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.
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.
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.
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 mL.kg-1.min-1) was significantly lower (P < 0.001) than during intermittent exercise alternated with active recovery (52.6 +/- 4.6 mL.kg-1.min-1). 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
Available from www.ncbi.nlm.nih.gov
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.