Fortiori Design LLC
Registered: 1355349061 Posts: 1,530
I am very biased, but nevertheless I like to give here some thoughts on the ongoing discussion we all have and questions we all have towards optimizing ( for me more individualizing ) any activity program, from Rehab of a ACL to a COPD patient to a post ops cardiac bypass rehab to a overweight person like to do some life style changes to a junior athlete planning to go as far as he can go to a world class athlete in any sport trying to maintain his top position and still stay healthy and play fair.
Now for me in all the above situation the question is on energy supply and demand. So who and how can I supply the needed energy to maintain the survival level of ATP production? Than the second question seems to be, whether I actually can use and convert the supplied energy to the ATP. Utilization. Now for me it can not be the goal to find out , where I hit the intensity , where one of the above reached the limitation and therefore the performance can't be maintained, or will drop to maintain the O2 supply ( ATP ) for the most important ( vital ) systems. Now in all the daily calls and emails an discussion most of the people absolutely agree and have the same goal in mind. All agree that this is crucial for an optimal training plan and it is crucial to see, whether the plan actually achieve the target we set out. Now so far so good. But that is about how far the discussion or better the talk moves towards. From now on there is a huge gab in fundamental ideas on how we may be able to achieve the common idea. Now my biased statement. Would it not make sense to try to track O2( as the key energy ) where it is used and where it has to go to and how it may " disappear " after we used this muscle ? So with NIRS we have for the moment the best and easiest way to get as close as we can to follow this idea. It is live and direct. So I have a huge problem for myself to keep discussion with people , when they argue that for example lactate is much better to track O2 energy supply and demand. So the desperate idea we all had to find the point , where all suppose to fall apart the LT. For sure lactate is closely related to metabolic reaction so is blood sugar and so are many many other ideas. One of the other is respiration . So the latest in the running c9mmunity is now to agree ( there is nothing to agree really ) that LT is worthless and that we all have to aim for VT ( ventilatory threshold and that we even can find out what muscle fibers are involved with the Ventilatory threshold. Here a great article from a famous runner site. What’s The Ventilatory Threshold, And Why Does It Matter? By Matt Fitzgerald, Published Oct. 16, 2013 .
They call it the ventilatory threshold. It’s that intensity of exercise above which your breathing becomes labored and you feel you just can’t draw in as much air as your body wants. Every runner is experientially familiar with the ventilatory threshold. When you run easy you breathe easy. As your speed increases, your breathing deepens, but gradually. However, as you continue to increase your speed, suddenly it seems as if a switch is flipped and your breathing races off ahead of your legs.
experience of the ventilatory threshold is familiar to every runner, the concept of the ventilatory threshold is less familiar to the average runner than is that of the lactate threshold. During exercise of gradually increasing intensity, the amount of lactate, an intermediate product of glycogen (carbohydrate) metabolism, increases in the blood as the muscles burn glycogen faster and faster. Just like the breathing rate, the blood lactate concentration increases gradually for a while and then, at a certain intensity, suddenly increases much more rapidly.
In fact, in most laboratory exercise tests, the ventilatory and lactate thresholds fall close to the same exercise intensity. Observing this coincidence led exercise physiologists to speculate that increasing blood lactate concentrations somehow trigger increased ventilation. But a study by Robert McMurray at the University of North Carolina proves it does not.
The design of the study was very clever. Knowing that the muscles’ ability to produce lactate is limited by the amount of glycogen they store, McMurray had a group of eight experienced triathletes perform incremental exercise tests in two conditions: once with normal muscle glycogen stores and again with glycogen stores depleted by low carbohydrate intake before the test. McMurray found that the relationship between blood lactate concentration and ventilation differed between the two trials, a clear indication that breathing rate and depth are not directly controlled by blood lactate.
So what does cause the ventilatory threshold? According to McMurray, the evidence suggests that it is the activation of fast-twitch muscle fibers. As you may know, there are three basic types of fibers in muscles: slow-twitch fibers with poor speed but excellent endurance that are used during low-intensity exercise (actually, they are used at all intensities, but they are used to the exclusion of the other two types at low intensities); fast-twitch fibers with excellent speed but poor endurance that are used only during high-intensity exercise; and hybrid fibers with a mixture and slow and fast characteristics that kick in at moderate intensities. Different brain cells are used to activate each fiber type. When the exercise intensity increases to the point where brain cells connected to fast-twitch muscle fibers must become active,
that’s when breathing rate and depth increase geometrically (as opposed to linearly).
What is the practical upshot of this finding for you?
It means that you shouldn’t bother to submit to blood lactate testing to determine your lactate threshold.
Your blood lactate levels during exercise are essentially meaningless. Instead, have your
ventilatory threshold determined through a VO2 exercise test. Or just pay closer attention to your pace and/or heart rate the next time you experience that loss-of-breath-control feeling. That’s your ventilatory threshold right there. Most of your training should be done below it; a modest amount right at it; and a small but consistent amount above it.
You can see where we go with that and I not even like to start ( yet ) to discuss how I can look at VT with NIRS. Yes again they are all connected as it is all about maintaining pO2 and ATP. So again the simple question is. Why do I not use something I can actually see the closest for the moment on how O2 reacts . Do I supply more than I utilize or can utilize, is supply and demand balanced and or is the demand so high , that I can not supply enough. 3 simple trends. Now based on this trends of SmO2 we add an additional live feedback on supply ideas tHb and now combine the feedback to get as close as possible to the reason why demand and supply shows up as we see it live and what is the limitation and what is the possible option to prolong the performance thanks to a possible compensation. VT is a perfect example on is VT produced due to a limitation or is VT a sign of a compensation. What do I talk about. Now LT VT and trend in SmO2 ( O2 Hb and HHb ) can be very closely related as all have some thing to do with energy supply and demand. Here a great example how this sometimes can overlap nicely but this nice pictures is not always the case. This is a paper and a work done a few years back in China for ma group who showed , that we can use O2Hb trend or HHb trend in some cases to replace lactate threshold.
Fortiori Design LLC
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wow a flood of emails but I would love to have many of the great feed backs on here. If you do not like to use your name or the name of your institution you work for create " artistic " name. Any feedback is great.
So here a short take on some of the discussion. In short VT ventilator threshold. For us it seems , that when respiration is a limiter Not to confuse with metaboreflex. Than we have an actual muscular limitation of the respiratory systems to move the needed VE and as such we have a too low VE for the CO2 which is produced in the working muscle's. This increases pCO2 and most likely as well as H + and lactate as well. So now on NIRS we have a shift in O2 Disscurve to the right, which is a short term great effective compensation to get more O2 as it is needed. So the re-lease in O2 is improved but the loading in the lungs to the blood not. ( SpO2 ) drop and it looks like a EIAH. Now the VT as an increase in VE shows often up as an increase in RF but a decrease in TV which makes the problem even bigger ( higher dead space volume ) Now yes we will see an increase in H + and for sure a drop in pH in the blood and some lag time increase in H + in the muscle. So we have a close link between VT LT and a drop in O2Hb increase of HHb ( see Chinese work ) and we often actually in this case have an increase in tHb ( vasodilatation. We see this often very nice in a 5/1/5 in the one minute rest. The high CO2 will show up with a delayed or lower recovery peak in SmO2 but a very nice recovery peak in tHb. In contrast to a metaboreflex respiratory limitation, where we have a tHb drop or less peak due to metaboreflex vasoconstriction and a fully recovered SmO2 peak. If respiration can be used as a compensator than we may see as well a VT as VE goes up but we see an increase of RF or at least a similar RF but the ability to increase TV or both. So now we have an option to get rid of CO2 and H + in the blood will be high so will be lactate as H + is shuttled out of the cell to keep H + in balance and we can keep going as long we can maintain this balance. So a great lactate shuttle system to move H + out and a great respiratory system to help with CO2 release will be able to prolong the performance. SO LT is showing up as a steeper incline thanks to great buffer help from lactate and lactate can claim nicely as we still produce and use lactate as we still have a balance situation for ATP production and us intracellular. I have to find the studies but there are nice studies done on this including muscle biopsies who support this idea respectively we go the idea form there . . In this case VT is not close to LT and VT is Not the place, where we know performance may fail but rather a great feedback on a great compensation work.
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Okay here the promised study form as you will see far back and it looks we just start to accept the information from the different groups. In the mid to end 1980- the buzz was LT and 4 mmol and individual anaerobic threshold and LT 1 and Lt 2 and lactate was bad ugly and the reason for all the performance loss.
So amazingly there where researchers out there with the scientific drive rather than the trend to adjust facts to theories. So here a great abstract section where we see, how H + intra cellular and in the blood can be very different but lactate not at all.. Threshold for muscle lactate accumulation during progressive exercise
J. Chwalbinska-Moneta , R. A. Robergs , D. L. Costill , W. J. Fink
Journal of Applied PhysiologyPublished 1 June 1989Vol. 66no. 6, 2710-2716
The purpose of this study was to investigate the relationship between muscle and blood lactate concentrations during progressive exercise. Seven endurance-trained male college students performed three incremental bicycle ergometer exercise tests. The first two tests (tests I and II) were identical and consisted of 3-min stage durations with 2-min rest intervals and increased by 50-W increments until exhaustion. During these tests, blood was sampled from a hyperemized earlobe for lactate and pH measurement (and from an antecubital vein during test I), and the exercise intensities corresponding to the lactate threshold (LT), individual anaerobic threshold (IAT), and onset of blood lactate accumulation (OBLA) were determined. The test III was performed at predetermined work loads (50 W below OBLA, at OBLA, and 50 W above OBLA), with the same stage and rest interval durations of tests I and II. Muscle biopsies for lactate and pH determination were taken at rest and immediately after the completion of the three exercise intensities. Blood samples were drawn simultaneously with each biopsy. Muscle lactate concentrations increased abruptly at exercise intensities greater than the “below-OBLA” stage [50.5% maximal O2 uptake (VO2 max)] and resembled a threshold. An increase in blood lactate and [H+] also occurred at the below-OBLA stage;
however, no significant change in muscle [H+] was observed. Muscle lactate concentrations were highly correlated to blood lactate (r = 0.91), and muscle-to-blood lactate ratios at below-OBLA, at-OBLA, and above-OBLA stages were 0.74, 0.63, 0.96, and 0.95, respectively.(ABSTRACT TRUNCATED AT 250 WORDS) So the key information is as well as followed :
COMPONENTS OF CELLULAR PROTON PRODUCTION, BUFFERING, AND REMOVAL
The cause of metabolic acidosis is not merely proton release, but an imbalance between the rate of proton release and the rate of proton buffering and removal. As previously shown from fundamental biochemistry, proton release occurs from glycolysis and ATP hydrolysis. However, there is not an immediate decrease in cellular pH due to the capacity and multiple components of cell proton buffering and removal (
Table 5). The intracellular buffering system, which includes amino acids, proteins, Pi, HCO3−, creatine phosphate (CrP) hydrolysis, and lactate production, binds or consumes H+ to protect the cell against intracellular proton accumulation. Protons are also removed from the cytosol via mitochondrial transport, sarcolemmal transport (lactate−/H+ symporters, Na+/H+ exchangers), and a bicarbonate-dependent exchanger (HCO3−/Cl−) ( Fig. 13). Such membrane exchange systems are crucial for the influence of the strong ion difference approach at understanding acid-base regulation during metabolic acidosis ( 5, 26). However, when the rate of H+ production exceeds the rate or the capacity to buffer or remove protons from skeletal muscle, metabolic acidosis ensues. It is important to note that lactate production acts as both a buffering system, by consuming H+, and a proton remover, by transporting H+ across the sarcolemma, to protect the cell against metabolic acidosis. To move this into a practical approach for all MOXY useres and users , who have a lactate analyzer. Bike in a balanced intensity. So wattage users on FTP 60 load, lactate users at Max Lass. and moxy useres at stable SmO2 , stable tHb. Now estabish the balance by testing your lactate level 2 x so by 5 6 min into the stable performance and by 8 min again. You should have a stable lactate and stable Wattage and a stable SmO2 and tHb.. Any of your choice. Than do a hypercapnic respiration for at least 2 - 3 min. so increase EtCO2 level. test after 4 - 5 min doing this. Test the lactate as well as look live SmO2 and tHb. as soon you have to quite this as you have to maintain a stable wattage go back to balance for 6 - 8 min than test again the lactate and MOXY info. Than go to hypocapnic respiration and do the same. Than assess what you see and it would be nice if you can show your findings on here so it is not from us. We did this in Boulder during our MOXY seminar about 1 year back. Fun results and fun to see, how theories should be replaced if facts show a different outcome.
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Short feedback to an emial I just got.
Lactci acid ? Biochemistry of exercise-induced metabolic acidosis
Robert A. Robergs , Farzenah Ghiasvand , Daryl Parker
American Journal of Physiology - Regulatory, Integrative and Comparative PhysiologyPublished 1 September 2004Vol. 287no. 3, R502-R516DOI: 10.1152/ajpregu.00114.2004
The development of acidosis during intense exercise has traditionally been explained by the increased production of lactic acid, causing the release of a proton and the formation of the acid salt sodium lactate. On the basis of this explanation, if the rate of lactate production is high enough, the cellular proton buffering capacity can be exceeded, resulting in a decrease in cellular pH. These biochemical events have been termed lactic acidosis. The lactic acidosis of exercise has been a classic explanation of the biochemistry of acidosis for more than 80 years. This belief has led to the interpretation that lactate production causes acidosis and, in turn, that increased lactate production is one of the several causes of muscle fatigue during intense exercise. This review presents clear evidence that there is no biochemical support for lactate production causing acidosis. Lactate production retards, not causes, acidosis. Similarly, there is a wealth of research evidence to show that acidosis is caused by reactions other than lactate production. Every time ATP is broken down to ADP and P
i, a proton is released. When the ATP demand of muscle contraction is met by mitochondrial respiration, there is no proton accumulation in the cell, as protons are used by the mitochondria for oxidative phosphorylation and to maintain the proton gradient in the intermembranous space. It is only when the exercise intensity increases beyond steady state that there is a need for greater reliance on ATP regeneration from glycolysis and the phosphagen system. The ATP that is supplied from these nonmitochondrial sources and is eventually used to fuel muscle contraction increases proton release and causes the acidosis of intense exercise. Lactate production increases under these cellular conditions to prevent pyruvate accumulation and supply the NAD + needed for phase 2 of glycolysis. Thus increased lactate production coincides with cellular acidosis and remains a good indirect marker for cell metabolic conditions that induce metabolic acidosis. If muscle did not produce lactate, acidosis and muscle fatigue would occur more quickly and exercise performance would be severely impaired. An increased ability to release H + over respiration ( CO2 ) would allow a longer increase in lactate without an increase in acidosis. · metabolism · skeletal muscle · lactate · acid-base · lactic acidosis
during intense exercise the increase in blood and muscle lactate and the coincident decrease in pH in both tissues has been traditionally explained by the production of lactic acid. Such a traditional interpretation assumes that due to the relatively low pKa (pH = 3.87) of the carboxylic acid functional group of lactic acid, there is an immediate and near total ionization of lactic acid across the range of cellular skeletal muscle pH (∼6.2–7.0) (
, 12 , 28 – 40 , 46 ). This interpretation is best represented by the content of numerous textbooks of exercise physiology, physiology, and biochemistry that explain acidosis by the production of lactic acid, causing the release of a proton (H 54 +) and leaving the final product to be the acid salt lactate. This process has been termed lactic acidosis ( ). According to this presentation, if and when there is a rapid increase in the production of lactic acid, the free H 27 + can be buffered by bicarbonate causing the nonmetabolic production of carbon dioxide (CO 2). In turn, the developing acidosis and the raised blood CO 2 content stimulate an increased rate of ventilation causing the temporal relationship between the lactate and ventilatory thresholds ( , 25 , 32 , 44 ). 53 Again the simple question is: What would be the best way to follow in practical terms the energy situation of O2 for any type of activity. Well what better thnaa live feedback over NIRS / MOXY. So where do we hesitate with this interesting option. Please give me some feedback where the hesitation is and why it is for practical use nearly a no brainer to work with live MOXY feedbacks ??? Is it the " fear" to changee ? or what is it ?
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Thanks Juerg for the great review. Just one more abstract that supports your view.
Is lactic acidosis a cause of exercise induced hyperventilation at the respiratory compensation point? T Meyer, O Faude, J Scharhag, A Urhausen, W Kindermann, Br J Sports Med 2004;38:622–625. Objectives: The respiratory compensation point (RCP) marks the onset of hyperventilation (‘‘respiratory compensation’’) during incremental exercise. Its physiological meaning has not yet been definitely determined, but the most common explanation is a failure of the body’s buffering mechanisms which leads to metabolic (lactic) acidosis. It was intended to test this experimentally. Methods: During a first ramp-like exercise test on a cycle ergometer, RCP (range: 2.51–3.73 l*min–1 oxygen uptake) was determined from gas exchange measurements in five healthy subjects (age 26–42; body mass index (BMI) 20.7–23.9 kg*m–2; VO2peak 51.3–62.1 ml*min–1*kg–1). On the basis of simultaneous determinations of blood pH and base excess, the necessary amount of bicarbonate to completely buffer the metabolic acidosis was calculated. This quantity was administered intravenously in small doses during a second, otherwise identical, exercise test. Results: In each subject sufficient compensation for the acidosis, that is, a pH value constantly above 7.37, was attained during the second test. A delay but no disappearance of the hyperventilation was present in all participants when compared with the first test. RCP occurred on average at a significantly (p = 0.043) higher oxygen uptake (+0.15 l*min–1) compared with the first test. Conclusions: For the first time it was directly demonstrated that exercise induced lactic acidosis is causally involved in the hyperventilation which starts at RCP. However, it does not represent the only additional stimulus of ventilation during intense exercise. Muscle afferents and other sensory inputs from exercising muscles are alternative triggering mechanisms.
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Nice article Jiri thanks so much,
Here not as a critic but as discussion point: The respiratory compensation point (RCP) marks the onset of hyperventilation.I would carefully disagree with this explanation ( not with the outcome of the study . Here why perhaps : Below is one of many definition of hyper ventilation : hyperventilation
hyper + ventilare, to fan resulting from an increased respiration rate, an increased tidal volume, or both. Hyperventilation causes an excessive intake of oxygen and elimination of carbon dioxide and may cause hyperoxygenenation. Hypocapnia and respiratory alkalosis then occur, leading to dizziness, faintness, numbness of the fingers and toes, possibly syncope, and psychomotor impairment. Causes of hyperventilation include asthma or early emphysema; increased metabolic rate caused by exercise, fever, hyperthyroidism, or infection; lesions of the central nervous system, as in cerebral thrombosis, encephalitis, head injuries, or meningitis; hypoxia or metabolic acidosis; use of hormones and drugs, such as epINEPHrine, progesterone, and salicylates; difficulties with mechanical respirators; and psychogenic factors, such as acute anxiety or pain pulmonary ventilation rate greater than that metabolically necessary for gas exchange, So in other words hyper ventilation basically never can show up in intensive sport activities like at the end of a race where we may see EIAH or during a step test like the above. If we hyper ventilate we actually will see the opposite a hypocapnia and a very low CO2 therefore with a shift of the O2 diss cuvre to the left and as such a nicety looking SpO2 and even SmO2. Hyper ventilation means you breath far more than needed and you get rid of CO2. In the study the athletes did the opposite , they had due a limitation in respiration ( VE ) reached a maximal level so the problem was to get rid of CO2 so they actually hypo ventilated for the intensity they did and would be needed to balance still CO2. They proof this by using NA Bi to help. This would not be needed if they could have reached a higher VE so CO2 would have been gone and not yet a big need of additional buffer options. Therefore they kept CO2 in pCO2 increased shifting the O2 disscurve to the right and as such initially helped to desaturate further SmO2 drops and problem to load O2 so SpO2 drops ( EIAH ) and the lack of release of CO2 created an out of balance H + which ended up with an increase in H + intracellular not just in the blood. This shift to the right is a functional help for short time option to gain time for survival. It is a " time bomb" and as such the now very low SmO2 reduced the option to rebuild fast and sufficient CP for additional help to maintain ATP levels. The H + than started to protect the ATP splitting by inhibiting the coupling of ATP Mg== and CA ++ as H + occupies the position of the Ca ++ and as such there is no more spitting of ATP to protect the level form dropping under a crucial situation which than would create a rigor, which never happens in sport situations. Now that doe snot mean I am right or wrong as it is far above what I could figure out. This is as always when we write something down we repeat something we learned somewhere and it sounded logical in the overall view of what we discuss. 2. Now the second part is : For the first time it was directly demonstrated that exercise induced lactic acidosis is causally involved in the hyperventilation which starts at RCP. That may be a point of discussion. What we know is that acidosis or H + situation creates a metabolic but it as well can create a repsirty acidosis. The lactate is most liley historically push into this discussion as the group is very striong connected with lactate threshold ideas. What we know is that the VT or RCP does not need lactate to show up. It needs h + dysbalance. The same probme we had with lactate is bad uf gly and should be get rrid of as fast as possible the sam eproblme is here. The theory on this seems to miss the facts. Here what I mean. Relationship between the lactate and ventilatory thresholds during prolonged exercise. Loat CE 1, Rhodes EC. Author information 1J.M. Buchanan Exercise Science Laboratory School of Physical Education and Recreation, University of British Columbia, Vancouver, Canada. Abstract
The anaerobic threshold is commonly measured by either blood lactate (lactate threshold) or ventilatory gases (ventilatory threshold); however, the relationship between these 2 methods is not conclusive. The lactate threshold has been characterised at either a fixed or variable blood lactate concentration (BLa). Recent studies have indicated a specific blood lactate concentration for each individual which considers the interindividual variations in lactate kinetics (individual anaerobic threshold), following either a continuous, exponential pattern or a discontinuous, threshold-like response. The ventilatory threshold is assessed using a variety of ventilatory parameters, many of which exhibit a threshold-like response during progressive exercise. Despite the apparent causal relationship between the stimulation of the ventilatory chemoreceptors and ultimately the ventilatory response and the accumulation of protons in the circulating blood, evidence does exist which refutes such a connection. Such evidence supporting a coincidental relationship examines no significant change in ventilation with significant increases in blood lactate concentration.
. The ability to perform at the anaerobic threshold is now recognised as an integral component of endurance events. Several studies have concluded that the ventilatory threshold is highly correlated with endurance performance, in distances ranging from 26 miles (41.6 km) [r = -0.94] to 5 and 10 km (r = -0.945). The lactate threshold, in particular the individual anaerobic threshold, has been examined from a performance standpoint. Much of the literature supports the individual anaerobic threshold as the exercise intensity at which performance is maximal and able to be sustained for at least 50 minutes. With the variety of techniques utilised in assessing the anaerobic threshold, caution should be taken in interpretation of the results as the different protocols may elicit a variety of responses during incremental exercise. Furthermore, it is essential to account for the individual's unique response to such exercise. Conversely, evidence from patients with McArdle's disease indicates that although no lactic acid is produced, these individuals do experience a threshold-like ventilatory response during incremental exercise So no lactic acidosis needed for this reaction. In fact we can create this reaction by just manipulating respiration so we can collect CO2 and keep it for a creation of a respiratory acidosis and you will see the same reaction of a hyper respiration trend ( Not hyper ventilation and pCO2 is very high. Easy to demonstrate with with a Spiro Tiger. Summary : Great article who shows the idea, that respiration can be a limitation. So ice hockey player who cam move 300 + Liter VE most likely can get faster back to normocapnic respiration when coming of te ice. In fact may not even create a problem on the ice and than we have better balance between O2 loading and O2 release as we are always normocapnic . Or we can manipulate even to go back on the ice slightly hypocapnic so it takes somewhat ( few seconds longer before we get hyper capnic again. Any feedback comment is great.