you can  make  interpretations.
We  do not  coach  nor  do we give any  advice on  how a training  suppose to go.
 NIRS/MOXY will help you  to   use your current ideas, than assess and  see, whether you  really  achieve  your  goal in increasing  the different  physiological  areas  you may like to improve.

 What I like to  try here to  correct some of may possible statements  in case  I got them  through as   wrong message.

to stimulate O2 delivery you reduce O2 utilization

Yes  and no.
Yes . If you  create a situation, where you can not  utilize  O2  anymore, than you create a  stimulation  where  you either  have to  quite  using this  specific   system, respectively the system will reduce performance.
 In  muscular view. if you hit a low   range  of  O2 delivery  so you    try to increase your utilization ability    and than you reach a    maximal utilization below   which you can not  drop  you either  may be able to maintain performance there (  cannot increase performance  , or you in fact may try  to find  another   muscle,  which may help you to maintain or    perhaps improve  performance. In other words  you  may have a  similar   utilization   ability in  one muscle  like the quadriceps  but the timing on when you may   use O2  in one head  compared to another head is different.
Example.
 SEMG    and NIRS  will show  in many cases, that we  first will use VL  to its   individual limit  and if we try to  push further  we  than will integrate  different other heads   so  RF  and  possibly intermedius.

 Now  it really depends  on the athletes or  person  ability to   maintain H +  balance  as  he or she pushes  more (  A  key element  to try to maintain H +  balance is   buffer  help  by  lactate  as well as  ability to get rid  of CO2 (  respiration options.
In our own  small studies  we  could start to see this option  to integrate RF   more into   leg muscle activity once we started  to look  closer  at respiration.

Here a  short  example  on  how we work on this.  We  compare  respiratory  trained athletes  with  respiratory  untrained athletes.
 Or  we  take  athletes, test  them   before we  train them   respiratorically  and than follow  them  up    every so many weeks  to see how the  integration of additional muscle groups  changes  with the ability  to   release  or move more CO2.

 I started  this  idea  many years back  with  COPD  clients. COPD  stands  for  chronic  obstructive pulmonary disease.
The unfortunate situations of the patients   is a " blessing "  for   physiological   controlled  training ideas. . So is unfortunately  a  cardiac  problem.
Why. Before we had   many of the here discussed  combinations and connections  we  needed  the  secure  feedback on what the real limiter  is .
 So in COPD  we had a  clear  idea   on the   current limiter. (  Or  so  we thought )
COPD people  are limited in their performance  and if they  walk too fast  or  they  do any activity , where there is an   increased  demand of  O2  and they reach a critical  " steeling " of  O2   from the   muscles  away  from their  vital  system like respiration we have the famous  ( Dempsey )  metaboreflex  , which will protect  vital system  by creating a  vasoconstriction to the leg  muscles as an example in walking   and the  client will have to slow  down or  even stop  to  get  the  balance in O22  supply  and utilization back.
 No the " classical " idea   in rehabilitation in  this cases is  to start  walking slow  and   than steady  try to increase the distance. So we know  we have a  delivery limitation  and as  such  any workout , where I try to push into this limit will initially improve  utilisation.
 We  as well see  in this  clients  a surprisingly  good integration  of many  options  of  muscles  contributing in one or the other way  for  the walking motion.
They  learn to  " tolerate"  higher CO2  levels  and as well    have a surprisingly good ability  to  destaurate.
 If you take SpO2  they   are   often   around  90 %  and  even lower  so   in a very hypoxic  SpO2  level  (3000 m above  sea level)
 A  chronic  " altitude " situation over time will not increase  mitochondria density but rather    you will loose  mitochondria . So before we  go too far here the short   story is.
 We    ass so often  offer the exact opposite , so   we have a classical  paid  COPD  rehab in town  and we  have our  private  offered ideas.
 In the  classical system  once people are regular  in a SpO2  90 %  and below they will start to walk  with an O2  tank  and end up  with an O2  supply  during the  night.

So  some people  do not like to go  already this   direction  and in a  small town  and with an increasing  numbers of  family doctors  knowing our  crazy ideas we have  clients, ready to pay  and try  another option. The option is : Stop  walking as a training idea  walk what you have to  do  for daily  task  but that's; it  forget  for the moment any additional  physical  muscle involved  activities.

Start training your   respiratory  muscle system instead.

In case Ruud is reading this   section. Here Ruud I will  help you to give you a feeling a COPD  client  has every time we push him  to walk.

Your  task.
Stand   or sit on the bike. Check  your  SpO2  and   breath with The  spiro tiger a comfortable  RF  and use  your 3 l  bag clamp it off  for  2.5 liter  and   as well  program  2.5  liter. Use  an intensity , where you feel  very relaxed so no problem at all.
So  if  he  is using a  2.5 L bag  and  let's  give him an easy RF  of  25 so  VE will be   with the system he  uses  Spiro Go  will be  70 l/min +-  if  he  keeps it in a  normocapnic  setting  )( only  bar graph  +-  maximal  an arrow  below or  above.)
 Now  do this  3  -  5 min  than  start either slow  walking or  as you are a  cyclist   start cycling   veyr low intensity  lets give you 100 watts. That's it, keep going and in your case  till you have to  quite. Important  you have to keep the bar  graph as you had in   sitting as we like to limit your  VE  to  70 l/ Min We basically limit your   VE  artificially   but in reality   an athletes may have a limitation of   120 l/VE.
 So  if the activity  you try to achieve or the performance you like to achieve creates a  CO2 production, which needs a higher VE /min than  what your limitation is , you simply will  accumulate  CO2 in your body  and the  end is   coming  fast   in your performance.
 Tell us  how it felt.

So  back to sport  and you may see the  connection.
If you  limit  delivery (  and   CO2  release is a  delivery limiter  problem )
than you will achieve a  short term  ability  to improve utilization. Once you bottom out of this ability   that's  it.
 You reach a VO2  max.
 Classical  workouts  based on  high intensity  all create a  delivery limitation. Classical test  ideas lie  Wingate  or   VO2 max  step test or  3 min LT  steps test  all create a  delivery limitation due to the  time restriction  we  force upon  our physiological systems.
 The  test results  will suggest an intensity which is absed ona  delivery limiting protocol  so you will when you us this intensities for sure improve  initially (  functional  reaction ) but you may miss any structural adaptation. The beauty on this idea is  fast  great improvement.
 
But ????
 BFR.  HIT  and other studies  show this  very impressive. The fast  change in 3 weeks studies   compared to  lower intensity  ideas over the same time  period..
 . Longer term   studies show a  reduction in   advantage  towards  slower  intensities  and  very long term studies  would shift the idea back to  lower intensity. the 80 / 20 ratio in cross-country skiing and rowing  and many other sports  would  be   a kind of  a back up  for  lower intensity  integration  compared to the attractive  fast changing reaction in functional loads.

So  the  athletes   where  followed or  many years  with  respiratory  changes  or   when we  compare athletes  we train respiratorically with  same   players in a team without  respiratory training we  can see the difference in  ability  to integrate  not just more muscles into te sport but as well  can push much higher  intensities  . And   can " tolerate" much higher  lactate.
 Last part is stupid  as they do not have to tolerate lactate. what we see is , that they  can  use lactate much more efficient  to   help to  buffer  so   shuttling H +  out of the cell  with help of  MCT  as well as  than  due to  a higher VE  can release  higher amount of CO2  which allows them  to   move  more H + into the circulation as the   H +  release is  very efficient  so less  or slower risk  of H +  accumulation.


COMPONENTS OF CELLULAR PROTON PRODUCTION, BUFFERING, AND REMOVAL

The cause of metabolic acidosis is not merely proton release, but an imbalance between the rate of proton release and the rate of proton buffering and removal. As previously shown from fundamental biochemistry, proton release occurs from glycolysis and ATP hydrolysis. However, there is not an immediate decrease in cellular pH due to the capacity and multiple components of cell proton buffering and removal (Table 5). The intracellular buffering system, which includes amino acids, proteins, Pi, HCO3−, creatine phosphate (CrP) hydrolysis, and lactate production, binds or consumes H+ to protect the cell against intracellular proton accumulation. Protons are also removed from the cytosol via mitochondrial transport, sarcolemmal transport (lactate−/H+ symporters, Na+/H+ exchangers), and a bicarbonate-dependent exchanger (HCO3−/Cl−) (Fig. 13). Such membrane exchange systems are crucial for the influence of the strong ion difference approach at understanding acid-base regulation during metabolic acidosis (5, 26). However, when the rate of H+ production exceeds the rate or the capacity to buffer or remove protons from skeletal muscle, metabolic acidosis ensues. It is important to note that lactate production acts as both a buffering system, by consuming H+, and a proton remover, by transporting H+ across the sarcolemma, to protect the cell against metabolic acidosis.

Once it is in the blood we  have one  great ability  to  get rid  of H + .

Respiration/Expiration

 

Respiratory training  / Spiro Tiger




Here some numbers.
 Grand tour   winner in  Pro cycling
 VC   with 15 years old  4.6 l/min
 with 17 years old  5.8 l/min
 with 19 years old   7.4 l / min
 Entering the pro  cycling ranks on the road .  independent measured  so not  from us  but  from the medical  pro team.  8.4  l / min
 VT  change  from 2.8 l min  and RF in races    where 55 +  to   full out  loads in the indepednent  test   where VT  was  4.2  liter  and  RF  was max  similar 50 +-

 check the VE  change.
 Can we   train the ability  to  retain  lactate  so we  can sue it in the next load  but  get  H + in balance.?

 If  we accept  that lactate is a veyr  potent  energy source, than the key  would be in intervals    or  in multiple   events in one  day  or  after a  race  to try   NOT  to  "cool down" to get rid  of  lactate but rather try to keep it  to  refuel  you liver ass  fast as possible.

So you like to balance  H +  but try  to not  get rid  of lactate !!!

Here some thoughts. Swimming Olympics. Some  top  USA  swimmers  had  multiple  starts in a  very short  row. Experts  argued  it  can't be done  but  coaches  and athletes   did it nevertheless.
 In some cases the races  where so close, that the  swimmer had  one race  in between his two races.
So  they not even left the pool deck they went over in the diving  tank  and where swimming super  slow  to than  get out  and  race again  with the surprising result of  actually swimming personal bests.

Now let,s look  at it  from a  physiological point of  view.
1. Cr.P  was  restored  in  1 - 2 min  and NIRS  SmO2  would have shown  that

2. lactate. Swimmers  have  compared to other sports very high VE. So  they get often not even planned  a  VE  which allows them  to help to get rid  of  a lot  of CO2  so  H +  balance is much longer maintain  and as  such  we se much higher  lactate levels in swimmers  than  for  example in   ultra distance runners.
As you see below the ability  to use  lactate  for  along time  to buffer  thanks to a great ventilation  increases  the end load  lactate level. So  after  a race we see a very high increase in circulating lactate  and it reaches in 5 - 10 min the highest  circulatory level.

 Strange is not it  after the race  they are  low in O2  so not even above 4 mmol so they suppose to be below LT !!  after  5 - 10 min they  are veyr high so above  4 mmol    above  T LT  and suppose to be " anaerobic "  no chance  to move  with 12 mmol lactate ?????
BUT  they moved  perfect. What happened in the  slow swimming in the pool. The slow motion movement   improves  the  slow deep breathing  which allows then  to get rid  of  CO2  in comparison to fats  and    low TV  breathing  we would  do on the dry land. The  super slow  movement  used veyr little  energy in the water  so  lactate was barely  touched  but H +  was  perfectly balanced  and    as they go to the start block they  even may  to some hyperventilation  so start with a veyr high pH   and get a  small advantage of that combined with a very high  circulating lactate ( energy ) compared  to their  competitor.

 



lactate post.jpg 
Below one off many cases studies  we did  to see, whether we  actually can  create this.

  
3min step test 1.jpg 



Just  to back up  the above and avoid  a  flood  of mails  here some independent  studies   to show these  reactions. Below  an independent lactate delay study   confirming the veyr old one I showed you above.
( Question,  how  can a  3 min or any  short term step test be  so  sure, that the lactate we  have is  from the step  we just finished ?)

lac delay.jpg The lactate we test is  the unknown  end result of  lactate appearance  and  lactate disappearance.. This depends   incredible on  muscle fibre  situation as well on   respiration ability to help maintain H + balance.

lac app and dissapp.jpg 


A  for example fatigues  respiration  will  fundamentally change the lactate   levels you tests in the blood. So will the O2  disscurve reaction  change  and with it  NIRS trends. It needs some major  number tweaking  to  fit a LT  idea into a NIRS trend  but is  that really  what we like to do with NIRS.

Below  the  statement  SmO2  can be  used under certain   situation  to  have a feedback on Creatine  refuelling. The  situation has to be in a  normal pH so  balanced H +  situation.
Below  refuelling trends in different  athletes. in Creatine
recovery  trends  in Crp.jpg 

Followed  by  an unpublished  case study  from us

overlap  smo2  CrP.jpg 
And last but not least  a small  overview  how respiration is an important  part of H + balance.
buffer H =.jpg 



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