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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
The regular reader knows  by now, that we believe that  both  groups have  very great valid  points  and we    show  since  over 15 years, how we look at this  ideas  as the so called ECGM  extended central governor model.
( See Blogs  in moxy website)
  Top give you some further ideas  why we  choose 5/1/5  and a  short term  assessments  exactly this.
  The regular  MOXY users  will see that in may 5/1/5  assessment your  client  does NOT  deoxygenate  very nicely  (  SmO2  can stay very high) but if you do  a  short high intensity test  you can see a much  further   deoxygenation. I like to show here a n example  from another group  who did a case study  and tested  at the same setup  one after the other  a  longer step version  5 min and a short step version.
 The   5/1/5  which would even show  where and at what step the  limitation may occur  would have been  even   with more  answers.
 nevertheless in  longer  assessments ( steps ) where we give the different physiological system a  fair chance to try to see, whether they  can adjust  or  whether they may have reached  the limitation    than we as well need the time    for  possible compensates  to try  to  respond.
  Example  HR. SV. LVET,   for cardiac responses  . SVR    vasodiltation  or  vasoconstriction for  circulatory systems.
 Inter  or  intramuscular  coordination  for muscular  and  neurological  systems including  motor unit recruitment  as well as RF  TV    and   O2  Diss curve  reactions  for the ventilatory system. So  5/1/5  will help us  to find limiter  and compensator  and often are information  controlled over the central governor  idea.
   Short term  loads  short steps   and so on  are more likley to give us   information or feedback on possible  peripheral limitations.
 The physiological system often  have not enough time  due to lag  in response  to adjust  so we will simply ( dig  deeper  into  O2  storage)  till we reach a critical  level of ATP demand  or use  and than we  may  have a feedback to the CG  to   stop the   utilization of ATP  down into a  dangerous   level.. Feedback loop  from peripheral  to central    or   Central to peripheral.
  Here a nice   study  form an accepted place,  who backs  up our  intentions  and practical applications.
  Both the  att  and the study  show  you  why we   use this 2 different ideas.
 The PP is a  simplification on the idea  of CG  and PG  as we name it ECGM as a part of our  seminar  scripts

Effects of short-term endurance training on

muscle deoxygenation trends using NIRS


Faculty of Kinesiology, University of New Brunswick, Fredericton, New Brunswick, CANADA; Faculty of Human Kinetics,

Allan McGavin Sports Medicine Centre, University of British Columbia, Vancouver, BC, CANADA; and Department of

Occupational Therapy, Faculty of Rehabilitation Medicine, University of Alberta, Edmonton, AB, CANADA


NEARY, J. P., D. C. MCKENZIE, and Y. N. BHAMBHANI. Effects of short-term endurance training on muscle deoxygenation trends

using NIRS. Med. Sci. Sports Exerc., Vol. 34, No. 11, pp. 1725–1732, 2002. Purpose: This study examined changes in cardiorespiratory

responses and muscle deoxygenation trends to test the hypothesis that both central and peripheral adaptations would contribute

to the improvements in V˙ O2max and simulated cycling performance after short-term high-intensity training. Methods: Eight male

cyclists performed an incremental cycle ergometer test to voluntary exhaustion, and a simulated 20-km time trial (20TT) on

wind-loaded rollers before and after training (60 min ! 5 d·wk"1 ! 3 wk at 85–90% V˙ O2max). Near-infrared spectroscopy (NIRS) was

used to evaluate the trend in vastus medialis hemoglobin/myoglobin deoxygenation (Hb/Mb-O2) during both tests pre- and posttraining.

Results: Training induced significant increases (P ! 0.05) in maximal power output (367 # 63 to 383 # 60 W), V˙ O2max (4.39

# 0.66 to 4.65 # 0.57 L·min"1), and maximal O2 pulse (22.7 # 3.2 to 24.6 # 2.8 mL O2·beat"1) during the incremental test, but

maximal muscle deoxygenation was unchanged. 20TT performance was significantly faster (27:32 # 1:43 to 25:46 # 1:44 min:s; P

! 0.05) after training without a significant increase (P $ 0.05) in the V˙ O2 (4.02 # 0.52 to 4.04 # 0.51), heart rate (176 # 9 to 173

# 8 beats·min"1) or O2 pulse (22.4 # 3.2 to 23.5 # 2.8 mL O2·beat"1). However, mean muscle deoxygenation during the 20TT was

significantly lower after training ("550 # 292 to "707 # 227 mV, P ! 0.05), and maximal deoxygenation showed a trend toward

significance ("807 # 344 to "1009 # 331 mV, P % 0.08), suggesting a greater release of oxygen from Hb/Mb-O2 via the Bohr effect.

Conclusion: The significant improvement in V˙ O2max induced by short-term endurance training in well-trained cyclists was due

primarily to central adaptations, whereas the simulated 20TT performance was enhanced due to localized changes in muscle




The physiological adaptations to endurance training,

both central (cardiorespiratory) and peripheral (local musculature), are well known (13,14,19,20,23).

More recently, the effect of short-term endurance training on physiological adaptations has been reported in a group of healthy (previously untrained) male volunteers (17,26). However, the relative contribution of the central and peripheral factors that influence exercise performance after highintensity been fully elucidated (29). Furthermore, although limited data have been published on intracellular PO2 levels measured directly in skeletal muscle during maximal exercise (29), direct data on oxygen availability and utilization during cellular respiration while performing high-intensity endurance performance is not available. This is largely due to the technical difficulty in measuring the relative contribution

of oxygen concentration at the cellular level for energy metabolism during endurance exercise performance. With the advent of near-infrared spectroscopy (NIRS) and its application to exercise, scientists have successfully used this noninvasive technique to examine changes in skeletal muscle respiration during a variety of exercise conditions including intermittent, continuous, isometric,

concentric and eccentric muscular contractions (3,6,7,16,15,18,24,25). NIRS is based on the differential

absorption properties of hemoglobin and myoglobin (Hb/ Mb) in the near-infrared range of 700–1000 nm. At 760 nm, deoxygenated Hb/Mb has a higher absorbency, and at 850 nm, oxygenated Hb/Mb has a higher absorbency (11,21). Therefore, the difference in the reflected signal between the two wavelengths indicates the degree and trend of deoxygenation at the level of the arterioles, capillaries, and

venules (3). The majority of exercise studies using NIRS have been descriptive in nature to ascertain that this technique can be used to examine alterations in muscle deoxygenation and blood volume (15) during short-term acute exercise. Several studies have shown NIRS to be a valid (10,21,27) and reliable (6,11) technique for measuring relative changes in muscle deoxygenation and blood volume.

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Development Team Member
Posts: 49
Hi Juerg,

Here's my attempt to respond to your questions!
1.  I would guess that its easier for SV to reach a higher volume in the first test because there is a slow increase in tHb, presumably this is due to a more gradual increase in load or a steady and long load that the athlete is responding too. I assume the heart will first increase its rate and then increase the amount it pumps per beat to respond to the demand. There is no barrier to the heart supplying blood to the muscle so it can function to its maximum capacity.

2. In the second test there is an initial increase in tHb and then a steep decline. I would guess that the decrease here is due to a peripheral limitation, such as vasoconstriction which forces blood out of the muscle.

In both these cases I'm using tHb as a proxy for SV, but I'm not confident that's a very good way to do it. Presumably if the heart increases its SV we'd see more bloodflow to the muscle, but if a peripheral limitation prevents bloodflow to an area presumably the heart could still have a large SV if its supplying blood to other parts of the body. In addition would the heart ever find itself in conflict with a peripheral limitation? If there's vasoconstriction would the heart work harder in attempt to overcome it? I can see that turning in to a negative feedback loop whereby the heart reaches its maximum very quickly and the periphery increases the vasoconstriction in response to increased pressure from the circulatory system.

Thats just a start for now, I'll try and add more with regards to your question about ATP production later on when I've had more time to think through the data. 
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Hmmm you are getting dangerous   close  to how we think ( Smile 0. That's' how we  work   getting through all this different options  . Your loud thinking is great. Now look as well at  other  systems  in the same idea    like the respiratory system  for example.
  Our  advantage in the past  was  that we always where looking at the same time   in Physio flow on the cardiac reactions  so we     had direct feedback  as well as  live on the respiratory reactions.
 What we  now   see is that   when   we  combine  many of the trends we  had in the past  we in fact    are able to use MOXY alone  to    get pretty close ideas on what the other equipment would show  us. Meaning , that you and  I can  go out using a MOXY  and  can give  a very close  information  , what we in the past only where able to do  by running NIRS, VO2  and physio flow.
 This is what we look for  a  cheap  simple  tool  to get pretty close    but not  exact  to what we normally   would do  with the great  expensive  equipment . This way MOXY  can help coach an athlete  to  do   the smaller    monthly  or  every second month test  at home  sending  files  to the coach  and reset the current program to the new situation ,instead of having 1  x  per year a VO2  max test  with no  ability to correct or adjust  programs  . Se  just running a program on a  calendaric  periodization ???? hmmm how much physiology is in that idea.
 Question: Is the MOXy   the start of the end  of calendaric  periodization.
  Last  very very hard question and we will for sure be back.
 Key words.
    Immediate  drop in SmO2    when we start an activity  meaning using O2.
  Lactate not the reason of fatigue  but great energy source ? Question  why  would we do a  " lactate tolerance training g"     Question?
 Is the so called  "classical "  anaerob alacticid    interval  perhaps more a aerob lacticid  workout.
 Give it some thoughts  why we where no able to test   or see lactate in the blood in this workouts ??  and why we thought  O2  is not used in this  workout    Lag times ????
 So if true  w e may  in fact improve oxygenation  resp  utilization of  O2  in this workout  and not  tolerance of  lactic acid, in fact due to the better O2 utilization we  can use  lactate  better as an energy source.
 At the end the question is only  whether we  can keep H + in balance  and as long we  can do that we  can increase lactate  and  maintain performance ???
 Just a  future  question .

Development Team Member
Posts: 49
Hi Juerg,

I've been reading a bit more about lactate since you posed your last question and I'm going to take a stab at answering it now. 

So I'm guessing the reason we don't see a lot of lactate in anaerobic alactic work is that the body is consuming it for fuel. I've been reading about George Brooks' theory of the lactate shuttle and while I'm a bit unclear about the bigger picture, from this and other posts you've made I'm assuming that the myoglobin provides the necessary oxygen for lactate to be used as fuel at the very start of a workout. This article that I've found appears to provide some support for that occurring during steady state exercise. In hard fast work like an anaerobic alactic interval presumably the body uses myoglobin instead of hemoglobin to provide the necessary oxygen for the reaction as the myoglobin is close and at hand. The quote below from an article about George Brooks puts it in simpler terms. 
"This is a fundamental change in how people think about metabolism," Brooks said. "This shows us how lactate is the link between oxidative and glycolytic, or anaerobic, metabolism."
He and his UC Berkeley colleagues found that muscle cells use carbohydrates anaerobically for energy, producing lactate as a byproduct, but then burn the lactate with oxygen to create far more energy. The first process, called the glycolytic pathway, dominates during normal exertion, and the lactate seeps out of the muscle cells into the blood to be used elsewhere. During intense exercise, however, the second ramps up to oxidatively remove the rapidly accumulating lactate and create more energy.

I'm hoping I'm on the right path here.
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Thanks for this great and in English  summary:
 Here  some  confusing add ons( please translate  in your words )   which may help, or  as  said ,confuse  more.

1. lactate in anaerobic alactic work is that the body is consuming it for fuel.
Yes , so  if we actually create lactate, which is  for sure, but we  can't  test it on the finger ( Lag time, too short  load  and  sufficient  recovery  in between ), than we  will argue  ( old  school ) that it is alactcicid  , as we  can't  show lactate  in the test equipment.. Question: if we start cold turkey ( low CO  and low VE ) we  can't show in the mask of a VO2  test immediately  a high VO2  use  so we argue  that we have an O2  deficit ??? 
How  can we show the immediate use of O2  (   ?????  )
 do we  really have an O2 deficit , when we  can take  form a storage area?
 So  an " anaerob alacticid"  workout  may in fact be super lactic. And that is great as we need the lactate  for buffer reasons.
  Anaerobe , well we use  O2  from within the  Mb  storage( Cant'  proof it with MOXY ),  as well   what is coming in and delivered  over blood  flow( Hb ). So we  not use  Hb  or Mb  we use O2  form Hb  or   and  Mb.  Depending, whether we  start " cold turkey "  low  CO  and low VE,  or whether we start  " warmed  up , higher CO  and higher VE  and therefor have a delivery  in full swing , versus  low delivery and the need  to take it  from the storage  area.( The  above  explanation is an important part  when designing  training ideas. Do you like to practice  the activation  to be able to utilize  from storage area  versus  avoiding this pathway  and  just use  it  from the delivery  options.?
 So  this part  is   perhaps nice and clear.  a  " classical "  anaerobe alactcid   workout is  in real    physiological   situation  most likely  aerob lacticid.
  This will throw  many coaches  out of balance, as  it may make not a lot of sense  to  argue  that you need a  lactate tolerance  training, when in fact  you need lactate   to  tolerate the training  (nice  dialectic  contradiction) 
That adds  some fun questions  to  some  interesting  ideas.
, Why , when doing an active "cool down"  lactate drops  faster , compared to a passive  cool down.
  Lactate is a  great  simple to use  energy, which during  cool down  will be the first  source  of energy  and therefor will drop faster, than when not moving.
 Critical question?
  Do you really like to get rid  of an energy  , which would refuel  you   much faster than any other energy source.( Perhaps  we  should get rid  of  H +  and not of lactate.???
Why  do you feel better  after a cool down.
 No not because you got rid  of lactic acid , but you got rid  of  H +  over  CO2. As you   jog your respiration will be   stronger ( VE higher), than when doing nothing , so faster release  of CO2  and faster re balance of  CO2  levels.
  BUT,  you got rid  of lactate as well. So how about get rid  of  H +  ( CO2  ) but  not  of lactate.  Better of both systems , faster refuel ling with the available lactate and faster  CO2  balance . 
How ???

  Second question   : is the drop of lactate in a cool down  really a  great tool  to  tell, whether you recovered better, when in fact keeping the lactate and converting  it  to  stored energy would be a  much better idea  for actual recovery    for the next load or performance to be ready???
 What is  out of  balance, when we  see lactate showing up.
 Lactate simple  tells us, that in the attempt  to  create ATP  some  other  pathways  besides the aerobic  pathways  have  kicked in  and we  have to try  somehow  to maintain the minimal ATP level.

One of  the   peripheral governor ideas is the protective  function of H +  to avoid a  critical low  drop of ATP  to avoid  muscular rigor.
  H +  stops the Ca++  from binding  with Mg --  to create the split  in  ATP  to P  and ADP.
  As soon the homeostasis of H +  is out of balance , we  have a shift in pH  and  the  external system will shut down.
 As long we  can maintain a decent H + balance  we  can  keep going.
  How  do we maintain  somehow longer a H + balance :
  One  part is an optimal shuttle service  over the MCT  proteins    together with lactate to shuttle   H +   from the cell  into the blood stream.
 lactate  binds  with H +  for a short  shuttle service   ( now  we have a short moment lactic acid.)
   Arrived in the blood H +   will be kicked off  and now we have  lactate and H + again  and  the respiration  can, if trained properly ,take over and  you expire CO2 if you have the  ability  to ventilate   sufficient air  with your respiratory system.
 last BUT NOT Least. look The YEAR  OF THE  ARTICLES    LATE 1980.
  look  when we  did  our lactate balance point idea,  try to explain that lactate is a bio marker and  we  can't use  absolute numbers  to  design intensity  zones.
  Well, a  quarter  of a century later  we have made very little if any progress.
 In fact  most   researchers  try  desperately  to force MOXY /NIRS  trends into an old " classical"   2  and 4  mmol  or LT / AT  system, instead of  looking  at new    ideas  and versions.

 Now you can see where we  have  some fundamental  difference in ideas  and  thoughts   for improving intensity definition  at an individual sport specific level..
 When you think  that thousands  of $'s  are  spent  in NHL teams,  CFL  teams NFL   to get VO2  max    tested on bikes  for this sports  and than believe we  can have any descent information or training ideas, than you see, why our ideas may  create  some  different reactions  and why  there will be a major   fight  against  an even close agreement on this.
 Can you imagine , if we  agree, that there is  a small chance  that we  can find a VO2  max.  how many PhD  works  and studies  may have to be redone or at least  revied  as  %  of VO2  max  an conclusions  may be  more than questionable.  Not even mention the studies where lactate  was used as  a base line  for intensity control ???
 Fun times  a head that's  for sure.

Solution to the above question.
 We have to be able to see live, whether a certain workout  will   use   O2  together  with O2 independent energy sources. or whether we push  to  move O2  down to its  current lowest accepted  utilization level  and than maintain performance  to  run hypoxic  and than  last but not least , whether we  rest  for    partial  reoxygenation, complete  re oxygenation  and  or  even   increase  re oxygenation.
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Feedback I got:
 "never  ever  was  reading, that  physiologist  would separate  lactate and H + "
 Is  there  any paper you  can  show, that it is not a  "goat  farmer's  "  dream.
  ha ha  I like this  I  just sent out today  what my dream  would be  here a  small inside  view.

 And here one of the interesting papers  you look for  and   build up from there.
 see  att. If you search  further you will s  find,  that if we can balance  H +    with different buffer options we  can  basically increase lactate  nicely  to  far above and beyond  easy    to achieve   values  over metabolic acidosis  workouts.
 You can combine  MOXY  and lactate  and you  can create  a  situation , where you can demonstrate  a nice increase in SmO2   ( Oxygenation of the tested  area  )  and in the same time  a nice increase in lactate   and   this  all on a person   who keeps  going very high intensity  and still smiles..
 Than you reverse  the   tryout  so you actually   see a  drop in SmO2    and you will see a  drop in lactate as well.
 How  can we  do that.
  If your question is :
  Can you show  accepted research papers ?
 Here the answer  no , no accepted research papers  just   own cooking   case studies but I know  many groups out there, who  made  this observation when playing  with Spiro Tiger and lactate  and respiration. Now  if the combine  MOXY  to the  game  than  they have the answers.
  Cheers   for now


Development Team Member
Posts: 49
Hi Juerg,

So just to restate what you wrote in your last response to make sure I understand.

1. Alactic Anaerobic Work - Previously people didn't think that any lactate was generated because when they tested for it the results would show up as negative. However this ignores the fact that the lactate was being consumed for fuel. As one would take a lactate sample from the finger or ear, the lag time in taking the sample after the short intervals and the fact that the sample wasn't taken directly at the source from the muscle meant that the lactate had been consumed by the body by the time the test was run. I think this formula is useful for understanding what we're actually measuring when we test for lactate.

Measured Lactate Level = Rate of Lactate Production - Rate of Lactate Removal.

The number our lactate meter gives us is the difference between how fast the body is producing lactate and how fast its removing it. So as mentioned in Juerg's previous posts, lactate production is likely incredibly high during "alactic anaerobic" intervals but the body is removing it just as fast for fuel. The Moxy Monitor can show us part of this reaction in that we can see oxygen being used for the consumption of lactate. Unfortunately we can't distinguish between myoglobin and hemoglobin with the Moxy Monitor so we don't have the ability to conclusively prove that myoglobin is providing the fuel in short fast/hard work like "alactic anaerobic" intervals. 

So this leads us to some interesting ideas for cool down and lactate production. If we're cooling down, using the drop in lactate as a marker for whether or not we're cooled down is silly. Lactate is fuel, if we've consumed the fuel how is that a useful marker for recovery? It merely means our body has used the fuel to feed our "cool down" workout. Instead the culprit for all the fatigue is H+ ions. These are removed from the body via CO2 delivered via respiration. 

So with regards to an effective cool down there are 2 key goals we want to achieve. Firstly we want to remove H+ ions, and secondly we want to conserve lactate for future use. This rules out doing a traditional cool down like an easy jog or bike. While the work we're doing is easy and we'll be able to clear H+ ions with our breathing as a result the body will still be consuming lactate to fuel the work that we're doing. My guess for an effective cool down based on this centers around simply controlling breathing properly and not doing any exercise. Breathing in a hypercapnic state where we stack more CO2 in the bloodstream to speed up H+ removal could be controlled with a device like a Spirotiger.

That's all I've got for now! 

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Thanks as usual.
 I like to add some more  thoughts  to this point.
Main reason is, as   there will be some major   discussion in the future,  on  the  ability to asses,whether  the " warm up " when assessing  from a metabolic  point of  view, as well as the cool down can be  changed  so it makes  more physiological sense.
 What we  have  to   think is,  on what besides  the metabolic aspect   may be important  in a  preparation for   training a race  or  event ?  ( coordination's inter  and intra muscular , Hormonal  control and balance    and much much  more.
 So simply   just looking on   my point of  lactate is not good enough but it makes as  thinking  at least.
So when we look  at   one  great summary   from the above post.

So this leads us to some interesting ideas for cool down and lactate production. If we're cooling down, using the drop in lactate as a marker for whether or not we're cooled down is silly. Lactate is fuel, if we've consumed the fuel how is that a useful marker for recovery? It merely means our body has used the fuel to feed our "cool down" workout. Instead the culprit for all the fatigue is H+ ions. These are removed from the body via CO2 delivered via respiration.

That is  pretty much a great summary, indicating as well, why  , when using  lactate as a  marker  for recovery, the question may  be allowed  whether it really indicates  recovery or whether we may be   less recovered  with a lower  lactate   than  when  we  would keep  the lactate .  Here a  more "educated"    information on that.

CHOI, D., K. J. COLE, B. H. GOODPASTER, W. J. FINK, and D. L. COSTILL. Effect of passive and active recovery on the resynthesis of muscle glycogen. Med. Sci. Sports Exerc., Vol. 26, No. 8, pp. 992-996, 1994. The purpose of this investigation was to determine the effect of passive and active recovery on the resynthesis of muscle glycogen after high-intensity cycle crgometer exercise in untrained subjects. In a cross-over design, six college-aged males performed three, 1-min exercise bouts at approximately 130% VO2max with a 4-min rest period between each work bout. The exercise protocol for each trial was identical, while the recovery following exercise was either active (30 min at 40-50% VO2max, 30-min seated rest) or passive (60-min seated rest). Initial muscle glycogen values averaged 144.2 +/- 3.8 mmol-kg-1 w.w. for the active trial and 158.7 +/- 8.0 mmol-kg1 w.w. for the passive trial. Corresponding immediate post exercise glycogen contents were 97.7 +/- 5.4 and 106.8 +/- 4.7 mmol-kg-1 w.w., respectively. These differences between treatments were not significant. However, mean muscle glycogen after 60 min of passive recovery increased 15.0 +/- 4.9 mmol-kg-1 w.w., whereas it decreased 6.3 +/- 3.7 mmol-kg-1 w.w., following the 60 min active recovery protocol (P < 0.05). Also, the decrease in blood lactate concentration during active recovery was greater than during passive recovery and significantly different at 10 and 30 min of the recovery period (P < 0.05).
These data suggest that the use of passive recovery following intense exercise results in a greater amount of muscle glycogen re synthesis than active recovery over the same duration

Now  we  could add some  additional interesting points here.


Med Sci Sports Exerc. 2004 Feb;36(2):302-8.




Passive versus active recovery during high-intensity intermittent exercises.Dupont G, Moalla W, Guinhouya C, Ahmaidi S, Berthoin S.




Laboratory of Human Movement Studies, Faculty of Sports Sciences and Physical Education, 9 Rue de L'Université, Lille 2 University, 59790 Ronchin, France.




Abstract PURPOSE:




To compare the effects of passive versus active recovery on muscle oxygenation and on the time to exhaustion for high-intensity intermittent exercises.








Twelve male subjects performed a graded test and two intermittent exercises to exhaustion. The intermittent exercises (15 s) were alternated with recovery periods (15 s), which were either passive or active recovery at 40% of .VO2max. Oxyhemoglobin was evaluated by near-infrared spectroscopy during the two intermittent exercises.








Time to exhaustion for intermittent exercise alternated with passive recovery (962 +/- 314 s) was significantly longer (P < 0.001) than with active recovery (427 +/- 118 s). The mean metabolic power during intermittent exercise alternated with passive recovery (48.9 +/- 4.9 was significantly lower (P < 0.001) than during intermittent exercise alternated with active recovery (52.6 +/- 4.6 The mean rate of decrease in oxyhemoglobin during intermittent exercises alternated with passive recovery (2.9 +/- 2.4%.s-1) was significantly slower (P < 0.001) than during intermittent exercises alternated with active recovery (7.8 +/- 3.4%.s-1), and both were negatively correlated with the times to exhaustion (r = 0.67, P < 0.05 and r = 0.81, P < 0.05, respectively).








The longer time to exhaustion for intermittent exercise alternated with passive recovery could be linked to lower metabolic power. As intermittent exercise alternated with passive recovery is characterized by a slower decline in oxyhemoglobin than during intermittent exercise alternated with active recovery at 40% of .VO2max, it may also allow a higher reoxygenation of myoglobin and a higher phosphorylcreatineresynthesis, and thus contribute to a longer time to exhaustion.   So  one of teh discussion  now is   teh great  situatin we  may have, whne lactate is  here to help rather thna  to create a problme.


The lactate shuttle during exercise and recovery.




Brooks GA.








Most (75%+) of the lactate formed during sustained, steady-rate exercise is removed by oxidation during exercise, and only a minor fraction (approximately 20%) is converted to glucose. Significant lactate extraction occurs during net lactate release from active skeletal muscle; the total lactate extraction approximates half the net chemical release. Of the lactate which appears in blood, most of this will be removed and combusted by oxidative (muscle) fibers in the active bed and the heart. The "shuttling" of oxidizable substrate in the form of lactate from areas of high glycogenolytic rate to areas of high cellular respiration through the interstitium and vasculature appears to represent an important means by which substrate is distributed, metabolic "waste" is removed, and the functions of various tissues are coordinated during exercise. During recovery from sustained exhausting exercise, most of the lactate accumulated during exercise will continue to be removed by direct oxidation. However, as the muscle respiratory rate declines in recovery, lactate becomes the preferred substrate for hepatic gluconeogenesis. Practically all of the newly formed liver glucose will be released into the circulation to serve as a precursor for cardiac and skeletal muscle glycogen repletion. Liver glycogen depots will not be restored, and muscle glycogen will not be completely restored until refeeding. This is because the diversion of lactate carbon to oxidation during exercise and recovery represents an irreversible loss of gluconeogenic precursor and because the processes of protein proteolysis and gluconeogenesis from amino acids are insufficient to achieve complete glycogen restitution after exhausting exercise.(ABSTRACT TRUNCATED AT 250 WORDS)












[PubMed - indexed for MEDLINE]

 Whe you think, that we know that  since the late 1980  so  can see,  where we  may go  with integrating   MOXY into  the common idea  of  controlling physiological testing.
  In teh workshops  and seminars  we will start in  2014  in europe, teh USA  and  Canada   we  will =have    some major  issues  with this   common  " classical  educated"   stabndards.
The beauty  will be  that we   will  show  inteh seminras  live prtactical  examples   and will not offer  an answer  but will ask teh    peopel    to give us  some explanartions.

  When we      try to stay out of teh lactate threshold, anaerovbic trehsold  ventilatory treshold   and FTP   ideas, thna   NOT becasue they  do not have some interesting points  but becasue MOXTY is a completely new direction  of   assessing information live   where all happens.
  So this  next  few  words  may help to understand  why  ideas we had  20 years backk with lactate inclduing our own LBP ideas  ahve to  be reveiwed  and put into a  smart context  with what we  can do now.

 Here  some more  to read.

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,


a delay could be expected between the beginning of lactate production within the working muscles and the parabolic rise in plasma [La-] in response to ramp exercise in a similar way that, in response to a short period of severe exercise, the peak value of plasma [La-] is only observed following a several-minute delay into the recovery period (see Hirvonen et al. 1987, 1992). Consequently, plasma [La-] concentration at a given t during a ramp exercise does not reflect lactate production in the muscle at that precise t and at the


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 correspondingwork 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 above. 

Now  take  any   short term test :  Wingate, Conconi,  1  2  3  minute  ramp tests,  Interval workouts  on the ice  and  so on.
  So when we  get into discussion  with  MOXY users  trying  to   show us  how  MOXY datas , no matter on step lenght , fit  together with lactate  information     and even in 1 min  and shorter    loads, than we  may have to step back  and  fair  and open  ask, whether an indirect  assessment of blood  over  your system  can be  used  to  " validate"  a direct info  through your skin  on a  working muscle.  Or  whether we  have  to separate the indirect  classical ideas  and  theories    and  look at new  options  with direct  info  we  have now  thanks to newer technology.

    Next  up  I    like to show, that  " cool  down"   has to  be observed  from different perspectives.
  1.  The metabolic  part we  just discuss here.
 2. The  respiratory  reaction , when we suddently  would stop .
 3. The cardiac  reaction on a  sudden stop.

 So here   the section to discuss:
Breathing in a hypercapnic state where we stack more CO2 in the bloodstream to speed up H+ removal could be controlled with a device like a Spirotiger.

   1. Do we   speed  up H +  removal, when we stack up CO2  ???

The  key is  to find out   after a  workout  or  a race,  in what situation the respiratory system  is moved  to.
a)  Is  the situation   so , that we have a  very very high RF  and a relative  low  TV  or the opposite.
  How  does this show up in the CO2  balance ( Hyper  or hypocapnic )  . Than if  we have the answer we  can look live  in MOXY trends  on the  reoxygenation  situation of the client.  Than the  "long term" situation.
  After a  400 m all out  race  every person  will   just have one   goal :  getting rid of CO2  and trying to get  pH  and  other  out  of balance    system back  to homeostasis.
 The question now is how long  does this take.
  One attempt  in the past  was EPOC.
  With the open question today, who  really has a  O2  depth.
 NIRS cleary shows  , that it is   NOT the muscle.
  There si no Deficit  at the start, as  we  not go into a defcit  but rather tahe it  from a  storage  ability.
   So is the increased  cardiac  reaction, respiratory  reaction  and  hormonal  reactions  to  get back into   start  situation the  main reason of the increase  O2  use  after an event.?
  When looking at recovery  we have a  recovery assessment, where  we  use   for example RRA  to see how   much after  a load  the respiration still is  out  of balance  and if it is  out  is the client    reacting   as a hyper  or hypocapnic  situation.
 Depending on this result we  will use respiratory  exercises  and interventions  to  try to speed  up   the time back to homeostasis.
 So stay tuned  for  recovery  or "cool down' on respiration and cardiac reactions.











Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Okay  here the follow up ideas.
 1.  We  know, that  when " cooling   down" we  will  stay  "  active"  and tehrfor  will need  to  still use  energy.
  Lactate is a very  great  energy source    and it is used nicley, whne we  ahve as well a  slightly   limited  O2  availability.. Now MOXY will  tell you  easy, whether  we  have  a  good or not optimal  O2  Bio-availability.
  In cases, where  the  load  was   a very high intensity   we  will use  lactate  for  movment  but as well    to use it as  soon and as fast as possible  for  reloading  essential storage  area.

Ann Physiol Anthropol. 1990 Apr;9(2):213-8.

Oxidative removal of lactate after strenuous exercise.

Hatta H.

Author information

  • Department of Sports Sciences, College of Arts and Sciences, University of Tokyo, Japan.


Metabolic fate of lactate after strenuous exercise which lasted 2-3 min was investigated in rats and mice. 14C-labeled lactate or glucose was injected into the aorta of rats through an catheter. 14C-glucose was injected intraperitoneally into the mice after supramaximal exercise. The mice ran twice with a 4 hr interval to investigate muscle 14C-lactate metabolism which was produced from muscle 14C-glycogen. A great deal of blood and muscle 14C-lactate was expired as 14CO2 after the exercise. The results indicate that oxidative removal is the major fate of lactate metabolism after strenuous exercise and that blood glucose is the major substrate for muscle glycogen resynthesis. Light intensity exercise after strenuous exercise (active recovery) enhances oxidative removal of blood and muscle lactate. Gluconeogenesis from lactate to glycogen within the skeletal muscle is not a major pathway of muscle lactate metabolism, while high intensity training can activate this pathway.


The result is  what we see,  active  recovery after  or between  loads  will  help to  drop lactate values  faster.
  To  argue  that this is a good  sign of  recovery is pushing  some   open  questions.
 Why  would  the  use  of a great  energy to move  and to reload   storage   for energy  be  great  to be used  to get rid of it.
  In fact  thanks to the buffer  ability  of  lactate we  are able  to get going.

 Respiration  and respiratory training, more than just for fun.




: "Because lactate is combusted [metabolized] as an acid (C3H6O3), not an anion (C3H5O3), the combustion of an externally supplied salt of lactic acid, CHO3H5O3- + H+ + 3O2 ¨ 3H2O + 3CO2 effects the removal of the proton taken up during endogenous lactic acid production (Gladden, L. B. and J. W. Yates, J Appl Physiol 54:1254-1260, 1983). A side benefit of alkalizing the plasma


by feeding lactate would be to enhance movement (efflux) of lactic acid from active muscles into plasma, a process which is inhibited by low (relative to muscle) blood pH.




(Brooks, G. A. and D. A. Roth, Med Sci Sports Exerc 21(2):S35-207, 1989; Roth, D. A. and G. A. Brooks, Med Sci Sports Exerc 21(2):S35-206, 1989). Moreover, maintenance of a more normal blood pH during strenuous exercise would decrease the performer's perceived level of exertion. The conversion of lactate to glucose in the liver and kidneys also has alkalizing effects by removing two protons for each glucose molecule formed, 2C3H5O3 + 2H+ ¨ C6H12O6. Thus, whether by oxidation or conversion to glucose, clearance of exogenously supplied lactate lowers the body concentration of H+, raising pH."(22)

So when  in February  all the reporters   and coaches and former  athletes   give their  live info  as  how the lactic acid  increases  and    is the reason  why they  are getting slower,   than we  have  to have a  gentle smile on our  face, as  it is  exactly the opposite. Thanks to the ability  to   generate lactate , we   see this  athletes  going  slightly  faster  and longer  compared  with the  opponent.
So  when we look  to many great studies  with NIRS  and the attempt  to  push the NIRS trend into a lactate  thrershold idea  we  actualy make a step backwards , trying to defend  or justify  some  ideas we had  and used,  instead of looking forward  to use  NIRS / MOXY  to show, that a  drop in SmO2   does not mean  always an increase in lactate  and  vica versa.

 Pushing   MOXY into a threshold  concept   would be  really loosing the ability  to move  forward  to develop some individual  ideas  of training  in any sport  . We  will see in teh future, how  " bigger  names' will come up "suddently "  with ideas, that  mOXY  coudl change teh way  we u  train  interall  as well as otehr  workouts.
.  It is all done  since many years  very practically  and Brina  from Next level pushes  thsi since many years in sprot schools  and team sport..
  Here just  for  fun  why  it  would eb a step backwards .




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.




This article contains a very concise summary of the concept of anaerobic threshold and how it is depicted in the literature. The implications of each individual statement are particularly important given the pre-occupation of many coaches with this concept. The major points of the article are discussed below. Further features are introduced in the "Implications" section.


The concept of anaerobic threshold itself is not universally consistent. Long dynamic exercise that is predominantly aerobic ranges between two extremes of physiological dynamics resulting in very different blood lactate levels.


  • At the lowest level, an exercise can be sustained for a very long time. After 2-5 min a state of overall oxidative energy supply is established where lactate production is balanced by lactate elimination at a low level. Fat (lipid) metabolism is the primary source of fuel. Exercise limits are mainly associated with eventual increases in internal temperature. Potential dehydration can be prevented by supplementation of water and substrate (carbohydrate and electrolytes) during performance. (p. 158)
  • At the highest extreme, the workload requires an additional formation and accumulation of lactate  better is H + ions to maintain power output. Exhaustion results through the disturbance of the internal biochemical environment of the working muscles and whole body caused by a high or maximal acidosis. Generally, accumulation of  H + limits performance to periods from 30 sec to 15 min. For example, the average time to exhaustion at the minimal velocity which elicits VO2max is 6:30 and is not correlated with the blood lactate level developed during the task. (p. 159)


Between these two extremes are transition stages, several of which are labelled similarly as "anaerobic threshold" or "lactate threshold." Thus, the same label is used for different concepts and their assessment protocols that lead to different values and training implications. Billat displays the various implications of this confusing situation. According to a variety of "authorities," changes in blood lactate accumulation are termed and defined differently as well as being associated with different levels and characteristics of accumulated lactate. H+ They are also differentiated by the protocols used to measure them. Some examples are listed below.


  • "Onset of plasma lactate accumulation" is established as being exercise induced levels which are 1 mM/l above baseline lactate values. [Farrel, P. E., Wilmore, J. H., Coyle, E. F., et al. (1979). Plasma lactate accumulation and distance running performance. Medicine and Science in Sports and Exercise, 11, 338-344.]
  • "Maximal steady-state" is displayed when oxygen, heart rate, and/or treadmill velocity produce a lactate level which is 2.2 mM/l. [Londeree, B. R., & Ames, A. (1975). Maximal steady state versus state of conditioning. European Journal of Applied Physiology, 34, 269-278.]
  • "Onset of blood lactate accumulation" (OBLA) occurs when continuous incremental exercise produces a lactate level of 4 mM/l. [Sjodin, B., & Jacobs, I. (1981). Onset of blood lactate accumulation and marathon running performance. International Journal of Sports Medicine, 2, 23-26.]
  • "Individual anaerobic threshold" is the state where the increase of blood lactate is maximal and equal to the rate of diffusion of lactate from the exercising muscle. Values range from 2-7 mM/l. [Stegemann. H., & Kindermann, W. (1982). Comparison of prolonged exercise tests at the individual anaerobic threshold and the fixed anaerobic threshold of 4 mM/l. International Journal of Sports Medicine, 3, 105-110.]
  • "Lactate threshold" is the starting point of an accelerated lactate accumulation and is usually around 4 mM/l and is expressed as % VO2max. [Aunola, S., & Rusko, H. (1984). Reproducibility of aerobic and anaerobic thresholds in 20-25 year old men. European Journal of Applied Physiology, 69, 196-202.
  • "Maximal steady-state of blood lactate level" is the exercise intensity that produces the maximal steady-state of blood lactate level and ranges from 2.2-6.8 mM/l. [Billat, V., Dalmay, F., Antonini, M. T., et al. (1994). A method for determining the maximal steady state of blood lactate concentration from two levels of submaximal exercise. European Journal of Applied Physiology, 69, 196-202.


Many scientists and coaches use the label "anaerobic threshold" interchangeably with these concepts confusing what is supposed to be a scientific coaching principle. Just because the same label is used does not mean analogous concepts are being discussed. Since there would be different coaching and performance implications from each of the above concepts, the blanket use of this term will foster many erroneous coaching prescriptions and procedures.


Lactate accumulation indicates a shift from solely oxidative to an additional glycolytic energy supply. Lactic acid production is due to the activation of glycolysis which is more rapid than activation of oxidative phosphorylation. This is indicated by a steep non-linear increase of blood lactate in relation to power output and time. That accumulation can be attributed to disparities in the rate of lactate production and removal, even for work intensities under those which elicit VO2max. Lactate production is not related to oxygen deficit but rather to the increase of the glycolysis flux. (p. 159)


Lactate is produced constantly, not just during hard exercise. It may be the most dynamic metabolite produced during exercise since its appearance exceeds that of any other metabolite studied. The constancy of the blood lactate level means that entry into and removal of lactate from the blood are in balance.


The turnover of lactic acid during exercise is several times greater for a given blood lactate level than at rest. For a given blood lactate level, lactate removal is several times greater in trained than in untrained persons.


Several factors are responsible for the lactate inflection point during graded exercise.


  • Contraction stimulates glycogenolysis and lactate production.
  • Hormone recruitment affects both glycogenolysis and glycolysis.
  • Recruitment of glycolytic fast-twitch fibers increases lactate production.
  • Blood-flow redistribution from lactate-removing gluconeogenic tissues to lactate-producing glycolytic tissues causes lactate levels to rise as exercise requires continually increasing power output.


Lactate values differ according to several variables: the activity being performed, the site from where the blood sample is taken, the environment itself (both physical and its effect on the athlete's psychology), and the state of glycogen stores prior to testing. Unless these variables and others, such as day-to-day cycles in general physiology, as well as variations in test administration and athlete performance of each test segment, can be controlled and made consistent between test administrations it is likely that score differences will be unreliable. The practice of attributing any observed lactate-test differences, no matter how small, to training effects or as revealing the trained state is extremely dubious at best.


Practical Implications


When scientists cannot agree upon a concept's definition, let alone the appropriate label to use, as well as the appropriate method/protocol of assessment, then the practical use of the "general implications" of the concept is foundationally prohibited. Until this situation is clarified and discrepancies removed, field testing for "lactate-threshold" should be avoided. There are more profitable and useful activities for athletes and coaches to be engaged in.


Of significance to coaching is the concept itself. The common misunderstanding that the anaerobic threshold is the state where aerobic activity is dominant and maximal and anaerobic activity constant but "insignificant" is very prevalent. There are few competitive activities or events where such a circumstance is desirable.


Most activities do not require all body parts to be involved in an activity at the same intensity level. A cyclist will work the legs extremely hard but, by comparison, the rest of the body will function comfortably in an aerobic zone of metabolic activity. A swimmer pounding out stroke after stroke in a 1500 m race works the arms at an intensity that employs a high level of anaerobic energy supply but the rest of the body is "relaxed" and functioning at quite a basic aerobic level. Even in running, in a marathon the legs work hard while the arms and upper body "save energy." In these activities, lactate is produced by the primary working muscles and resynthesized by the muscles engaged in mild supportive activity. Those muscles cleanse or "sponge" out lactate so that the blood supply to the hard working muscles is quite low in acidity when returned to those muscles. Thus, any lactate measure is a measure of the "general functioning" of the body, not the actual work performed by the primary sporting muscles. Differences in technique most probably would account for a significant portion of many inter-individual differences in lactate assessments than work levels or movement economy.


In many "aerobic" sports the actual prime mover muscle groups work at an anaerobic level rather than aerobically as is inferred from anaerobic threshold testing. The common perception of anaerobic threshold does not give any information or understanding of what actually is happening in important aspects of a performance. Even the slightest improvement in movement economy (technique) in the "anaerobic prime movers" could make a significant difference to performance.


Of all the concepts of anaerobic-type thresholds or measures that are proposed perhaps the maximum lactate steady-state (MLSS) is the one that is most applicable to the field of sports. In cycling events of one hour, athletes have been measured to "tolerate" and demonstrate sustained lactate levels in the region of 7 mM/l. In most events where "effort" is required as part of the competitive strategy, lactate levels will be sustained in a competitive performance in excess of the anaerobic threshold (if one can be demonstrated). There is a much greater proportion of many competitive performances that is more anaerobic than is generally acknowledged. If appropriate and sane anaerobic training is ignored then an athlete will not be trained optimally and a theoretically "best" performance will not be possible.


How can one test for maximum lactate steady state? Simply ask trained, experienced athletes to perform a task equal to the duration of their competitive event and they are likely to produce a performance that is close to demonstrating the MLSS. To be sure of this, if performance intensities, usually velocities, are performed at an increment above and below the first trial, verification should be forthcoming. Repeating many trials usually is not necessary. Is this too simple of a concept for complicated science? In practical circumstances it works. But since this could be a procedure that is implemented by coaches would it be endorsed by scientists which would seemingly remove a coach's dependence on them?


But a central perplexing question still remains: what does one get from measures of lactate and performance? What do they tell more than is already known? If lactate values are specific to the task/testing-protocol/event there can be no inference beyond the observations themselves.


When two athletes with the same physiological capacities perform the same activity, one using arms only the other using arms and legs, the performance results are often different, particularly when energy supply is an important aspect of the task demands. In this case, it is not the "anaerobic threshold" that differentiates the two but the movement economies, one using more muscle mass to produce a performance outcome. An attempt to shift the anaerobic threshold by further training of a particular type in an hypothesized metabolic zone with appropriate heart rates is clearly the wrong approach to solving the less-efficient athlete's problem. A skill element change to reduce unnecessary movements would result in greater movement economy and would shift the velocity that supports the MLSS to the right.


It is dubious to attribute shifts in anaerobic threshold values to physical training. Given that so many variables render field tests of this phenomenon practically unreliable, what is attributed to score differences obtained between two tests is more of a guess than an informed judgment.


Sport scientists can produce graphs of swimmers, runners, rowers, etc. showing an "inflection point" that occurs in a region of performance velocity. Equally, other athletes tested with the same protocol do not show any inflection or exhibit measures that cannot be interpreted in terms of a traditional anaerobic threshold. A few selected demonstrations do not prove the existence of a phenomenon that can be applied universally. The trend in field testing is rather one of more people not demonstrating a clear "anaerobic threshold" than doing so. Complicate that further with deciding upon which threshold protocol fits the sport from the existing array of definitions and confusion results rather than a clearly usable training tool.


Anaerobic threshold results must be reliable, that is, capable of replication. When a particular protocol is used for a series of periodic assessments, as is commonly followed in "sport science testing" programs, if that protocol is altered, the previous results cannot be used for comparison purposes. A protocol change will produce unrelated results, often different response phenomena, and above all different implications and interpretations. The definitions and discrepancies listed above all originate from different testing protocols. Thus, results from one protocol to the next, no matter how small the change is explained to be, should not be compared. Essentially, a new data base is developed.


An unavoidable dilemma. Sport scientists are ethically bound to represent the worth of lactate testing and the inferences that are commonly proposed. This is what is known.


  1. Lactate concepts and measures are limited/specific to each testing protocol.


  1. Results from one protocol cannot be used to generalize or infer values to other testing protocols.
  2. If one cannot infer from one lactate testing protocol to another then it is illogical to generalize lactate testing results to a competitive performance.
  3. It is a greater stretch of the imagination to leap conceptually from an inferentially-limited measure under controlled conditions to the dynamic circumstances of a competitive or practice setting.
  4. At most, lactate and lactate threshold measurements reveal changes but have limited to possibly non-existent inferential capacities about future performances (even training performances let alone competitive performances).
  5. Lactate and lactate threshold measurements can reveal that they have changed as a result of training, but, if those changes are unrelated to competitive performances what is their value?
  6. There are no national or international competitive events that reward medals for lactate threshold changes, levels, or testing protocols.


A story. During the spring of 1996, this writer attended the ARCO Training Center in Chula Vista, California. One day a USOC testing group had completed lactate threshold and aerobic parameter testing sessions on the US men's heavyweight rowing eight that was to compete later that year at the Atlanta Olympic Games.


The eight had just completed a European tour and performed worse than at any time in the previous three years. Based on comparative racing performances, it was a boat in trouble.


The head USOC scientist related that the members of the eight were still improving in fitness as the measures that were taken were better than previous test results.


Despite improved "fitness measures" the eight recorded a performance that was worse than any in the previous four Olympic Games, and compared to the boats that it had raced during the recent European tour, it had also degraded in racing capability. The fitness measures indicated that training was progressing satisfactorily. Unfortunately, racing performances were declining. Training improvements in physiological indices were negatively correlated with racing achievements. In 1994, the eight were world champions, in 1995 world bronze medalists, and in 1996, when they had the best testing results, were fifth out of six at the Olympic Games.


Just what is the value of lactate and lactate threshold/MLSS testing for making coaching decisions that relate to competitive performances?"

 Lactate  is  and can NOT  be  compared  with a live  info   like MOXTY  without taking  other  aspects  like respiration into account. See pic  from a workout , where  lactate  went very very different  from what we would expect  as we manipulated  the  O2  disscurve during a workout'

. We will show  and practically  proof in our  2104  seminars  all over the european  and  north america continent, that  respiration combined  with MOXY  will  answer  many open questions.
 Here a pic  from a  workout  we  did  2 days ago  with an athlete  showing him, how he  can  gain  another  2 - 6  seconds  top performance   at the end of a load,  when  using his brain  combined  with his respiratory system..
  Or  he    makes  no technical mistakes   though the last   few  gates in a  slalom  during a downhill race  and so on.

  You see SmO2  and   tHb as  2  nice indicator  of  Bio availability of O2  as well as tHb  as the  blood  flow trend.
  Look at the picture  and  alone the picture  will show  you  the changes.
  The load was a  " warm up " to the current  optimal SmO2  and tHb  on that day.
 5 min 100 watt  followed  by 5 min 150 watt  followed  by 81/2 min 200 watt  followed  by 11/2 min  rest  and than   all   loads  are 300 watt  for 30 seconds  with 11/2 min rest.
  Some loads  where   just the way he would do it, followed  by  3  and 4 loads  same  wattage  same duration but with  specific interventions  to show  him  how  to  create  an additional advantage  on bioavailability    during  a  race  and or   at the end of a race.   So I  as usual  got lost  but will be back   on how we  solve the  cardiac  and respiratory problem, when  not  using activity  to  " cool  down"
  Here just to finsih  of teh   thought  on MOXY  and  threshold.


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.




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