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Juerg Feldmann

Fortiori Design LLC
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.

While the 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.
china  lac nirs  co2.jpg 

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
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.
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
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 :


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.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
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 Pi, 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, 4046, 54). 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+) and leaving the final product to be the acid salt lactate. This process has been termed lactic acidosis (27). According to this presentation, if and when there is a rapid increase in the production of lactic acid, the free H+ can be buffered by bicarbonate causing the nonmetabolic production of carbon dioxide (CO2). In turn, the developing acidosis and the raised blood CO2 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  ?

Jiri Dostal

Development Team Member
Posts: 51
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.


Attached Files
pdf NaHCO3.pdf (58.06 KB, 16 views)

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
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 :



Etymology: Gk, hyper + ventilare, to fan

pulmonary ventilation rate greater than that metabolically necessary for gas exchange, 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

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 CE1, Rhodes EC.

Author information

  • 1J.M. Buchanan Exercise Science Laboratory School of Physical Education and Recreation, University of British Columbia, Vancouver, Canada.


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. 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. 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.


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.

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