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juergfeldmann

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 #16 
Rachel  you are a lucky  girl  having Sandy  as your coach , as she is the  leading endurance  coach in that    section of  Canada  and we  have   always great feedbacks  from her , so  she  gives us many great  data  and  great to discuss options  with her. Keep us  updated.
 If you have a 5/1/5  can you sent  or  tell Sandy  to sent the  csv  file  as  II like to look at some  tHb  trends in your  assessment.
Rachel

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 #17 
I agree that I am lucky to have her as my coach!  She's fabulous.  I just did a 5/1/5 last week so I'll ask her to send it along.  Thanks again!
fitbyfred

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 #18 
Folks, hi, g'morning.

Regarding the discussion below for high delivery -vs- limited utilization during a 5/1/5, 

My brain goes in a few directions: 

- What's causing this ? 

With endurance trained is it an issue related to their low body mass (generalizing here) along with having great movement specific coordination, especially on a treadmill ? So less tHb reaction due to much less muscle compression ? mostly red muscle fibre type recruitment until the near end of 5/1/5, etc. etc.

How are folks using the MOXY for finding useful info here ? 

- Is this situation same for different exercises / loading options ?   

- Is the situation driven by resting breathing habits, which could possibly create a dysfunctional Bohr Effect and maybe limit final stage of O2 delivery ?

Without a resting respiratory screen prior to the 5/1/5 how are folks using the MOXY to find helpful info without interfering with the 5/1/5 ? 

ryinc

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 #19 
Clint thanks for the webinar found it really interesting. One thing of particular interest was going into more detail about giving ideas how one might respond to a limiter e.g. in the weninar using spirotiger as example.

Can you or Jeurg ( or anybody else) elaborate on some further ideas on the types of training and tools that you would use in instances of other limiters. The intention is not to create a "cook book" as Jeurg would state it but i am trying to understand some practical examples of how one might say train cardiac system without stressing respiratory or muscles. Or train, muscle strength without stressing other systems. Or more generally train utilisation without stressing delivery, or train delivery without stressing utilisation?
juergfeldmann

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 #20 
Thanks  for  both  feedback  from Fred ( Fred is a  very advanced  MOXY user  in  Halifax  and  people  form this area  hey  visit him as he is unique in his approach  and as you see  critical in what we / he is doing.
 \Thanks  as well to the last post  with the   absolutely  crucial  question  he asks  on specificity of  training.
 I am really  really surprised, that this questions  never  showed  up many years back.
 I am not surprised  as it comes  from somebody  who  tells me in another  post , that he  has a limitation in physiological  knowledge. We  all have  and that's'  why this is a crucial question.
  If we follow  general believes  we take a cook book  take a 75  %  form something  as the cookbook tells us that what  works  , we do not ask this questions, we do not look  whether we  can get a feedback  and we do not reassess, whether it worked.
 Sorry wattage users in the cycling community   but there   thousand  if not more  of  cyclist out there  calculation the CP  or  what ever  and than  follow the cookbook  with relative  limited  critical  questions on why. Reason it is simple  it is  clear  there are no  questions to be  ask  as  220 watt i s just that all the time  and there is never  anything to question on this.
 Not a  critic  but a reality and a reason , why   bio feedback information will need some time  to  be used in  sport  but the hundreds  of  mails I am getting  shows , that there is a growing interest in this.
 Now  to the specific  question  on how  you  do  what  be avoiding overloads. I will try  to  give  some feedback  but like to avoid    cookbooks  so  people  do not go out  and try  without having the specific information, whether it makes  sense.
 I just sent a long mail to Rachel's  and Rachel;s  coach Sandy Musson in Toronto  to show  some option  for the   utilization stimulation if that is needed.
. To Fred. The  trend we see in Rachel  and in many top  endurance athletes  has some very interesting  contradiction  feedback.
 Her a  hint  where and  what I am working on.
 Every ACL  TKR  and  other operation I get in  I  do a  left Right  NIRS. I like to see the  what people may call detaining  reactions.
 Now  we know in scoliosis that the convex  side in idiopathic  long lasting  scoliosis  has  a  high %  of FTF  fibers ( biopsy  researched )  and the concave  side  has  FTF x or FTF G  fibers.
  Why ?
  well no matter why  but there are somewhere a reason ?   I look how  NIRS  reacts  and    when trying to load  symmetrically how the respond is.
 Unfortunate  for the moment the respond is not  as I  expected  or  had  hoped  for as I would have  an immediate explanation.
 based ion classical  education.
 But  it does not make   sense I  we would ahve to change the  facts  so that it fits  the theory. I  do NOT have enough examples  or  numbers  yet  as I only have about 60 - 70  cases  properly assessed  so just a trend  but nothing to  be proud  of  as of yet. Will need as in all cases we look at  500 +-    cases  do be able to  argue   or better debate  in case it  contradicts  the established  believes.
 So  we need to be somewhat  more patient  but time  works  for us.
 So will be back  on some of the great points  which where made.
ryinc

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 #21 
I am not sure i follow Rachel's post. She and her coach identified she has a utilisation weakness (relative to strong delivery perhaps) but then also says respiratory system is the limiter. I would have expected with respiratory limiter delivery not utilisation would be the weaker aspect?
Ruud_G

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 #22 
Hi Juerg. Tnx for the reply as usual. The reason I asked for monitoring of changes and used %FTP was just to set one parameter as set for comparison reasons. And yes. Other situations need to be more or less constant as well to make comparisons overtime. Same as you show with the examples. Same workouts out of perspective of trying to repeat and see differences.

And with trend information some point will be above and some below the line but that's OK. In that sense I believe it is in the big picture and that when it comes to training and improvements there are some general guidelines. If the details were that important they would be guidelines and not details.

Wrt CP, FTP, negative W'bal etc. due to wrong CP, etc. Yes I agree. Trying to fit everything in a mathematical model is not like it goes on reality. But there is also value in these metrics. Am I improving? Where am I improving? Etc. It gives hints (and not more) on why you improve (or don't). And yes, I agree it isn't the full picture. But at the same time SmO2 and ThB also isn't the full picture. It's all value as a whole: it's one big orchestra. (Als think about blood values, protein/carbo, etc etc and other parametes which - as a normal person- you don't track daily).

Wattage. Wattage is output. SmO2, HR, etc make the cranks go round. If these values are 0, my wattage is zero, and my family won't be happy I guess. (They are happy when wattage is zero, but not the SmO2, HR, etc [wink]

juergfeldmann

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 #23 
m running  far behind  with  feed backs  on many great ideas on here on the  forum . Will try to  catch up in all the  section  but as well here  and where ever I miss feed backs. So please  remind  me  and my messy brain  if you expect a feedback , but  I miss it and  nothing comes from my  side. Sometimes it may be " selective  reading"  but I hope to  avoid this.  Here a  feedback  form this section  before   we go back to Ruuds   ideas  . here what  I refer  to.
I am not sure i follow Rachel's post. She and her coach identified she has a utilisation weakness (relative to strong delivery perhaps) but then also says respiratory system is the limiter. I would have expected with respiratory limiter delivery not utilisation would be the weaker aspect?

Absolutely great point  and    as well  clear  why it is  confusing.
 Yes  Rachel  seems to have  ( will   if  I am allowed  to show a  5/1/5  assessment  fresh  from her on her ) a great    delivery system.
  Than  the " confusing"    statement to  work on her  respiration. let's see , whether I  can get  that right.
 again I like pictures due  to my  Swenglish. Below a  very nice  pictures  from the Swedish  group  Holmberg  on VO2  max  limitation.

limitation of performance.jpg 

I use  a similar  picture in  our  workshops  but I lie this  because it shows the fundamental difference   where  we  have in a  very specific  aspect  of  Performance.

let's start  on the top  and  go clock  wise.
VO2  max  , we  would use  VO2  peak tested. Old  and ongoing discussion. The discussion on  genetic  limitation of VO2  max.
 Genetic  means it is given and can't  be changed , like your body height  or  your eye  col our  and so on. For us VO2  max   can change. long discussion so we  go more towards VO2  peak tested.
2 central  circulation. This  is  where we  sue  Physio flow  to assess the feedback  and where  we  than  compare   reactions on Stroke volume  and  HR    with NIRS  reactions. Example (  drop in tHb in more than  one moxy placement to have a  systemic  reaction [wink] and  the potential  compensation  of increase in HR . as CO = HR  x  SV  so if  preload  drops ( thb )  drops  or  goes up  due to venous  occlusion  ) than  SV  often  drops  or  is  stable  and  to  push a higher  CO  we  will at that moment increase  HR.

 This  section is a part of  the DELIVERY  system.

4. Muscle metabolize  This in  simple terms    can  be  look at the  SmO2  reaction  so  more O 2 delivery  than  utilization ( SmO2  increase,  equal  delivery  and utilization SmO2  flat  and  dropping of SmO2  as a  sign of a higher utilization  situation  than delivery. 

So really this part is  what we  all look  since  ever the intensity , where we  have a problem  with O2  delivery   to maintain   performance. The  difference is  simply that w e had  no  optimal  tools  for this  so we  took blood  and assumed , that lactate  is  only produced  when we  go into a  higher utilization than delivery.  Turns  out  that this has to be  reviewed  as lactate is produced   as well when  enough O2  is available  and turns  out  that  this is  not always the case as we may  produce  lactate but it never shows  up in the finger  as  utilization of lactate  is  so  fast , than  there is nothing left   once w e test blood in the finger.
 Nevertheless it was a great  step forward  to the  right time.
 Now  we used  the idea of lactate threshold exactly out of this reason, finding the  " golden"  point  where we  had  a problem in O2  delivery  and utilization  would take over  in a higher rate  as delivery  so we started a  " time bomb "   for  performance.
 So  s we know , that lactate  was  an idea  to  look indirectly  for this  critical  point  but it is not optimal  and now  we  can look live directly when this happens, why  would I  try  to validate  NIRS  to lactate  when we  would have to validate lactate  to  NIRS.
 It is about    using  an d MRI  and I see a   ACL tear  , than make  an older  x ray  and can't see the  ACL  tear  and argue  that MRI is not validate d  to a  normal xRay  because  I can not see the ACL tear in the x  ray . Hmmmm    can you see  what I mean ????  Why  would I abuse  NIRS technology  to move it back  to a  great but outdated  idea of lactate ?  Why  would I  read  a  ice hockey  game report when I  had  the  choice  to go to  the live  game ?

 now in  4.  muscle metabolism  one  part  we miss is  under energy stores   ( glycogen )  the  ability  to store  O2  ( in MB  and  what is  already there.
 Do we store  O2     most likely yes  on Mb  and  to  see, whether that is the case  we  can make a  sudden occlusion   at rest  so stop any potential delivery  and we  see with NIRS the immediate  drop in SmO2  or drop in O2Hb  and increase in HHb  as  the  part of  the  immediate  O2   integration in the   plan  to maintain ATP  base levels. The  dilemma discussion on  anaerobe  and aerobe.  Now  this  really basic  experiment  with occlusion shows , that there is no  such thing like anaerobe  as we  see O2  utilization  immediately  and without  any  further delivery.
 How long  can we   keep occlusion.  basically till we kill the   occluded  part  and that  take s place  once O2  is gone  or  reaches a  critical low level  so that w e can not maintain ATP  baseline level.
 Now  we may be  anaerobic  but   most likely not what we like  to do   as a part of our  exercise  program ? So  point  4 on the picture  is a part of  UTILIZATION and a little bit  of  delivery  ( capillary  density in the muscular  area.)  tHb  can give us  some feedback on the capillarisation in the  1 min rest  period in  a 5/1/5 .

 3  regional blood flow  that is really where NIRS  shines   the   utilization  and  delivery in the regional muscle setting. as we  know  we have  still limitations  but  we  are a  big step forward    when  we  add NIRS feedback  to  classical feedbacks  and put them into perspective  how they interact together. Remember  :  SmO2  can increase   so it appears  to  have more O2  delivered  than  used  but we still may see  lactate increase.  Why ?
 so  understanding the  interaction is  what I mean. 

now  point  1
lungs.  I  would rather use the word  respiration. The lungs  on their own have some limitation   but the respiratory  system is  what counts.
Now  Delivery :  Yes  the respiratory  system is a part of  the delivery  system  like the  heart. So  why  would we in Rachel  case  consider to  work on the respiration..  It is   due to the fact , that we mainly think O2  when we  talk respiration, so how  do I get O2 into the system. Now all VO2  users  know the value  of FeO2  %  the %  of  O2  we   breath out  after we  took O2  in. simple  numbers  21 %  of the  air we take in has O2  and FeO2  % is  somewhere around 14 - 18 % in  many cases  with exception. meaning , that we  breath a lot of  O2   out  again    after we    breath it in.  Now  2   options  we  forget. I  the delivery  system respiration as well "delivers"  CO2  out of the system.  Now  this reaction  may be in many cases underestimated. CO2 is absolutely crucial  to keep the O22  diss  curve in balance. Or in simple terms  CO2  will decide  how easy it is to load O2  form the lungs  to the blood  but as well from the blood  to the   cell. So  when we  talk  about  O2 Diss curve than we  talk about this O2  reactions  or stickiness..  If  CO2  is out  of balance  so let' s ay  we  breath much  more than needed  so hyperventilate , than  we  drop the needed optimal CO2  level  and we  talk about  hypocapnia. Now  easy to try   out  and you will  get dizzy. Too low  pCO2  and you  will  easy load O2  from the lungs  to the blood but you will have  a problem  to take it  from the blood to the  cell. Easy  to show  with a  MOXY on  any muscle.  SmO2  will go up as you load but you can not use it  O2  bioavailability. So despite  a high SmO2  you  may  work  hypoxic  and that's  when we   may see lactate increasing.
So you can do  a  short term simple  hypoxic  workout  with  using a great trained  respiratory system  to manipulate O2  disscurve. Now in this case the SpO2  sensor is  worth less , as it will be  very high. By the way  the  extreme  respiration you see eafter a  400 m run or rowing is NOT  hyperventilation this is  hyperpnoea  with  hypercania  and will move back  to  normal breathing  and normocapnia  as soon  H +  is balanced . H + is  balance d far before  lactate is  dropped  to resting values  which is a nice  section to show that they may show up  +-  the same time but they have very different dynamics  as  one is  not  related  directly  to the other.  one is a buffer    of  H +  . As  long  CO2  or  H + is not balanced  we  will have a higher respiratory  work  and as such  a higher O2  demand  after  a laud  which is not a  O2   deficit  pay  back  but a  part of the EPOC..  With NIRS  we will see a  delayed  increase in SmO2   but a nice  overshoot  of tHB  if  we have a respiration  limitation  due  to inability  to  move  CO2  out. High CO2  allows  easier use of O2  as the O2  discurve is now  to the right so easy unloading  from blood to  cell but  harder to load  form lungs  to blood. SpO2  will  drop  so will SmO22  drop. As  we use  O2  easier  now  or better available  we will have  an initial  drop in  higher lactate level  for a  certain  time  frame. so   again a different reaction than we  sometimes  would expect.

So in Rachel  case  2  option  for  respiratory  delivery    limitation.
a) if  she  as many ultra distance athletes  has  an incredible developed vascular  system  and an incredible  mitochondria density.  than  she may crate  a problem  for  the delivery  of O2  as the   muscles  may simply be able  to demand so much O2  that  the delivery systems  can not keep up  so  the  heart  may  increase   CO  but   it is not enough as there is a limitation in O2  intake over the lungs  and we create the famous  metaboreflex. meaning that the central governor   protect the vital system  from  a  too low  pO2  and a  such has to make the decision to  reduce the blood flwo to  all the muscles  who demand O2  y to keep a save eO2 level  for the vital systems.
. If this is the case , than we will see a systemic  vasoconstriction  in   2 moxy sites or  we may in some cases see  a vasoconstriction in some less involved muscles   to  shift the blood  to the needed locomotors area. Juts to finish the picture. If  there is a cardiac limitation CO  level  we  see  either a  reduced  recruitment of  motor units or  if  we have  an incredible   big  vascularisation we  will see a  drop in tHb  due to  BP  control ) Blood pressure control )
 b)  She may  have a  simply  weakness of  the  respiratory  system  and is not able  to maintain   over  along time  the high VE  demand  so  the  main  respiratory  muscles  will fatigue  ( diaphragm  which leads to a  drip in core stability  and as such  loss of    movement efficiency , This leads  to more O2  demand  and you can see the  problem . A higher muscular  work now  creates  a higher CO2    situation, which triggers  a  higher respiratory  work  which  than  can not be maintained so TV  drops ( tidal volume  as the   amount  of  air  moved  per breath )  so TV  drops  and  respiratory  frequency goes up  and now we have the opposite  form hyper ventilation  with  a  hyperpnoea with a    not sufficient  relase of CO2 as a  part o the H + balance  and now   exercise is  soon over  or performance has to be  strong reduce.
 This is a  completely  underestimate    situation and the  big and long  discussion on EIAH  is    for sure partially  to be blamed on this reactions  in high  performance athletes  as respiratory  limitation  due to  respiratory muscle  not being trained properly.
 Summary. In Rachels  case  we have to give it a  closer look at this  respiratory  situation  as a part of  CO2  release. True  we would expect, that  if  she can not release  CO2  SmO2  should drop but in  respiratory weakness the system  seem  just to shut down. If  we  have respiratory  trend  athletes  who  can move   control  VE  form 40  to 240 liter  when ever they decide  to increase TV  or RF  or both  than they can play  with this  compensator  and  use this  as an additional tool. If  respiration is the limiter than  there is  little  or no hope to play around  and the  physiology  will force  you in what ever is needed.  So  bad  word  delivery   for respiration  as it is as well " get rid  off"  Hope  that  all makes a little bit  sense  other wise please  come back.







juergfeldmann

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 #24 
Ruud  great  debate  and great points  well taken. Absolutely  true   zero  wattage makes  your family very happy  as you are there with  an  output  of HR  and SmO2  and as  such a much more important  output than wattage  (  at least  for the family [wink])  I  just get an answer or  better some graphs  ready  for your   feedback    for  endurance  workouts. So   please  look at it  critically  and add more feed backs  and  ideas  to it  so we  can get forward  in this points.  As  well yes   performance data's  are  absolutely critical  and  yes  it  has to be a  full concert   NIRS  alone is  great  but  lot's is missing. Wattage  and  math  is great but as well a lot  is missing  the key  would  be to  have the  different  ideas put together  to be used  as a  team approach. The interest in some   cycling software   programs    with  MOXY  and in discussion  shows  that  more and more   people see that  value  of  integration  of physical  and physiological feed backs. Over the next  few  month there will be  a Greta shift into this   interesting  and exciting direction. So stay tuned on all  this  coming up.
Rachel

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 #25 
Absolutely, please feel free to share my 5/1/5 test.  
juergfeldmann

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 #26 
Okay  here  the long promised  information  to  discuss together form a great  suggestion made  by Ruud.

any graphs or something which relates to monitoring the Moxy output related to wattage workouts (and I assume some same kind of workouts (same wattage level, same duration etc) done over a period of time) which could really show that HOW the wattage was produced actually changed (like by seeing a trend in better utilization, better delivery, different thb reactions?) 

So will try , and Ruud please  come  back  and  tell me  whether this is  what you where looking  for.  Short intro.
Some  may think we  " hate  " wattage . not  at all  and we use  and need wattage to see ,as Ruud  so  often  and   friendly pointed out , performance  as  an objective tool  to  show  at least  for us , that what we  try to improve  on limiters   at the end  of the  day  really shows  up as  a performance improvement.  Now  sports  where  we  an measure wattage have  an incredible  advantage  and as  such  as well  carry the risk to  stay to  much  focused on  wattage performance only. Using HR  as  a guide  has the  risk  to  just look at  HR    and use this as a gospel. Combining wattage  and HR  is  already a big  step  forward.
 Now using  NIRS  feedback only  and  there  just SmO2  has as well the same negative  risks  as  any one sided  use of  any  markers.
 It is ,as we  always  try  to point out , a  full team  who  tries to reach  a  great  end  result  performance  and to achieve this  we need  all team members  to be able  to contribute to the  overall performance. The first  member  who may interfere  with this  idea  is the LIMITER. That is where we  focus  the  main time in a  training program,  but   always  keep in  mind  to not loose the great   ability  from the   compensator.
 Here  a  simple practical example. Your  4  men rowing team  has a  guy in, who can  maximal  row a  stroke rate of 39. Now  to achieve  the next level  in the overall performance they have to get  to 43. So  they  can not  go out  and row  with this goal as the overload  and kill always the same  guy. So. We  take him out  and  practice alone  with him on this goal . The other three  to not  loose their 43  ability  go   without  him  and  can maintain or  perhaps  even improve  upon their ability.
 Now there is a  time, where  they still have to get together  and   you may not be able  to wait  till the 39  has  443. So you use some other options. In this case you make it easier  for  39  so he  can go 43  by having an or  with holes in it so less resistance  and easier    to go 43  so  they can practice  the overall performance.  Now  can you imagine on how the established  rowing  community will react?

So  if the Team is your body  and you  have  for example a  coordination  or a  strength limiter, than you  never will push the respiration  to the level you may need or like to do., So   there will be days  where  you may simply push the respiration  alone  all out  for  30  min  or  5  x  x min  or  RF  pyramid  form  30  to 64  RF / min  and back  or TV  from 2 L  to 6  L  and so on. On this days your coordination or strength   part will have a  complete  break or recovery day  where as  you can push  and or  at least maintain the  compensator  respiration  so you  still benefit in a race  from this option. Just to finish the thought. Why is it good  to have a great respiration system if u you have  a stent  or coordination limitation. a ) coordination limitation. You loose  efficiency  of the motion  and you may  either start to integrate   less important  muscle  for your sport  but  as you are not  stable  you may need them  for balance  purposes.  Example  cross country skiing you need  the arms  to maintain bale  and a  such  loose the  forward  propulsion option    because you make side potions  for  stability  Needs O2  but not  for     the actual motion but  to  keep  balanced.

 Strength  limitation.  If this is the case and you reach a  certain intensity  you start creating  too much  compression on blood vessels  and as such  tHb  drops  and you may need  more CO  to try  to  keep  blood  flowing to avoid  occlusion. Nevertheless  you  start to increase  H + production  and  now  you need  to keep this in balance  and respiration is the only    option in the  sort  run to  do this decently efficient. Yes I see already the question. So respiration is always  pushed  as it  always  has  to  compensate. True but  an optimal  coordination workout  or  strength workout  should not  ask  for compensation as you like to overload this system   and nothing more because you do not like that  the compensation arm  or so  is  getting activated  as it destroys  the efficient  technique.

So  to Ruuds  graph.
 Key guidance  was  FTP  . meaning  that we use  the latest  FTP   wattage level  to  design the   workload  steps.
 We  than  use  always the same wattage   or  ( yes you  have it  here) the same FTP  % . So  we always  " warm up  with  FTP 60 % in this athletes  case    for 10 min followed  by FTP  80 %  for 10 min followed  by  FTP  for  10 min  and than  we will make a decision as we  go along  as we have a live feedback So this is  for reassessing  and basically  we do this daily as it is a part of the " warm up. This way  we have  immediately a feedback  in the first  10 or 20 min whether FTP    today is still 100 %  or whether the workout  from yesterday  change  the current FTP  wattage level. So  this way  we  can establish the same physiological  stimulus  but immediately  can see that the wattage  changed  ( higher   or  lower or is the same. )
 So we  can get some feedback of performance development on a  daily base  and over time.
 What we  collect , if it is a high  performance athlete  , we  use VO2   data  so RF  TV  VE,  Physioflow  for SV  HR  and EF  and sometimes  LVET trend.
 We use  SEMG  Myoexcersier  2  channel  and we use Capnometer  as well as  NIRS  now  most often 3  MOXYS instead of  one portamon. One moxy on a leg one on a  minimal involved  muscle and one the intercostal 7/8  for respiratory feedback . Than just for fun and because we  have free lactate strips  as the main distributor  of lactate Pro  we use  lactate  and sometimes  ammonia  and  blood sugar. That depends whether the athlete likes to be  poked  and whether we like to show  some ideas like delay  of   blood  and VO2  information.  Now   I like to show you , that this  looks  great sounds  good  and costs  a lot of  money  and is  simply not applicable  for a  decent  coaching idea  due to the time  and effort.
 So  what we   now  use is  one MOXY  to start out   and than again lie  to show  you based on hundreds  of test we did  with all this equipment, why  we  can  create some  connection  from    NIRS  trends  to this   incredible equipment.  Now  Ruud  made some good point  somewhere on  carbs  as well another reader once  pointed out that  carbs  loading or storage could be a limiter  and with NIRS  we do not get a handle on this. A  whole other issue   for another time . Here just a question to this  point  to think about.
 Do you us e carbs  or  glucose  to create ATP  or  do you may as well need O2  to  convert it ? So  if you  may go  with O2  plus  carbs  than  NIRS is already somewhat involved  as it tracks  O2   trends.
 If you go a   stable performance  and you run   short of   glucose  you may  try  what ?
  So if you keep  performance you may see what  and why ? What needs more O2   to create ATP   G  or  F ?  Lets  go back.
 So   here a  6 month  comparison  of the  workouts . The goal  was  an increase in Cardiac  out put  over    if possible  a  stroke volume increase. Limitation in a 5/1/5  was  a  delivery limitation or  a   too  string muscular system  . I show you    values  with  one MOXY  and  a  HR  monitor    and we sued peripedal. So keep in mind  4  stages  at 10 min each step no rest  from one step to the other  and 60 %  80 %    FTP  and above FTP + 20 lets  see, whether you can se e what happened. The   goal was to  work out  as many times  per week as possible   with an intensity we where hoping to create a  SV  stimulation. The  average   workouts  we  where able to  do   so that we had this stimulation was  2  to 33  x  per week. We had  forced  resting  days   so we  simply where not able to create the targeted  stimulation  and we  often had this  feedback after   the first or  second  step in the warm up.If  we  had the  feedback no SV training today  we  would  only  focus on coordination, when  the athlete  was keen to bike  or we  would  focus on  respiration of the bike or   we would do  a  hypoxic  hypercapnic  workout on the bike  with a wattage  of 40 %  of  FTP  So her the simple  4  steps  in one comparison.

improvemnt  perigraph.jpg  
your  comment.
 Than below  just  a  comparison as we overlap this in a different  excel program. so the last  two  assessments.
improvemnt  perigraph hr thb smo2.jpg 
Top is  HR   middle is  SmO2    and bottom is Thb trend. And just to top it  up  but not  needed if you have a  MOXY  the  view  if you look at  actual  cardiac  hemodynamic.

Top is  biased  graph  and in simple terms what we look is  whether the distance  between  blue  and red is  getting open as a  indication of great delivery  or  closer. as  an indication of   reduced  delivery. If it crosses than we  drop  below  what we started out  so  not optimal delivery  and  uses   utilization as a compensation. But as you  can se e    all output  form just  one MOXY  an a  HR monitor  and yes a  good power meter in this  case to be sure we had  stable performance in each step.

improvemnt  sv co hr  and bias.jpg
Above just an  example of  a  6 month SV  workout  and  specific   assessment protocol we  did in this case.  light colors is start levels  and dark is   6 month later  No  be carefull we  can do this  in a  day  as well when we  create  a plasma  expansion.
 So  to be  sure we have a  actual structural  change  you have to  do this  2   to three days ina  row  and see, whether the SV  stayes    clear higher  with a nd or without  plasma  volume   change.
 Lect  blue is  HR trends. middle is  Stroke volume  and  right side iss  EF %  ejection fraction %  . This is how much you throw  out iwht one beat  form what you got in. So  your EDV  ( end diastolic  volume) may be  100 ml  and you have  an  EF %  of   you  throw out  70  SV. Use this  as it is  easy to calculate in my head not  because it is a good number. Now  your  turn.
 Don't  ask  for the training program  as  we are not  a franchise  we are or try to be chefs.

Ruud_G

Development Team Member
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Posts: 279
 #27 
These kind of things is what I am looking for yes, because these graphs clearly show a delivery improvement. To utilise the better delivery is / will be a next chapter as you pointed out (often with good endurence athletes, good delivery not so good utilization).

if all improvements go in this way training outcome becomes more "obvious" and predictable. I was in that respect "happy" with your statement " hoping to create a SV stimulation", because I think it is not that easy to actually . Especially not if you consider a "normal" cyclist nowadays with a powermeter with numbers, HR numbers, cadence numbers etc. Let alone if a rider should constantly wear equipment while training.

Given the above I also encourage users to post similar graphs in which they show: 1) the "problem" or limiter/ compensator from an assessment 2) how they went on to work on that limiter/ compensator and 3) show outcomes of first assessment and later assessments to show whether what they worked on actually improved and finally (of course) 4) the actual results in terms of improvement (because end of the day that's what it's all about (and of course, focus should not be solely on outcome but also (especially) on the proces to get there).

In this way you have a very nice loop and other readers will actually see how it might work. It becomes more tangible. This does give ingredients (read ideas for others) to start cooking, but by experimenting you can put your own flavors to it so your meal will just taste a bit different than "normal".

I know that these things are scattered around the forum and if you look closely you will see there often is this kind of structure. But given my own experience (almost a year now) it is sometimes hard to find that structure. Not a critic, but just to help.
ryinc

Development Team Member
Registered:
Posts: 359
 #28 
Jeurg, thank you for your detailed reply which was really informative. 

As a reminder, my question was in relation to Rachel's case whether there was any contradiction in respiratory system being the limiter but the overall delivery being strong and there is perhaps a utilization problem.

To make sure that I (and others) understand the key points you have made:

1. CO2 balance (and H+ balance) is a key issue in relation to oxygen delivery/utilization, because it determines whether the dissociation curve shifts left or right. In simple terms - the "stickiness" for O2 of the blood.

When C02 is high: The O2 dissociation curve becomes more O2 "sticky"/O2 affinity (shift to the left). This makes it easy to transfer O2 from the lungs to the blood ("delivery") but difficult to transfer O2 from the blood to the muscle (form of utilization).

(Please confirm in such a situation MOXY would show high SmO2 reading?)

When C02 is low: The O2 dissociation curve becomes less O2 "sticky"/O2 affinity (shift to the right). This makes it difficult to transfer O2 from the lungs to the blood ("delivery" issue) but easy to transfer O2 from the blood to the muscle ("utlization" issue).

2. The respiratory system has a key role in re-balancing the dissociation curve, as it is the mechanism that gets rid of CO2 from the body (i.e plays a role in the utilization part of the "orchestra"). So if the respiratory system is not effective at getting rid of CO2, it is actually a utilization limiter. There is a circulatory problem here as well because the respiratory system is the only system that can be the compensator i.e.  the respiratory system starts to work harder to get rid of the C02, then it creates more C02 because of the muscles in the respiratory system working harder, which makes the C02 imbalance more etc....

Have i understood correctly or totally misunderstood?

If the above is correct, the the training intervention to such a limiter problem would be to try to train the respiratory system to become more efficient in releasing C02? Not sure what such training would look like, but will think about it. Initial (perhaps completely wrong) thoughts:
 - Altitude training
 - Focused breathing training with strong focus on exhalation 



juergfeldmann

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Posts: 1,501
 #29 
Great  great   respond . Here some add on  to see whether  we get this great idea  going.
 (Please confirm in such a situation MOXY would show high SmO2 reading?) You may have the right idea  but look at the   pictures.

 Below  I like to show  the FULL  O2  dissociation curve. In most cases  we never see the complete  right section as you will see in the next picture. You can see that MB is  more  to the right than left indicating , that at a start  of a  load  we    will take  advantage of this  and we  can sue the O2  which is  stored   in the working muscle cell. This   fact is  completely   push under the table  when we  talk about using  stored  energy  like  ATP  and Cr.P  and glucose. Why  would nature store  O2  on MB  when it is  never  o  only used  absolutely  at the all out  before   end  load. No it is   used as well immediately  at the start as it is used  for the ATP  maintenance  . See the   Dilemma  of   MOXY  section.



o2 diss  real.jpg 

Now  to make a  picture  of your summary :
  here the typical  O2  disscurve we see.

02 diss curve 2.jpg 

or  just to have some option

O2 DISS CURVE.jpg 


So  right  shift  towards  decreased  affinity  ( less sticky ) so  high to very high CO2  will allow  you
to get easier  O2  from the blood to the cell.
 Your  experiment  at home.
 Fix  a MOXY on  any muscle or  2  MOXYs  on very different muscles.
 CO2  is  most often  ( not a  cook book ) a  systemic  reaction . So one MOXY  on  leg  one on  arm.
 Now hold your breath  and wait. It will take  some time  Lag time of  CO2  accumulation  and therefor different XCO2  level sin the blood  , and in the expired  air. In fact we may  have three different  CO levels   P arterial  CO2  p  alveolar  CO2  and so called EtCO2.

 This is  why RQ  (  measured in the blood )  and RER  used   in VO2 test    measured  in the mask  can be  but are often not the same.
 You need a  time  frame of  6 - 8 min   to "balance"  CO2  in blood  and  in your VO2  mask. and you have to be  very  quite  or   minimal  motion.
 As  soon you move your RER  and RQ  is off and your RER  is    extremely depended on your respiratory  ability  and whether you breath  always  with the diaphragm or sometimes  more  papilla  with   auxiliary  muscles.  This  fact   throws  a lot  of critical questions  out  to  what we  do  with RER  and the " calculation  based on RER  on  use  of Fat  or glucose  and so on.
 It is a great impressive   concept  will see great  but is it   actually  working ?
 Hard  to explain  why sometimes  RQ  (  which really is RER in VO test  drop  as harder  we go  which would indicate more Fat use  in a  hard  section.) 
Here  for  all " critics"  a case study  from Prag  from Jiri  Dostal

kindlyman  VO2  VCO2.jpg 

look at  dark  bleu  RER Which  many VO2  equipment sellers sell as RQ ??? In this  case  as you can see it was a step test  with rest in-between RER  was high at the start  and drop as harder the athlete   got pushed  so   in " nutritional " metabolic terms  ( classical ideas ) this athlete  started out  with Glucose  and ended  with FAT. In fact  an RER  number of  0.7  would indicate  fat use  and an RER number  of 1  would indicate  glucose   use  only. Numbers  above  1.0 ????
  So now  your experiment  with holding breath  will :
 a ) increase ????
CO2 levels duirng holding breath.jpg 

Below the  picture  of this experiment. Keep in mind  this  person  is very  good respiratorically trained.  . Case study  courtesy  of Brian Kozak  Next level   ice  hockey    expert. MOXY  expert  as well as  respiratory   Spiro Tiger  expert

holding breath  3  x.jpg 

Now  you can do the opposite You  can breath  super intense   ( hyperventilate )  and see  what happens  to SmO2. So  yes  we  can  manipulate  with a  proper  respiratory  system  whether we like to load  O2  form lungs to blood  (  so u you have to breath ???? ) or  whether you like to  get some  more O2  from the blood to the cell  you have to breath how ????
. Now  if your respiration system is okay   you  can barely try it out. If  your respiration is  a limiter  forget it.   and this   under  workload  it is  even  harder  and a  reason  why most coaches  say it  can not be  done.


2. The respiratory system has a key role in re-balancing the dissociation curve, as it is the mechanism that gets rid of CO2 from the body (i.e plays a role in the utilization part of the "orchestra"). So if the respiratory system is not effective at getting rid of CO2, it is actually a utilization limiter. There is a circulatory problem here as well because the respiratory system is the only system that can be the compensator i.e.  the respiratory system starts to work harder to get rid of the C02, then it creates more C02 because of the muscles in the respiratory system working harder, which makes the C02 imbalance more etc.... 

Absolutely. But  some   debate on the respiration. 
 Key  questions is :
 What is  the respiratory  main muscle.
 Besides  respiration ( inspiration he is the main  and key  core  muscle  for core  stability.  so yes  a  weak    diaphragm  will ask  :  for  a loss of  optimal core stability  and therefore efficiency in any sport. This creates  more muscle activity  more CO2  and  asks  for  auxiliary muscle to  try  to compensate  for  weakness in diaphragm  which leads  as mentioned  above  to more  CO2  and  you see where we  end up.


efficient in releasing C02? 

focus on exhalation 

 You only  can exhale  as much as you inhale. Exhalation   is getting a big help  from a great inhalation (   loading  rip  intercostal muscles  and  so on   so  as you relax  you exhale  out normally  passive. During sleep you only inhale  really  with a muscle  contraction the rest is  " passive"  now  an increase in  exhalation alone will create a  dysbalance  it  has to be a balanced  / inhalation and exhalation  work  and  by inhaling properly  you will get forced  to exhale  decently.  Question :  would you as  an endurance athlete  buy a  leg press equipment or a  treadmill to  get  better in endurance  ability ?
 So  would you  use a  respiratory  device ,where you can do 10   to 15  extreme inhalations  and force full exhalation ( leg press  for the  respiratory  muscles )  or  do we think  respiration may  be an extreme  endurance  muscle. As  usual  some  exceptions  like COPD for example. Hope  this  adds  to some of  the many questions we  started  in this  section



ryinc

Development Team Member
Registered:
Posts: 359
 #30 

 

Jeurg,  thanks for the reply. The pictures helped, but I am still confused about some things – please be patient with me – no background in physiology.

 

In my post I said:

When C02 is high: The O2 dissociation curve becomes more O2 "sticky"/O2 affinity (shift to the left). This makes it easy to transfer O2 from the lungs to the blood ("delivery") but difficult to transfer O2 from the blood to the muscle (form of utilization).

(Please confirm in such a situation MOXY would show high SmO2 reading?)”

In your post and also from your pictures

“So  right  shift  towards  decreased  affinity  ( less sticky ) so  high to very high CO2  will allow  you  to get easier  O2  from the blood to the cell.”

In other words, In my post it is the wrong way around – I should have said

When C02 is high low: The O2 dissociation curve becomes more O2 "sticky"/O2 affinity (shift to the left). This makes it easy to transfer O2 from the lungs to the blood ("delivery") but difficult to transfer O2 from the blood to the muscle (form of utilization).” And naturally the opposite when C02 is high"

I think I understand the above, and that’s how I actually originally had it when I was first writing the reply. However what then confused me was the athlete being discussed with high C02 case in this discussion:

  • ·         Athlete respiratory system has problem getting rid of CO2

-> Problem getting rid of CO2 = High CO2

-> High CO2 = Disscurve shifts right

-> Disscurve shifts right = Lower oxygen affinity/”stickiness” in hemoglobin

-> Lower oxygen affinity/”stickiness” in hemoglobin = Difficult to transfer O2 from lungs to blood but easy to transfer O2 from blood to cell

-> On Moxy,  once enough time has elapsed this would show as a low SmO2 (?)

Now here is the problem/confusion for me – I thought in this type of athlete we were seeing high SmO2.

Rachel: “My 5/1/5 looks pretty similar to that one you posted.  Sandy said I have great delivery but I'm just not utilizing it.  My limiter is respiratory so we are going to do some work with that.  I'm eager to learn, train and see how I can improve with all the great info from the Moxy.  “. I thought she was referring to the graph where you showed SmO2 of top endurance athlete where it increases and then stays high.

Then finally to answer your questions:

“Now you can do the opposite You  can breath  super intense   ( hyperventilate )  and see  what happens  to SmO2. So  yes  we  can  manipulate  with a  proper  respiratory  system  whether we like to load  O2  form lungs to blood  (  so u you have to breath ???? ) or  whether you like to  get some  more O2  from the blood to the cell  you have to breath how ????”

Based on the information, you posted, thinking out loud I think the answers are:

  • If you wanted to get more O2 from the lungs to blood, in effect you want the disscurve to shift left, which increases O2 affinity/stickiness. One way to do this would be to reduce C02 which (in theory) can be achieved by breathing intensely (i.e. opposite of holding your breath)
  • If you wanted to get more O2 from the blood to the cell, in effect you want the disscurve to shift right, which reduces O2 affinity/stickiness. One way to this would be to increase CO2 which (in theory) can be achieved by holding breath for longer

Unfortunately don’t have Moxy yet, to try the experiments above. Again, if the answers above are correct, then I am confused about the case of top endurance athlete (and for which Rachel's picture is similar according to her) where SmO2 values are persistently high implying that transfer of O2 from lungs to blood is good, but transfer from blood to muscle cells not as good (as this would imply CO2 too low, not CO2 too high).

Sorry not sure what i am not understanding - thanks for your patience.

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