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juergfeldmann

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 #1 
Hmm  got  already 2 mails back  after my short critical  view  on lactic acid.
 I  decide  to go this  route . Let's use the    words of the counterbalance  to Mader  and  Holmann  to explain  somewhat simple but nice  the the myth of lactic  acid  started  and w y we may have to review  this 
Here we  go  again.
 

fitbyfred

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 #2 
Thanks, Juerg. 

Such a nice chat to share. 

I especially like Brook's casual thoughts on areas to stimulate, specifically around 15:40.  

FBF
juergfeldmann

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 #3 
And I like  the  miss concept  from the girl    who is doing the interview  and the politeness of  Brooks  not  to intervene. She  talks  about  respiration and the limitation f getting the O2  in, when he  talks  about respiration  nd the limitation to get rid  of CO2 s a part of the H+  buffer ability.
 This is what we see all the time. Respiration =  O2  that's' it , when in fact there is much more to it and NIRS  shows it   very nicely.
fitbyfred

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 #4 
To help her better understand, he could get set her up on a tread at/above LT (your favourite) [redface]) and coach her to release breath ? 
hourerg

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 #5 
Great interview. I have a great amount of respect for the "girl who is doing the interview" Dr. Rhonda Patrick. She is definitely someone to keep an eye on.
juergfeldmann

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 #6 
Thanks  for the nice feed backs on here. I got some as well as  emails but more towards a trend of  trying to  maintain status  quo on LT or anaerobic threshold..


 I like to add some additional  critical reading to this we showed  already  many times  so here we have a all together.
 First a very critical     paper   and look how far back  it is.

ANAEROBIC THRESHOLD - A RELATIVELY USELESS CONCEPT FOR COACHING

Billat, L. V. (1996). Use of blood lactate measurements for prediction of exercise performance and for control of training: Recommendations for long-distance running. Sports Medicine, 22, 157-175.

And here a  slightly  less aggressive   wording.

Chest. 1997 Mar;111(3):787-95.

Dangerous curves. A perspective on exercise, lactate, and the anaerobic threshold.

Myers J1, Ashley E.

Author information

  • 1Cardiology Division, Palo Alto Department of Veterans Affairs Medical Center, Stanford University, Calif, USA.

Abstract

A number of general observations can be made from these recent studies. Lactate is a ubiquitous substance that is produced and removed from the body at all times, even at rest, both with and without the availability of oxygen. It is now recognized that lactate accumulates in the blood for several reasons, not just the fact that oxygen supply to the muscle is inadequate. Lactate production and removal is a continuous process; it is a change in the rate of one or the other that determines the blood lactate level. Rather than a specific threshold, there is most likely a period of time during which lactate production begins to exceed the body's capacity to remove it (through buffering or oxidation in other fibers). It may be appropriate to replace the term "anaerobic threshold" to a more functional description, since the muscles are never entirely anaerobic nor is there always a distinct threshold ("oxygen independent glycolysis" among others has been suggested) Lactate plays a major role as a metabolic substrate during exercise, is the preferred fuel for slow-twitch muscle fibers, and is a precursor for liver gluconeogenesis. The point at which lactate begins to accumulate in the blood, causing an increase in ventilation, is important to document clinically. Irrespective of the underlying mechanism or specific model that describes the process, the physiologic changes associated with lactate accumulation have significant import for cardiopulmonary performance. These include metabolic acidosis, impaired muscle contraction, hyperventilation, and altered oxygen kinetics, all of which contribute to an impaired capacity to perform work. Thus, any delay in the accumulation of blood lactate which can be attributed to an intervention (drug, exercise training, surgical, etc) may add important information concerning the efficacy of the intervention. A substantial body of evidence is available demonstrating that lactate accumulation occurs later (shifting to a higher percentage of Vo2max) after a period of endurance training. In athletes, the level of work that can be sustained prior to lactate accumulation, visually determined, is an accurate predictor of endurance performance. Presumably, these concepts have implications related to vocation/disability among patients with cardiovascular and pulmonary disease, but few such applied studies have been performed outside the laboratory. Blood lactate during exercise and its associated ventilatory changes maintain useful and interesting applications in both the clinical exercise laboratory and the sport sciences.


However, the mechanism, interpretation, and application of these changes continue to rely more on tradition and convenience than science.

 

hourerg

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 #7 
Years ago, when I was doing the LBP tests, it occurred to me that we should try doing step tests in reverse order. By that I mean, start off our first step at a high intensity where there was a high lactate reading. The next step would be a slightly lower intensity yet still produce a higher lactate reading. Continue the steps decreasing intensity till there was a lactate reading that was no longer increasing. Of course, there was problems with the lag time of lactate testing but I wonder if now with the Moxy, we would learn something by trying the same test.
juergfeldmann

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 #8 

I   assume  you are aware  who  developed the LBP  ( lactate balance point or FaCT test .
 So  you can imagine  what the first   idea was, when I had the first time a  NIRS in my hand.
 The shocking  result  was, that the idea  with LPB  fell apart    with every single  step we added and challenge.
 20 years of  lactate  ideology  form my side  with over  hundred  thousand  of  lactate sampling  simply  crumbled in front  of  my eyes.
 I  had  to take  my own  " religion" apart  and exchanged  some  of  my "gods".
Well  first I tried for  awhile to   manipulated the NIRS  data's   to fit into my  old ideas. but  as harder I tried  to   fit the  facts into a  wrong theory  as worse the end result   was.
 We  as well where able to  explain some   results  form LBP , now  where before we  simply  where pushing the possibilities  under the table as they did  not fit  our  believes.
The first  thought was:
 Can we replace  lactate  testing  with NIRS. 
 terrible thought , as we  sell hundreds of thousand  of  lactate strips in  north America.
So  why  would we search  for a replacement of lactate.
 Well even worse was  when we  started  to think  even more critical on lactate as  I did in our   MLSS discussion on this forum.
 Two  world  collided.
 The  reality  that LBP  was  a great step forward  to  find  why  it does not work  and  second the    interesting feedback of  live bio markers, which showed,  that SmO2  not   runs   always  with lactate trend.
 Again we can have in a NIRS data  SmO2  increasing  so    seems to have more O2  but lactate is going up . or we can have  SmO2  decresasing  so less O2  and yes lactate goes up  but as well we can see SmO2  decreasing but lactate goes  down.
Some trends  due to the  lag time of lactate  reaction   and how  and where we test  for   but as well due to physiological reactions.
This creates  an interesting  situation, that I sometimes  get called to the phone in the fact office  to explain  people  that yes we  can sell you  lactate strips. If you use it  for sepsis early detection great . If you use it  for   sport assessments.  well I can sell it but I   can not help you what you can  use it for besides  some nutritional feedbacks. Than if they ask  for a NIRS  equipment to   test  for LT  I  as well can not sell him a  NIRS  equipment.  as NIRS  does not test  lactate it simply gives a feedback ove the   light spectrum what  happened under the   placement of the  probe in  connection  with O2  dynamic. Does  lactate and NIRS feedback  have something in common.
 Sure both are  feedbacks in their own rights on  energy  trends. One is live and direct the other one is a    systemic  end result  with   some open  questions.
 Is  NIRS better  than lactate.
 No it is different.
 Is  lactate  ideas easier to use.
 No  it is  a mind set on how much  we like to invest  to critically  learn  as we   get new ideas and equipment.
 Is  LT  easier to sell.
 For sure  as nobody asks  critical  questions  and   many believe  it is the golden standard.

Shall I change  to NIRS  and give up lactate.
 
No  not at all.
Start  to combine it and make  your  own  step by step  findings  when  and where your  experience  together with the  b values  you find   can help to make a  better decision  for your client.
 Than you decide, when or whether you may   use one or the other  alone or together.
 Never throw  out your experience but  always be ready to  change your believes. 
 Remember the old   gods.
  Thunder and lighting  was  caused  by angry  gods  fighting with their  swords.
 Well  great  idea but once  there was  an explanation  some of the goods had to be retired.
 Only  religion has the privilege  to  create stories  we  not have to back up  with facts.
 . Not sure whether  this   should   be applied  to  exercise  physiology  or science ?

juergfeldmann

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 #9 
I got some  very nice  feedback  and one of them  really   asked a  great  question.

We know  by now , that lactate  is very strong influenced  by energy  demand  and utilization .

Is there a  connection  to NIRS  and if   how ?

Answer  is yes, as both  NIRS feedback  gives a feedback on O2 supply and demand   as well lactate gives a metabolic  feedback on needs  for buffer  and  possibly energy  shuttle.  The interesting part off  this is,  that  lactate , when used ass a classical  model  for a lactate curve  without integration of the physiological knowledge , may lead to very  different conclusions, where as  SmO2 trends  show the actual   real information on  O2  supply  and or   utilization.
 I like to show you a  " classical"  graph  including some very interesting  " features  on it.

lactate curve bsx.jpg  Above is a  typical lactate  curve  with the idea of  finding LT  where we have a  1 mmol increase in lactate over  two steps in a  row. Now here some critical points.
 
a) look  at the LT interpretation . Do we fit the facts  so it fits the theory
2. Accuracy  of any lactate testing  equipment is   O.2 +-  mmol  for positive thinking people  and slightly higher for more critical people.?
 The likely hood , that the blood sample was in  exactly at the same  second is slim  and it does  possibly not matter  at all anyway.
 But give +- 0.1  to 0.2 and   see, how  performance  at LY  would change. ?


Now the above graph  explains, that a  right shift   of a lactate  curve indicates  an improvement in  performance. Which   may be true  but is not  always the case.

3 kurven reichert graz lactate and diet.jpg 

The  explanation  on the graph  top empty  circles  glycogen rich
Full  circles middle graph average normal  food  ( what ever normal means )
and   most  right curve  is glycogen  poor  or unloaded.
So  extreme right shift  but  most likely  less  good  performance ???

True  the   experience  lactate user  will have a specific  point  when comparing this  2 graphs.  why it is clear , that the top graph indicates a  shift in  performance improvement , where as  the lower  a  sign of  glycogen depletion.
What is the  argument we  can use  for this statement ?

 So in case you come up with that argument.  apply it to the  test result below  and see, whether  it  can be defended ?
r summary 3 tests.jpg
Now  use  any of  the current  LT  theories  and apply it  to   any of the three examples I showed  and   honest  tell your  self or  even on here,  what you come up  with ?
 
   Now   look the below graph  form a rowing  website.
rowing lactate.jpg 

Questions:
a) where is LT  1 In rowing  they use  2 mmol. In  other  groups they use  the  start value  as abase line and when it  passes this  value again there is  LT 1
LT  ( or LT  2)  above.
 1 mmol increase in 2  follow  up steps  so it would be 225 watt  4 mmol ?  . ).1   measurement error  and we  shift again .

Now  it is  even more fun see below.

triathlon lactate.png 
 Now depending on the theory  they like to apply  LT1  =- 45  %  VO2max
 If  we use  2 mmol we have 2 lT1  one by +- 60 % and one  just above  70 % Now  LT    they are lucky it fist  with 1 mmol idea and it is  exactly 4 mmol   tested. Needs a lot of  skills  to  actually hit 4.00 mmol  lactate value. Even  with   thousands  of tests we never got  down to that science  and accuracy.
  In fact the " father" of  4 mmol  lactate idea  G. Mader  never got it either

$ mmol tabelle amder.jpg 
 Sorry  he was better, he got  2 x 4.00 in the lactate steady state  and once in the  3 min step test. Interesting to see how he shows , that  step length may  screw up the  result  and in fact the 5 min step test  was closer  to 4 mmol than  the usually used 3 min step test.

Summary.  Lactate  dynamic  and trends  and  shift in the curve  are  incredible  dependent on many different reactions  and  are  most likely not easy to apply  during a   workout.

 So  where is NIRS  coming in.
 1.  Live feedback  and  not  fixed on absolute numbers.
2. The   option to find a  LT  and a BP in a nirs   is getting very hard to find, if  we take the glycogen  rich poor  and normal example.
 . As less glycogen  as more  likely we may see a  shift  of the lactate curve  to the  right
 
 As less glycogen,  as earlier or  as more we may  need  fat metabolic  help , which needs more O2  for same performance so  the  NIRS  " curve  will shift to the  ????????

 Here  a case study  from the very early  days  of NIRS  and lactate.

NIRS  and  lactate curve.jpg 


You can see where we have some  honest problems to fit  a BP  if there is one  to a  theory of LT.

BUT  the bright  side is  that you  can see how a live feedback of  O2  trends  may  in fact  change the way  we may work out.?
 Or  so I hope


sandor

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 #10 
Juerg, i just re-read something i had forgotten as well - that utilizing fatty acids is more oxygen hungry than utilizing glycogen.

1 mol fatty acid yields 129 ATP but uses 31 mol O2 (4.2 ATP per 1 mol O2)
1 mol glycogen yields 38 ATP but uses only 6 mol O2 (6.3 ATP per 1 mol O2)

this morning i was contemplating how this sizable difference in O2 consumption could show itself with a device like Moxy...



This, to me, is the exact example of how discrete SmO2 monitoring (ie monitoring the fuel usage of the engine) can be much more exciting, but also more complex, than monitoring the systemic lactate levels (ie monitoring the exhaust output of the engine)
juergfeldmann

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 #11 
Nice  add on . Thanks  Sandro  great
In defense  of lactate   in case we look at this  resting  and post break fast lactate is  an interesting  concept.
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