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.
- 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 .
ANAEROBIC THRESHOLD - A RELATIVELY USELESS CONCEPT FOR COACHING
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.
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.
- Lactate concepts and measures are limited/specific to each testing protocol.
- Results from one protocol cannot be used to generalize or infer values to other testing protocols.
- If one cannot infer from one lactate testing protocol to another then it is illogical to generalize lactate testing results to a competitive performance.
- 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.
- 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).
- 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?
- 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.