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Development Team Member
Posts: 168
Juerg, this reply is helpful, thank you. See attached MOXY image. This treadmill running assessment is perhaps 100% opposite of the VO2 max test at the start of this topic. By shear length, it was obvious the client started out way too easy, resulting in too many steps.

Using your advice on viewing tHb first as possible sign of delivery challenge, I can see the quick drop early on and a continued steady drop for several steps. During the 1 min unload it's easy to see the tHb response upwards during periods of rest, PLUS as the client is increasing pace / moving smoother, the tHb is rising some towards the end the 5 min loading phases.

So client started moving too easy, creating a less smooth stride and more impact, resulting in muscle compressions that decreased blood flow ?


Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Fred,    Great feedback as usual.  We  can use  if you not mind this assessment for some more in depth  information.
 If you can sent me the csv file  raw data's  as well as the  actual performance of the step test  and if possible  HR . If you did it  on peripedal  you can sent me the peripedal  file converted  to the  MOXY.
  Cheers Juerg

Development Team Member
Posts: 168
Juerg, hi. Yes I did make a peripedal copy of the file, and it's at my conditioning centre while I am home for today with a nasty cold. I do recall the treadmill speed began at 7.1 km/h and increased by .5 km/h each binary jump. So final speed = 10.6 km/h. Today I do have a copy of the Fitmate data, which has the HR info. See attached xlsx

I'm keen to discuss open and welcome others.


Attached Files
xlsx FBF_Jan_2_MOXY,_FITMATE_&_STATISTICAL_INFO.xlsx (498.23 KB, 37 views)

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Fred  take  care in Halifax. no rush  so as soon you  have access to the   MOXY raw data's  it will be  fun to look at them  somewhat different. Than we  can take   both VO2  as well as MOXY info  and I can give some general ideas  when using 5/1/5 in running assessments.
Here for people using VO2  data collection and MOXY  and the TIP ( 5/1/5  idea.
 Here let's see, whether I can get that through properly but I am sue   one or the other regular reader may be able to translate  my Swenglish.

 If you look  at a TIP trend, than you can see, that we always  have  after a 5 min load  a  1 min rest.
 a)  at the start  ( no warm up ) we have the situation , that the Delivery systems.  CO, VE  and capillary bed  are  lagging behind the sudden start  from zero load  to  any step  you start first.  So  for example  from o watt to  sudden  100 watt load. Despite  "only " 100 watt it is   the biggest sudden performance  step we have in the whole assessment.
  So the  immediate  need  fro energy  (  any  type of energy )  shows up in the most extreme use of  O2 in the whole test . We have a big drop in SmO2    . But we as well have a big drop in tHb. SmO2  drops as a sign of a  short fall of delivery ( Low CO , low VE  and  not yet optimal vascular bed situation. This is paired with an initial  muscle compression  due to the sudden start. As we know by now VO2  will lag in reaction. So VO2  curve  slowly increases. This  NOT as a sign of an O2 deficit but as a sign of a delayed reaction of the delivery system form  0 load  to a sudden 100 watt load.
 The O2  is available on Mb  and Hb  and  we use what we have " saved " for situations lie that.
 A deficit is , when we go  form nothing into negative  and nor when we  go  form a lot  to less. The old idea , that the slow increase in the VO2  curve indicates an " anaerobic " process is  wrong and we see now thanks to NIRS, that we use  actually a lot of  O2,

As soon the delivery system reach  and often overreach the needed  level of  performance ( HR overshoot , RF  overshoot )  we  than settle  down  and have the needed CO  and VE   and  nearly but not yet optimal blood flow in the vascular bed

 Now in this  5 min or  somewhat less. " steady state "  resp  often  increase in tHb  and SmO2  as we  deliver somewhat more O2  and more blood as such as needed  , we than  come to a sudden stop. This means that the working muscles  sudden ly  do not demand  anymore the same amount of O2  as they just did seconds before.
 The  "  so called " deficit  which is  just a reloading  back to a better  level of  O2 is long reached  in this initial  levels.
 So the sudden stop   stops  immediately the need  fro O2  from the working muscles.
But the delivery system CO . VE  and capillary bed  do NOT  react the same way. The where just in the midst  of  have an optimal delivery, which now  suddenly is not needed  anymore, but it is still going on  for a  few more seconds ( depending on the intensity level )
 Now  you see where I go with this. We have  an immediate overshoot of SmO2 in the rest phase  as well as  an overshoot of tHb. The SmO2  overshoots, as we still deliver a lot of O2  but it is not used    at that moment from the resting muscles. So the " overshoot  "  from the SmO2 level  immediately before the stop  to the actual level during the stop is the % of O2  the muscle work needed in the step. We can look at this  and look  at the VO2 info as well.
 The tHb overshoot is a sign , that the muscle tension is gone  and we have  good delivery  and free flow  due to no  or very reduced muscle tension.
 Now  as you rest  CO VE  and vascular bed  will come  back to a lower  level as well. Now as you  suddenly start again we have an other alarm phase  and the lag time  of CO  and VE  and  capillary bed is again the reason  why we see a drop in SmO2  and tHb.
So  the drop level  from the top SmO2  at the bets situation in the rest period  to the lowest level  before it  moves back up or is flat or drops  further is the amount of O2  you s=use  due to the lag time of the delivery system. As long delivery can pick up to compensate   and  delivery more O2  or equal O2  we will see an increase in SmO2  or at least a plateau. Again you can see the VO2  in that case.
  I hope you see where we go with this. The load intensity trend   and the deload   trend  combined will tell you  about  delivery  and utilization. The deload  rest  trend  in SmO2  and tHb  will reveal a lot more than most  can see. Most NIRS user look at the load trend and reaction. We look at both load  and deload reaction as they  connect with each other depending on limiter and  or compensator. Look through the many 5/1/5  assessments we showed here on the forum  and get  some thoughts  to what I  tried to explain above. Cheers Juerg


Development Team Member
Posts: 168
Yes, Juerg, thank you it's very understandable. Especially when comparing the above graphics with this image from the forum:

It's early AM here in Halifax, NS and I'm nursing a fever while I read, and I may try a little thinking outloud:

If a delivery situation" is the lag time of CO, VE and capillary reaction, plus an undershoot of volume ?? Correct ?

Next then, clearing a delivery issue is identifying the system who ??? And, if we only had MOXY to work with to identify ???


Attached Images
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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Fred  take  care . Short  help needed.  I  out  of my  own stupid  can't open you  fit mate  excel  file  sheet. Can you sent it  somewhere  different    to my email  so I  can play  with it  and later show how you can combine  Fit mate  and MOXY in a 5/1/5  info.

Development Team Member
Posts: 168
Juerg, here is the peripedal file of the 5 1 5. The first minute standing starts at with the beginning of the MOXY info--around 3:30. 

Copied to your email address too.

Attached Files
csv FBF_5_1_5_Jan_02,_2014.csv (177.54 KB, 13 views)

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Fred  thanks it worked.
 I like to finish  somewhat of this topic  n VO2  and will move your one on a  new  Topic  to separate the two  ideas.

To ,  at least ,  get a  certain  finish in the VO2  max  discussion  we have opened  here   with a great start  form Kyle. I like to give it some  additional critical  thoughts on what  went through our minds  many many years back , when  the first time  the discussion was coming up, that  certain " classical'    ideas may need some  more critical reviews. 
Here just  some key words  to start out.
- Lactate not the reason of fatigue ( Brooks / Gladden  and more )
- VO2 peak  rather than  VO2 max.
 - no such thing like anaerobic
- Anaerobic threshold  a  relative useless concept .
And much more critical  ideas we  already discussed  since many years  on different forums.

So I like to use this opportunity  to just  think loud on some of the key words, as they are  not easy to digest. I like to use  our  first  part of this topic  , where we have the direct comparison  between a VO2  max test  and a simple MOXY data collection.  I like to use  the wording  form the contributor   to show the fundamental difference between   exercise physiology  as a practical application an the theoretical believes  and calculations.
 See  once more the  2 pictures  below.
 1.  MOXY assessment with the same   protocol. ( Which was not a great idea  and you will see  why in the discussion )
 2. The result of the same VO2  max test  with 30 sec  average  data's.

Our  take .
  MOXY test results  show  an individual trend ( not optimal with this type of protocol )  on  this  persons oxygenation reaction to create  ATP.
 In a physiological  sound protocol  we  will see  three  different reactions.
 a) increase in SmO2    as a sign of  an optimal sufficient  delivery of O2  , in fact  a more "over-delivery " of O2.
b) a relative  flat  situation   indicating a  balanced  delivery  and utilization situation.
 c) a drop in SmO2  indicating  an insufficient  O2  delivery  but a still optimal utilization.
 See  a  test on the same topic  by  Fred.

 So  from a  MOXY data collection we  have a n individual information on  Zoning.
 From a VO2 max  with  this  type of protocol  we have an individual endpoint  of  the test. This is called  VO2 max  ( better would be  tested VO2 peak.

 This is all what we have  on an individual base.
  So  what  do we do here.
  See answer  taken  from our first  post.

What would I do with this Data?

You can use the measured V02 to assist in calculating exercise zones as well as compare with measured lactate 
  True  we have  an additional suggestion

Because no Lactate was measured, it’s not possible know the exact point that Lactate Threshold was achieved  Lactate was not measured during this assessment and it’s important to note that lactate threshold typically occurs at 70-80% of V02max in top athletes (And might be as low as 50% is untrained persons).

So  with an  " all out test"  we  can calculate   something, based on ????? ( statistic )  and assuming

people when working ion 70 %   working with the same physiological load  and limitations ????

True we  could  have taken the lactate to get the individual lactate threshold. Look at the ramp test.below

The ramp test started at 100w and climbed one watt every three seconds. I was able to maintain this at an RPM of 95 until 400 watts.


I  do  lactate testing since  over 30 years  and possible   over 10'000 tests  or sampling with any available lactate analyzers.

  Tell me how you  take and when  you take lactate in a  test protocol like this.
  Yes you can take blood.
 Question. The sample ( result you have), to what  wattage ,performance or HR  or VO2    number  do you assign it.
 How  can we believe  , that a  sample taken  anywhere   in a finger or earlobe  or where ever  during a protocol like this  can be  assigned to any of the other    values.
  How  can we  believe, that the lactate  produced  some where in some muscle cell  at  any given time  is representative  to any  other value HR watt  VO2    at the  moment of  the sampling ??

This is just  super hard to believe , that we  can do that  and sell it  without  any scrutiny.
.  Besides  the pen question on  what defines  a lactate threshold in the first place.
 See   back to the key words.



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.

See the date on this critical question 

Thirdly, an alternate or a complementary explanation to the pattern of plasma ]La-] response to ramp exercise can be suggested. According to this explanation, lactate is produced in the working muscle: (1) as soon as the exercise begins, as suggested by Brooks (1985); or (2) following a delay, according to the theory of the anaerobic threshold (Davis 1985). Under both hypotheses the onset of lactate production within the working muscles occurs at comparatively low work rates. At that time: (1) the amounts of lactate produced and the gradient between muscle [La-] and plasma [La-], and the amount of lactate released from the muscle remains small; (2) cardiac output and muscle blood flow are also low and do not favour lactate release


from the working muscles and its distribution into S; and (3) the small amounts of lactate released are diluted within the comparatively large S, thus resulting in a very small increase (if any) in plasma [La-]. Therefore,



exact corresponding work rate, but at a previous t minus ~ of unknown and probably variable length, and at the corresponding work rate. This phenomenon might have been overlooked in the development of the theory




of the anaerobic threshold which implicitly assumes that plasma [La-] at a given t reflects lactate production and thus the metabolic state of the muscles at that precise t, and at the exact corresponding work rate. This is very unlikely to be the case, particularly during the exercise protocols of short duration and with steep increase in work rate used for the detection of the anaerobic threshold (Anderson and Rhodes 1989). In this type of protocol, where VO2 significantly lags behind the value expected for the corresponding work rate (Whippet al. 1981), it may be expected that plasma [La-] also tracks the metabolic state of the working muscles with a significant delay, particularly at the beginning of exercise for the reasons presented


So the question really comes  up:

Lactate efflux is unrelated to intracellular PO2 in a working red muscle in situ.


Connett RJ, Gayeski TE, Honig CR.




Blood flow, lactate extraction, and tissue lactate concentration were measured in an autoperfused pure red muscle (dog gracilis). Muscles were frozen in situ during steady-twitch contraction at frequencies of 1-8 Hz [10-100% of maximum O2 consumption (VO2max)]. Myoglobin saturation was determined spectrophotometrically with subcellular spatial resolution. Intracellular PO2 (Pto2) was calculated from the oxymyoglobin-dissociation curve. Tissue lactate was well correlated with VO2 but not with Pto2. Lactate efflux increased markedly above a threshold work rate near 50% VO2max. Efflux was neither linearly correlated with tissue lactate nor related to Pto2. Pto2 exceeded the minimum PO2 for maximal VO2 in each of 2,000 cells examined in muscles frozen at 1-6 Hz. A small population of anoxic cells was found in three muscles at 8 Hz, but lactate efflux from these muscles was not greater than from six other muscles at 8 Hz. Our conclusions are that


1) the concept of an anaerobic threshold does not apply to red muscle and


2) in absence of anoxia neither tissue lactate nor blood lactate can be used to impute muscle O2 availability or glycolytic rate. A mechanism by which the blood-tissue lactate gradient could support aerobic metabolism is discussed.



and last but not least even the big  fathers  of VO2  max  testing ideas  recognice  that, to have a decent abiltiy  to  say  somethig about  respiration and circulation, which is all what we have  when  working out,  needs  some decent  time.

Oxygen uptake during the first minutes of heavy muscular exercise




1.   Per-Olof Åstrand1 and




2.   Bengt Saltin1




+ Author Affiliations




1.    1Department of Physiology, Kungliga Gymnastiska Centralinstitutet, Stockholm, Sweden








Oxygen uptake, heart rate, pulmonary ventilation, and blood lactic acid were studied in five subjects performing maximal work on a bicycle ergometer. After a 10-min warming up period work loads were varied so that exhaustion terminated exercise after about 2—8 min. Peak oxygen uptake and heart rate were practically identical (sd 3.1% and 3 beats/minute, respectively) in the experiments. The heavier the work was and the shorter the work time the higher became the pulmonary ventilation. There was a more rapid increase in the functions studied when the heaviest work loads were performed. It is concluded that aerobic capacity can be measured in a work test of from a few up to about 8 min duration, severity of work determining the actual work time necessary. Duration of work in studies of circulation and respiration during submaximal work should exceed 5 min.


In  conclsuion.
  VO2  max testing  and VO2  max testing  with lactate   needs  some  critical review   and this certainly in a  time, where we have  easier to use , less expensive  and more  powerfull  information gathering equipments  like a  MOXY.
 Any  center  with a VO2  max equipment may   or should consider adding  some more  and better individual  data gathering to their tool box . This will  possibly change the way  we look and work  in te future in   rehabilitation and  sport.
  Any  additional comment are very welcome , as a critical  help on where we  go   in the future in practial sport applications.









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Posts: 266
Hi Juerg,

Your conclusion that VO2 max testing needs some critical review seems consistent with some thoughts expressed on USA Triathlon's website by Dr. Alexander Hutchison.

In that article, Dr. Hutchison states:

Although VO2max is a clear measure of physical fitness, it provides little useful information for training by itself.

He goes on to state that Lactate Threshold testing is useful.

The LT, however, provides a definitive anchor point for training. If the test is done correctly, you will be given a heart rate range at which your LT occurred. You can use these values to train at, or just above your LT. There is no guesswork involved, and that is a great benefit to you as an athlete.

I have seen that there are many different definitions of Lactate Threshold.  It seems that few people subscribe to a definition of >4 mmol any more.  Most of the definitions I see in use today are more related to a point where lactate production rate exceeds lactate removal rate so there is a lactate accumulation.

Dr. Hutchison defines LT as:

Lactate threshold is defined as the intensity of exercise at which lactate begins to accumulate in the blood at a faster rate than it can be removed.

You sometimes argue that Lactate itself is a fuel source and it's not a bad thing for the athlete.  It seems that Dr. Hutchison would agree with this argument at least to the point that lacate is "not really" a waste product and that it does not cause muscle soreness as he states below.

Lactate has gotten a bad rap for the past several decades. Many refer to it as a metabolic waste product (not really) and blame it for the muscle soreness that can plague us several days after a hard workout (not so, actually inflammation).

Even if the precise role of lactate is not always properly understood, it seems that main stream thinking (as represented by Dr. Hutchison's article on USA Triatholon's website) is that lactate testing does provide useful information for setting training intensity zones.

We have also seen that muscle oxygen information can be correlated with some definitions of LT or at least Maximal Lactate Steady State as in the paper below.  A strong correlation would suggest similar usefulness of information.

Moxy has some practical benefits compared to lactate testing because it provides continuous data and doesn't require a blood draw.  I also recognize that Moxy can be used for more that determining optimal training intensity.  So only focusing on the usefulness of data for determining training intensity zones:

Question #1 - Aside from the practical benefits, does Moxy provide less, the same, or more valuable information than blood lactate testing if we only consider the goal of setting intensity zones?

I have a Question #2, but I'm still thinking about it so will ask later.


Juerg Feldmann

Fortiori Design LLC
Posts: 1,530

 great  nice feedback.
  I was  actually hoping to avoid  this ongoing  discussion on the topic  of VO2  max  and LT, as it is  hard  to believe we still do  that and I am doing this  since the late 1980.

 The main problem is  as  you pointed  out in the word  believe.
 We believe,  because we read something.  so  let's stay  with that  but I will suggest  for  open minded people to stop  with the believe  and do some of the suggestions  I will give you below to see , so you   can stop  believing.

1.  Short( very short ) repeat of historical introduction of LT  or  better AT  and ANT  and Max lass.

The idea  to look  for a  marker, who tells us, whether we  go  " anaerobic  " or "aerobic "was one of the big goals, as this  may or  would be the key to understand " fatigue "  or  failure to increase performance.
 So the drive was out there to find the  magical   product or  hormone  or   chemical, which would  explain all of this. Reality is, that we have this days a huge amount  of definition of fatigue  and what may cause  the   stop  of performance   due to the different "fatigues."
 Lactate was one of the   chemicals, which  was in this magic believe
 Lactate, as   we  saw  with Hill  and Meyerhofer , was the reason   or believe  of the  end of performance.
  This   was than moved on and on  and  we had some  rebirth of the idea, that we  could use lactate  ( the  bad  guy )  and  adjust a number to it  to  argue that once  we reach this concentration of " lactic acid"  we  will see an end of performance.
 The main push  was coming  from Mader  with his suggestion of  4 mmol and 2 mmol lactate concentration.
  Now  we got stuck  but  very soon after many  found, that the numbers simply did not  add up, but the theory  was great, we simply adjusted the facts   to maintain the theory  of anaerob  and aerob. So the individual  LT  was born. It was a feast  for many new  ideas on how to find the LT.
 So    where ever you worked or when ever you needed a publication you " invented  " another  formula   or ideas to find an individual lactate threshold.
  I have a whole booklet  written  many many years back on the different option to find  your individual lactate threshold.
 The problem:
 The  function of lactate changed  and it is not  what it  suppose to be.  It is a metabolic  product   produced in the normal metabolic  breakdown to help to  achieve  an acceptable ATP level or to maintain an acceptable, needed  minimal ATP level.

 Meaning, the idea  to be able to use lactate as a  marker  for intensity  , built on the idea, that it is  the limitation  for performance , disappeared.Now we know  that lactate can be used  as a marker  for  metabolic trends, where it can indicate, that the intensity reached  a level, where the O2  dependent energy supply line needs some help  from the  O2 independent  energy supply  line in a way, that it is more than    before  and the breakdown of glucose   will show up as  an overflow  of lactate not used  in the working   cell due to different reasons, but  at least  used  as an  energy shuttle  and a part of the buffering options  for H +
  What did not disappear is the idea, that we have to train   for lactate tolerance. See in many articles.
.  Now  do we have to train  for glucose  tolerance , or pyruvate tolerance or  creatine  tolerance  or fat tolerance?
 All  energy  sources  , as  is  lactate.
  We  just had a great  contribution  from another source  sending us  lactate  and  blood sugar   curves  and this is a perfect example, to show  how they react very similar.
 Here  a few  other examples from very early times.
 Ask your question.
 1. Why did we not  created  a Fat threshold see pic  1
. The  "curve  "  would be just in a  different  direction.
2.  Or a pyruvate threshold  pic  2   
3. pic  where  do you take the lactate as the trend  and sudden increase is different depending where we  take it  as some lactate is getting " lost " used in the one option 
4.or an  adrenalin threshold ( Thanks Per  for this contribution )
5.a blood sugar threshold.( Thanks Per  for this  contribution)

Now  as  you can see,  any  reaction in   a  physiological system, concerned  of a potential problem in ATP  production  for performance  and in specific  for   the maintenance  of a needed  minimal ATP level , will react very similar, as   everything is   about  energy production  and utilization. So, any system will try to be a part of an efficient   and smart contribution to supply  help ( energy )  to  get the final product  going.
 Oxygen  is one of this  energy sources.

So the fact , that we  talk about lactate threshold is based  purely on the historical  mistake,that lactate may be the reason of  fatigue  and not on the fact, that lactate will   increase in situation , where  we  have enough glucose  so it can be a part of the" splitting " process to maintain energy delivery and if needed can be used  as a buffer  of H +  and as a   additional help  to be shuttled  to other energy needing   organs or  places.
 So  does  adrenalin  react    and nor adrenalin. So  does FFA  react  just reverse  as in higher intensities the supply   is not that   needed    but is still ongoing, So does pyruvate show  up and as you can see  Blood sugar as well.

You can see, that there are much cheaper options to create a  curve, which than depending on ideas and theory can  be used to find a threshold in some or the other way?
 Now  all of the above  have one  big    and the same problem.
They are all indirect information's on  the situation of  energy delivery  and utilization somewhere in the working body.
 We    check most of them  somewhere  far away    build in the circulatory blood.You can see the difference venous  versus  arterial lactate trends.  Why.?
   . We all know , that this  reactions  and the time needed  to have a  concentration  as close as possible to the concentration in the working cell ( muscle )  will be    time dependent and  we do not know  how fast this time   will be  or how long it may take.
  So any of the results  in any of the current" classical "  tests  will have this open question.
  Is the lactate value , blood sugar  value ,  adrenalin value     and more ,are they really the values in the working muscle . or is the blood value we read out and test really  from the intensity perhaps produced  a few steps earlier?  

 The answer is  not even close so you have to believe  or you do it.
  . A . Make a  VO2  max  as suggested with a steady increase in watt every  few  seconds  till  end of  test.
  Take lactate by the   Wattage   or as close  as you can.

B) repeat with the same person a 1 min step test  with fixed  wattage  for 1 min  and take lactate.
 c )  make with the same person a  3 min step test  same   idea.
 Than make a 5 min step test  same idea,  and compare , where and when you see the  lactate " threshold ?
 Than make a test , where you allow more time like a  TIP 5/1/5  and see what happens there.
  See pic below, where we   did a 3 min step test  and a  TIP  look where in the 3 min steps test you may have speculated the  LT  could be .   2 options. Than look where you see or what you see in a 5/1/5. If  we would not allow  more time the lactate  would somehow steady increase  and no lactate Threshold is visible.    if we allow  a  longer   time we may be able to   drop lactate after an initial increase as it is now possible,thanks to  compensation,to  go back to  a .;balanced  or  optimal  energy supply  without the need  to get  incredible help  from the O2  independent energy supply
As  such. all this  energy sources  are in one or the other way related to each other  and are all taken indirectly. With  one exception.????

All have the same limitation ( time lag  and  most of them  have  some problem  to be accurate  or to be repeatable based on nutritional baseline.  Whit one exception ????

 See a summary   from Maders own research  , where he asks  the critical question, whether we  actually can use  lactate   as a   way of  finding a   number or  what  if we  make  three test in a row on the same day or  on different  days. see   studies.

 So let'  get a break here  with a very simple question

 If  you could  test your energy trend  directly , where it takes place  and noninvasive.   would you not prefer this  to avoid the discussion  and open questions we just opened  above.???
Why would we   boder to  go through all this questions when we   just can watch  on our screen or   HR monitor whether i my  supplying more energy than  I need, whether i reach somewhat a steady state  and balance  or whether spent   more than I  actually can afford  over a long time.

 How  about the question, that the idea of LT  was great  at the time, and it was a great  direction but we learned more and more  and now  may have to be  looked upon more critically because we have  an alternative  direct  testing option.????  MOXY

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Here some additional  reading
This to Balance out  Rogers info  offered  by Dr. Hutchinson.
The  question  of  finding LT.
This is  an interesting  topic  and is discussed   in  long  evenings  since  25 years and longer.
  The point is  whether  we  can see in any blood sampling a real  trend of "deflection" of a value and can use that as an information on what is happening  in the body's  working area.
 The word  document is  the full  article . Here  to just make you hungry to read it .


·         During a ramp test (such as the ones carried out in the laboratory in which the runner must run at a regularly increasing intensity until exhaustion], the blood lactate concentration never appears as a threshold, as some people argue. The curve obtained shows no deflection (Figure 3). To see one, a very fertile imagination is required. It is true that many sports scientists (whose fame is somewhat inferior to the revenues they obtain from the tests they conduct) unscrupulously possess such an imagination but, in reality, the shape of this curve is most likely the result of a delay in the appearance of the lactate in the blood (PERONNET and MORTON, 1994)".

To support this group I like to take another  study in  from some  great  critical researchers  I showed  already many times.

 Read  carefully. Do you see the  word  VO2  max "" 

Is it replaced  by ????

 Do you see, the info  , that lactate may be an energy supplier ( fuel ) and as such  as discussed  above  any  blood test of  any  fuel  could offer the same  information of a  curve. Which  with some  fantasy  may offer us a  threshold ???
 Depending on the  protocol we  can  force  a possible threshold easier, than in other  protocols.

Lactate and glucose interactions during rest and exercise in men: effect of exogenous lactate infusion


1.   Benjamin F Miller,


2.   Jill A Fattor,


3.   Kevin A Jacobs,


4.   Michael A Horning,


5.   Franco Navazio,


6.   Michael I Lindinger* and


7.   George A Brooks


+ Author Affiliations


1.    Department of Integrative Biology, University of California


Berkeley, CA 94720, USA


2.    *Department of Human Biology and Nutritional Sciences, University of Guelph


Ontario, Canada N1G 2W1


1.    Corresponding author
G. A. Brooks: Exercise Physiology Laboratory, Department of Integrative Biology, 5101 Valley Life Sciences Building, University of California, Berkeley, CA 94720-3140, USA. Email:




To test the hypothesis that lactate plays a central role in the distribution of carbohydrate (CHO) potential energy for oxidation and glucose production (GP), we performed a lactate clamp (LC) procedure during rest and moderate intensity exercise. Blood [lactate] was clamped at ≈4 mm by exogenous lactate infusion. Subjects performed 90 min exercise trials at 65 % of the peak rate of oxygen consumption (O2,peak; 65 %), 55 % O2,peak (55 %) and 55 % O2,peak with lactate clamped to the blood [lactate] that was measured at 65 % O2,peak (55 %-LC). Lactate and glucose rates of appearance (Ra), disappearance (Rd) and oxidation (Rox) were measured with a combination of [3-13C]lactate, H13CO3, and [6,6-2H2]glucose tracers. During rest and exercise, lactate Ra and Rd were increased at 55 %-LC compared to 55 %. Glucose Ra and Rd were decreased during 55 %-LC compared to 55 %. Lactate Rox was increased by LC during exercise (55 %: 6.52 ± 0.65 and 55 %-LC: 10.01 ± 0.68 mg kg−1 min−1) which was concurrent with a decrease in glucose oxidation (55 %: 7.64 ± 0.4 and 55 %-LC: 4.35 ± 0.31 mg kg−1 min−1). With LC, incorporation of 13C from tracer lactate into blood glucose (L → GNG) increased while both GP and calculated hepatic glycogenolysis (GLY) decreased. Therefore, increased blood [lactate] during moderate intensity exercise increased lactate oxidation, spared blood glucose and decreased glucose production. Further, exogenous lactate infusion did not affect rating of perceived exertion (RPE) during exercise. These results demonstrate that lactate is a useful carbohydrate in times of increased energy demand.

So  when we " cool   down"  what is the reason  that lactate drops  faster, than  when we  "breath down"  to get rid of H+
 Do you really like to burn the lactate of ? or do you like to balance  H +    back  to norm ?

This  will create a  very interesting question:
  Why  would I buy any nutritional supplement  and or drink , who claims on the label , that it  will get rid  of lactate.  Or why would we go  to a massage ,   who claims they get rid or flush lactic  acid  out.
If  lactate is an enrgy source  we in fact should go  an  add lactate to the  intake.

" Stretching/Self Massage Helps to flush lactic acid build up, maintain muscle length, prevent injury - " 

Lactate Ingestion May Increase High-Intensity Bicycling Performance


Submitted by: Jean Nick 2011-08-29 00:00


Eating calcium lactate (the form of calcium commonly found in foods) has been associated with increased exercise performance and researchers wondered what effect taking calcium lactate supplements would have on performance in trained competitive bicyclists, as well as on blood levels of bicarbonate (a possible mechanism). They recruited 11 competitive cyclists (including 2 women) in their early 20s and had each visit the lab four times. On the initial visit each cyclist performed a maximal exercise test to measure VO2max and maximal power output (MPO) and then practiced a specific interval performance test. On the next three visits they had an initial blood bicarbonate test; drank either plain water, water with aspartame capsules (as a placebo), or water with calcium lactate capsules (120 mg/kg of body weight); and rested for 70 minutes. Then each completed the interval performance trial with blood samples taken periodically to monitor bicarbonate levels. Blood bicarbonate levels rose significantly after the 70 minute rest after taking calcium lactate but not after taking aspartame or plain water. Time to exhaustion and total work were significantly higher, an average of 17% higher, during the lactate trial than during the aspartame or no supplement trials. The authors conclude that a pre-exercise dose of calcium lactate can increase performance during high-intensity exercise, but that the mechanism is unclear as correlation between blood bicarbonate levels were weak. More studies are needed the determine optimal dosing and underlying mechanism of action.."

At least  we have  to  get somewhat more critical , when using  calculator  and  optical illusions  when setting up training zones.
 Would it be not very interesting to  actually find  your  bodies  own indvidual reaction, when  he has to shift  to a differemt  or more efifcient  way  in moving   energy  ( O2  )  and I see, that directly  form the muscel  who is working or in an endurance sport  from the  muscels    in the overall system.
  In endurance sport there is a huge  activity going on in energy shuttle  and shifts  and blood  supply.
   The end result is the same  as  so often.
 Survival.  When ever  working  extremity  muscels  start to " steel ' too much O2  '  we will have a survival  reaction feedback  to limit  the  O2  use  for non  essential  activities
  By using a simple device  ,we  can get a  nice hint  at least, whether the limiter is  central or  peripheral  and as such  have an individual  information on Zoning  rather thna a  calculated   speculation.

1.    Saltin et all


       Submitted 20 June 2002.


       accepted in final form 5 September 2002. 







To study the role of muscle mass and muscle activity on lactate and energy kinetics during exercise, whole body and limb lactate, glucose, and fatty acid fluxes were determined in six elite cross-country skiers during roller-skiing for 40 min with the diagonal stride (Continuous Arm + Leg) followed by 10 min of double poling and diagonal stride at 72–76% maximal O2 uptake. A high lactate appearance rate (Ra, 184 ± 17 μmol · kg−1 · min−1) but a low arterial lactate concentration (∼2.5 mmol/l) were observed during Continuous Arm + Leg despite a substantial net lactate release by the arm of ∼2.1 mmol/min, which was balanced by a similar net lactate uptake by the leg. Whole body and limb lactate oxidation during Continuous Arm + Leg was ∼45% at rest and ∼95% of disappearance rate and limb lactate uptake, respectively. Limb lactate kinetics changed multiple times when exercise mode was changed. Whole body glucose and glycerol turnover was unchanged during the different skiing modes; however, limb net glucose uptake changed severalfold. In conclusion, the arterial lactate concentration can be maintained at a relatively low level despite high lactate Ra during exercise with a large muscle mass because of the large capacity of active skeletal muscle to take up lactate, which is tightly correlated with lactate delivery. The limb lactate uptake during exercise is oxidized at rates far above resting oxygen consumption, implying that lactate uptake and subsequent oxidation are also dependent on an elevated metabolic rate. The relative contribution of whole body and limb lactate oxidation is between 20 and 30% of total carbohydrate oxidation at rest and during exercise under the various conditions. Skeletal muscle can change its limb net glucose uptake severalfold within minutes, causing a redistribution of the available glucose because whole body glucose turnover was unchanged





Juerg Feldmann

Fortiori Design LLC
Posts: 1,530

After the above  more scientific  backed up  information on the discussion  on VO2  ( max )    rather peak and lactate  rather  an energy fuel  than a  substance  for training zoning support.
  I like to add a more practical  support to our ideas.
  We  strongly  see MOXY as  a tool  for  sport   and activity specific  testing  and  training   support.
 MOXY  not only  finds  your individual  " Zoning"  but as well guides  you during a workout  or  race  to the  individual current ability  to supply  O2   to the working muscles.
. The discussion  we have  since  many years.
 Why  would I ever test a n ice hockey player  on a bike f for his bike related VO2  peak.
 There is no transfer  to  his sport.
  No  normal thinking  top cyclists  would  accept the be tested  and  get a training program  by testing him on the ice   for VO2  max.

 The other point is, . If  I test in the lab  an than   find

 zoning"  based on VO2  and or  lactate.  How  do I know during the workout in the field, whether my 72 % VO2 max intensity really is  this 72 %  max intensity. There  are very few  athletes running around  with a VO2  max   mask. Here ho it looked  many years back.  at least  for  lab ideas.  Okay true  they are looking much   slicker this days. K42B.  Fro 24'000 $  you get a  to run  with a VO2  mask. Problem . You still have no love feedback.
  For   1000 $  plus  you  can have  alive feedback on your Oxygenation situation.

 Here  to enjoy  a nice  article. supporting some of our  ideas  on Performance  has to be tested sport  and a activity specific.

VO2 max: Not the gold standard?


Tony Leyland


In my article on exercise science in last month’s CFJ, I highlighted the difficulty of scientifically determining optimal training methods. Most often, it is coaches working hands-on using a trial-and-error methodology that actually push the science ahead. Eventually, scientists notice that most coaches are doing a particular thing with success and then design a study to determine why it is effective.


However, coaches’ practical, field-tested insights and clinical experience don’t necessarily translate into the realm of scientific testing and study design. I was recently contacted by a coach working with the Canadian National wrestling team. One of the wrestlers was competing in the 62 kg class, but the coaches thought that if he could drop down a weight class he would be able to medal at the Olympics. They wanted him to drop from 62 to 55 kg, but realized that he was, understandably, concerned about how he would perform after dropping over 11 percent of his body weight. So they wanted him to get a few weight-cutting practice trials in before he actually had to do it in competition. He was to act like it was a wrestling meet and cut down for weigh-in at 6 p.m., rehydrate overnight, and then go through some physiological fitness tests in the morning. They wanted to see how his body handled the cut-down and hopefully give him confidence that he could maintain fitness and perform normally while dropping that much weight. That is where I come in: they wanted me to conduct the morning fitness tests at my university.


The tests they wanted to use were a VO2 max test (aerobic capacity measured while working to exhaustion on a treadmill or stationary bike) and a Wingate test (a bike test designed to assess both anaerobic pathways). Not a good idea in my book, as those tests do not mirror the performance required by the wrester in his sport. They would not very effectively test the wrestler’s ability to perform at the tasks required for his event—which was the whole point of the experiment.


So why did they suggest tests that are clearly not the best to assess the athlete’s performance? I think it is because we all have a tendency to work with standards that are universally accepted. (Maybe this is why CrossFit is viewed with suspicion by some: it doesn’t put much stock in the standard tests for evaluating fitness. How can people compare CrossFit’s methods and results with others? How can they evaluate and quantify the fitness it produces? Nobody else uses tests called “Fran,” “Linda,” etc., to measure progress. The unfamiliar is always suspect.)




VO2 max: Not the gold standard?




The VO2 max test on a treadmill or stationary bike measuring gas exchange is considered the “gold standard” of laboratory tests to assess VO2 max (the conventional measure of aerobic fitness), which is why the wrestling coaches wanted to use it for their athlete. But does it transfer to a wrestling match? Olympic freestyle wrestling bouts consist of three rounds of two minutes each. Wrestling is an exceptionally demanding sport using multiple lines of action (pushes, pulls, and static grips with both the arms and legs) and demanding both cardiovascular endurance and muscular stamina, so why not asses all these abilities in one test? You could do three two-minute rounds of one minute of thrusters and then one minute of pull-ups (like a Fran), or maybe three sets of two minutes of clean and jerks (like a Grace). This would tax the cardiovascular system as well as muscular strength, power, and endurance, and the athlete’s scores for each would measure changes in his fitness. You could also develop a continuous six-minute test similar to Fight Gone Bad that would cover many of these aspects and be indicative of the wrestler’s VO2 max. To break the testing into a VO2 max test (which would quantify how well he pumps blood to his leg muscles and the stamina of those muscles) and a Wingate test (which is a 30-second maximal-output bike test to assess phosphagen and glycolytic energy pathways) doesn’t adequately test the demands of the sport.


If you wanted to assess other energy systems separately, you could test the phosphagen system with a maximal sprint (say, 60 meters) or, if you wanted a very short-duration power test, you could use a vertical jump or clean and jerk. As for the glycolytic system…well, I think any self-respecting CrossFitter could think of something extremely intense using multiple muscle groups that you could sustain for only 90 seconds before collapsing in a heap on the floor.


When I discussed these issues with the wrestling coach, I got a very positive response. It made a lot of sense to him (as did the thought that he wouldn’t have to pay for expensive tests). Also he now has complete control on the timing of the test and he can repeat it more frequently than relying on my university to conduct the test.


Athletes are competitive by nature and love to challenge themselves, so I frequently get calls asking me to measure VO2 max and body fat percentages. As with the wrestling coach, I usually tell people to save their money. There is no need for expensive tests to measure these variables and there is good science to prove you shouldn’t. I’ll talk about percent body fat at another time but this month I want to focus on VO2 max.


VO2 max is a measure of your body’s ability to take up and utilize oxygen. VO2 max is measured by determining the amount of oxygen in the inspired air and the expired air. The difference is the amount of oxygen used by the body. This is usually done by analyzing inspired and expired gases while having the subject run on a treadmill with ever-increasing speed and/or incline until exhaustion.


At sea level, the most important physiological factors that determine VO2 max in a given person are:


the ability of the heart to pump blood


the oxygen-carrying capacity of the blood (hemoglobin content)


the ability of the working muscles to accept a large blood supply (amount of capillarization within a muscle)


the ability of the muscle cells to extract oxygen from the capillary blood and use it to produce energy (number of mitochondria and aerobic enzymes)


Delivery of oxygen to the blood via the lungs is important, but at sea level it is not a limiting factor. Most people can get adequate amounts of air into the lungs. The last two points in the list above are really why I thought that a running or biking VO2 max test for the wrestler wasn’t a good idea. A runner may have a large stroke volume (amount of blood pumped by the heart per beat, #1 above) but if you put him on a bike, his VO2 max measurement will come out lower than when he is tested on a treadmill. Similarly, a cyclist will not do as well on a treadmill. This is because of the difference between systemic adaptations to the training impulse and peripheral adaptations. Both runner and cyclist have large stroke volumes but the runner’s quads cannot accept as large a volume of blood and extract oxygen as efficiently as the cyclist’s quads. Likewise, the hamstrings and especially the ankle extensors (gastrocnemius and soleus) of the runner are able to receive larger amounts of blood and extract oxygen more effectively than those of the cyclist. So VO2 max is specific to what you are doing. In truth, there is no single, movement-agnostic




VO2 max. There is a “running VO2 max,” a “cycling VO2 max,” a “thruster VO2 max,” etc.


The highest VO2 maximums recorded are for cross-country skiers, as they utilize the most muscle tissue in their event. I wonder what the VO2 max of an elite CrossFit athlete would be while doing thrusters. You could have a series of barbells set up with different weights and increase the weight being thrusted every three minutes until the athlete couldn’t sustain that power output (similar to increasing the speed and/or inclination of the treadmill). Not an easy test to administer, but it is interesting to consider. The VO2 max recorded would undoubtedly be a very high value.


Another important point to keep in mind about measuring athletic performance is that there is daily variation in our physiological parameters. If you measure your heart rate upon waking each morning, it will vary from day to day. So will the maximum heart rate you can achieve on any given day. It has been reported that there can be up to an 8% variation in the VO2 max due to this natural daily variation (we are not robots responding to stimuli exactly the same way every time). So why pay for one VO2 max test when you are trying to determine change? You need at least two measures. But even two tests aren’t ideal, as the difference is likely to be affected by daily variation and other factors such as hydration, nutrition, and environmental temperature, rather than changed VO2 max per se.


So the best thing is to have simple tests such as a 5k run that you can easily repeat six or seven or more times a year. If your time improves consistently, you know your running VO2 max has improved. Over the year and multiple tests, variation due to factors other than improved running VO2 will cancel out. This is why it is so easy to test yourself while following CrossFit: the benchmark workouts become the standardized tests. You might not hit a PR every time, but you will see which direction you are heading in and how steep the trend curve is.


If you actually want a specific numeric measure of your VO2 max (in ml of oxygen utilized per kg of body weight per minute), you can run a 1.5-mile test (6 laps of a standard 400-meter track) or run for as far as you can on the track in 12 minutes. The links below will take you to calculators that will estimate your VO2 max based on your results:


Sure, there are errors in these predictions compared to a test that actually measures the O2 content in your inspired and expired breath (the gold standard of testing, remember), but they are free and repeatable whenever you can find a 400-meter track and a stopwatch.


Not a runner? Test yourself at 150 wall-ball shots for time. If over the year your time decreases, your VO2 max for wall ball has improved. And that is good to know. However, you must be able to sustain any movement you want to use to test VO2 max continuously for about 6 minutes or more. If wall ball with a 20-pound ball overloads your arms so that you have to break sets and rest, it wouldn’t be the best choice for evaluating VO2 max. Using a lighter ball (and maybe even adding to the number of shots) so that you can work continuously for 6 minutes or more would make it work as a test of your wall-ball VO2 max. So for anyone thinking of getting an expensive fitness test done, don’t bother. Spend your money on useful things, like the CrossFit Journal or another medicine ball or another set of rings so your friends can join you in actually improving your fitness rather than worrying about how to quantify it.




Tony Leyland is Senior Lecturer at the School of Kinesiology at Simon Fraser University in Vancouver, Canada. He has taught at the university level for 24 years and has been heavily involved in competitive sports such as soccer, tennis, squash, and rugby as both an athlete and a coach for over 40 years. He is a professional member of the National Strength and Conditioning Association, a Canadian National B-licensed soccer


Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
I like to add some support  to the people  looking  at a confirmation  why they use lactate threshold.
 Here  an article  from a university
( short  section.)  You  can see in red  below  where there  are some fundamental difference  between Ph.D. guys  and Ph. D  guys.
 So as a practical coach  you will sit  simply in between  and it is more a  question of religion  believe  for the majority out there, than on  what do we see.
  If you  have a tool  whee you actually could see,  by what intensity  you supply more O2  than you need,  by what intensity you may be a  a nice  balance between utilization and  delivery  and by what intensity you may in fact run earlier  or later in a  energy  delivery  and utilization problem
\ Would you not have a better   option  , than  juts hoping  on what you believe  may work  based on Ph. D  publications.
 How  about  using a MOXY  and  see what  you do.

Explanation of Lactate Threshold and Vo2max

-by Trent Stellingwerff-

-PhD, University of Guelph-

Lactate Threshold (or anaerobic threshold)

When increasing running pace or workload there is a point at which lactic acid begins to accumulate. This is a crucial workload, as lactic acid can inhibit muscle contraction and energy production and cause pain and a burning sensation. The point (heart rate or running pace) at which lactic acid begins to accumulate is called the


Lactate Threshold. This measurement is also sometimes called the anaerobic threshold or onset of blood lactic acid.

The lactate threshold measurement is very valuable as it is one of the more sensitive indicators of fitness level. For example, if training is ineffective the lactate threshold will be reached at a relatively low running speed; with more effective training the threshold.. 

So back to the  idea, thab lactic acid is the limiting  factore  and reason for fatigue ???

hmmm confused.

Lactate per se improves the excitability of depolarized rat skeletal muscle by reducing the Cl conductance


  1. Frank Vincenzo de Paoli1,
  2. Niels Ørtenblad2,
  3. Thomas Holm Pedersen1,
  4. Rasmus Jørgensen1and
  5. Ole Bækgaard Nielsen1

+ Author Affiliations

  1. 1Department of Physiology and Biophysics, Aarhus University, DK-8000 C Denmark2Institute of Sports Science and Clinical Biomechanics, University of Southern Denmark, DK-5230 M Denmark
  1. Corresponding author
    O. B. Nielsen: Department of Physiology and Biophysics, University of Aarhus, DK-8000 C, Denmark.  Email:



Studies on rats have shown that lactic acid can improve excitability and function of depolarized muscles. The effect has been related to the ensuing reduction in intracellular pH causing inhibition of muscle fibre Cl channels. However, since several carboxylic acids with structural similarities to lactate can inhibit muscle Cl channels it is possible that lactate per se can increase muscle excitability by exerting a direct effect on these channels. We therefore examined the effects of lactate on the function of intact muscles and skinned fibres together with effects on pH and Cl conductance (Gcl). In muscles where extracellular compound action potentials (M-waves) and tetanic force response to excitation were reduced by (mean ± s.e.m.) 82 ± 4% and 83 ± 2%, respectively, by depolarization with 11 mm extracellular K+, both M-waves and force exhibited an up to 4-fold increase when 20 mm lactate was added. This effect was present already at 5 mm and saturated at 15 mm lactate, and was associated with a 31% reduction in GCl. The effects of lactate were completely blocked by Cl channel inhibition or use of Cl-free solutions. Finally, both experiments where effects of lactate on intracellular pH in intact muscles were mimicked by increased CO2 tension and experiments with skinned fibres showed that the effects of lactate could not be related to reduced intracellular pH. It is concluded that addition of lactate can inhibit ClC-1 Cl channels and increase the excitability and contractile function of depolarized rat muscles via mechanisms not related to a reduction in intracellular pH.



  • (Received 18 July 2010; accepted after revision 24 September 2010; first published online 27 September 2010)

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