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
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”