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juergfeldmann

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 #1 
Seems an  endless discussion but  at least  people start to discuss, despite   the fact that the discussion started  to  taper of  end of  the  1990. At least i the  exercise physiological world.

Now  for people  working on the idea , that they may   use physiological feedback  for physiological training ideas  , than  we have to understand  the lactate history,  but as well the latest  in what lactate  actual  tells  us. This is crucial to understand   the  interval  planning  and what we like to achieve.

 It is  clear since  that  time, that lactate is not  what we  where hoping  for   after  G. Maders  interesting 2  and 4  mmol  concept  got introduced. And unfortunate i think  the  populist approach to sell  NIRS  equipment  refueled  the idea  of using a relative useless concept  for   training  intensity ideas  and even worth  for  interval  planning  . (  Intensity ,  duration rest period  and   repetition )
Just as a reminder.
When we  used lactate  for intensity control we  learned  the idea, that lactate is the reason  of fatigue  and  all the problems  we have  with performance loss. So  we learned  concepts  like you have to get rid of  it  with massage  or  " cool down"  and we have to avoid it  and there is a  critical point  where  we  have  to keep in mind  LT 1 and Lt 2. This all created  specif  workouts  and 25 different ideas on how to find  the  elusive  LT  1 and LT 2.

So here to have some key notes on one  thrash  for new  readers  to  think through ..

see the year  of  this great  critical   paper
1.

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.


Well about  10 years before. G . Brooks  postulate b the  lactate shuttle  idea. So  lactate  production under  hypoxia  is  more  the exception  than the rule.


At  that time  they  easy  showed, how lactate values  at the end of a high intensity    will not show up as  values  we may have produced.

lactate post.jpg   


So    looking at the above post load lactate dynamic  from the  1980  we have to ask our self  ,  on what value  do we have  after   or during an interval  workout  when we see this very different time  delays  for   values. ?

Than  you read below  again.

Thirdly, an alternate or a complementary explanation to the pattern of plasma ]La-] response to ramp exercise can be suggested. According to this explanation, lactate is produced in the working muscle: (1) as soon as the exercise begins, as suggested by Brooks (1985); or (2) following a delay, according to the theory of the anaerobic threshold (Davis 1985). Under both hypotheses the onset of lactate production within the working muscles occurs at comparatively low work rates. At that time: (1) the amounts of lactate produced  and the gradient between muscle [La-] and plasma [La-], and the amount of lactate released from the muscle remains small; (2) cardiac output and muscle blood flow are also low and do not favour lactate release

from the working muscles and its distribution into S; and (3) the small amounts of lactate released are diluted within the comparatively large S, thus resulting in a very small increase (if any) in plasma [La-]. Therefore,

a delay could be expected between the beginning of lactate production within the working muscles and the parabolic rise in plasma [La-] in response to ramp exercise in a similar way that, in response to a short period of severe exercise, the peak value of plasma [La-] is only observed following a several-minute delay into the recovery period (see Hirvonen et al. 1987, 1992). Consequently, plasma [La-] concentration at a given t during a ramp exercise does not reflect lactate production in the muscle at that precise t and at the

exact corresponding work rate, but at a previous t minus ~ of unknown and probably variable length, and at the corresponding work rate. This phenomenon might have been overlooked in the development of the theory

of the anaerobic threshold which implicitly assumes that plasma [La-] at a given t reflects lactate production and thus the metabolic state of the muscles at that precise t, and at the exact corresponding work rate. This is very unlikely to be the case, particularly during the exercise protocols of short duration and with steep increase in work rate used for the detection of the anaerobic threshold (Anderson and Rhodes 1989). In this type of protocol, where VO2 significantly lags behind the value expected for the corresponding

work rate (Whippet al. 1981), it may be expected that plasma [La-] also tracks the metabolic state of the working muscles with a significant delay, particularly at the beginning of exercise for the reasons presented above.

  Now  add this  fun study  to it  and lactate as a feedback is  even more or better less likely to help.



       Submitted 20 June 2002.

       accepted in final form 5 September 2002.

       Saltin et. all

 

Abstract

To study the role of muscle mass and muscle activity on lactate and energy kinetics during exercise, whole body and limb lactate, glucose, and fatty acid fluxes were determined in six elite cross-country skiers during roller-skiing for 40 min with the diagonal stride (Continuous Arm + Leg) followed by 10 min of double poling and diagonal stride at 72–76% maximal O2 uptake. A high lactate appearance rate (Ra, 184 ± 17 μmol · kg−1 · min−1) but a low arterial lactate concentration (∼2.5 mmol/l) were observed during Continuous Arm + Leg despite a substantial net lactate release by the arm of ∼2.1 mmol/min, which was balanced by a similar net lactate uptake by the leg. Whole body and limb lactate oxidation during Continuous Arm + Leg was ∼45% at rest and ∼95% of disappearance rate and limb lactate uptake, respectively. Limb lactate kinetics changed multiple times when exercise mode was changed. Whole body glucose and glycerol turnover was unchanged during the different skiing modes; however, limb net glucose uptake changed severalfold. In conclusion, the arterial lactate concentration can be maintained at a relatively low level despite high lactate Ra during exercise with a large muscle mass because of the large capacity of active skeletal muscle to take up lactate, which is tightly correlated with lactate delivery. The limb lactate uptake during exercise is oxidized at rates far above resting oxygen consumption, implying that lactate uptake and subsequent oxidation are also dependent on an elevated metabolic rate. The relative contribution of whole body and limb lactate oxidation is between 20 and 30% of total carbohydrate oxidation at rest and during exercise under the various conditions. Skeletal muscle can change its limb net glucose uptake severalfold within minutes, causing a redistribution of the available glucose because whole body glucose turnover was unchanged

 

Now lets  look  at some more  specific   sport reactions.

 

Med Sci Sports Exerc. 2006 Jun;38(6):1165-74.

Muscle and blood metabolites during a soccer game: implications for sprint performance.

Krustrup P, Mohr M, Steensberg A, Bencke J, Kjaer M, Bangsbo J.

Author information

  • Institute of Exercise and Sport Sciences, Department of Human Physiology, University of Copenhagen, Copenhagen, DENMARK.

Abstract

PURPOSE:

To examine muscle and blood metabolites during soccer match play and relate it to possible changes in sprint performance.

METHODS:

Thirty-one Danish fourth division players took part in three friendly games. Blood samples were collected frequently during the game, and muscle biopsies were taken before and after the game as well as immediately after an intense period in each half. The players performed five 30-m sprints interspersed by 25-s recovery periods before the game and immediately after each half (N=11) or after an intense exercise period in each half (N=20).

RESULTS:

Muscle lactate was 15.9+/-1.9 and 16.9+/-2.3 mmol.kg d.w. during the first and second halves, respectively, with blood lactate being 6.0+/-0.4 and 5.0+/-0.4 mM, respectively. Muscle lactate was not correlated with blood lactate (r=0.06-0.25, P>0.05). Muscle glycogen decreased (P<0.05) from 449+/-23 to 255+/-22 mmol.kg d.w. during the game, with 47+/-7% of the muscle fibers being completely or almost empty of glycogen after the game. Blood glucose remained elevated during the game, whereas plasma FFA increased (P<0.05) from 0.45+/-0.05 to 1.37+/-0.23 mM. Mean sprint time was unaltered after the first half, but longer (P<0.05) after the game (2.8+/-0.7%) as well as after intense periods in the first (1.6+/-0.6%) and second halves (3.6+/-0.5%). The decline in sprint performance during the game was not correlated with muscle lactate, muscle pH, or total glycogen content.

CONCLUSION:

Sprint performance is reduced both temporarily during a game and at the end of a soccer game. The latter finding may be explained by low glycogen levels in individual muscle fibers. Blood lactate is a poor indicator of muscle lactate during soccer match play.

PMID:

16775559

[PubMed - indexed for MEDLINE]

 or 



Studies of high intensity exercise also show that different interventions produce fatigue at different blood lactate concentrations in the same subjects, such that ‘‘considerable inter-individual differences must exist in the pH sensitivities of the various processes involved’’, thus ‘‘if acidosis makes any contribution to the fatigue during performance of this (high intensity) type of exercise, it is an indirect one…..’’

. Elevated blood lactate concentrations also do not contribute to the slow component of the rise in oxygen consumption during high intensity exercise and hence to any possible effect that this may have on the fatigue process.

 

More significantly, the study of Nielsen et a would seem to show that lactate and H + enhances rather than inhibits skeletal muscle contractile function when the extracellular potassium concentrations are also high.

 This would be most probable if lactate is one of the preferred fuels for skeletal muscle metabolism as it is for cardiac muscle when extracellular lactate concentrations are elevated, for example during high intensity exercise. It seems paradoxical that the same substrate that is the preferred fuel for the maximally working (lactophilic) heart is supposedly toxic to the maximally working (lactophobic) skeletal and respiratory muscles (fig 2). 

or 

Lactate efflux is unrelated to intracellular PO2 in a working red muscle in situ.

Connett RJ, Gayeski TE, Honig CR.

Abstract

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.

 

And again the  question is on how  many more  accepted  papers  do we  need to   see, that we  used an interesting concept  based on  some   not optimal conclusions  and now have a  heck of a problem  to  try to  use the best of it but get  rid  of some mythological ideas.
 What is  wrong with  progress due  to new  knowledge  ?









xcskier

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Posts: 46
 #2 
[This is an opinion of a practitioner and someone with science background
who reads sports physiology papers...]

What I have consistently observed over the years is a lack of understanding
of physiology, energy systems and how different training types affect different
systems. This includes both athletes and coaches. In my younger years,
coaches kept talking about "threshold" and other fancy terms without
understanding them themselves and without explaining them to athletes.

For years, when I was on serious and competitive teams, we did VO2max / lactate
profiles 2-3 times a year and yet we never did any lactate tests during interval training.
This is quite astounding, because I never really got a feel for what "threshold" means.
It was always some mystical HR that everybody had to follow. I remember coaches kept
telling us HR=165 was threshold...

I know there are good coaches out there who know their stuff and educate
athletes (especially in Scandinavian countries) so that they learn about training
process, etc. But, there's probably a larger group of mediocre coaches
who just parrot some party line or training orthodoxy without knowing why.

Second, how many athletes actually regularly use lactate meters during training?
How many athletes/coaches actually know how to interpret the numbers and put
them in context (apart from 2.0/4.0 party line)?

Another big issue is terminology itself. We throw around fancy terms LT1, LT2,
aerobic threshold, anaerobic threshold, MLSS, OBLA, etc. and without thorough
understanding we blindly follow coaches (who may or may not know) or
in this day and age numerous blog posts and online articles.

> i think  the  populist approach to sell  NIRS  equipment  refueled  the idea  of
> using a relative useless concept  for   training  intensity ideas  and even worth  
> for  interval  planning  . (  Intensity ,  duration rest period  and   repetition )

It seems that some very successful athletes are using lactate for training planning.
Norwegian endurance sports (rowing, X-C skiing, orienteering, etc.) have
standardized their terminology (training zones) and are using lactate extensively
for interval training. They seem to have a huge success with this method.
Whether their success is a result of this training methodology and intensity
monitoring or a result of something else may be up for discussion.

The bigger issue, in my opinion, is a sheer number of different studies and
papers that show results of various training methods and hey can be
conflicting. For example:
1. Somebody may advocate 4x4 intervals [Hoeff - Helgerud]
2. Another not to train much in the zone between LT1 and LT2
http://www.tradewindsports.net/wp-content/uploads/2014/02/Neal-12-6-wk-polarized.pdf
Intervals done at 90% VO2max
https://www.researchgate.net/publication/46403553_What_is_Best_Practice_for_Training_Intensity_and_Duration_Distribution_in_Endurance_Athletes

3. And yet another empirical study to train fair amount in the zone between LT1 and LT2
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0101796

While there are certainly many ways to skin a cat and many ways to train,
we are not doing ourselves any favors with various training methods
without really understanding what "intensity" is (on paper) and how it
translates to "feeling" when an athlete is training. As Juerg points out
with "physiological zones" feeling and intensity may be quite different
from day to day.

I have read countless papers on the above three training variations
and yet still don't know what training intensities should be and how
they would be set for an individual athlete. And how I would actually
effectively monitor them. We may not have access to expensive
equipment or help of assistants that take various measurements
during training.

This said, it seems that Norwegian skiers/biathletes have a great success
with lactate-based training. And the same with east African runners (although
they go by "feel" instead of actual lactate numbers). But it could be that the
devil is in the details, as usual.



sebo2000

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 #3 
This is great discussion, I think there is no "perfect workout"  "perfect intensity" same as there is no "the best car" "best bike" or "the best glue" (beside crazy glue [smile] it is all creation of today marketing.

We need to understand what we are training for:
Discipline wise: Cycling is not really cycling..., we have BMX, CX, Track, Road Racing, Criterium, TT, IM. yes they use legs, but those disciplines are so different...

And even as precise training as course wise: we have one crit in Toronto that requires different fitness from Crit in Buffalo...

Not only each sport will require different training, but we can go as far as training for particular course.

Now, once we understand what effort we will approximately be doing, we need to assess where our body is, what are our limiters, from deepest hole to least, and start training based on how our body react to training.

What is happening now in most of the places is: people sign up for some "cycling classes" they do lactate\VO2max test because it feels they are pro\serious and start pedaling without any bloody sense.

When questioning why, they will be intimidated with response: Last year road champ was training with us, we must be doing something right....(yeah this is really answering my question why we do this....)

Untrained people will improve no matter what they do, problem is that they might be creating imbalances in the process, that might be very hard to fix later on. But since they are getting faster they are happy.

I see super fast kids in youth clubs, that are so fast they already need puffer or they will have "asthma" attack at the end of the race. Doctor gives them puffer, parents say he has exerciser induced asthma...He will not win the race without the puffer...

Nobody says: their legs are so big and strong at 12 or 13, that respiratory system can not keep up, it is not asthma attack...If you tell them something, you are jealous your kid is slower...

Education by showing simple examples might change that...

Just to add to this: It might happen that based on physiology person is simply not suitable for certain disciplines, you might not be good at Crits, but you are world level at Tri. 



juergfeldmann

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Posts: 1,501
 #4 
Nothing to add  than. YES

 and  I hope this week  I find  some time  to  move forward  with  some critical  views in the SWINCO  section. 
xcskier

Development Team Member
Registered:
Posts: 46
 #5 
Quote:
they do lactate\VO2max test because it feels they are pro\serious and start pedaling without any bloody sense.


Yes, exactly! And unfortunately this is not just a problem with "amateurs"
(and I mean this in a good way, "enthusiasts"). This problems persists
at serious competitive levels even now. You do all the tests, but most
of the time people don't know what to do with them.

Quote:
When questioning why, they will be intimidated


This is a again a result of lack of knowledge and deep understanding.
A good coach will be able to explain why you are doing something,
and what is the purpose of a workout.


I do understand your comment about cycling being really many different disciplines potentially requiring different training. This is also true for skiing where maybe certain courses (or even snow conditions) favor some skiers
(due to technique, physiology, etc.)

On the other hand, I have noticed that in some sports (in particular
cross-country skiing), coaches in North America complicate
quite a bit with training. If you look again at the Norwegian analysis of their
gold medalists, their program for skiing/rowing is remarkably simple.
Olaf Tufte in his gold winning year repeated the same interval training
session over 60 times...

While I am very enthusiastic about NIRS, I also want to remain cautious 
about overcomplicating things. Maybe training should be more complex,
with more complicated interval sessions and periodizations. But maybe
they don't. That's what makes this so fascinating.


juergfeldmann

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Posts: 1,501
 #6 
2 very important  and great points  to support.
 But  first some  additional    points. 

A  country   who  dominates   over many  decades a sport  is often a  country  where this particular sport  is  very important  and success in this sport will give  you fame and money.
  example. Ice hockey and Canada. 
The reason  for the  depth in   good players is based on numbers  and  very  little on  training  ideas. In fact the   majority of training's in  Canadian  ice hockey are rooted  over 1 /2  century back. The goal is  " suck it  up and keep going "
 Speed  skating is  the sport in  Holland besides  biking.
 Soccer in  Brasil, mountain biking in Switzerland, Cross country skiing in Norway.
 This  traditions  bring as well a  wealth of  experiencin  which is so important. Mixing this  experience  with   scientific   information than moves  people  often ahead of  the  crowed.

now  great pi oints : 
 1. Olaf Tufte in his gold winning year repeated the same interval training 
session over 60 times...

a )
  first how  do we know  he   repeated  physiologically  the   workout 60 x  thee  same.
 An external number  of a  workout  like 5  x  30 seconds  all out  may never be  really  physiologically the same workout  as we  steady   adjust. We  have the initial functional reaction and I showed  the  idea many times   you need  to repeat  a  certain amount of time a functional stress  to create  the functional reaction to have a chance  that we  will create a structural adaptation.

Even if  the workout on the paper looks the  same   we   will have  every time a different  situation. Now that  where we like to known what happens.  Below an example.
 4  loads  and easy to see 2  loads   are different so 2  x  the same load. The goals where very different and the loads  where  the  same in all 4 loads  from outside so  same  wattage  same speed or what ever we use  for an objective outside load  idea.





prio 1 thb  smo2 close  section.jpg

N
ow below the opposite   2 very different loads,  but  with the goal to desaturate   down to the same level.

same SmO2  drop  but differetn load.jpg


N
ow you  can add  tHb  and that's it so very simple. .
Questions. 
1 . from a  O2  point of  view( energy ) do I like to  stress utilization  or  delivery.
2.  from a  blood flow point of  view: Do  I like  to  create  utilization  stimulation or  do I keep  the flow  so that I  can deliver.  so  60 x  the  outside same looking workout  can be very different or  very equal, depending on   what you like to achieve  with the same workout.
 I  can , to make it simple, do 50  interval session  all  with 100 w easy loads  for 60 seconds   followed by  1 min 350 loads. So  from the training log all the same, but I can completely change the physiological stimulation effect in the same interval  very very easy. So   what looks  the  same is not the same  at all.
If  it is planned  I  have the  feedback  why I may improve or  why I stop to improve. If  I  believe it is the same I can only hope.
 

While I am very enthusiastic about NIRS, I also want to remain cautious 
about overcomplicating things.


Absolutely  and it is  as you see above very simple. No tests  needed  just a  goal before the workout and your live feedback  will tell you what happens. Than it is up to you to decide, yes  today  the   idea is to  create a   utilization stimulation , so   reduce  the delivery.  Now  you can do this over  muscle tension  or over  O2  ( muscular intervention) you can do it over cardiac intervention  or over  respiratory intervention, what ever  you like to   add to the  stimulation or like to  keep  out  of the overload.  That it. The SmO2  will give you the live feedback  whether  you are successful the tHb  as well  whether  the option you  try to choose  are actually working.

xcskier

Development Team Member
Registered:
Posts: 46
 #7 
Quote:
first how  do we know  he   repeated  physiologically  the   workout 60 x  thee  same.


I obviously don't know, I was just referring to anecdotal claim that he 
did 6x10' intervals over 60 times. Whether it was the same intensity,
I have absolutely no idea. 

For cross-country skiing, the intervals would be very simple and the training plan prescription would be also be very simple. For example, the plan could just say
5x8min, 2min recovery, Zone 3 (~3.5mM). Or: 2 hours (easy, zone 1). And as Juerg
points out, even when you are in Zone 1, you can be working different energy systems,
so instructions like: "easy, zone 1" seem very ambiguous at best.

Back to intervals. Now there may be some variation in duration (eg, 7x6min, 4x15min, etc.), but if the intensity (say 3.5 mM) is the same and you only vary duration (5x8 vs 7x6 vs 4x10) are you still training different systems or you are always working the same thing over
and over?

This brings me to another question. According to Jan Olbrecht's "Science of Winning",
"During the first 1 to 2 weeks of a new training cycle the body adapts quickly to the new stimulus. In the next few weeks the power of this same stimulus to provoke an adaptation will progressively fade to end up completely after 6 weeks."

This seems to imply that you have to change interval training (intensity / duration) every
few weeks. So, if you were doing the same intervals over the course of the year, it
seems that your body would stop adapting pretty soon (even if you have a new 
"lactate profile" every few weeks). Yes?


juergfeldmann

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Registered:
Posts: 1,501
 #8 

Some  fascinating points  and i like to give  some thoughts and questions  to   some of them.


5x8min, 2min recovery, Zone 3 (~3.5mM)


This  is  what we all did  a  time  or distance based load  without  any  actual physiological  justification  or reasoning  why 8 min is better  than  7 min  or  why 5  reps  are better  than  7  reps.
But it looks organised  at least. So  my  question  would be . What  do I like to achieve  so I  have or I like to stop  by  8  min  and I  have or I like to  stop  after 5  sets. 
Or  why 2 min  rest  what is  the goal  of the rest in between. Reoxygenation  or  " supercompensation   or insufficient  recovery  ?  or  is  the   8 min and 2 min rest a very  convenient  timing as it is  easy on the ski  to see, when 10 min are over to go  again  and  after  I  have not  finger left on my hand I know the training is  over  .

 3.5  mmol  or any mmol as a target intensity

Here one of  the classical   examples from wooww  long time ago.
2 athletes  getting 3    time loaded  with a  step  load. But first  3.5 mmol load   during an on snow  ski.
a)   you ave to take blodo  (  timing )  than  you have to take that blood  at lest 2  x in the same load  so  after  5  min and than  after 8 min  when you stop.
 Now  lets be lucky  and after   5 min  your  lactate is  3.5  but after  8 min it is  4. 3 ?????
 same effort  same HR  Than  you may have  the same HR  but  due to  the  terrain  you may  shift  the effort   from legs  more  to  arms.
 Here  where my thoughts   move  to . 3.5  from where  and   why  and when

Am J Physiol Endocrinol Metab. 2003 Jan;284(1):E193-205. Epub 2002 Sep 11.

Leg and arm lactate and substrate kinetics during exercise.

Van Hall G1, Jensen-Urstad M, Rosdahl H, Holmberg HC, Saltin B, Calbet JA.

Author information

  • 1The Copenhagen Muscle Research Centre, University Hospital, Denmark. gvhall@cmrc.dk

Abstract

To study the role of muscle mass and muscle activity on lactate and energy kinetics during exercise, whole body and limb lactate, glucose, and fatty acid fluxes were determined in six elite cross-country skiers during roller-skiing for 40 min with the diagonal stride (Continuous Arm + Leg) followed by 10 min of double poling and diagonal stride at 72-76% maximal O(2) uptake. A high lactate appearance rate (R(a), 184 +/- 17 micromol x kg(-1) x min(-1)) but a low arterial lactate concentration ( approximately 2.5 mmol/l) were observed during Continuous Arm + Leg despite a substantial net lactate release by the arm of approximately 2.1 mmol/min, which was balanced by a similar net lactate uptake by the leg. Whole body and limb lactate oxidation during Continuous Arm + Leg was approximately 45% at rest and approximately 95% of disappearance rate and limb lactate uptake, respectively. Limb lactate kinetics changed multiple times when exercise mode was changed. Whole body glucose and glycerol turnover was unchanged during the different skiing modes; however, limb net glucose uptake changed severalfold. In conclusion, the arterial lactate concentration can be maintained at a relatively low level despite high lactate R(a) during exercise with a large muscle mass because of the large capacity of active skeletal muscle to take up lactate, which is tightly correlated with lactate delivery. The limb lactate uptake during exercise is oxidized at rates far above resting oxygen consumption, implying that lactate uptake and subsequent oxidation are also dependent on an elevated metabolic rate. The relative contribution of whole body and limb lactate oxidation is between 20 and 30% of total carbohydrate oxidation at rest and during exercise under the various conditions. Skeletal muscle can change its limb net glucose uptake severalfold within minutes, causing a redistribution of the available glucose because whole body glucose turnover was unchanged.

 

Now  here  the   grphs  of the  2 athletes.
 You can see that both  to  keep  3.5 mmol   have to go  harder.  so they chnage the intensity   to keep 3.5 mmol but  do they maintain the same  training stimulus ?

glucogen speicher.jpg 
now look  the individual change in HR  of the  2  and ask  whether  that is the same cardiac stimulus  still by the  same 3.5 mmol lactate  and so on  or in any lactate number. Now  lets go a  step  further  , what do we  do  when we have  by the target   HR  we had  from a test  by 3.5 mmol   now  after 5 min   a lactate of  2.3 and  after 8 min 2.1 ????? but stable  HR  accordingly  to the test. 

Summary . 
Even  though  top   scientist in sport  still   defend  the lactate   idea   for me   this si a  great example of a great looking bloody mess on the snow  without  any  evidence  at all , that it  works.
 We have minimal control  by taking lactate  sampling  whether we ave a  stable physiological situation  and  1  sample  somewhere  at the end is   ridiculous  and during the  8 min in snow  even more as it will take   30 +- seconds   to rest  and take the sample  and if  you take it at the ear in the winter  or  at the finger    at the same time you will have +- 0.5  difference. Which one is the proper  3.5  mmol lactate ?

 7x6min, 4x15min, etc.), but if the intensity (say 3.5 mM) is the same and you only vary duration (5x8 vs 7x6 vs 4x10) 

As lactate is a  small  feedback  of  some metabolic  reactions  which have taken  place  somewhere  between the start  and  the blood sampling   having at the end  3.5  on both  workouts  means   little. You can change the  lactate  value  by maintaining the same  intensity  ( speed ) by  changing intermuscular coordination  and more  and in skiing this is very very  common.  We used in preparation  or the 1988  winter Olympics  lactate  to  find the  efficiency in athletes  with changing to different pattern . Was it the  reason  for  gold and silver . I  do not think so  at all. We  simply where lucky and had  some very very smart  athletes  who gave incredible  great feedback  and as  such  as so often  right moment  and t the right place  and we  could blame  the lactate  for the success. 

This brings me to another question. According to Jan Olbrecht's "Science of Winning",

With all due  respect  to Mr. Olbrecht,  but there where some great  brains before    that statement  and  he  just took some fundamental ideas  from people like

Lamarck.jpg 


The  fundamental idea  at the  time was  and I try to  translate it into  a hopefully  understandable  English.

Adaptation  is a  dialectic  contradiction.
 You stimulate a physiological system , which will create  an adaptation. The adaptation is the Reason  for progress , but because you adapted the same stimulus  now is the reason  for  stagnation or  even  regress.

This leads  us  to the functional and structural  reactions or  adaptations. Below  a graph I presented  25 years ago in a  training camp in Spain and I  do not know   what I would change  today.

F  and S.jpg 

If  in simple term  we miss the  switch  from red  to green  we  lost the   timing, where a  great functional stress  was able to  create some  structural changes.

Now  to   find  that timing and than adjust the   stimulus  we need  physiological feedbakcs  and NIRS is one of  them.
 This is  where the " periodization"  based of   weeks and moth or  days is getting  very  conflicting reviews.
 Why would I   stop a  so called  basic endurance period  when I see an athlete makes  still great progress after  8  weeks . or  why would I maintain   the  same  period , when I see an athlete does not respond  at all   on the idea of the  stimulus.

That Leeds  us to the end 
This seems to imply that you have to change interval training (intensity / duration) every
few weeks. 

Physiological  training means  there is no such thing like weeks or  training intensity  like speed  or  time duration. It is  the guide  of your physiological reaction who  decides  now  as you do it  whether you stimulate  what you have panned  or whether  you stimulate  something  without  knowing.  Than last but not least  changing intensity   does not mean  going harder  it means changing intensity for  your target physiological system  by changing  what you pkann  for exampel  reduce  the O2  availability  by  a  lower intensity  instead of going harder  to  force a O2   availability  due to intensity.


xcskier

Development Team Member
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Posts: 46
 #9 
Your points are well taken.

Quote:
Physiological  training means  there is no such thing like weeks or  training intensity  like speed  or  time duration.


Interesting! So, how do you then determine "duration" an "intensity"?

Can we be concrete and look at two typical workouts that
I mentioned earlier:
a) 2 hrs, Zone 1, Lactate 1.2 mM
b) intervals 5x8' with 2 min rest Lactate 3.5 mM

How would these two sessions get translated from HR/Zone/lactate paradigm into physiological  zones paradigm? Can we stay simple and concrete
(if we can)?

If I understand correctly, you would first choose the energy system you are
training in the session and then decide how to train it.


juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #10 
Question back :
 Can we be concrete and look at two typical workouts that 
I mentioned earlier:
a) 2 hrs, Zone 1, Lactate 1.2 mM
b) intervals 5x8' with 2 min rest Lactate 3.5 mM

Can you explain  concrete  why 1.2 mmol and what happens  if  you may ski  with 1.5 mmol or if  with 0.8 mmol

Why do we know  the speed where  you are stable  at 3.5 mmol  is  higher  besides actually  testing the  speed or  feeling it.  1.2  can be a balanced   intensity  and  I  could have   by the same intensity 3.5  as  the numbers  only tell that  somewhere I may have  created  some   higher   production than    usage ,  but may balance in so  now  a stable 1.2  or  3.5  means  that  production and removal are balanced.


So  concrete  what  do you stimulate   with 1.2 mmol    and what  do you stimulate  by 3.5 mmol
Why  do I need to ski  2 hours  when I have 1.2 mmol  and why  do I have to ski 8 min  with 2 min rest when I choose  3.5 mmol. What is  th physiological reasoning behind  this    and what would change if  I  ski only 1h 30 min  or  3  hours  or  when I  reduce  the  interval t 5  min.  Please no  copies  off  explanation  on paper  of Zone 1  and  zone 2   simple  physiological facts  what happens  and why  it has  to be  at this lactate levels  and where  do we have the studies  who show  that in this lactate levels  (  which are  metabolic  indications ) we really create this  stimulation )

How many times in a 2 hours   load  do we  have to take lactate to  see the  1.2 mmol level. 

In a physiological  workout  I look  for example  that I  do not reach a cardiac limitation    so  that I may have to shift  blood from the arms  to the legs because I may  work on my   upper  body  lower body  optimal, coordination.  Or  I may like to shift  the load  form  arms  to legs  and back  depending on the technique  I choose  so 15 min arm dominant  than shift to leg  dominant  than    back to  both  optimal   and so on.

Again  what is  the   workout goal

Lactate Accumulation

During intense exercise, muscle and blood lactate can rise to very high levels (10). This accumulation above resting levels represents the balance of production and removal.

 It says nothing about whether accumulation is due to an increased rate of production or decreased rate of removal, or both.

 Similarly, if lactate concentrations in the blood do not rise above resting levels during or immediately following exercise, it also infers nothing about lactate or lactic acid production during that activity.

 It may be that lactic acid production is several times higher than at rest but that it is matched by its removal showing no net increase (26).

A common misinterpretation is that blood lactate or even lactic acid, has a direct detrimental effect on muscle performance. However, most researchers agree that any negative effect on performance associated with blood lactate accumulation is due to an increase in hydrogen ions. When lactic acid dissociates it forms lactate and hydrogen ions - which leads to an increase in acidity. So it is not accurate to blame either lactate or lactic acid for having a direct negative impact on muscular performance.

The increase in hydrogen ions and subsequent acidity of the internal environment is called acidosis. It is thought to have an unfavorable effect on muscle contraction (10) and there has been considerable research to demonstrate that this is the case (11,12,13,14,15,16,17).  

 

.

 

juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #11 
Here  just t add some  additional thoughts  to the  discussion on lactate values  below  and above  what some  will call LT.
 
ed Sci Sports Exerc. 1998 Sep;30(9):1424-9.

Lactate distribution in the blood during steady-state exercise.

Abstract

PURPOSE:

The purpose of this investigation was to examine the plasma to red blood cell (RBC) lactate concentration ([La]) gradient and RBC[tongue]lasma [La] ratio during 30 min of steady-state cycle ergometer exercise at work rates below lactate threshold (<LT = approximately 40% of peak cycle ergometer O2 uptake ¿VO2peak¿) and above LT (approximately 70% of VO2peak).

METHODS:

Eight subjects (cycling VO2peak = 41.6+/-1.6 mL x kg(-1) x min(-1); LT = 57.9 + 1.2% VO2peak) performed 30 min of cycle exercise at intensities < and > LT. Blood samples were taken from a heated forearm vein, immediately cooled to 4 degrees C in a dry-ice ethanol slurry, and centrifuged at 4 degrees C to separate plasma and RBCs.

RESULTS:

During >LT, plasma [La] rose to 8.8+/-1.1 mM after 10 min and remained above 6 mM. RBC [La] (4.9+/-0.7 mM) was significantly lower than plasma [La] at 10 min and remained lower throughout exercise. As a result, there was a sizable [La] gradient (approximately 3.5 mM) from plasma to RBC during most of >LT. In <LT, plasma [La] increased only slightly from rest (1.6+/-0.2 mM) after 6 min (2.4+/-0.3 mM) and then declined to approximately 2 mM for the remainder of the trial. The plasma to RBC [La] gradient averaged approximately 0.8 mM throughout <LT. Despite drastically different plasma to RBC [La] gradients in <LT and >LT, the ratio of RBC [La][tongue]lasma [La] was the same for both (0.58+/-0.02) and not significantly different from rest.

CONCLUSIONS:

These results refuted our hypothesis that the RBC[tongue]lasma [La] ratio would decrease at the onset of >LT exercise because of muscle lactate release exceeding the ability of RBCs to take up the lactate.
Instead, there appears to be an equilibrium between plasma [La] and RBC [La] in arterialized venous blood from a resting muscle group as evidenced by the constant RBC [La][tongue]lasma [La] ratio.

xcskier

Development Team Member
Registered:
Posts: 46
 #12 
Quote:
what  do you stimulate   with 1.2 mmol and what  do you stimulate  by 3.5 mmol


The purpose of easy session (at 1.2 mM or below) is recovery or increase in capillary density
(for a very long session, say 3-4 hours). 1.2 mM is chosen based on the test result
to be at or below resting lactate.

With the "threshold intervals" (3.5 mM or maybe even a bit lower), the point is to
a) increase "lactate threshold"
b) recruit both slow twitch and fast twitch oxidative fibers
c) etc.

As I have indicated in my earlier posts, taking lactate is useful
to get a "feel" for certain intensities. You get a pretty good 
feel prety quickly.


juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #13 
I was  hoping or I was  afraid  the  answer would be  that    with little evidence  of  the  possibly  science. Here just a  very short   direction as it goes  far above  what NIRS  interpretation is on this  forum
 he purpose of easy session (at 1.2 mM or below) is recovery or increase in capillary density
(for a very long session, say 3-4 hours). 1.2 mM is chosen based on the test result
to be at or below resting lactate.


There is not one  study   who can confirm  , that  the reason of   vascularsiation is becasue we  avoid  lactate  build up. in fact we  not even know whether we  avoid  this  as  1. mmol  dos not mean  that we  do not  create a lot of lactate in the metabolic  path  way,  it only indicates, that we  not  accumulate in the circulation. 

ngiogenesis. 2012 Dec;15(4):581-92. doi: 10.1007/s10456-012-9282-0. Epub 2012 Jun 3.

Lactate stimulates angiogenesis and accelerates the healing of superficial and ischemic wounds in mice.

Abstract

Wounds notoriously accumulate lactate as a consequence of both anaerobic and aerobic glycolysis following microcirculation disruption, immune activation, and increased cell proliferation. Several pieces of evidence suggest that lactate actively participates in the healing process through the activation of several molecular pathways that collectively promote angiogenesis. Lactate indeed stimulates endothelial cell migration and tube formation in vitro, as well as the recruitment of circulating vascular progenitor cells and vascular morphogenesis in vivo. In this study, we examined whether the pro-angiogenic potential of lactate may be exploited therapeutically to accelerate wound healing. We show that lactate delivered from a Matrigel matrix improves reperfusion and opposes muscular atrophy in ischemic hindlimb wounds in mice. Both responses involve lactate-induced reparative angiogenesis. Using microdialysis and enzymatic measurements, we found that, contrary to poly-L-lactide (PLA), a subcutaneous implant of poly-D,L-lactide-co-glycolide (PLGA) allows sustained local and systemic lactate release. PLGA promoted angiogenesis and accelerated the closure of excisional skin wounds in different mouse strains. This polymer is FDA-approved for other applications, emphasizing the possibility of exploiting PLGA therapeutically to improve wound healing.


Now     this is  as well on humans and one direction in cancer research is to avoid   vascularisation. and one of  the  steps  they  research is avoid lactate   to  be moving  to the cancer cells.   so they  work on  manipulation  MCT  carriers. 


More  questions to  come  and  this is NOT a  critic  on anybody  but it is a  direction, that if  we like to move towards physiological  training immunization  we  have  to get clear  with seem  classical mythological ideas. 

REMEMBER
 The  whole  concept  of lactate threshold  was developed under  the  information , that lactate is  the reason of  fatigue  and it is bad  ugly  and we have to get rid of it. 

So  again  why  do we cool  down,  why do we have to learn to " tolerate " lactate     and many more ideas we  still  hang  on  and YES it is hard to  get rid of  them as  many  do not   know how to replace them for now

juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #14 
Woww  fast reaction and a  call just know. Here  the     direction  .

So  for many readers her    who hate  that I  talk lactate, not even  follow  this  ideas , as it is very frustrating to read  some  really  interesting research.  if we  are not ready ( yet )  to  rethink  some ideas  [wink] but without  really   digging into  this direction   there  is no  way   we ca consider physiological stimulation as a possible interesting idea for training planning and  stimulation

  NIRS  and with it the SmO2  reaction combined  with lactate  information  and  understanding on  how lactate  at  NIRS  interact  is he  key  for   vascularisation. 

The problem we have  that there are  other groups out  who  take SmO2 interpretation    very  simple  and  argue, that when  we see a drop in SmO2   or  they call it  SmO2 break point, we start to  go " anaerobic" . May be,  but really a  drop in SmO2  means we use more O2  than we  can deliver  so  it is the opposite really ( if  we believe  NIRS  shows  what  e hope )    so  it i  exactly than  when we  are  sure we use  O2  where others  believe  we   do not use    O2. A  flat  even very high SmO2  could be that we have a problem to  use  O2.


    So  again back  to the   1.2 mmol  idea  and  the   statement  a what it suppose to  do and the lack of  studies  confirming the reason  for  the  possible vascularisation and  the  idea  to  " avoid " lactate.
 

We use   SMO2  tHb  and therefor   metabolic stimulation of  lactate  for that specific reason. 

Adv Exp Med Biol. 2008;614:73-80. doi: 10.1007/978-0-387-74911-2_9.

Lactate, with oxygen, incites angiogenesis.

Hunt TK1Aslam RHussain ZBeckert S.

Author information

Abstract

Lactate has been reconsidered! As we now know, most is produced aerobically We report that lactate accumulation commonly occurs in the presence of oxygen and is sufficient to instigate signals for angiogenesis and connective tissue deposition. These include vascular endothelial growth factor (VEGF), transforming growth factor beta (TGF beta), interleukin-1 (IL-1), and hypoxia-inducible factor (hif-1alpha). This paper, a mini-review, is occasioned by new data showing increased presence of VEGF and angiogenesis in an oxygenated site by adding a slow-release source of lactate into Matrigel and implanting the Matrigel subcutaneously in mice.

  Antioxid Redox Signal. 2007 Aug;9(8):1115-24.

Aerobically derived lactate stimulates revascularization and tissue repair via redox mechanisms.

Hunt TK1Aslam RSBeckert SWagner SGhani QPHussain MZRoy SSen CK.

Author information

Abstract

Hypoxia serves as a physiologic cue to drive an angiogenic response via HIF-dependent mechanisms. Interestingly, minor elevation of lactate levels in the tissue produces the same effect under aerobic conditions. Aerobic glycolysis contributes to lactate accumulation in the presence of oxygen, especially under inflammatory conditions. We previously postulated that aerobic lactate accumulation, already known to stimulate collagen deposition, will also stimulate angiogenesis. If substantiated, this concept would advance understanding of wound healing and aerobic angiogenesis because lactate accumulation has many aerobic sources. In this study, Matrigel plugs containing a powdered, hydrolyzable lactate polymer were implanted into the subcutaneous space of mice. Lactate monomer concentrations in the implant were consistent with wound levels for more than 11 days. They induced little inflammation but considerable VEGF production and were highly angiogenic, as opposed to controls. Arterial hypoxia abrogated angiogenesis. Furthermore, inhibition of lactate dehydrogenase by using oxamate also prevented the angiogenic effects of lactate. Lactate monomer, at concentrations found in cutaneous wounds, stabilized HIF-1alpha and increased VEGF levels in aerobically cultured human endothelial cells. Accumulated lactate, therefore, appears to convey the impression of "metabolic need" for vascularization, even in well-oxygenated and pH-neutral conditions. Lactate and oxygen together stimulate angiogenesis and matrix deposition.

 

xcskier

Development Team Member
Registered:
Posts: 46
 #15 
I am not arguing whether there is a solid science behind any of the lactate
numbers or lactate training. Most of it is clearly based on old science
and myths.

The points I was trying to make are:
1) There are only a few ways to practically monitor intensity:
a) heart rate (continuous measurement)
b) lactate (5-6 per session at most)
c) power (for some sports, continuous)
d) NIRS (continuous)
e) VO2 (a few times per year at most, very unrealistic scenario, may be difficult to
measure for some sports due to equipment constraints)

2) Most people are still using HR/lactate as a measure of "intensity" whether 
it's correct or not. So, that answers the question of the post:
YES, lactate can be used for interval planning and control.

3) What I have been trying to learn is how to translate
(perhaps a better word would be relate or map) from traditional
HR/lactate zone training (eg, the two workouts I explicitly mentioned)
to a different monitoring system using NIRS.

For NIRS to be useful to a practitioner, there has to be good ideas
about how to change the training so that people (both athletes and
coaches) are willing to try it. It's all too vague at the moment to
dummies like me.

The reason why people still use HR is because it's easy to understand
and to follow. The same with lactate. There's a decades of distilled
knowledge, practical prescriptions and experiences. They may all be
wrong and based on wrong science, but they are there.

And many athletes have successfully used lactate-based system to win countless medals.
Perhaps it's a total fluke and their success is attributed to a wrong reason and they would
be even more dominant if they used different monitoring / planning.  But, they are using 
some sort of system that is coherent (and could be completely wrong or inadequate at best).

So, let's try to change this.



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