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xcskier

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 #1 
What are muscle oxygen saturation thresholds (ST1 and ST2)?

How are they determined (ie, is there a protocol)
and what are their meanings?
juergfeldmann

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 #2 
Need help on this. Where  did  you  found  the  ST  1 and  and ST  2. ?
I   would argue  if that is  around  it is  to try  again  to  link  LT  1 and LT  2  and VT  1  and VT 2  all in the same  bucket.
  There are no thresholds  as  people like to have. There  are areas  of  overlap  and this is  used  since  the  2  and 4 mmol lactate threshold introduction, where exercise  people very  fast  understood,  that there are no punctual  situation and that's  why they  used   at that  time the so  called aerobe  / anaerobe  transition area.
I will give some thoughts, on that when we look at lactate ideas like to confusing idea on LT  1 and  LT  2. To  make a  ST  1  and or  ST  2  by using  one specific  muscle  and than  use that  for what ever sounds a  big step  backwards  with NIRS.
 Again, as in one  example we  had.  SmO2  alone  does not give the   full picture  as  tHb  is needed as  SmO2  is   a  %  of  tHb.
Finding any  magical point in an assessment and  than run training ideas on this  is  what we did in the past. 
 We  use  NIRS  to find physiological limiters  and potential  compensators , so we know  where and  what  to stimulate.
 The intensity and how to stimulate this limiters is not bound to a  magical tested point.
 As  this points  can change from yesterday  to  today.
   The  training intensities are based on your  training/ stimulation goal. So , as  so often mentioned, you may like to have a specific desaturation workout, but you do not like to stress the cardiac system  too much with it. So  you   choose a  very low intensity and manipulate  the O2  bio availability.  Traditionally  we  would use  desaturation workouts  by  making any kind  of a HIIT. Traditional HIIT is   paired  with  high load  ( wattage in  biking )  but we look  HIIT  as  the idea  to  stimulate one  targeted  area  very intense so  high intensity  for one area and  if  planned,  avoiding  an overload  in an other system.    
xcskier

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 #3 
I came across ST1 and ST2 in a marketing blurb for another NIRS sensor 
and its analysis software:
http://www.oxy4.com/en/performance-diagnostician/software/
It doesn't say anything what it is.
juergfeldmann

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 #4 
Question
 I  try  to  figure out  why  this interesting  question on ST  1  and ST  2. I  looks to me , that  we  try  to hang on the idea  of  LT  1  and LT 2   and  than find a  way to use NIRS  to kind of  copy  the LT  1  idea  for the  slower and longer training  units. Remember  lactate  or glucose or  epinephrine  or norepinephrine or what ever we like to use, are blood values and as   such  have a lag time and  are a feedback on something  which  may have happend locally like lactate  or systemically  like epinephrine,  but at the end it is a  blood  drop to give some feedback on some energetic  reactions. Smo2  alone  has  to be taken  carefully  and better  you use it in combination with tHb  trends.   Even than it is  from a specific muscle  and if we like to have more feedback  we  may have to get a second one  to see possible systemic  or  more local reactions.

The other interesting  situation is,  that lactate trends and SmO2 trends can go in very different  directions.
 The best  way to look at this is   with  glucose  loading or unloading.
 The same  can be used to proof  that VT  can be  but often is not  LT

Here  an old  case study   at thee  beginning of  trying to replace  lactate poking  with NIRS information. Below one  of initial  hundreds  of  test step test  where we  though wooww there is a connection ( and it is )  so we  can create a " lactate curve  with  an SmO2 trend. But than we  had  to look more critically . So  depending on what muscles  we  would use it was  completely off. As well  depending on the step length we  where  of,  depending on  the  sport  so if  we had to stop to  take lactate we where off. BUT  the stop  gave us  some interesting other  NIRS feedback.  ( Can  you smell  why we   moved  towards  5/1/5 ?)
And many  more reasons.  .So  we  moved  back to the   glucose  loading and depleting as we  did  when we worked  on the lactate balance point idea. 
 The fact  that  a  lactate curve  moves  to the  right , indicating a better performance when in fact performance  dropped,  was  a key  question. Why?. If we  move  more towards  fat metabolic  situation because we run out of  optimal  glucose  supply,  what  will happen  with NIRS.  With lactate we knew  it would imply a  right shift,  but  using more  fat  than  glucose would ask  for more O2    so  this would indicate that  the " SmO2  curve " may shift to the left.

Below a  single   old test


roach lac and SmO2.jpg 


Now  belwo  three  tests  with different glucose  loading/  deloading  and  average   load.

NIRS  and  lactate curve.jpg 

 The reason  why  we  trend towards  physiological   stimulation and live feedback is  exactly  the dilemma  we have  or  had  with LT  1  or  LT  2.
 . Why  LT1  and what is  LT  1 .   one of  the most common   reason  we  gave is  you should have  no lactate in the system. Well  finger  sampling may tell there is not  a lot   of lactate circulating, but you may  produce  nicely in some muscles  and  use  it in the some  other muscles.
 Well what is  wrong  with lactate  after  it  got  debunked  as  being bad.
 So  the  question  for people  who  try to find  a LT1  replacement   is    much more on what  is the physiological reason  for this  long  slow  training hours ?
 ? . That's where the physiological ideas  come in on how  to stimulate  a vascularisation.  than  to use  NIRS  to actually have the feedback  to support  the different ideas or methods we believe  we  can   create more blood vessels  . And than assessment and reassessment to  see, whether we  actually increase  the vascularisation

xcskier

Development Team Member
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Posts: 46
 #5 
So, if I understand correctly ST1 and ST2 is an (possibly misguided) attempt
to define some sort of training zone based on SmO2. I couldn't find any
reference to this concept in the literature.

This question may belong in a different thread, but

Quote:
much more on what  is the physiological reason  for this  long  slow  training hours ?


are you saying that long slow hours (in some sports like rowing, skiing) are unnecessary
and have dubious physiological benefit? Namely, with proper (and different) stimulation,
the same benefit could be achieved with lesser training hours?


sebo2000

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 #6 

 That website is really cool, it is very exciting to see people are exploring physiological monitoring instead of performance based markers.

 

I’m asking myself about Lactate, why did we use it, what for? I think lactate was allowing us(me) to organize\categorize our training regime\plans "better."

 

For years people were using lactate to define physiological load/stress. Is it precise method? No, it is not. Is performance based FTP method precise? No it is not.

Can it help in training, yes, it can because it brings structure. As long as we see gains it helps. Is it the most efficient method? No it is not.

 

As long as we see gains we can use it, problem starts when we do not see gains, we start to believe we peaked… and I’m sure we are very far from peaking, we just do not know how to unleashed our potential because we look at wrong numbers. With Moxy we can look much deeper than ever:

 

  1. Physiological systemic adaptation/changes.
  2. Very localized changes adaptations, we can be super granular.

 

Understanding sport/discipline and demand for it, is the key, also careful body observation is a must.


In the past I would do lactate test, define my lactate at eg 280W, based on that I would have further zones defined. In my build period I would be riding Z2 and Z3.

Problem is that those zones are dynamic based on current training overload, events, and many other factors, sleep hydration, temperature etc.

Normally I like to stay in my Oxy/balance zone, for what ever reason... In translation to the numbers: at 230W my SmO2 is solid line growing very slowly over time of 20min.

 

Just recently: I had some velodrome session/races on the weekend

 

Next day I’m jumping on the bike, ergo set to 230W started pedaling and see my SmO2 not only dips deeper than usual, but also is jerky, it seems my delivery systems are fighting utilization/delivery changes….line is slowly dropping.

 

It seems my lactate zone 3 is not zone 3 anymore, I dropped the load 15W same thing, I dropped it another 15W, same thing, I dropped another 15W watts, same nice steady slowly growing SmO2 line.

45watts lower @185W lactate/FTP world that is totally different zone now, but from physiological perspective my body is I correct "zone" I wanted to be, and it feels the same despite the fact it is 45watts less.

 

Would I be able to perform on the fly adjustment like the one above with lactate? Not really, I would have to go over ramp lactate test to see if my lactate changed, that’s totally not realistic.

 

My biggest questions, and I know we could debate this to death, but still would nice to hear different opinions:

 

Let’s consider we have well balanced athlete, his cardiac/respiratory and utilization system is in sync. We want to work on utilization or delivery (I do not want to be specific, hence no specifics)

 

Is it better to overload those system on the “edge of the overload/balance” or just go all in and hit it hard? If we hit it hard, most likely we will not be able to perform the same next day, we can alternate with some other workout. Consistently overloading at smaller level will allow us to do more similar workouts every day.

 

So the question is: what brings bigger gains? I understand we probably do not have right answer, but what people experience what people think? Switching between systems and high overloads or more consistent training on each system with lower loads?

 
Real life actual racing “wish” I always had for many years, materialized just few days ago thanks to Juerg awesome questions (this is gold for an racer):

 

After a race my respiratory system was always very heavily overloaded, understandably. After a race I was always coughing mucus quite a lot, few hours after the race or intensive Velodrome session, I was always having very clean airways, super clean, I was always thinking to myself, this is way too late, if I could only breathe like that BEFORE the race I would place much better.

As we all understand having super intensive session just before the race would be plain dumb, it would help with respiration but it would kill my legs…

 

Juerg persistent examples and questions made me experiment with breathing, I did 2x10min sessions requiring zero “muscle effort”, I was actually seating at my desk,  my airways are cleaner than ever before, last night I was coughing quite a bit.

My wish came through, this will be exercise I will be doing week before the race day for sure.
I will not say what I have done besides experimenting with breathing (no tools needed, you can do it with your body only), because Juerg didn't relay gave me any specific exercise.


juergfeldmann

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Posts: 1,501
 #7 
are you saying that long slow hours (in some sports like rowing, skiing) are unnecessary
and have dubious physiological benefit? Namely, with proper (and different) stimulation,
the same benefit could be achieved with lesser training hours

Not at all  . I think it is needed , but I  do not  think  the benefit  is  that we  create really  more blood vessels. We may but a lot  of  time    and we coud  do this in much  shorter time  the same as we see in classic a HIIT  VO improvement.
 I will  come back in here, why I  would do  longer    slower workouts  but I would  look what I target  with this and not  looking on lactate, but on  many other   parts ( efficiency )  for endurance sports  energy  shift   and much more.
Oleksiy

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 #8 
Hello,

"  The  training intensities are based on your  training/ stimulation goal. So , as  so often mentioned, you may like to have a specific desaturation workout, but you do not like to stress the cardiac system  too much with it. So  you   choose a  very low intensity and manipulate  the O2  bio availability. "

Was there are any studies done to do so with those breathing restriction "Altitude" masks? And what would be a proper use of those?

Thanks for another interesting thread!
juergfeldmann

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Posts: 1,501
 #9 
There  are many studies  out  there  and I did many   experiments  with all  possible  respiratory  devices  and combined  them   with  VO2, cardiac , blood and NIRS  and SEMG  devices as usual  to allow  to  see as much as possible  and avoid   to hasty  conclusions..
.The  results seem to very  regular  the  same.  And if  you  do some  physiological  thinking  you may reach  t  your own  conclusion.
The  results  are not surprising. What surprises  ( well not really ) is  why people   go an by  ant  equipment  if it is  in a certain price  range   because it is in a certain price  range  and not   because  they did  some home work.
Sometimes  there is a reason  why  you have to pay   more  money  for   equipment. I  had a   huge amount  of  e mails  on reaction of interval and  HR  / lactate guided
  as well a   lot of  questions on  cardiac  training.

Again  this is NOT a training  consulting   forum it is a tool  to try to understand interpretation of  NIRS  devices  and what the  data's  can reveal .

I will  show  in that direction  some  ideas  and  it is up  to all the great coaches  using  this information here  to   apply  if  they like in their  own already successful training  guidance.

The same  is  for  this  " altitude " masks to  find out  what  they stimulate  if .

 Question , what is  hypoxia  or  altitude  stimulation  triggering on physiological  reaction we  can test  for ?.
 If  you have the answer, that is   what you test. 
Oleksiy

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 #10 
Dear Juerg,

Thank you for your answer. If you noticed i put "Altitude" mask in parenthesis for a reason. I'n not really after simulation altitude. Just wanted to get your opinion on this case when we restrict delivery system by utilizing this kind of equipment (regardless of marketing price). What happen then? most likely you'll see SmO2 goes down significantly, but it's not because of the utilization, right? How does this play in the big picture?

Sorry if i'm asking stupid question. Just ignore me next time.
juergfeldmann

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 #11 
No  it is a really good  question.
 There is a fundamental difference  between  restriction devices  and  normocapnic  hyperpneu. Restriction devices  due exactly that they restrict  the  airflow  either in expiration or inspiration or both.  So   they are basically a leg press equipment if  you would be a runner   and you can either   have  myo metric   or pliometric  motion   or both. As heavier  you load  as more  ATP  you will ask  for  and  as higher chance, that  you   finally will create more  CO2  and  you will breath more  intense  but there is a limitation how heavy you can load. So  this is a  strength training  for your legs  as a  runner. You may  need  that  for certain reasons.
 Now  you can  get a  treadmill and now  you  run  on that one  which is a different kind of a  workout. Same  with restriction  respiratory  devices  versus   normo capnic   hyperpneu.
 Now  restriction you can  do  with many different options ( cheapest  version   breath through  your nose only  . next one a  towel  in front of the nose  and mouth ,  and  depending on the intensity  you run or  walk  yo may start to have a problem to get  rid  of CO2  and  you will shift  the  O2  disscurve to the  right. This  than will  make it harder  to load  O2  on Hb  and SpO2    will drop.
 There are  some advantages  and  dissadvantages.
 You are limited  how much VE  you can move  and  you are limited  how deep  you can breath or  how shallow so  to not  get hyper  or hypo capnic.

This creates  a  limitation how long  and how  far  down  you can drop your  SpO2 .  The  normocapnic  hyperpneu is   now  what   controlled  the  pCO2  so  you can breath incredible  deep  and    a lot of VE  without  having the risk of  going hyper or hypocapnic.
In both  versions you can choose  to  " cheat " and use  auxiliary muscles  if that is the plan  or  you can try  to integrate  the diaphragm only in inspiration with intercostal muscles. 
The key is  to  know  whether you like a  high pressure  or a low pressure  see the  graphs  we showed  in resiration in and around  your  alveoli.
Summary 
Respiration options  and variation allow  you  to shift  the O2  disscurve  and a  such   you can manipulate the O2 bio  availability  nicely.
sebo2000

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Posts: 227
 #12 

Oleksiy, I’m very interested in this as well, I think they renamed the “Altitude” mask to training mask.

 

From my short testing experience, I can confirm what Juerg said, any mask works like resistance device. When I go in my Oxy zone eg. 170W with mask on, I do not see any changes in SmO2 or SO2. It is just harder to breath. When I increase power to be in balance zone about 230-240W it will be super hard to take a breath, I will feel my auxiliary muscles working hard and Smo2 will slowly decrease and SO2 will go down, but I will not be able to hold this for more than 5 min, I think this has more to do with the way I breathe than mask itself, And I’m very limited to the power of 240W.

 

If you breathe hard you will not get both: hypoxic (decrease O2) and hypercapnic effect (increased CO2) if you breath hard you will have O2 and fairly high level (at altitude we do not have a lot of O2), you would have to start breathing shallow to decrease O2, and I think you can do that easier without the mask on, I’m still experimenting with that [smile]

 

At high altitude we have the same % of O2 but because of low pressure there is less O2, so I guess if we want to simulate that we can’t take deep breaths and hold them, or use mask (a lot of O2) we should be taking shallow breath or actually exhale kind of half breath, to simulate low O2. I might be totally off base, I’m just sharing what I see in my moxy experiments, and each day I have more questions that answers, but I love it [smile]

xcskier

Development Team Member
Registered:
Posts: 46
 #13 
If I return to my original question about "thresholds", I have finally
found a paper that discusses it:

http://jap.physiology.org/content/87/1/348.full.pdf+html

I don't know if there was any further research done.
juergfeldmann

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 #14 
Good paper  and you look back  far in the forum we showed  the Grassi  paper  already.
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