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Kirill

Development Team Member
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 #16 
I'll bring a source with the calf for fiber types and the resynthesis of creatine phosphate. For, the terrible mistake of most athletes is to count the shin with an aerobic muscle. Perhaps 10-30% of motor units of gastrocnemius and soleus aerobic, I do not argue. But everything else - wildly acidified, does not have any special outstanding abilities. Consequently, the use of ultra-rigid training on the lower leg is one of the main reasons for the lack of growth of the shin. She needs to train exactly the same way as a quadriceps - with a rest of 10 minutes, without superseries.
http://dx.doi.org.sci-hub.cc/10.1002/mrm.26329
The pH Heterogeneity in Human Calf Muscle During
Neuromuscular Electrical Stimulation
Norman Stutzig,
* Reinhard Rzanny,
Kevin Moll,
Alexander Gussew,





LYdZJBfSzKI.jpg 


Рисунок1.png 

Kirill

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Posts: 93
 #17 
And see this
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5132121/



xbdv0o2oYP0.jpg 
NBM-29-1825-g004.jpg 

pgc1_sdh.jpg

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Kirill

Development Team Member
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Posts: 93
 #18 
And this.
https://vk.com/doc212236790_437041868

Type I fibre dont create metabolic sterss without occlusion (or norelaxation exercise)

ENERGY METABOLISM IN SINGLE HUMAN MUSCLE FIBRES DURING INTERMITTENT CONTRACTION WITH OCCLUDED CIRCULATION BY PAUL L. GREENHAFF*, KARIN SODERLUNDt, JIAN-MING RENT AND ERIC HULTMAN

rRtE5oTrdBw.jpg  

And, dont growth
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1479884/

Skeletal muscle hypertrophy and structure and function of skeletal muscle fibres in male body builders
Giuseppe D'Antona,1 Francesca Lanfranconi,2 Maria Antonietta Pellegrino,1 Lorenza Brocca,1 Raffaella Adami,1 Rosetta Rossi,1 Giorgio Moro,3 Danilo Miotti,3 Monica Canepari,1 and Roberto Bottinelli1,4



mBBXh_HS_mg.jpg  P1f3EAW5xHk.jpg
juergfeldmann

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Posts: 1,501
 #19 
Nice  feedbacks and super interesting as all this stuff is.
Thanks  for all your  time on here and they greta interesting critical  contribution.
Here   a  thought:

http://dx.doi.org.sci-hub.cc/10.1002/mrm.26329

 we  see in studies  that they indicate  that the different muscle fibers  react to different electrical  stimulation  and have therefore different  wave length    as a pattern  for reaction. I  cannot find  in this study that they  tried  different   frequencies  just one single one.  wave length  they used or  frequency  for the  stimulation  . 
 Help  and show  some  studies  where they used  different stimulation pattern. See in their paper as they agree with that point.

a)       Furthermore, the activated muscle area depends on the stimulation intensity, that is, electric current 

but  as it seems  as well on Hz  and ms. ( my comment)

 

b)      Go  and look  for some interesting reading  from companies  like Compex  Originally  Switzerland  or myotron. They all argue they have the different   frequencies so  you stimulate specific  the targeted  fiber  type. 


c)        They used one specific  frequency  from the literature. What would have happened if they used another one where perhaps   other fibers  would  have reacted   different . ?

 

The muscle was stimulated using a pulse frequency of 40 Hz, pulse width of 200 ms, stimulation train duration of 1 s, rest time between trains of 1 s, and current strength of 72 mA. The stimulation parameters were chosen based on literature.

 

So   if  the different   stimulation pattern theory opens  the question  , whether this  specific   frequency   was the preferred one for a specific  fiber  type and therefore this one had  the highest ATP need  and   reaction ???

 

Kirill

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Posts: 93
 #20 
In order to accurately determine the recovery of muscles, it is possible to do isometric squats before the parallel, and according to the trend of deoxygenation, assume that the muscles consume oxygen as before or not. Of course it's not every workout, but only as a one-time event.

So, hypothetically, the ability of muscles without tremors to keep isometric indicators of their health, freshness. If there is a tremor or oxygenation does not fall to zero, if there is a growth of Thb, then the muscles are in poor condition.

I read the studies of runners at medium-distance international level, where they were offered to hold 3 kg fixed on an ankle sitting on a chair.

Overtrained athletes were registered with a tremor and they did not have a burning sensation, EMGs were accompanied by high-frequency peaks, signal loss. This was caused, in particular, by the long running in the competitions.

Normally, the refusal to work was due to burning, without tremors and fallouts/high-frequency peaks of the EMG signal.

Therefore, according to the muscles that can not work properly, they will constantly flow blood and oxygen, which will be seen on the sensor.

Andri

Fortiori Design LLC
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Posts: 65
 #21 

Thanks Kirill for the links and topic expansion. 

A few questions/or points about some of your remarks that I am not sure about, and maybe you can elaborate on.

  1. "the ability of muscles without tremors to keep isometric indicators of their health, freshness. If there is a tremor or oxygenation does not fall to zero, if there is a growth of Thb, then the muscles are in poor condition"


In am not sure if this is a language or understanding problem but this is what I am getting out of this statement. If you do an isometric contraction and you have SmO2 tremors, SmO2 does not go to 0%, and tHb increases during the contraction your muscles are in poo condition. Is “poor condition” a general statement about the muscle or is it a statement about the current state of muscular fatigue? Then when you say isometric, at what ability? MVC? I have a lot of data with untrained to highly trained, from endurance to power sports, that show many different responses in isometric contractions, and many variables play a factor in the response. 

My assumption is that what you are trying to say is the following: If you have a well trained individual who is fully recovered and completes a isometric MVC we would expect to see clear drop in SmO2 to values very close to 0% and a complete occlusion meaning no change in tHb. This I agree with.


2. “according to the muscles that can not work properly, they will constantly flow blood and oxygen”

 

This point, again I think is a little difficult to understand but ties into the previous points. If a muscle is recovered and well trained and is then contracted to a high degree, lets say MVC, you should see occlusion tendencies, ischemia, low SmO2 values, etc. If a muscle is fatigued or not well established contraction force well not results in this ischemia and therefore you will have continuous blood flow and therefore continuous oxygen supply. This is most likely a true statement. What I want to make sure that other readers do not get confused about, blood flow restrictions caused by voluntary contractions is a result of the amount of force the muscle is producing on the vasculature. Being aware of this is important when using the Moxy, but also very important when considering the activity/intensity of training, or thinking about the sport one competes in.

Practical example. If you are cycling for an extended period of time having regular blood flow to youe working muscles is vital, and therefore factors that impede blood flow (for example high muscle force, but also things like positioning) need to be taken seriously and avoided when possible. However, if you take a sport like alpine skiing, this avoidance of blood flow restriction is near impossible, as the forces involved and the isometric contraction from the aerodynamic position will automatically generate this. Here is much more about a quick “recovery”/release when possible and a buffering of the system for the duration of the event. 




Kirill

Development Team Member
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Posts: 93
 #22 

Yes, you understood me correctly.

The study that very frequent muscle tremors occurs in overtrained runners I read in the library in Russian, observations were made on the USSR national Olympic team.

So there are works, perhaps you are well-known that when EMG signs of poor muscle relaxation appear very soon, a sprinter can tear muscles if he does not allow them to recover.


Muscle tremor - I call it when the muscles begin to tremble very often during isometric tightening or during normal exercise. Look at the moment 2:54 in this video, if you look closely you can see how the trembling starts, can also start quickly and quickly in different directions to twitch the feet.



youtu.be/eqnBIvYvQis?t=174

There are crazy people who with such a "tremor squats" for 200*10 kg. This is the way to complete muscle break from bone, in my opinion. I believe that Moxy will score the alarm before the tremor begins, on the appearance of abnormal trends of Smo2 and ThB.

Example - I squat without weight in a short amplitude without muscle relaxation, while the muscles are in good condition, and I see a Moxy "bug"

If i squat with ~60% 1RM i not see Thb rise

Graph_djprmt8z.png


1
 - squat without weight
2 - squat with With rubber creating resistance of 54 kilograms
3 - This is the same rubber folded in 2 times


Kirill - 2017-03-18T08-44-18 - Snapshot - копия.png 

juergfeldmann

Development Team Member
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Posts: 1,501
 #23 
Here an add on  to  confirm  Kirill's  and Andri's  greta information.
I use  SEMG  combined  with NIRS  (  first Portamon   now MOXY )  daily in rehabilitation and  now as  well often in report  to  insurance companie s and return to work assessments.
During the  rehabilitation we  can motivate  the patient  and see as well the    value  of  how many reps. 
 The  classical  rehab we often   completely underestimate the recovery time needed  of a  d rehabilitation leg  ( muscles ) as well the  amount  of  reps  needed  to make progress.
 It is more a  question of  quality of   contraction   if we look at strength regain , than a  question of quantity  which may be important  m in the case of regaining coordination .
 The   nice   part of NIRS involved  rehab is the live feedback   and therefor the  diretcfeedbackc of the  quality of the rehab.

So here  an example  of a  ACL  rehab  with   comparison of  operated  leg  to healthy leg. Portamon  print out 7 years back .
ACL  rehab 12  weeks  post ops. 
Left is  ops  leg.
 White  top  trace is  TSI  %( Tissue  saturation index)
Green is tHb on here
Red is  O2Hb  and blue is HHb. The  thick  color is  T3  so  the depth of a MOXY   reading  in the muscle . The  thin  color is T1   so  more toward the skin  O2  reaction.

Untitled.jpgLeft leg compariosn.jpg  Easy to see that in the "healthy right leg the   isometric  muscle contraction quality allows  an initial compression outflow  of tHb followed by  an arterial occlusion due to a  good  contraction force  ( quality ) Than at relaxation  a  back flow  of blood into the test area  with some overflow  as a typical occlusion trend reaction.. The  contraction quality  was  so good , that we never  had a moment of  a short venous occlusion pooling. 
The  ops  leg left  shows as well the initial  outflow  compression tHb reaction but then a  much less   quality  contraction  which lead sot a venous  occlusion ( outflow restriction ) with a   " tremor  "  and not  a great  hard   contraction sign , followed   at relaxation by a  tHb  drop as a  feedback of a pooling outflow.

Here a  second  example.
 Squatting  done by an extreme endurance athlete  and a strength athlete in Santa Monica  ( Red bull seminar) including  blood  test( I stat ) .

Blood values  and strenght.jpg



L
eft is  endurance athlete  three squatting  right is  a  strength athlete. The EtCO2  was tested  after  the  loads  and represents  the highest value  which showed  up  30 - 60 seconds  post workout.( Emma  capnometer used )
Blood was taken immediately  at the end of  the load.
O2  %  =  SpO2  sensor  taken    after the load  and is the lowest value  we  were reading.

And hre a  super interesting   real  action  results  on snow.(  Swiss ski athlete gold medal winner in Sochi  tested  and assessed  by Andri  in Zermatt  switzerland )

I  show  just one relevante feedback in  connection with this  discussion.  The athlete  had a severe complex  knee surgery   prior. Look at the  tHb   trace  and " contraction "  quality  and   try to   guess which  brown is the operated leg  and why ?

Here  a load  during a  training  run in a   fast corner at the  start  ( fresh)


r closer look 2    push off thb.jpg 



Now here  somewhat  later in the test  run. Explain  for yourself  what you may see in  contraction quality between the  2  legs .


r closer look 3    push off thb.jpg

Kirill

Development Team Member
Registered:
Posts: 93
 #24 
Another example "muscle tremors" and SmO2 

see 0:40 MOxy Phantom Chair.mp4 www.youtube.com/watch?v=xcNYhZ1GlS8

When I say "squats in a shortened amplitude without muscle relaxation," I mean what's shown in this video:

Kirill

Development Team Member
Registered:
Posts: 93
 #25 
Returning to the kinetics of creatine phosphate. In my opinion, useful information for building a model that occurs in the muscles

Cross bridges account for only 20% of total ATP consumption during submaximal isometric contraction in mouse fast-twitch skeletal muscle

http://ajpcell.physiology.org/content/291/1/C147.long

Shi-Jin Zhang, Daniel C. Andersson, Marie E. Sandström, Håkan Westerblad, Abram Katz

It is generally believed that cross bridges account for >50% of the total ATP consumed by skeletal muscle during contraction. We investigated the effect of N-benzyl-p-toluene sulfonamide (BTS), an inhibitor of myosin ATPase, on muscle force production and energy metabolism under near-physiological conditions (50-Hz stimulation frequency at 30°C results in 35% of maximal force). Extensor digitorum longus muscles from mice were isolated and stimulated to perform continuous isometric tetanic contractions. Metabolites of energy metabolism were analyzed with fluorometric techniques. ATP turnover was estimated from the changes in phosphocreatine (PCr), ATP, and lactate (−2ΔATP − ΔPCr + [1.5Δlactate]). During contractions (2–10 s), BTS decreased force production to ∼5% of control. Under these conditions, BTS inhibited ATP turnover by only 18–25%. ATP turnover decreased markedly and similarly with and without BTS as the duration of contraction progressed. In conclusion, cross bridges (i.e., actomyosin ATPase) account for only a small fraction (∼20%) of the ATP consumption during contraction in mouse fast-twitch skeletal muscle under near-physiological conditions, suggesting that ion pumping is the major energy-consuming process.

Muscle metabolic responses to exercise above and below the “critical power” assessed using 31P-MRS

Andrew M. Jones, Daryl P. Wilkerson, Fred DiMenna, Jonathan Fulford, David C. Poole

Muscle phosphocreatine concentration ([PCr]) responses to <CP (•) and >CP (○) knee-extension exercise
http://ajpregu.physiology.org/content/294/2/R585

F2.medium.gif 


Typical kinetics of oxyhemoglobin/myoglobin (Hb/MbO2) level and PCr concentration during resting metabolic rate measurements. Sample recordings are shown from 1 subject for RMRmus determination. Tracings of Hb/MbO2 and PCr measured by NIRcws and 31P-MRS, respectively, are shown during arterial occlusion. This ischemic condition caused an immediate decline in Hb/MbO2, which plateaued ∼5 min after the start of occlusion. At this point, PCr began to decline linearly, which continued until the end of the 15 min of arterial occlusion.S R, slope at rest; OD, optical density.
http://jap.physiology.org/content/90/1/338.long

F3.medium.gif 



juergfeldmann

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 #26 
Nice feedback and great for us  after all this years  to have some accepted  studies   showing the validity  of  NIRS  and  why we do what we do Here the discussion which is  super interesting as well.

The next  step we hope  we will see is  more confirmation in  what we  term limiter and  compensator idea  and how NIRS  combined  with up to date physiological ideas  can  ,as we  do , guide   coaches and athletes in a very new  direction of  physiological guided  workouts  versus  performance guided  workouts. 
 This is the start  of the end  of training zoning as we know it . ????? This is the start of  live feedback  training intensity control as we  go  a long.
  

DISCUSSION

RMRmus measurements.

Measuring RMRmus accurately was one of the most important parts of this study for estimating the absolute values ofV˙o 2NIR(30). Blei et al. (4) and Hamaoka et al. (12) reported that the resting PCr breakdown rate after the complete depletion of muscle O2 stores by arterial occlusion at rest reflected RMRmus. In this study, as in previous studies, there were no changes in intramuscular pH and ATP concentration along with no O2utilization during RMRmus measurements. Because the contribution of the glycolysis to the PCr synthesis was negligible at rest (8), it is reasonable to conclude that the PCr breakdown rate after O2 depletion reflects RMRmus (Fig. 3). The average value of RMRmus in this study was 0.0076 mM ATP/s, which is similar to both 0.008 and 0.0073 mM ATP/s previously measured by31P-MRS (412). This result is also comparable to the value of 6.3 μmol · min−1 · 100 ml−1 measured invasively (17).

Validity of NIRcws measurement.

Several studies have shown that the Q values measured by31P-MRS reflect the rate of oxidative ATP production (6161721). The high correlation between Q(30) measured by 31P-MRS andV˙o2NIR(30) measured by NIRcws under the same conditions demonstrates the validity of NIRcws as a quantitative measurement of muscle O2 consumption. Several studies have used NIRcws to estimate oxidative metabolism (101218), and one study correlated NIRcws with a standard invasive measurement (18). To the best of our knowledge, this is the first study to show the validity of the quantitative values of V˙o 2NIR measured by NIRcws. The muscle oxidative ATP production rates obtained in this study [Q(30)] ranged between 0.041 and 0.209 mM ATP/s, which correspond to between 5.6- and 28.2-fold higher than the RMRmus. The initial Q for PCr ranged between 0.067 and 0.341 mM ATP/s. The intramuscular pH at the end of exercise ranged between 6.37 and 6.96. The wide range of these parameters would suggest the effectiveness of NIRcws measurements for evaluating muscle oxidative metabolic rates at various metabolic levels. To look into the wide range of the metabolic rates, we used different muscle loads. The possible reason of why different metabolic rates were obtained at the given intensity was the varying physiological and metabolic properties in the individuals. Blei et al. (4) reported that the average Q following fully excited muscle contraction was 0.28 mM ATP/s. Hartling et al. (17) reported that forearm O2uptake during maximal forearm dynamic exercise was 201 ± 56 μmol · min−1 · 100 ml−1, which is equivalent to 0.2 mM ATP/s (17). In this study, Q values from the three subjects were equivalent or higher than the values measured by Blei et al. (4) and Hartling et al. (17). This result indicates that the finger flexor muscles, which served as the measurement site in this study, were maximally activated in some cases and confirms the feasibility of the measurement of maximum muscle O2 consumption by NIRcws.

Advantages and limitations in measurements.

NIRcws has several advantages as a method of evaluating muscle oxidative metabolic rates compared with 31P-MRS measurements, which are currently held to be the gold standard. First, the portability of NIRcws allows it to be used anywhere it is needed. This characteristic allow for more opportunity to examine both clinical and nonclinical (experimental) aspects of energy metabolism. Second, NIRcws has a higher sensitivity to changes in muscle metabolism because NIRcws is a more direct measurement of the changes in O2content compared with the indirect measurement made by31P-MRS. In other words, NIRcws can be applied for measuring muscle oxidative metabolism even in the case where there is a lack of a significant decrease in PCr such as very low-intensity exercise. Third, NIRcws has a higher time resolution than31P-MRS in the measurements of muscle oxidative metabolic rates. The time resolution of NIRcws used in our study was 1.5 s; however, improvements in technology have increased the time resolution to 0.1 s. On the other hand, the time resolution for one data point by 31P-MRS in our study was 10 s, which was the same or even higher than the other studies (425), although there were some studies in which 31P-MRS was able to be measured every 1 s (5). Furthermore, to measure muscle oxidative ATP production rate using 31P-MRS, the postexercise Q has to be determined. When the rate constant of PCr recovery is used to calculate Q, PCr kinetics postexercise has to be monitored for at least 5 min (42125-27). Some studies achieved a much better time resolution in which the initial Q values were measured directly from the changes in PCr concentrations between successive time points (520); however, it was pointed out that obvious random error occurred in the case of Q calculated in 10 s following exercise (5). Furthermore, it was suggested that a solution to this error would be to use a window of PCr resynthesis wider than 10 s during recovery because it would provide greater signal-to-noise ratio (5). In other words, the ideal condition is essential to calculate the oxidative metabolic rate within 10 s following exercise using 31P-MRS. In our setup, better reproducible results of the rate of PCr resynthesis were obtained when the rate constant of PCr recovery was used rather than when the changes in PCr concentrations between successive time points were used. On the other hand, as already shown in this paper, NIRcws takes 6 s and would take even shorter when NIRcws with a higher time resolution are used.

Although there was a significant correlation between NIRcws and31P-MRS measurements, the average value ofV˙o 2NIR(30) measured by NIRcws (0.092 ± 0.051 mM ATP/s) was smaller than the average value of Q(30) (0.113 ± 0.052 mM ATP/s) measured by 31P-MRS (P < 0.001). One possible explanation for this is the technical limitation of the NIRcws equipment used in this study. The declining rate of Hb/MbO2gradually decreased with time during postexercise arterial occlusion (Fig. 5). Four consecutive data points (6 s) were required to obtain the regression line for the rate of Hb/MbO2 decline in the postexercise measurements. If the slope was calculated using two data points, the slope would be steeper and less valid. To overcome this possible underestimation, it is necessary to develop NIRcws with a higher time resolution that can be used in validity studies along with31P-MRS. Another possible reason for the underestimation inV˙o 2NIRis that the arterial occlusion was initiated when the Hb/MbO2 level was extremely low. To avoid this, in this study, theV˙o 2NIR was measured 30 s after the cessation of exercise so that Hb/MbO2levels would have fully recovered to resting levels by this time.

In conclusion, the high correlation between NIRcws and31P-MRS measurements supports the validity of the quantitative evaluation of skeletal muscle oxidative metabolic rate using NIRcws. Therefore, NIRcws can be used as a valid method for quantitatively measuring exercising muscle metabolism , and its portability and accessibility make it a useful alternative.

Acknowledgments

We acknowledge the help of Kelly McGrath and Toshio Kimura in writing the English manuscript.

Footnotes

Andri

Fortiori Design LLC
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Posts: 65
 #27 

Let’s look at this graph that Kirill posted, which helps us understand our logic, and hopefully also the success we have seen using NIRS for HIIT. Now, what still stands, as Kirill nicely highlighted earlier, there is always a concern about muscle and tissue heterogeneity, but also about how different muscle tissue interact with one another bioenergetically (consider lactate shuttle theory). In the graph, we see that PCr and muscle oxygenation data as gathered by NIRS stand in some relation to on anther. Something that is also know is that the higher the intensity of the muscle work the greater the difference in muscle re-oxygenation and PCr recovery. This is very important in strength work for example. If we look at the graph it can help us understand the following points:

  1.  that the further and longer we deoxygenate the further PCr stores drop (better said slower replenishment)
  2. Keeping deoxygenation intervals shorter I more likely to keep PCr stores/replenishment intact

Therefore, as proposed by the Moxy HIIT trainings, intervals like the desat-resat SIT, should not maintain low levels of deoxygenation, and therefore should be more likely to keep PCr intact, and therefore making the time frames offered by SmO2 more rebust. This also holds true for a submax gradual desat. Where we run into problems is with an extended desat. Protocol where we really push low SmO2 levels. Here it is very likely, and in practice you will see this quickly, pure muscle re-oxygenation does not work to assess recovery. While several factors can be the reason for this, the graph can help us add to these reasons, PCr is just not recovered. 




F3.medium.gif

Kirill

Development Team Member
Registered:
Posts: 93
 #28 
[6bf4fb1ef2af4d04a9c2f72c2e2c6456]

The Time Course of Phosphorylcreatine Resynthesis during Recovery of the Quadriceps Muscle in Man 1976 R. C. HARRIS 1, R. H. T. EDWARDS 2, E. HULTMAN 3., L.-O. NORDESJO 4, B. NYLIND 5, and K. SAHLIN 1 




AND from http://jap.physiology.org/content/90/1/338.long



[image] 
Andri

Fortiori Design LLC
Registered:
Posts: 65
 #29 
Thanks Kirill for presenting the data. Did you want to comment for the group?
Kirill

Development Team Member
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Posts: 93
 #30 

Personally for me it is an illustration of the fact that anaerobic glycolysis or doesn't take part in resynthesis of a PHOSPHOCREATINE, or its power is very small, or he resynthesis only ATP directly.

And it is very evident pictures for understanding of extreme importance of delivery and consumption of oxygen for resynthesis of PHOSPHOCREATINE and ATP.

And why to a Moxy is the magic device for an assessment of metabolic processes in muscles.

In the 2 picture reflects that when in the middle of PHOSPHOCREATINE restoration blocked a blood stream the complete recovery PHOSPHOCREATINE came from the oxygen taken from a myoglobin.

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