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Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
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With the reluctant  acceptance, that lactate  may be not  that  ugly  and bad  as we   all got educated    and the fact, that lactate  may in fact be a  great energy source  and  with out   its development  we may be  much less able  to get  to the high intensities  we actual;. can go, we  hav3e reached  an interesting discussion.
.  What if  lactate is   just  an additional part of   survival  . A survival  with the goal  to maintain the needed  ATP level on a stable base line  and if in trouble  find  ways  to reduce the demand of  ATP production rather  than to find  additional  ways  to create more.
. What if  we  have some answers  to what we did   in the late  1980  , when we  where  looking  at  lactate trends  ( lactate balance  point )  rather than  absolute numbers  )  and what if we  would take glucose   ( blood sugar  rather than lactate.
. This is what we did  and    we  had the trend. that glucose ( blood sugar  ) would show a very similar trend      compared to  lactate. In fact, when we  compared  lactate  in a " classical step test" to blood sugar in a classical step test  the   blood sugar   gave a much more interesting trend info  than lactate which  simply increase  in a  curve. The curve  was  mainly influenced  by the test protocol rather than any other   ideas.
 So  by  starting with a " normal blood sugar  and seeing the trend. we reversed  at that time the lactate by  created in   high lactate level  )  pre test )  an than   followed up by a  " step test, which than created  the LBP  idea.  .   Interesting is that now  1/4  century  later I  have some great discussion on this again  and here a very short  review  and inside  view  on some  e mail exchange we have in an internal group.  This is an example , how we could discuss  many topics  with integration MOXY here on this forum.

  Here  for a  short peak inside    on what we  do  and discuss:

This  is a great examples     why we did  originally the LBP ( lactate balance  point )in the late  1980 . We  where looking , where blood sugar  would   stop dropping and increase again. (  blood sugar  balance point )( as the strips  where much cheaper ).

  So we argued , that  when we start we  use   glucose  so    levels  will drop  and  the drop  comes  from the  glucose  circulating in the blood . Once the level drops  critically we release  form the liver  and now  more   release than utilization. ???

Once we  kick in  the  stored  glucose  from the liver  it will increase     and we have  what we seem to see here.

 There was  as you can see many open questions.

 So we did  the opposite  and  loaded an athlete first to create lots  of lactate  and than  deloaded   and  reloaded again with a second step  test. We argued  that as  long he has more  O2 than he needs  he  will be able to drop lactate and once there is  an “ anaerobic “ situation lactate will go  up  and than he has to quite because of lactic acidosis !!!!  smile .

 You know by now where we  went wrong. What we tried to avoid is the LT  or  2  and 4 mmol and we went  just with lactate trend..

  Today  we know, where the weak part was or is  and why   blood sugar  from a certain moment increases  as well like  lactate.( or  at least  we hope  we know )

So the question than was.

  Who  or what creates  the reaction for an increase.

 Is it the incredible demand   for  energy supply to  be sure we  have  enough energy    for ATP  demand so we   over  react  by splitting glucose   and  one of the   products  is lactate  if    there is  too much  glucose  splitting

 So as long  we have  enough O2 supply  for the working muscles  we can use it , as soon we  run into H +  production  we try to keep H + balanced  and now we use   lactate as a shuttle of  H +  buffer on the one side  and as a helper  for other muscles   looking for a great energy source.

 . So why is glucose increasing.  Discussion of  an overshoot of   glucose release  from the liver as long we have this option.  A   limitation at the end of  glucose  use-ability  as lactate is  readily available    and no need  to break down further glucose  and  better save it  for vital areas  like the brain.

  And many more feedback questions.

 As you can see in Per’s great picture That  we may have lactate influencing the blood sugar  or  do we have blood sugar influencing the lactate. ????

 ???  what do you think  , who reacts  first  and     how much is the difference  as both have indirect problems  of  delayed  information  in the finger. ???.

  Blood sugar may in fact show  a better  trend in  change due to the  dip  we  can see  rather than a steady increase in lactate  with no real indication ,  just based on   statistical options like 2  and  4 mmol In  every  step test  you will have a blood sugar  dip  . In lactate you can have it by doing our old idea of LBP ( lactate balance  point )test.

 Goggle; lactate balance point  and you will be surprised on the hits  of  this concept.

 

Cheers juerg the   examples  are In the att.  word  document   Here   a short summary from a historical review   just  for  refreshing  where we  may have got stuck in what we  often still do and believe.

 

HISTORICAL DEVELOPMENT OF THIS MODEL OF PERIPHERAL FATIGUE 

 

( Summary out  of  T. Noakes  historical review on current classical  believes.)

 

 

 

“The origins of this belief can be traced to the pioneering studies of Fletcher and Hopkins, and Hill and colleagues  in the 1920s.

 

The classical theory, since defined as the cardiovascular/anaerobic/catastrophic model of exercise physiology, postulates that fatigue during high intensity exercise of short duration results from a skeletal muscle ‘‘anaerobiosis’’  that develops when the oxygen requirement of the active skeletal muscles exceeds the heart’s capacity to further augment oxygen delivery to exercising muscle by increasing the cardiac output. As a result, any additional increase in energy generation in the active muscles can come only from ‘‘anaerobic’’ metabolism, leading to fatigue because the ‘‘maximum oxygen intake is inadequate, lactic acid accumulating, a continuously oxygen debt being incurred, fatigue and exhaustion

 

Setting in’’ 

 

 Since than  we take   this  idea  and squeeze it into a  current theory  by  abusing  any  new facts  to be  adjusted  so they can accommodate  the ‘classical “ believes. No matter    on whether the original idea was ever properly assess   on how and why we created this model of anaerobe and aerobe.   This despite the fact, that with much more advanced technology we can show now, that there is no such thing like anaerobe situation. 

 

 

 

“Richardson et al have concluded that: ‘‘…intracellular pO2 remains constant during graded incremental exercise in humans (50–100% of muscle VO2max)’’ so that: ‘‘With respect to the concept of the ‘‘anaerobic’’ threshold, these data demonstrate that, during incremental exercise, skeletal muscle cells do not become anaerobic as lactate levels suddenly rise, as intracellular pO2 is well preserved at a constant level, even at maximal exercise’’ (p. 63168). They also conclude that: ‘‘Net blood lactate efflux was unrelated to intracellular pO2 across the range of incremental exercise to exhaustion’’ but was ‘‘linearly related to O2 consumption’’ (p. 62768). Another study confirmed these conclusions: ‘‘…consequently these data again demonstrate that, as assessed by cytosolic oxygenation state (deoxy-Mb) during incremental exercise, skeletal muscle cells do not become ‘‘anaerobic’’ as lactate levels rise, because intracellular PO2 is well preserved

 

at a low but constant level even at maximal exercise’’

 

Interesting is to note, that we  simply  accept the fact   despite  some conclusion made by Hills  which were great based on theory  but where overruled  some years later  when  more  in detailed information was discovered concerning  energy  pathways.

 

“Hill believed that the ‘‘lactic acid’’ generated by ‘‘anaerobic’’ conditions in skeletal muscle served two opposing functions. Its initial production stimulated muscle contraction; in the presence of an adequate oxygen supply, the oxidative removal of lactic acid produced the ‘‘neutralization’’  necessary to allow muscle relaxation. However, at the higher exercise intensities at which skeletal muscle ‘‘anaerobiosis’’ developed, lactic acid could no longer be neutralized but accumulated progressively.”

 

 

 

“Of course, Hill and colleagues could not have surmised that ‘‘fatigue and exhaustion’’ was caused by a progressive failure of ATP generation in the active muscles, as Hill’s model evolved in the period before the detailed metabolic pathways for ATP

 

generation were described; indeed ATP itself was discovered in 1929, 6 years after Hill’s model was first proposed. In addition, the role of ATP and phosphocreatine in providing energy for muscle contraction had yet to be described.

 

Hill could not have known that ATP depletion, rather than lactic acid accumulation, causes skeletal muscle rigor.”

 

 

 

 

 

HISTORICAL DEVELOPMENT OF THE OXYGEN AND ENERGY DEPENDENT ‘‘LIMITATIONS’’ OR

 

‘‘CATASTROPHE’’ MODELS OF EXERCISE FATIGUE

 

 

 

“The role of ‘‘anaerobiosis’’ and ‘‘lactic acidosis’’ The real origins of the classical Hill cardiovascular/anaerobic/ catastrophic model can be traced to the pivotal influence that the original study of Fletcher and Hopkins1 at Cambridge University exerted on the thinking of Hill and colleagues in Manchester. Fletcher and Hopkins1 wished to establish

 

whether or not: ‘‘within a muscle itself, means exist for an oxidative control of its own acid formation, or for the alteration or destruction of acid which has been formed, either there or by muscular activity elsewhere in the body.’’ They were perplexed by the consistent finding at that time that lactic acid (lactate) concentrations in excised skeletal muscle preparations were always high, regardless of the experimental conditions, for example, whether the excised muscle came from rested, exercised, fresh, or preserved tissue.”

 

 

 

Now Fletcher and Hopkins never ever had the goal or the idea to see, what is going on during exercise in skeletal muscles. They simply did some lab test to learn how to conserve certain tissue sampling for   additional research projects.

 

 Their sampling was completely of any option to be a part of a feedback loop as we have during exercising and activity. So any conclusion based on their observation was completely taken out of context to what we really see and do in exercise physiology.

 

So it is very  astonishing, that this great work   was taken  out of context  and forced into a   interesting “ classical ‘ model  which  still survives  up to this days.

 

 

 

 

 

“Fletcher and Hopkins did not conclude either that ‘‘anaerobiosis’’ or more correctly, no perfusion anoxia, was the sole reason for increased lactic acid production by amphibian muscle or that the ‘‘increase of lactic acid’’ caused fatigue. They merely described these separate phenomena whilst developing a novel technique (immediate immersion

 

in ice cold alcohol) for the accurate measurement of lactic acid in biological samples. It is important to stress that their primary interest was not the effects of exercise on skeletal muscle metabolism.”

 

 

 

I  wonder if  Fletcher  and Hopkins  would have  taken  glucose  instead of lactate  to test, whether we  would talk  this days  as instead of a lactate threshold   from a Glucose threshold  and instead of   lactic acid    from “Glucosacid”

 

 

 

 
Attached Files
docx Per_red_bull_glucose_and_lactate.docx (184.90 KB, 17 views)

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