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juergfeldmann

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 #16 
Here an add on what we see in practical applications.
 In  mitochondrial myopathy patients we see an incredible increase in blood vessels despite the fact that  the  target   cell is not working. This indicates a  stimulation of  blood vessels  buildups    from other reasons  than hypoxia. This leads us  back to  some great  studies  from Schoen et all, where they had additional stimuli  than hypoxia  which  can lead to angiogenesis.

Now   I had  2  myopathy clients  where I did  NIRS  and it is  interesting, that we have a great tHb reaction but a minimal  to no explainable   SmO2  level  which  did not changed  at all or  minimal  despite the fact , that the client had  to give  up  the motion. No  if we  to excessive pliometric  workouts  we have  for a few  days a similar  NIRS picture  which than moves  back to " normal" . This can be used in strength  workouts  to plan  load  and recovery  very nicely.
CraigMahony

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 #17 
Juerg, I am trying to understand what you are saying here. 

Now   I had  2  myopathy clients  where I did  NIRS  and it is  interesting, that we have a great tHb reaction but a minimal  to no explainable   SmO2  level  which  did not changed  at all or  minimal  despite the fact , that the client had  to give  up  the motion. No  if we  to excessive pliometric  workouts  we have  for a few  days a similar  NIRS picture  which than moves  back to " normal" . This can be used in strength  workouts  to plan  load  and recovery  very nicely.

So your clients were working muscularly and tHb (muscle compression, muscle pump, etc) reacted but SmO2 did not? If this is so it implies no or little use of O2, yet there was an energy demand. It sounds like it was close to being fully anaerobic, but as has been explained in this forum, the aerobic system supplies energy quickly.  So I am not understanding something here. Could please please explain it again? Can you also indicate further how this applies to pliometric (plyometric is the same?) workouts?
Kirill

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 #18 
"This indicates a  stimulation of  blood vessels  buildups    from other reasons  than hypoxia"

I read ~500+ articles about capillarisation build.

ROS activate VEGF. Mitomiopathy generate ROS

This is an example, in so factors dozens, dozens of nutritional factors. Even mechanical squeezing stimulates the growth of capillaries and their strength, as an example in the practice of weightlifting, bruises on the hip from the impacts of the rod bar are no longer appearing.

If we look at rats without myoglobin, they live and run along the path. This is like an extreme case for the evaluation of the link. Suppression of capillaries through VEGF (- / +) animals can not practically overcome, they can not completely compensate.

My total opinion - higher levels of myoglobin and capillaries are useful, but they do not say anything about the level of the athlete. To show the result you must have developed all the mechanisms at the same time, and the irony is that some can be grotesquely developed, for example 1 per 100 people can have an oxygen delivery of 8-10 liters, and consumption is only 3-4 liters.

Example of superdelivery - Chris Froome tests, 580 watts at hr 160. If extrapolate - 9 liters delivery!
juergfeldmann

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 #19 

This indicates a  stimulation of  blood vessels  buildups    from other reasons  than hypoxia"

Thanks Kirill for your great feedbakcs  and  here   you can use Kirils  summary  of my short but incomplete feedback on blood vessels stimulation and the many different reasons  where this  can happen

My total opinion - higher levels of myoglobin and capillaries are useful, but they do not say anything about the level of the athlete

Absolutely and you  simply agree with the  statement  from Andri in his respond.

Andri
 1. I agree of course with how this point starts. The best athlete is the one that wins the competition or wins various competitions the majority of the time. Physiology measures do not determine the best athlete, this holds true for VO2 or blood lactate, and also of course for Moxy. That is why we have athletic competitions and not lab testing events.


And I like to add on here that this is the reason  why we  do NOT test  we assess  and we   assess as  close to the real  activity as possible.
 Lab tests   offer little  to no help  for  practical application as we  do not get any live feedback on any current reaction  we have  at any specific  day  where we  work out. So that's  where we hope  with NIRS  and  combinations we  make a huge  step  forward in real targeted  stimulation ideas with real  live feedback versus  calculations  and hope.
With NIRS  we are  a nice step closer to this ideas  but  not optimal yet. But for sure closer  than with lactate or any otehr  calculations  we used in the past.
juergfeldmann

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 #20 
Craig  here another  try.

Thanks  for the  question. . One section I can give a  very  exact answer, the second  part is  what we observe  and  has to be  studies  in many more cases  so take it with a grain of  salt.

1. Pliometric  ( not  plyometric  training )
1938 Hubbard and Stetson  explained  in their  work  how muscle  most likely  work  and created the  definition of the three  possible  muscle contraction reactions.

 mio metric, plio metric,isometric
 This work  ding  are taken  as  so often at that  time  from Latin or Greek. In this case   from Greek.
 Mio = means  shorter
Plio  = means  longer
 Iso = means  the same
This was  the exact   observation they ha d for the muscle reaction.
Than somewhere  later some  " smarty  guy " decide  that Greek is out   and we need some "English" definition  and   they created  for example eccentric

So below  the  definition for  eccentric  help   me  whether you see see that this  definition makes  any sense in connection with muscle contraction ?

ec·cen·tric

ikˈsentrik/

adjective

  1. 1.

(of a person or their behavior) unconventional and slightly strange.

"my favorite aunt is very eccentric"

synonyms:

unconventionaluncommonabnormalirregularaberrantanomalousoddqueerstrangepeculiarweirdbizarreoutlandishfreakishextraordinary; More

  
   
  1. 2.

technical

(of a thing) not placed centrally or not having its axis or other part placed centrally.

  •  
  •  

noun

  1. 1.

a person of unconventional and slightly strange views or behavior.

"he enjoys a colorful reputation as an engaging eccentric"

synonyms:

oddity, odd fellow, characterindividualistindividualfree spirit; More

  1. 2.

a disc or wheel mounted eccentrically on a revolving shaft in order to transform rotation into backward-and-forward motion, e.g., a cam in an internal combustion engine.

 

 To  the second much harder part we  base on observation paired  with  studies  like the one  Kirill  stated  as well on myopathy.

Some may remember at the start of NIRS intro in this forum we made the claim, that we see  extreme  situations like  a cardiac limitation in either  top  athletes or  people e with cardiac  problems . 
 The reaction is the same  the performance level is just very different. This way  by assessing originally people  with know  limiters  like cardiac people or  respiratory  diseases  or muscular diseases  we got some ideas on how NIRS  could identify this limitation. Than we  moved  to " healthy " people, but as  well healthy people have a limiter, it is just  not    critical as it  is not about life and death there, but just about bragging rights  in one or the other event.
 I am often kidding in presentations  , where i argue, that the training challenge is the  same in this  2 groups. No difference  at all.
 the only difference is  the timing for the payment for the training program.
 In disease  people you better charge in advance  to your program in case you make a mistake . In athletes  it  doesn't matter  as he may simply change the coach  and  does not pay you.

Kidding aside.
 If  we look at some  NIRS  example we showed  from 100 mile runners  we see that  they have a very high SmO2  and minimal change,  even if they  go all out. They as well show an  incredibly good  and high tHb trend in recovered  situation.
 We  argued  that they most likely  have a very high  mitochondria density   and therefore  as well a very high   myoglobin  content.
 Now remember the O2  disscurve  for  Hb and MB.

 Here as a reminder.



oxy and myo o2 curve.jpg

NIRS / MOXY  does not  discriminate  between Hb loaded  whit O2  O2Hb  and Myoglobin loaded  with O2.
 So look  at the left side  the arrow  and  orange area. It needs a every very low pO2  till we  actually call upon the myoglobin to release  O2  and  in  many endurance athletes  this may simply not happened  due to the way  they train or the body works. But we    can in any case get SmO2  down  to   zero  as we know.
So we have a  very  great delivery from cardiac  and  respiratory  and piping ( blood vessels system in this athletes  and we have a very good utilization when it comes  to use O2  which is   steady delivered  by Hb. But we  keep a very high SmO2  %  due to the very highly  mitochondria  and therefore Mb  density , which  is not  triggered  so easy to release.
 Now  id we  do a  race or  workout where they have an uncommon high %  of plimetric  muscle activity  like running very long downhill and never trained this  we see a severe muscle damage  the following days.
 Now  when we  do a  SmO2 tHb  assessment and compared  with  recovered  once  we see no a  much lower  start  and   over level of SmO2. Why ?

 Now in muscle myopathy  there are chronically in this " damaged " muscle situation  so not just functionally. They seem to try to compensate  by producing more blood vessels as we often see in athletes  initially an increase in blood vessels  so supply line before we see an increase in mitochondria. On the opposite site  after an injury so in rehab we see first  the reduction of  mitochondrial  density  and than  later a reduction in blood vessels  as they are not used  due to the lack of demand. ?
Similar in COPD  where  due to the chronic  hypocapnia we see  an overload of  the right ventricle , where as in athletes it is   initially just a functional reaction.
 Now in myopathy  they have a  very good vessel density situation so an incredible great deliver and often as well due to the   demand of  O2  a very good  CO and even respiration. But we have nobody  who actually  can use the  O2  optimally.So  they may have  ( not sure )  much less  MB  due to the disease  but a huge amount of Hb  circulation loaded but  can no unload  ( O2 is not bio available.
So  SmO2  high here  due to high loaded  Hb  and in  endurance athletes  due to high loaded MB  , so it looks the same but  the O2  is much less bio available the one group than the other which than clearly shows  up in performance.
 So under load  they deliver as it is a huge demand  and the  delivery is far better  than what they can utilized  and therefor even if they go very hard  they  can not  drop  SmO2  significantly  before  other problems show  up so the CNS  will shut down  further  ATP use  as they may reach a  critical low  for survival needed  ATP level.. But again in an occlusion test we  can drop them all the  way  down. So  the use  of NIRS in thee 2  cases  created  this  discussion and idea. This   clients  where sent  for aggressive  rehab  and strengthening but in my assessment  and after the result I  sent them back  with the  question for potential myopathy. Initial reaction  from the  med  community was no way  that this  works , good  connection help to get them tested and unfortunately both had  mitochondrial myopathy. Possibly luck  and coincidence  but at least very interesting  and the  med  community could try to make a bigger study out  of  an idea like this as it may save a lot of  diagnostic headache  and time  perhaps.  For  the  practical coach  they could  use  this  possible reaction  for their planning  of muscular recovery after specif  workout. Track  tHb  and  SmO2  after unconventional and new strength loads  with potentially lots of pliometric  loads.  Craig hope it makes  better sense  otherwise  come  back  and I give it another try.

 


Kirill

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 #21 
Interesting work with the use of NIRS. Gives food for thought, how important and necessary, or do not need O2 oversupply.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5269414/

Intracellular oxygen tension limits muscle contraction‐induced change in muscle oxygen consumption under hypoxic conditions during Hb‐free perfusion
Hisashi Takakura, 1 , 2 Minoru Ojino, 2 Thomas Jue, 3 Tatsuya Yamada, 2 , 4 Yasuro Furuichi, 2 , 5 Takeshi Hashimoto, 6 Satoshi Iwase, 7 and Kazumi Masudacorresponding author 2
Author information ► Article notes ► Copyright and License information ►
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Abstract

Under acute hypoxic conditions, the muscle oxygen uptake (mV˙O2) during exercise is reduced by the restriction in oxygen‐supplied volume to the mitochondria within the peripheral tissue. This suggests the existence of a factor restricting the mV˙O2 under hypoxic conditions at the peripheral tissue level. Therefore, this study set out to test the hypothesis that the restriction in mV˙O2 is regulated by the net decrease in intracellular oxygen tension equilibrated with myoglobin oxygen saturation (∆PmbO2) during muscle contraction under hypoxic conditions. The hindlimb of male Wistar rats (8 weeks old, n = 5) was perfused with hemoglobin‐free Krebs–Henseleit buffer equilibrated with three different fractions of O2 gas: 95.0%O2, 71.3%O2, and 47.5%O2. The deoxygenated myoglobin (Mb) kinetics during muscle contraction were measured under each oxygen condition with a near‐infrared spectroscopy. The ∆[deoxy‐Mb] kinetics were converted to oxygen saturation of myoglobin (SmbO2), and the PmbO2 was then calculated based on the SmbO2 and the O2 dissociation curve of the Mb. The SmbO2 and PmbO2 at rest decreased with the decrease in O2 supply, and the muscle contraction caused a further decrease in SmbO2 and PmbO2 under all O2 conditions. The net increase in mV˙O2 from the muscle contraction (∆mV˙O2) gradually decreased as the ∆PmbO2 decreased during muscle contraction. The results of this study suggest that ΔPmbO2 is a key determinant of the ΔmV˙O2.
Kirill

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 #22 
A number of interesting studies for you in the field of mitochondria.

http://sci-hub.cc/10.1097/00042752-199801000-00012
http://www.ijppp.org/files/ijppp0000411.pdf
http://jap.physiology.org.sci-hub.cc/content/jap/121/3/636.full.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3065478/
https://www.researchgate.net/publication/261190102_Three_dimensional_reconstruction_of_the_human_skeletal_muscle_mitochondrial_network_as_a_tool_to_assess_mitochondrial_content_and_structural_organization
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3208215/

oilQUIVJWXw.jpg  ySxHqJDn7dM.jpg

Kirill

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 #23 
http://jeb.biologists.org/content/218/21/3377.long
Local capillary supply in muscle is not determined by local oxidative capacity
Alessandra Bosutti, Stuart Egginton, Yoann Barnouin, Bergita Ganse, Jörn Rittweger, Hans Degens
Journal of Experimental Biology 2015 218: 3377-3380; doi: 10.1242/jeb.126664

    ArticleFigures & tablesInfo & metrics
    PDF

ABSTRACT

It is thought that the prime determinant of global muscle capillary density is the mean oxidative capacity. However, feedback control during maturational growth or adaptive remodelling of local muscle capillarisation is likely to be more complex than simply matching O2 supply and demand in response to integrated tissue function. We tested the hypothesis that the maximal oxygen consumption (MO2,max) supported by a capillary is relatively constant, and independent of the volume of tissue supplied (capillary domain). We demonstrate that local MO2,max assessed by succinate dehydrogenase histochemistry: (1) varied more than 100-fold between individual capillaries and (2) was positively correlated to capillary domain area in both human vastus lateralis (R=0.750, P<0.001) and soleus (R=0.697, P<0.001) muscles. This suggests that, in contrast to common assumptions, capillarisation is not primarily dictated by local oxidative capacity, but rather by factors such as fibre size, or consequences of differences in fibre size such as substrate delivery and metabolite removal.

EQXUoXoTAnY.jpg  P-hr6LlhKmQ.jpg 

Kirill

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 #24 
See page 7 and 8
http://www.zmpbmt.meduniwien.ac.at/fileadmin/zbmtp/Dateien/Arbeitsfelder/MR/Spectroscopy/dynamic_31P_MRS_in_soleus_muscle.pdf
345324543.png 



_aaQ3-LhPbU.jpg 

Kirill

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Posts: 93
 #25 
90% of people from a typical, full-amplitude training with muscle relaxations are not inside type 1 muscle fibers:
  1. No CrP depletion
  2. No metabolic stress
  3. No signalling
  4. No RNA
  5. No Protein synthesys (With the exception of the regeneration of damaged slow fibers)
  6. No growth Type I CSA

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3365403/figure/F4/
AkizhHcxdLs.jpg

Kirill

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 #26 
http://jap.physiology.org/content/113/2/199


p-ylNUi1Pio.jpg  ZJ0ar4a13N4.jpg 

Kirill

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Posts: 93
 #27 
HjvF7oTZlFw.jpg  xK4bHR_6X6Y.jpg


limits-of-respiration2.png 

Kirill

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 #28 
I use this data to rest. I rest 5-10 minutes.

http://dx.doi.org.sci-hub.io/10.1007/s00421-007-0394-y

The effect of rest interval length on metabolic responses
to the bench press exercise
Nicholas A. Ratamess

345324554643.png 

Kirill

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 #29 
Summarizing the research data, for me personally Moxy is an extremely interesting tool for find the keys to hypertrophy of slow muscle fibers, speaking broadly - a means for hypertrophy of all motor units active on VT2
Kirill

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Posts: 93
 #30 
 If  we look at some  NIRS  example we showed  from 100 mile runners  we see that  they have a very high SmO2  and minimal change,  even if they  go all out. They as well show an  incredibly good  and high tHb trend in recovered  situation.
 We  argued  that they most likely  have a very high  mitochondria density   and therefore  as well a very high   myoglobin  content.
 Now remember the O2  disscurve  for  Hb and MB.


Maybe this athlete use 20-30% of delivery?

So far, all studies have shown that, other things being equal, a more complete oxygen extraction should be considered a favorable indicator.

In general, most stayer do not know how to hypertrophy muscles, and all of their trainings are a waste of time, except for the extraordinary and completely useless development of the transport system, they are not leading - VT2 does not grow.

Data Concept2 from elite athlete, olympic level http://www.medscape.com/viewarticle/834570

r_6caArvWCs.jpg 

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