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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
When private  independent groups  do research  they will face some  very common challanges.
1. We are dependent on  independent groups, having their own great ideas and a great amount of knowledge outside the BOX.
 That's why they work independent and are not " educated" groups, meaning, they are not used to repeat what they have to repeat but rather use their brains to  think ideas and options through.
 Here a nice example  and as well an example why we run somewhat behind with data collection.
 I great group leader writes :
 " I am happy to add lactate samples to a standard step test starting at 60 watts, in order to support this study, but am interested in whether we are doing this to simply prove once again the lack of value of traditional lactate threshold testing, or for some other reason. It seems both a waste of resources and money to simply pay and extra $20-$30/test, and submit an athlete to additional invasive testing, without a clear understanding of what the protocol is trying to accomplish. "

 The part of interest is really :
 "but am interested in whether we are doing this to simply prove once again the lack of value of traditional lactate threshold testing"
This is a group , who since years understands the  information lactate  can give or better will not be able to give, when approaching " classical" step tests.

So our mistake in this case was, that we did not clear enough explained , why we need the step lactate values.
  Here in very short first, but I will explain in much more in depth later today.
 Simple Idea :
 Can we  see in NIRS / MOXY  the trend in "lactate"
  -  possible information, when we shift  the metabolic demand die to change in oxygen demand and delivery. With lactate as an invasive test we can assume, that when lactate  is increasing in the system, that we  made somewhere in the participating muscles a metabolic shift towards the prodcution of lactate. As Andri pointed out there is than as well an assumption made, that there is a shift in H + dynamic and  additional dynamics  like P inorg.
 What we know now since over 20 years is, that lactate per see si not a reasoning for "Fatigue " but a sign , that somehow it worked as a shuttle and one of the shuttle options is H + shuttling  from the intracellular are into the blood stream.
  The key question than is rather, whether in the process of helping to buffer possible H + over- production to keep  ATP production going . or whether H + may  fall out of homeostatsis, or not. There are different  helpers to try to avoid this, with lactate one of them, the other one easy to use in sport is the respiratory system over CO2 expiration.
 One of the interesting studies, and Andri may come later  more to the science, is, that as long H + seems to be in a state of homeostasis , it does not matter at all what the lactate value test shows.
 In fact adding lactate to the system improves performance.
 So in very short term:
 Cooling down active will ,as proven over and over again, reduce lactate  relative fast compared to sitting still.
 Why ?:
 well when moving we need energy and lactate is a fast and easy to get energy after an all out 400 m run in an intervall. So it is very clear , that lactate will decrease  much faster.
 BUT ;
 Do we really like to get rid of the so great energy source .
 Perhaps we should get rid of the H +  by not using up to much lactate.
How ?
Well think and we will  come later back to this.
 With MOXY ,we in fact can look at this  situation.
 Are we completely nuts now?. Here a short  abstract of an interesting study backing us up and  I am sure more will come.
 Tradition will fight back as there has to be an active "cool " down to get ride of the lactic, acid as it is very evry bad.????

 Here an inside view. Now think in this study outside the box.
 Key words.   and questions: Energy , oxygenation ,O2 Diss curve, respiration ,CO2

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.



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 phosphorylcreatine resynthesis, and thus contribute to a longer time to exhaustion.


 1. Where does  lactate as a fuel possibly stay higher ?
2. Where do we possibly can change O2 diss curve easier with the respiratory system.
3. Why do we see a better reoxygenation  in passive recovery ( Think  CO2 levels and O2 Diss curve.)

 Now here an opposing study , who thinks active reovery is better.

Journal of Sports Sciences (2008)

Volume: 26, Issue: 1, Pages: 29-34

·         PubMed:17852681

Available from

or Find this paper at:


The aim of this study was to examine the effects of active versus passive recovery on blood lactate disappearance and subsequent maximal performance in competitive swimmers. Fourteen male swimmers from the University of Virginia swim team (mean age 20.3 years, s= 4.1; stature 1.85 m, s= 2.2; body mass 81.1 kg, s= 5.6) completed a lactate profiling session during which the speed at the lactate threshold (V(LT)), the speed at 50% of the lactate threshold (V(LT.5)), and the speed at 150% of the lactate threshold (V(LT1.5)) were determined. Participants also completed four randomly assigned experimental sessions that consisted of a 200-yard maximal-effort swim followed by 10 min of recovery (passive, V(LT.5), V(LT), V(LT1.5)) and a subsequent 200-yard maximal effort swim. All active recovery sessions resulted in greater lactate disappearance than passive recovery (P < 0.0001 for all comparisons), with the greatest lactate disappearance associated with recovery at V(LT) (P= 0.006 and 0.007 vs. V(LT.5) and V(LT1.5) respectively) blood lactate disappearance was 2.1 mmol l(-1) (s= 2.0), 6.0 mmol l(-1) (s=2.6), 8.5 mmol l(-1) (s= 1.8), and 6.1 mmol l(-1) (s= 2.5) for passive, V(LT.5), V(LT), and V(LT1.5) respectively. Active recovery at VLT and V(LT1.5) resulted in faster performance on time trial 2 than passive recovery (P=0.005 and 0.03 respectively); however, only active recovery at V(LT) resulted in improved performance on time trial 2 (TT2) relative to time trial 1 (TT1) TT2- TT1: passive +1.32 s (s= 0.64), V(LT.5) +1.01 s (s= 0.53), V(LT) -1.67 s (s= 0.26), V(LT1.5) -0.07 s (s = 0.51); P < 0.0001 for V(LT)). In conclusion, active recovery at the speed associated with the lactate threshold resulted in the greatest lactate disappearance and in improved subsequent performance in all 14 swimmers. Our results suggest that coaches should consider incorporating recovery at the speed at the lactate threshold during competition and perhaps during hard training sessions


Now the part that teh lactate levels dropped by this intensity is not surprising at all as it needs energy to go that hard.

 The fact that teh  performance improved is not surpsiing either as at this  trehsold intensity we have the highest but still most controlled respiration ( Ventilatory threshold and as long the respiration is NOT the limiter we  have teh  biggest effect in  uisng repiration as a  helper to get H +  9 pH ) back into balance so this helps  clearly to recover.
 The question here is. What IF they would not swimm but  breath in teh intensity they would breath at this threhols level, moving this amount of VE and therefro this amount more of CO2 and tehrefor beeing able to use respiration to balance out H + easier. BUT  keep teh good energy of lactate  in their system ?
 Just a question . now last but not least  here  an intersting  articel about fuel .


 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)"      


Some 30 years of research at the University of California, Berkeley, however, tells a different story: Lactic acid can be your friend.


Coaches and athletes don't realize it, says exercise physiologist George Brooks, UC Berkeley professor of integrative biology, but endurance training teaches the body to efficiently use lactic acid as a source of fuel on par with the carbohydrates stored in muscle tissue and the sugar in blood. Efficient use of lactic acid, or lactate, not only prevents lactate build-up, but ekes out more energy from the body's fuel.


In a paper in press for the American Journal of Physiology - Endocrinology and Metabolism, published online in January, Brooks and colleagues Takeshi Hashimoto and Rajaa Hussien in UC Berkeley's Exercise Physiology Laboratory add one of the last puzzle pieces to the lactate story and also link for the first time two metabolic cycles - oxygen-based aerobic metabolism and oxygen-free anaerobic metabolism - previously thought distinct.


"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.


Training helps people get rid of the lactic acid before it can build to the point where it causes muscle fatigue, and at the cellular level, Brooks said, training means growing the mitochondria in muscle cells. The mitochondria - often called the powerhouse of the cell - is where lactate is burned for energy.


"The world's best athletes stay competitive by interval training," Brooks said, referring to repeated short, but intense, bouts of exercise. "The intense exercise generates big lactate loads, and the body adapts by building up mitochondria to clear lactic acid quickly. If you use it up, it doesn't accumulate."


To move, muscles need energy in the form of ATP, adenosine triphosphate. Most people think glucose, a sugar, supplies this energy, but during intense exercise, it's too little and too slow as an energy source, forcing muscles to rely on glycogen, a carbohydrate stored inside muscle cells. For both fuels, the basic chemical reactions producing ATP and generating lactate comprise the glycolytic pathway, often called anaerobic metabolism because no oxygen is needed. This pathway was thought to be separate from the oxygen-based oxidative pathway, sometimes called aerobic metabolism, used to burn lactate and other fuels in the body's tissues.


Experiments with dead frogs in the 1920s seemed to show that lactate build-up eventually causes muscles to stop working. But Brooks in the 1980s and '90s showed that in living, breathing animals, the lactate moves out of muscle cells into the blood and travels to various organs, including the liver, where it is burned with oxygen to make ATP. The heart even prefers lactate as a fuel, Brooks found.


Brooks always suspected, however, that the muscle cell itself could reuse lactate, and in experiments over the past 10 years he found evidence that lactate is burned inside the mitochondria, an interconnected network of tubes, like a plumbing system, that reaches throughout the cell cytoplasm.


In 1999, for example, he showed that endurance training reduces blood levels of lactate, even while cells continue to produce the same amount of lactate. This implied that, somehow, cells adapt during training to put out less waste product. He postulated an "intracellular lactate shuttle" that transports lactate from the cytoplasm, where lactate is produced, through the mitochondrial membrane into the interior of the mitochondria, where lactate is burned. In 2000, he showed that endurance training increased the number of lactate transporter molecules in mitochondria, evidently to speed uptake of lactate from the cytoplasm into the mitochondria for burning.


The new paper and a second paper to appear soon finally provide direct evidence for the hypothesized connection between the transporter molecules - the lactate shuttle - and the enzymes that burn lactate. In fact, the cellular mitochondrial network, or reticulum, has a complex of proteins that allow the uptake and oxidation, or burning, of lactic acid.


"This experiment is the clincher, proving that lactate is the link between glycolytic metabolism, which breaks down carbohydrates, and oxidative metabolism, which uses oxygen to break down various fuels," Brooks said.


Post-doctoral researcher Takeshi Hashimoto and staff research associate Rajaa Hussien established this by labeling and showing colocalization of three critical pieces of the lactate pathway: the lactate transporter protein; the enzyme lactate dehydrogenase, which catalyzes the first step in the conversion of lactate into energy; and mitochondrial cytochrome oxidase, the protein complex where oxygen is used. Peering at skeletal muscle cells through a confocal microscope, the two scientists saw these proteins sitting together inside the mitochondria, attached to the mitochondrial membrane, proving that the "intracellular lactate shuttle" is directly connected to the enzymes in the mitochondria that burn lactate with oxygen.


"Our findings can help athletes and trainers design training regimens and also avoid overtraining, which can kill muscle cells," Brooks said. "Athletes may instinctively train in a way that builds up mitochondria, but if you never know the mechanism, you never know whether what you do is the right thing. These discoveries reshape fundamental thinking on the organization, function and regulation of major pathways of metabolism."


Brooks' research is supported by the National Institutes of Health.


And last but not least

How taking SportLegs afterward helps recovery: "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)"

Now what  has this all to do with our study idea.
 Everything. We like to see how NIRS can be used to see " reloading ( recovery of local O2 situations and in the same time the trend when  more O2 is used than can be delivered.
 In simple terms. A very  different approach to look at training intensities based on direct infos versus indirect speculations.


Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Than there is one additional more direct challenge we have :
  same group writes :
 "It seems both a waste of resources and money to simply pay and extra $20-$30/test"

 As you can see  the 20 - 30 $ is a big challenge  in private research.
 Wonder how much money we spent in the last 25 years trying to come up with some ideas we than freely share here on this  and other forums. saving  many hours and many wasted strips  by  sharing information than rather cooking in the   own kitchen.
 Here to put this all into perspective a group  who is working on a similar approach

A dedicated laboratory is available for clinical and volunteer studies as part of MOG research activities and includes equipment for monitoring heart rate, arterial oxygen saturation (pulse oximeter), automated rapid cuff inflation (Hokanson) and online real time blood pressure (Portapres).


Research in the group is supported by the following grants:

Leverhulme Trust Research Grant

“Gas signalling and biological energy”


Wellcome Trust Project Grant

“Integrating monitoring and modeling for real-time tracking of cerebral circulation and metabolism”


British Olympic Association

“Development of a portable optical device for improving sports performance”


EPSRC Fellowship

“The Magic of Blood: Shining Light on Chemistry, Physics & Bioengineering”


MRC Project Grant (Co-investigator)

“Novel noninvasive optical methods to characterise cerebral oxygen delivery and utilisation after traumatic brain injury”

£277, 435

Spending  not just 20 - 30 $ but having fun over  30 years on this topics and buying out of  our own pocket any available  top upgraded  equipment to see, whether the latest  ideas could go , including MOXY affordable  NIRS idea is what we look for.
 So for any otter participating group  who  needs  stripe for  20 - 30 $  otherwise they simply can't do the study , please email me and I can make a private donation to  your group so you still can do the study and  enjoy a meal at the end of the day on your table.
 That's why I have goats so I for sure  have  a glass of milk in the evening .

 Be ready to get more inside view as we promised on research as it takes place.
 Last  fun example.
 On a flight down to Vancouver ( payed on my own ) I met a university researcher  as we waited for the plane.
 I was working on some NIRS graphs and picture and as it happened he sat beside me and immediately understood the traces and graphs and started to talk to me.
 Woo  what a great information on NIRS data's,  at what university  do you do this great research.
 My answer. in my goat barn south of Prince George.
 He thought I was kidding. Only goats   are j=kidding .
 Short story after a great conversation.
 He has a research place at a  University for NIRS and is applying  since over 34 years for a grant to but the Portamon I had  there in my pocket but he can't get the Grant, but is paid  since 4 years from the tax payer top do a study with an equipment he does not have.
  Year wage above  100'000 $. So  he asked me how I  could do this.
 My answer. Having fun and is a hobby.
 My answer as well was.  If a welder comes to my House with a certification as a welder, but he has no welding equipment but a duct tape to fix my water pipe, would I hire him , after the explained me exactly  know how it would go but nobody paid him  to buy the equipment so I have to wait till somebody sponsors his equipment to do his job ?
 In my age I can have fun discussing this   as  the only  part we look forward is to have fun on what we do.




Fortiori Design LLC
Posts: 65
To add to the discussion, and underline the point why a discussion involving lactate and pH balance is taking place. 

As already mentioned in many other posts, blood lactate accumulation was and still often is seen as a result of anaerobisis in working tissue. The idea was then that tissue hypoxia resulted in anaerobic energy production yielding H+. The accumulation would then eventually lead to a shift in pH denaturing working tissue and activity  would stop or slow down. This idea lead to many modern training concepts. The problem is that studies of the last decade have shown that many of these assumptions are possibly incorrect and therefore reanalysis is needed. One study by Richardson and colleagues "
role of intracellular Lactate efflux from exercising human skeletal muscle" (1998) does a nice job addressing a large portion of the statement above.

Firstly, the notion of true active muscle hypoxia leading to fatigue due to anaerobic energy production is questionable as Richardson shows. He identifies that intracellular PO2 remains constant during graded incremental exercise between 50-100% of VO2max. A possible explanation for this, presented by Richardson, could be that muscle blood flow compensates for reduced arterial O2 content during  hypoxia, and therefore O2 delivery was not different from normoxia at each intensity. This suggests transfer  of O2 was not responsible for the difference in PO2 between hypoxia and normoxia, but that the diffusive component of O2 was more likely affected. In other words, active muscles never truly lack oxygen for ATP production and therefore local tissue hypoxia is definitely not a reason for change in pH or blood lactate production. On this point, data does indicate that with increasing work rate at a given fraction of O2   lactate efflux is unrelated to cytoplasmic PO2, however it is also true that efflux is higher in hypoxia than normoxia. This goes back to the explanation by Gladden that while lactate accumulation does not imply hypoxia, hypoxia does in a sense promote lactate accumulation.  Richardson suggests that that a systemic and rather than an intracellular PO2 is responsible for increases catecholamine responses to hypoxia and therefore is also responsible for corresponding higher net lactate efflux. Use of lactate to identify hypoxia, could therefore be associated to critical errors, especially when someone believes that this lactate is a sole result of peripheral muscle activity. 




Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Here just a very shorty add on to this topic, as we will for sure come back , once we look at more critically what the classical ideas actually use.
 Try to think somewhat deeper on the fact when we use a VO2 equipment spitting out a "Threshold" result or taking FeO2 % or any indirect  blood gas information to  look great sound smart and ?????
Is what we do mainly for business or is it really a physiological information based on individual reactions. Here to enjoy

Anaerobic threshold: review of the concept and directions for future research.

Brooks GA.


The concentration of lactate in the blood is the result of (1) those processes which produce lactate and contribute to its appearance in the blood and (2) those processes which catabolize lactate after its removal from the blood. Consequently, the concentration of lactate in the blood provides minimal information about the rate of lactate production in muscle. The accumulation of lactate beyond the lactate threshold [T(lact)] does provide an indication that the mechanisms of lactate removal fail to keep pace with lactate production. Lactate is produced in skeletal muscle as a direct result of increased metabolic rate and glycolytic carbon flow. Factors which influence lactate production in muscle include: the Vmax of lactic dehydrogenase (LDH), which is several times greater than the combined activities of enzymes which provide alternative pathways of pyruvate metabolism; the kM of LDH for pyruvate, which is sufficiently low to assure maximal stimulation of LDH in the conversion of pyruvate to lactate; and the K'eq of pyruvate to lactate conversion, which exceeds 1000. Recent studies on dog gracilis muscle in situ clearly indicate that lactate production occurs in contracting pure red muscle for reasons other than an O2 limitation on mitochondrial ATP production. In addition to failure of the essential assumption of the anaerobic threshold [T(an)] hypothesis that there exist limitations on O2 availability in muscles of healthy individuals during submaximal exercise, several groups of investigators have produced results which indicate that parameters associated with changes in pulmonary minute ventilation [i.e., the ventilatory threshold, T(vent)] do not always track changes in blood lactate concentration. Therefore, the T(an) hypothesis fails on the bases of theory and prediction. A series of kinetic tracer experiments to better understand lactate kinetics during exercise is proposed.



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