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DanieleM

Development Team Member
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Posts: 264
 #1 
I understand that the Moxy Zone is telling you what is actually the physiological/physical reason for the output (power/velocity), but I would like to know if there is some correlation with the "old" zone method.
I am referring here in particular to the Aerobic Threshold or first turnpoint of the lactate, where I was planning to focus during my boring winter aerobic base.
Even if I realize there is nothing bad with the increase of lactate, I see this point as a different shift of the energy store for the exercise.

In the "Moxy Zone" I am quite sure it is on the STEI, but this zone could be quite large.
My rough guess is that could be a step where it can be seen a decrease on the Sm02 base level compared to previous step, but that would still lead to a flat SmO2.

Hope the question is relevant.

Daniele 
Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #2 
" but I would like to know if there is some correlation with the "old" zone method."

 In short   NO. !

We would like to  completely  separate  what we did  many years back and still is done  with what and where we  like to go with physiological assessments  and training control.
 Here  a part of  our   philosophy.
  In the olden day's  when we used some very different ideas of trying  to  control  workout intensities  we had  no  such luck  to get  a hand  on physiological affordable testing and assessment equipment.
 It was  in   some lucky situation an option to get into a lab  to get some physiological indirect methods  done  like VO2  and or lactate or combination of both.
 Real time info was  hard  to come by and was all invasive.
. So NIRS   and in specific MOXY  now opens this option for anybody on the road. . There however is a problem.
 Traditional   education and thinking versus  potential   new  and  different information's.

Predication  and zoning  and so on  are   all historically based on the situation, that we  had  no access to physiological feedback. So we where  basing the information on  experience  and changes in performance  as a physical feedback. As long this performance was improving we  where happy  and despite the lack of scientific  backups  we  accept this as an empiric    truth.
 The problem only  is getting relevant , in cases, where we had no progress  and therefor  needed  some kind of  an explanation to  accept  this idea of  Zoning  an its  impact.
 reality    shows  and  scientific    assessments  proof  , that a 60 %  load  from 2 people with the same VO2  max ( or better peak )  is not    always the same physiological   stimulation .
 In Lactate ideas we know , that 2 mmol   lactate is not    the same  load  for   2 people despite the same  10'000 m end  time. Many more situation are    showing this  situation.. Zoning is based on a mathematical model , where we use a  single assessed  or  calculated point  ( lie 220 - age)  or  VO2 max tested , of  4 mmol   lactate   produced  with a  " curve"  an than we  simply    decide, that 60 %  suppose to achieve this  and 80 %    suppose to achieve that.
 There are  no  studies  proving this .
 Nevertheless  we  use it as it is  easy no questions asked  and  nothing really to discuss.

Here not  to   get  too negative  but  a  nice  discussion over  1/4  century old.

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.

So    what is with the zoning based on the ANT ?

Here another fun  section as a picture  .
Thiebaeult lactate.jpg 


Never the less  we pay nice money  to get a  AT  or LT  test done. The result from a big company looks  like this.
lactate  rightination.jpg 

True with some imagination you may  find a   AT  or ANT in this three curves.
 The right shift  was done  over a certain amount of time.  there a picture,w here they saved a lot of time  for the same shift right
3 kurven reichert graz lactate and diet.jpg 


And  here, where they did that right shift  by simply changing surface.
heck lactate.gif 

Despite this  facts, we have  now  situations, where   NIRS  is  completely abused  to  try to hang on  with bare  live on a  idea  and   belief, which was great at the time  due to lack of  ability to  see, what really  happens..
 This created an interesting  situation  and I like to   use  an very different example  form a very smart  paper  I will add on as a pdf  file.
 Here the  example:

The behavior of baseball umpires helps define the issues. There are three types of umpires. The first

type says: "I call balls and strikes as they are." The second says: "I call them as I see them." And the

third says: "What I call them is what they become." 



With MOXY  we try to be the first umpire
With  Lactate  and VO2  we  where  with some luck  the second  but  we  often in discussion will meet  with the third  one.

 The  would reflect in 
 :

What distinguishes the types of umpires is not the situations in which they find themselves, but the

attitudes that they bring to their work. As a result of those attitudes, they practice umpiring differently. The first type claims truth;; the second, perspective;; and the third, power.


So the   main discussion we  ave  for now  is not , whether  NIRS is  actually  working as much more   :
 

PROFESSIONAL SCIENTISTS usually respond to new findings with a profound skepticism that goes beyond the specifics of the research. When first confronted with new work, gatekeepers judge it

according to how well it fits with prevailing beliefs. Therefore, the more novel and unexpected a

discovery, the more likely that other scientists will reject it-­-­precisely because it contradicts current

understanding. When they were initially proposed, ribozymes, prions, and cold fusion all looked like

long shots.


As you can see , the  situation is  very  interesting.
 We  believe, that there is   no such thing like a  zoning    we can plan  for, but a  physiological intensity we  can see,   now live, whether we  are in that intensity.
 Now  we  can    repeat this over a certain amount of training units  and than re-asses and see, whether my idea  of  developing a certain functional reaction  and  than follow up with a structural change   is really happening and if  it changes into the planned  direction or not.
 No mater what the outcome is, I now know , what stimulation  I create  with a certain  workout  creates  what kind  for a physiological respond.
 If it is the planned one  great , if not  great as well as I now know , what  this workout actually stimulated in my body  and I  can change now  to another physiological intensity  and see, whether this is doing the planned adjustments.
   We are now a  nice group world  wide using this  idea, looking   what happens  and not  what we  like to see  and we are well  underway to understand  more ( Not all ) on what  loads  and what physiological   stimulation    create  what out come.


 This is not    only true  for  endurance  but as well for strength, where  the 1  Maximal rep  idea  as 100 %  and than taking    80 %  from that has the same   missing physiological  information  as  the % in open discussion.' Follow the promised PDF file,.

durnace workouts.
 Again why should  I   run 60 min  or  5  sets    1 min  or 400 m     or 50 m swim. This are all  simple  organisational ideas  with out any physiological logic  behind  at all.
 The energy supply  ( delivery ) and utilization feedback is what creates a   stimulation  to our  body  to react accordingly to the  overload  we apply.
 Hope this make s some sense  but please come back  with great and critical feedback's.
  This is what creates a healthy discussion
 follow the  promised PDF

DanieleM

Development Team Member
Registered:
Posts: 264
 #3 
Thanks Juerg, I understand your valid point.

Regarding my specific question (Aerobic Threshold) I found this research:

Blood lactate accumulation and muscle deoxygenation during incremental exercise



Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #4 
Thanks again for the great feedback. Yes the Grassi's paper was  an interesting   study  and we have it some where on this forum  at the beginning of our discussion.
 i  tried  or we  try to avoid    further discussions on lactate as we  do this  now  since the early 1980. The main interesting situation is, that  we   somehow  accept these fact , that lactate is not what we  learned  in school ( but  we still have a problem to get rid  of the  use  of the old idea in sport.
 How  come that we still have  so called lactate tolerance  workouts, when in fact we know, that  if we add lactate  to a working muscle we  can go longer  and faster ???
 What is the reason  we learned  in school why we should cool down ???
 Well if  lactate is not the reason anymore  what is  the new  reason.
 Why would we like to drop lactate after a  workout, when in fact it is a fast  option as a shuttle   to refuel  the liver ???
 And many more  question we  collected over the  last  over a quarter of a century.
  Yes there is  a  connection with lactate and SmO2    reactions as both  have a  connection to   energy production over  O2.
  I will look back where we did  many years back the same. We  desperately tried  to hang on  to the lactate idea ,  Threshold idea  and so on  and we tried  over  hundreds  of test  to  create a LT  threshold with NIRS (Portamon )  but as longer we  tried  as worse  was the outcome as we started  to  understand more ( not all yet ) how O2  utilization  and energy  production  are influenced.
  We  think it is great , if people try  to use  NIRS    to  do a noninvasive lactate test?  The question simply is up  for discussion on  how to I  find a lactate threshold if  perhaps there is no such think like a lactate threshold, and if there is one  what  concept  do I use  ( Simon , Keul , Kindermann, Bunc, Broumann ,Tegtbour  ????)  but a great imagination may always find something..
 Depending where we go here  I may  copy some of many  many hours  of discussion on lactate on here as we go along.
 Our idea  simply is to look what  MOXY is doing , what we  can measure  and what  it tells us, without trying to force it in any existing  theory we  may simply like to defend  out of many different reasons.
   As  such I like to how here a  very short perfectly written summary in where lactate really  seems to be  and to go.
 Have  fun  and great discussion  and  yes many different options.
 

Lactate metabolism: a new paradigm for the third millennium

L B Gladden

Department of Health and Human Performance, 2050 Memorial Coliseum, Auburn University, Auburn, AL 36849-5323, USA

Corresponding author L. B. Gladden: Department of Health and Human Performance, 2050 Memorial Coliseum, Auburn University, Auburn, AL 36849-5323, USA. Email: ude.nrubua@blddalg

Author information ► Article notes ► Copyright and License information ►

Received November 25, 2003; Accepted April 29, 2004.

Copyright © The Physiological Society 2004

This article has been cited by other articles in PMC.

Go to:

Abstract

For much of the 20th century, lactate was largely considered a dead-end waste product of glycolysis due to hypoxia, the primary cause of the O2 debt following exercise, a major cause of muscle fatigue, and a key factor in acidosis-induced tissue damage. Since the 1970s, a ‘lactate revolution’ has occurred. At present, we are in the midst of a lactate shuttle era; the lactate paradigm has shifted. It now appears that increased lactate production and concentration as a result of anoxia or dysoxia are often the exception rather than the rule. Lactic acidosis is being re-evaluated as a factor in muscle fatigue. Lactate is an important intermediate in the process of wound repair and regeneration. The origin of elevated [lactate] in injury and sepsis is being re-investigated. There is essentially unanimous experimental support for a cell-to-cell lactate shuttle, along with mounting evidence for astrocyte–neuron, lactate–alanine, peroxisomal and spermatogenic lactate shuttles. The bulk of the evidence suggests that lactate is an important intermediary in numerous metabolic processes, a particularly mobile fuel for aerobic metabolism, and perhaps a mediator of redox state among various compartments both within and between cells. Lactate can no longer be considered the usual suspect for metabolic ‘crimes’, but is instead a central player in cellular, regional and whole body metabolism. Overall, the cell-to-cell lactate shuttle has expanded far beyond its initial conception as an explanation for lactate metabolism during muscle contractions and exercise to now subsume all of the other shuttles as a grand description of the role(s) of lactate in numerous metabolic processes and pathways.

Introduction

In 1950, von Muralt distinguished four different eras in the development of muscle chemistry: pre-lactic acid, lactic acid, phosphorylation, and myosin. The pre-lactic acid era began in 1808 with Berzelius's discovery of an elevated concentration of lactate in ‘ the muscles of hunted stags’ (see Brooks & Gladden, 2003). Although there were several studies of lactic acid (HLa) in the next 99 years (see Brooks & Gladden, 2003), confusion reigned until the landmark studies of Fletcher & Hopkins (1907). Their paper ushered in the lactic acid era during which A. V. Hill's studies suggested that HLa was the immediate energy donor for muscle contractions and Meyerhof demonstrated that glycogen was the precursor of lactate (La) (e.g. Meyerhof, 1920). Between 1926 and 1932, ATP and PCr were discovered and investigations were begun to determine which of these phosphagens might be the direct energy donor for muscle contraction (see Brooks & Gladden, 2003). These discoveries and new ideas changed the field of muscle energetics so profoundly that A. V. Hill (1932) called the experiments over the 1926–32 time period ‘the revolution in muscle physiology’. Accordingly, the 1930s marked the beginning of the phosphorylation period of muscle chemistry. In 1939, the myosin period began with the finding that the enzyme responsible for ATP hydrolysis was associated with the muscle protein, myosin (see von Muralt, 1950 for details and references). By the early 1940s, the full Emben-Meyerhof (glycolytic) pathway had also been elaborated.

If we restrict our considerations to HLa and its metabolism, we might term the period from the 1930s to approximately the early 1970s the dead-end waste product era. During this period, La was largely considered to be a dead-end metabolite of glycolysis resulting from muscle hypoxia (Wasserman, 1984). Lactic acid was also believed to be the primary cause of the slow component of the O2 debt (Margaria et al. 1933) and a major cause of muscle fatigue (Hermansen, 1981). Since the early 1970s, a ‘lactate revolution’ has occurred. At present, we are in the midst of a lactate shuttle era which began in 1984 with the introduction of the lactate shuttle hypothesis by George Brooks (1985a).

 

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #5 
I am getting the ongoing emails with the reaction  of the  picture  from Perronet and Morton 1994
They  had  the guts to write :  Unscrupulously  process of  imagine a threshold. :
  I like to add here to their  version the  next interesting trend we see,  as we try to defend the lactate threshold versus the direct feedback NIRS  can give  by  " abusing " the NIRS  information into the imaginary  options of a  lactate  break point  or threshold.
 You are the judge  from this  fun  picture  form a  very great group    trying to   create a noninvasive  idea  of lactate  threshold  found by  NIRS.   can YOU see the breakpoints  where they see it ?

VO2 lav and TSI % UK.jpg

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