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Andri

Fortiori Design LLC
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 #1 

In a review by de Salles et al (2009) titled "Rest intervals between sets in strength training" an review of 35 studies was made looking at the effect of rest intervals on different strength components. The investigation clearly demonstrates that recovery between sets is defining factor into the results of a strength training, and should be considered to the same degree of importance as the exercise and intensity itself. The question is how to control recovery, as most recovery protocols are based on non-physiological time duration, that are not individually specific. This is where Moxy can fill the gap very nicely. Moxy can at an individual basis determine recovery of oxygen levels following a strength set. The question then is how to determine rest periods using the Moxy. Well for this an ebook will be published in the foreseeable future but here are a few things to think about. A paper by Haseler et al. (1999) show that sub-maximal efforts illustrate a highly similar curve for PCr recovery and oxygenated hemoglobin recovery and therefore state that during sub-maximal efforts PCr recovery under normoxic conditions is limited to oxygen recovery. Considering this for all endurance strength protocols, rest periods should be in tune with oxygenation recovery in the muscle. Considering this recovery rate, and data that determines long rest periods between strength endurance sets do not yield greater strength endurance gains a very clear cut approach to a strength endurance recovery protocol is laid out. Using a Moxy a strength endurance protocol would demand SmO2 recovery to baseline value no longer or shorter. This guarantees individualphysiological based recovery for a strength endurance training. In a following post I will talk quickly about maximum strength training as this requires some variation. 


Andri

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 #2 
As mentioned in the previous post, submaximal effort show a near identical trend in PCr recvoery and oxyhemoglobin recovery leading to the statement that "oxy-hemoglobin recovery is rate limiting for ATP synthesis, evaluated as the rate of PCr recovery after sub-maximal exercise" (Hanada et al. 2000). Considering this SmO2 would then be an excellent parameter to determine recovery between sub-maximal strength effort during strength training. However, maximum efforts appear to be somewhat different as described by McCully et al. (1994) in the paper titled "Simultaneous in vivo measurements of HbO2 saturation and PCr kinetics after exercise in normal humans". The recovery rate of PCr is dependent on some other factors, one for example, as McCully points out, is pH. With decreasing pH the recovery time for PCr increases. Now, with the hb dissociation curve shifting to the right with increasing pH it is also true that oxygen unloading is done more readily and therefore recovery time increases as well. However, in McCully's investigation the recovery of PCr was still greater during maximal efforts and decreasing pH than o2hb recovery. What this means at a practical level for strength training is that a recovery following a maximal effort, to then complete another set of maximal effort, requires not only SmO2 recovery which is related to PCr recovery even at maximum efforts, an actual extended recovery beyond SmO2 recovery is needed. Using the Moxy we have titled this a super or enhanced recovery protocol.
Juerg Feldmann

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 #3 
The recovery rate of PCr is dependent on some other factors, one for example, as McCully points out, is pH.
pH is  influenced  by the accumulation of  H +. H +  is not all that bad. It is  as pointed out  by Lennartz nearly 50 years ago H +  may be the  one  protector  to avoid a  drop of ATP below a critical level.
 So  one of the keys of recovery is the  ability to maintain  or  recover  from a H+  dysbalance.  The one way of H + buffer is over  lactate  ( MCT) protein , as well as over respiration  ( CO2 release.) What we see in ice hockey loads  and testing. The better the respiration the faster the recovery of SmO2  and the faster  a SmO2 overshoot. If you can breathe efficient 150 L VE  that is not bad , if you can breathe 250 L VE than 150 L feels like nothing.
Andri

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 #4 
I completely agree. The idea is that PCr recovery is related to oxygenation, but other factors play a role. O2 intake and consumption is closely linked to CO2 production and output. The fact that the ability or lack of ability to release CO2 will then effect O2 intake and consumption due to the Hb dissociaiton curve, in conjunciton with a shifting pH shows how the entire system is related. Therefore as you explained; proper SmO2 recovery is a great  indicator of recovery following strength efforts, and nicely illustrates what we can do to achieve a greater capacity for recovery.

Juerg Feldmann

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 #5 
Here  some interesting add ons.
  A great  study  looking at the different  reactions of  load  and recovery. As you can see in the list  , it is a great study  but  for  most of  the coaches  and personal trainers  it will be a great study  with very little practical applications , as there  is  or better was  now way on assessing the recovery  besides  feeling  and  certain experience.
 Now  with MOXY we  actually have a tool  to assess depth of load  as well  duration of recovery  in strength training  but as well for interval  and  acyclic  sports like  Ice hockey  and so on.

CrP  and SmO2.jpg 


One  big part of recovery is the  bio availability of O2  and as  such the normalization of the  CO2 level  as well as the pH  and so on.

Here some thoughts on that  situation
 The  picture  shows you the ability to maintain a certain performance, when we  where allowing the body to get rid  of CO2  and as  such  H + buffer help.
  First we inhibited the  CO2  release  than we allowed  a proper  CO2  release.
 The case study  was  done  by Nick Mc Lean a  graduate  of the University of Kelowna  satellite of  UBC  Masters program.
He did some one leg  squatting  to  subjective  exhaustion.
Red is  accumulation of H +  and  not allowing to get rid of CO2
  Blue is free  release of  CO2.
 Red where 8  single leg  squatting, Blue  where  31  single   leg squatting


r leg spiro.jpg 


There seems to be a direct  connection between  SmO2  trends,  O2  Diss  curve  and  recovery . And therefor as well a  possible  nice  ability to use  NIRS/Moxy  for   individual training for load  and recovery.

There as well seems to be a critical  CO2  concentration and timing  where  we  will see a  change in SmO2  reaction.
 The following picture is a   case study   sent to use  By Jiri  and his  great  team in Prag.
  It shows   the CO2  levels and the  reaction in this case of O2  release  SmO2  drop during a  6 min step test, where  the first 3 min in each step the client was breathing so called " normal'  and the second  3 min in each step   he was  or she was asked  to breathe   intense  and more VE.

Jili CO2 Smo2.jpg 

Grey is the trend  in CO2 levels, step length where 6 min  on a bike  3 min  "normal " respiration  followed  by the same  load  but 3 min  intense respiration.
Dark green is vastus lateralis  SmO2 trend, light green is  SmO2 trapezius  trend.

Here  another one 

Pospisilova. co2  smo2.jpg

Grey  CO2. Dark green  Trapezius  and light green  is  quadriceps Trends.    I will follow  up with some critical questions concerning some traditional ideas on "cool downs  " and recovery   markers.

Andri

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 #6 

These are the same trends I have seen collecting data. The rationality problem I have had, and discussed with others is the inability to untangle co2 increase with a decrease in oxygen uptake. For example if I inhibit CO2 release by holding my breath or slowing exhalation down dramatically, and then do a resistance exercise is the variation in SmO2 a result of an increase and CO2 (thereby change in Hb dissociation curve), or is the impeded oxygen uptake effecting the curve. This would be the same with any respiratory manipulation, somehow decoupling CO2 change with oxygenation change; if this is possible. I hope the position I am making is understandable. Anyways, in order to look at this more closely, as it was a concern, we did a short study that attempted to, very simply, illustrate the difference in oxygenation with changing CO2 values. I attached a PDF of the study abstract. The data nicely shows that change in respiratory manipulation will significantly effect SmO2.

 
Attached Files
pdf abstract.forum.pdf (97.92 KB, 106 views)

Juerg Feldmann

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 #7 
For the regular advanced  MOXY user   you can try the   respiration idea  to shift   SmO2  towards increase  or decrease  as well by doing hypocapnia  work instead like in this  study above  hypercapnia  work. In many cases it is easier     than holding your breath  for 60 sec.  You simple  have to hyperventilate  and  see how  SmO2  may  be reacting.
Juerg Feldmann

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 #8 
Got some great feedback's  from strength coaches  and   game sport coaches  as they use  MOXY  for   interval and strength e=sets  fro the recovery in between.
 Here again  some paper  to have  all in one place.
 Here  a  nice  picture  to show you  that when you do the same  idea  60 - 90 seconds  hard load  with this three groups  you will see a basically identical trend in SmO2  recovery as you can see here in PCr. recovery  trends  in Crp.jpg      recovery.

 So you can see , why for   out of the "classical ' box thinking  coaches  a  MOXY is a   great tool  for live feedback on recovery   and load  planning.  It is not anymore a  question of time but a  question , whether   we keep up  with fitness centers  who understand  that they increase motivation and quality of  workouts  under the title individual  training  by simply  using MOXY on their customers during workouts  and they can see that on a TV screen like Fred is doing it in Halifax.

Juerg Feldmann

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 #9 
And here an additional nice feedback, that we have more an more support for our crazy ideas.
 As  so often mentioned, that " classical ' idea  of ATP/CrP/ glucose  as  energy  path way has to be reviewed. Here a great   study showing  the surprise of the group , that O2  is involved  from the beginning in sprinting  and a Wingate  test.
 It  is as well an additional  explanation I gave  in another  section on , why  sometimes    clients  drop SmO2  nicely but than in an endurance  test not.
 It is  all about muscle mass  and deliver  and timing to  get  delivery going  as well. here to enjoy


Sports Med. 1997 Nov;24(5):308-20.

Determinants of oxygen uptake. Implications for exercise testing.

Poole DC1, Richardson RS.

Author information

  • 1Department of Kinesiology, Kansas State University, Manhattan, USA. poole@vet.ksu.edu

Abstract

For exercise modalities such as cycling which recruit a substantial muscle mass, muscle oxygen uptake (VO2) is the primary determinant of pulmonary VO2. Indeed, the kinetic complexities of pulmonary VO2 associated with exercise onset and the non-steady state of heavy (> lactate threshold) and severe [> asymptote of power-time relationship for high intensity exercise (W)] exercise reproduce with close temporal and quantitative fidelity those occurring across the exercising muscles. For moderate (< lactate threshold) exercise and also rapidly incremental work tests, pulmonary (and muscle) VO2 increases as a linear function of work rate (approximately equal to 9 to 11 ml O2/W/min) in accordance with theoretical determinations of muscle efficiency (approximately equal to 30%). In contrast, for constant load exercise performed in the heavy and severe domains, a slow component of the VO2 response is manifest and pulmonary and muscle VO2 increase as a function of time as well as work rate beyond the initial transient associated with exercise onset. In these instances, muscle efficiency is reduced as the VO2 cost per unit of work becomes elevated, and in the severe domain, this VO2 slow component drives VO2 to its maximum and fatigue ensues rapidly. At pulmonary maximum oxygen uptake (VO2max) during cycling, the maximal cardiac output places a low limiting ceiling on peak muscle blood flow, O2 delivery and thus muscle VO2. However, when the exercise is designed to recruit a smaller muscle mass (e.g. leg extensors, 2 to 3kg), mass-specific muscle blood flow and VO2 at maximal exercise are 2 to 3 times higher than during conventional cycling. consequently, for any exercise which recruits more than approximately equal to 5 to 6kg of muscle at pulmonary VO2max, there exists a mitochondrial or VO2 reserve capacity within the exercising muscles which cannot be accessed due to oxygen delivery limitations. ### The implications of these latter findings relate to the design of exercise tests. Specifically, if the purpose of exercise testing is to evaluate the oxidative capacity of a small muscle mass (< 5 to 6kg), the testing procedure should be designed to restrict the exercise to those muscles so that a central (cardiac output, muscle O2 delivery) limitation is not invoked. It must be appreciated that exercise which recruits a greater muscle mass will not stress the maximum mass-specific muscle blood flow and VO2 but rather the integration of central (cardiorespiratory) and peripheral (muscle O2 diffusing capacity) limitations.

 

 

###  This is not just  because of limited  muscle mass versus  big muscle mass but as well   when we have limited  delivery of  O2 like in a start  and  where we have a  big delivery situation  like at the end  or  explained  after eccentric  muscle loads

 

Andri

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 #10 
We are back to basic VO2 which is a function of both delivery (cardiac output) and and supply or arterio-venous difference (pulmonary loading ability and muscle utilization ability).

Therefore all of these parameters can limit local muscle performance. To follow up on Juergs last comment about muscle mass as mentioned in the paper, I would argue this is relative as Juerg aims to point out I believe. The size of the muscle that needs to be so called restricted is dependent on the ability to supply. A greater supply system can maintain a larger muscle mass with a "maximum VO2"; or a poor muscle mass can be maintained by a smaller supply as well. This is the balance between O2 demand and supply Moxy attempts to make people aware of during live athletics, and not in the laboratory. 
Juerg Feldmann

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 #11 

Thanks  for  all the additional   info's.
 I like to show  some intriguing  pictures  to    motivate  strength coaches  and  coaches, who use MOXY  to   design interval workouts how  and why  we use SmO2    the  way we suggest.
 1. Remember  :
 I  " hate" when research is designed  on  time  and or  performance but it is  what it is. The problem is , that we create a cookbook by forcing  physiological reaction into a   protocol  so the  physiology  often can't react accordingly.
  So here what I mean with this  and why  we use  individual feed backs  rather  than timing. The timing  and performance is used  to see  progress in absolute   numbers, the  physiology is here  to create this performance improvement.
 Here the recovery study I showed  before.
recovery  trends  in Crp.jpg 

 Now  we have here  three groups  of  clients  who where tested.  I think it is  fair to assume, that the Elite athlete  is in better   " shape  " than the overweight person.
 So a  90 second all out load  is as well  hard  for an elite athlete  and there is no  way  he can sustain this all out  in the way of a  stable performance. If he goes all out he will in  15 +- seconds  start to loos e dramatically performance . Now  if I repeat  this a few  times  with not optimal recovery in between ,I create  with  a top athlete a  picture like we see in a beginner in a  too long single overload .
 Now the same  will be the case  for  an overweight  client untrained  somewhat faster loss  of   top load , if he  actually can create  top load.
 But for sure  90- seconds  is a  very very hard  task  for an untrained  person.
 The second part is  muscle  contraction quality. A  top athlete is used  and trains  to have a very great intra  muscular coordination , a  untrained person not  at all  so the contraction quality will be not here. (  so  in top athletes  we   may see not just a compression (tHb  drop ) but  possibly as well a  venous  and perhaps  depending on the discipline  we  do this 90 seconds  an arterial occlusion.
 So no inflow no   outflow  and as  such  a  better   or  more needed  " survival'  energy  from  PCr.
.
 Now here  an internal study I like to show in this  discussion.
 We did this in  Ft. Bragg with the  USA  Army. We  " changed  a top athlete   to an  " overweight " persons  reaction !!!

3 stes  smo2  like  Crp.jpg 
SmO2  trend of a  30 second  all out load  by the same  athlete   just three in a row.
 Now look below.
overlap  smo2  CrP.jpg

We  " create the three  categories  in one   person really. So  just because  we  have a top athlete  " recovering fast  and  an untrained  not does not mean   that this is ail ways  the case. In fact SmO2  is used  to  decide , when we like to quite  a load  and how long we like to rest  in between loads.

 In fact  when we load  an untrained  person hard but much much shorter time  we see as  well a fast increase in SmO2  and CrP  after one load.
    Now   why is this . Because as  Andri pointed out it is all about energy   so delivery  and utilization.
.
 And this is  depending on the ability  after one load  to  again try to deliver  and try to utilize.
  So here  a  closer look in our  example on the delivery section , tHb  as  so many time mentioned  is  a great indication of delivery.
 So same three loads    with a view  on how  the delivery reacted  during  and after the    all out performance.
3 sets  thb   like  15 Crp.jpg


And below  delivery and utilization  together  and you can see how the " quality of the contraction " changed  over  time . The question is  now  , how do we plan this  situation.
  Can we really  just take a  time  and  design an interval or strength workout  and than have  10 people use the same   template of a workout  . Than  can we expect the same end result based on this type of a   workout. ??
 Or  do we  better look at  physiological feed backs    and therefor  may have a beginner workout  15  seconds  all out  and a top athlete  45  seconds   and both may set the same stimulus  just on a very different performance level. Or    if both workout  45  seconds  is the beginner really stimulating the same  physiological  responds  than the top athlete ? 
 You give the answer .

Juerg Feldmann

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 #12 
I got  some mails  with the question : What is the practical application of the information.
 Here some ideas.
 . SmO2    and if you use  a  high definition  peripedal  screen  for short loads  off 3 min will allow you  live ( practical  to decide, whether you reach your  goal  you have  set for the workout.
 Goals  could be :
 a).  muscle contraction intensity so that we still maintain in  and outflow.
b)  intensity , where you like to maintain inflow   but  reduce  outflow.
 c) intensity  where you like to  stop in and outflow.
 This  would be  controlled over tHb  feedback.

 If you like to use  SmO2  only   you could have the following goal setting.
 1.  Reload  once you reach  calibrated  baseline.
2. Incomplete recovery so  you load before  SmO2  reaches  baseline.
 3. Over compensation  so you load  when you reach the highest value  after  the   calibration base line.

4. You  wait till your overcompensation is back to calibration baseline.
This  type of workouts  can  be done as well with a Garmin watch  and you simply use  the HR  mode  and alarm  for  upper and lower  HR limits    with MOXY by changing the MOXY on the MOXY app to a HR  monitor    version. ( Do not forget  that the SmO2  number  will now have a  1  in font  so 135 SmO2  means  really 35  % SmO2.

 Here  2 examples  and you    move  it into what  the coaches  tried  to achieve  or  how they guided  the ,l load.  It is both  form a swimming workout in the water.
3  loads SmO2    decrease  low end.jpg

swim ipahr.jpg


 

Juerg Feldmann

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 #13 

some answers or feed backs to postings on here 20.04 and the 2 additional once. But first wow thanks to come back on this old postings, which shows me, that many people actually work through my mess here and read it very critical . Thanks so much. 1> The graphs in the post , where we show CO2 ( ETCO2 reaction and SmO2 reaction. The question I got is a very great one. In the post we wrote, that the client was breathing normally at the start 6 min followed by a very intense breathing. So the clear question is : Would intense breathing , not create the opposite meaning EtCO2 would drop so hypocapnia so less CO2 and shift to the left by the O2 diss curve and as such a higher increase of SmO2 and not a drop? Absolutely great question. Now the possible answer or thoughts for a discussion will in the same time take one of our own case studies apart and will show how easy we get caught up in some fixed or less good ideas. Here my part to this discussion. a) the same problem in the study. If we measure SmO2 we test in the muscle , where all may take place. When we use SpO2 we test in the arterial blood where it may take place or has taken place. and if wee test EtCO2 we test far away from where all took place. So different locations and therefor different time lags. EtCO2 is not always Pa or PA CO2. it takes some time to have a balanced EtCO2 close to a PA and Pa CO2. And this only can be achieved in resting or very low intensity motions, otherwise it iss off. So the situation had a stable CO2 over the full time but not a stable and clear difference in SmO2 in the 2 situation can reflect my above statement. The change in SmO2 takes place, when we have a change locally of H + and CO2. and not because we have in the expired air a high CO2., I can breath in a bag in and out till I have a high CO2 in that bag. I close the bag and now I inspire the bag volume in so I have a high EtCO2 not caused by activity but by using this bag. So Emma will show a high EtCO2 but there is no change in SmO2. ( Or if there is one it takes a relative long time.) . Now the CO2 reaction in the 6 min step test. Hard breathing ? You can breath very fast and optically hard and you may show a low EtCO2 in Emma or capnometer , but you may actually have a high CO2 in the blood and muscles. There is a difference between hyper ventilation and hyper respiration. Hyper ventilation means you breath more or you ventilate more than needed , so you actually ventilate the lungs as a whole and you will create a hypocapnic situation and CO2 is therefor down with all the not optimal feelings coming from this. On the other side you can hyper respirate, meaning you breath far too fast but not deep enough so you move mainly dead space and not a lot from the actual air in the gas exchanged area . So lots of O2 and little CO2 is in the expired air and it appears they are hypocapnic , when in fact CO2 wila accumulate in the blood and muscle. To be sure people breath the way you like to have them in connection with CO2 you have to check not just RF but as well TV ( tidal volume.) This is what you see as well in people with a respiratory limitation. They may show aN increase in VE and as such create a so called Ventilaory threshold, which compnies, who use gas exchnage use as lactate threshold as it seems lactate threshold is what we can sell. So in this case RF may go up but TV may drop due to an actual muscle weakness and they in fact may have a decent looking EtCO2 but may have a very high CO2 collection in blood and muscles and a very strong drop in SmO2. On the other side people who use respiration as a compensator may as well show a ventilator threshold where VE suddently goes up, but this time not as a limitation of the respiration but rather as a compensation with respiration. So RF will go up as well but they as well will increase TV so VE makes this threshold as well but this time this reaction will prolonge the performance as this athletes can balance H + much longer. These athletes as well will show higher lactate values. You can do this easy as a test and you can show how lacatate at the same load is very very different. In fact you can have a relative high lactate level and you start breathing slow and deep to collect more CO2 and you will see a drop in SmO2 but as well a drop in lactate.??? So in one case ( which one? the VT may look like LT, if we believe in LT and in the other not at all. That's why we see studies rejecting the VT = LT or some who argue there are responders and nonresponders. ????' Summary: The information we often get on the TV when an athlete is going through the finish line ( often inc cross country skiing and rowing ) and they collapse and breath really really hard , they do NOT hyper ventilate, they actually are hypo ventilating at the particular moment and they have to stop moving to try as a priority to get rid of CO2 . So if they could breath much more they would be much faster normocapanic but they are

after the finish very high hyper capnic which allows them to breath very hard and not get dizzy but better, in contrast if they would hyperventilate. This athletes show a drop in SmO2 after the finish line ( rings a bell ) and it will change to an increase in SmO2 as soon they are ???????) This same athletes as well show a low SpO2 after the finish line which will get corrected as soon they ?????? ) So now search for some studies with EIAH exercise induced arterial hypoxia. How could we name it as well perhaps EI A H and H would stand for ????? In tis athletes how would a TIP look like in connection with SmO

Kirill

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 #14 
1) The rapid kinetics of smo2 is not yet a fact that will always reflect the "best athlete". A runner at medium distances with the largest VO2MAX (We omit that that VO2MAX a bad indicator of qualification) can have a more !prolonged! recovery. Similar data, that the higher the VO2MAX the longer the recovery was found for people with pathology of the heart and lungs. https://www.ncbi.nlm.nih.gov/pubmed/23604001

2) These averaged curves of resynthesis of creatine phosphate can not be used! It is necessary to take data where they look separately for recovery in type 1, in type 2A, type 2B. And in untrained people in 2B recovery can take up to 20 minutes.


Therefore, since typical strength training only develops type 2B. In the best case, another 2A hypertrophy, the recovery of which is also very slow, and is practically not noticeable on the curve of smo2, in this case it is necessary to focus on the restoration of repetitions, on the rate of increase in working weights month to month. And here the minimum is about 5 minutes, and the top lifters (deadlift/squat 250-300 kg+) should use 10 or more minutes, even 20. Remember Paul Anderson, I read that his rest was up to an hour.

Only if you train slow muscle fibers you can focus on reoxygenation, if you break its recovery, do not give enough rest then it leads to trauma.


https://www.researchgate.net/figure/49711638_fig6_Representative-kinetics-of-creatine-phosphate-CrP-recovery-in-subjects-with-different

Representative-kinetics-of-creatine-phosphate-CrP-recovery-in-subjects-with-different.png 

Andri

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 #15 

 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. However, It is clear that understanding how and what type of physiology generates the best performance for a given sport will help guide training and enhance chances of successful training outcomes.

About the remaining assertions made about the difficulty understanding physiology, and what you would I assume identify as a contradicting statement (largest VO2 max elite runner has a prolonged recovery, as do pathological heart lung patients). Firstly, I think there is a misunderstanding about what Moxy measures. Moxy, as stated above does not measure good or bad, it measures real-time oxygen supply and demand relationships. We see similar trends and curves in people with very different physiological parameters (age, sex, training status, etc.). Why? Simply, oxygen supply and demand is an individual response that can go either way, the difference is how and when does the relationship change. Let’s take your example of the elite runner. If this elite runner shows a prolonged O2 recovery meaning, he in simplified terms is having trouble recovering from the much higher O2 demand than supply. This can be true for the exact same reasons for your identified lung or heart patient, in that his supply is having trouble recovering from the high demand (again simplified). In both cases, they are having problems with the supply side of the equations, the difference is the performance output being yielded by the physiology. In essence your elite runner is a heart/lung limited performer at a really high level, whereas your heart and lung patients is a heart/lung limited performer at a really low level. This is how we understand limitations.

Quick side note; SmO2 recovery dynamics is a result of many different factors, and even though it is a contradiction to your presented data (or might be, I don’t think it is), we see the longest recovery delays in high level power athletes that exert themselves maximally for an extended period of time. Summary, the way you test or protocol you run effects data.

Below, for all those interested is the abstract from the article Kirill mentions in his first point; and I added another one that contradicts that statement.

Slower recovery rate of muscle oxygenation after sprint exercise in long-distance runners compared with that in sprinters and healthy controls.

Nagasawa T1.

Author information

Abstract

The purpose of this study was to examine whether differences in aerobic capacity and training status influence muscle reoxygenation after sprint exercise. We hypothesized that the muscle reoxygenation rate after sprint exercise is slower in long-distance runners with a high aerobic capacity. Five male long-distance runners, 5 male sprinters, and 6 healthy male controls performed a 30-second sprint exercise on a cycle ergometer. Oxygen saturation in muscle tissue (StO2) in the vastus lateralis muscles was measured by near-infrared spectroscopy. The muscle reoxygenation rate after the exercise was evaluated at half the time required for StO2 recovery (T1/2 StO2). Aerobic capacity was evaluated by measuring maximal oxygen consumption (V[Combining Dot Above]O2max). The T1/2 StO2 in the long-distance runners (25.0 ± 4.5 seconds) was significantly longer than that in the controls (15.9 ± 1.6 seconds; p < 0.01) and in the sprinters (18.0 ± 4.6 seconds; p < 0.05). In all the subjects (long-distance runners, sprinters, and controls), the T1/2 StO2 had a significant positive correlation with the V[Combining Dot Above]O2max (r = 0.75; p < 0.01) and was longer in subjects with a higher V[Combining Dot Above]O2max. These results suggest that reoxygenation after sprint exercise is influenced by aerobic capacity and training status, and that the subjects with a higher aerobic capacity have delayed muscle reoxygenation after sprint exercise.

 

Effect of endurance training on performance and muscle reoxygenation rate during repeated-sprint running.

Buchheit M1, Ufland P.

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Abstract

The aim of the present study was to examine the effect of an 8-week endurance training program on repeated-sprint (RS) performance and post-sprints muscle reoxygenation rate in 18 moderately trained males (34 ± 5 years). Maximal aerobic speed (MAS), 10 km running and RS (2 × 15-s shuttle-sprints, interspersed with 15 s of passive recovery) performance were assessed before and after the training intervention. Total distance covered (TD) and the percentage of distance decrement (%Dec) were calculated for RS. Between-sprints muscle reoxygenation rate (Reoxy rate) was assessed with near-infrared spectroscopy during RS before and after training. After training, MAS (+9.8 ± 5.8%, with 100% chances to observe a substantial improvement), 10 km time (-6.2 ± 5.3%, 99%), TD (+9.6 ± 7.7%, 98%), %Dec (-25.6 ± 73.6%, 93%) and Reoxy rate (+152.4 ± 308.1%, 95%) were improved. The improvement of Reoxy rate was largely correlated with improvements in MAS [r = 0.63 (90% CL, 0.31;-0.82)] and %Dec [r = -0.52 (-0.15;-0.76)]. Present findings confirm the beneficial effect of endurance training on post-sprint muscle reoxygenation rate, which is likely to participate in the improvement of repeated-sprint ability after training. These data also confirm the importance of aerobic conditioning in sports, where repeating high-intensity/maximal efforts within a short time-period are required.

 

 

2. Thank you very much for bringing this article up again, its one I read a little while back, and it was a great re-read. Again, I think you make a really good point, and some caution needs to be taken when applying Moxy. This is true with all the measures we use to test and monitor training.

First, maybe you can help me. In the article the graph you highlight is not from a published paper, but perhaps it has been published now. I could not find it, and therefore using this as a basis for an argument is difficult as I do not know how these results came to be so. If you have access or know where I can find it please send me a link. The reason I say this is if muscle fibers are being investigated in vitro the translation of this information in vivo is always difficult. If you read the entire article, this is something nicely identifies, that in vitro experiments lead to many of the misinterpretations we see readily used today. Now, it is very plausible based on the physiological make up of different fibre types that some will have a slower PCr curve on their own, since Type II fibers oxidative properties are lower, PCr recovery is ultimately linked to oxidative capacity (a point we made earliers in this thread). However, these fibers do not function in an isolated manner , and we know for example based on findings like the lactate shuttle theory that a rapid and constant exchange takes place between cells and fibers. Also, during maximum efforts, or long endurance activates a range of all fiber types are used and it is not so that during strength only type II are used, and during endurance type I. For this reason, It would be interesting to see how the data you present was actually acquired; in vivo or in vitro.

Finally, I think to get to the point you wanted to arrive at, and I agree with. In terms of strength training and Moxy, we need to ask ourselves what does Moxy measure. SmO2 is a bioenergetics parameter, and if you are doing high strength workouts it is more likely that your limitation is CNS related rather than bioenergetics related, and therefore the application of Moxy is questionable. However, if you are doing strength, sprint, or interval work hoping for adaptions associated with bioenergetics like; hypoxia/dysoxia, ischemia, etc. then Moxy combining both SmO2 and tHb can be very insightful.

Finally, I recommend that everyone reads the paper Kirill linked at the end of his post, as it nicely highlights the things we have been saying for many years now, and why we think the Moxy is important. Some of the juicy highlights:

“glycolysis [glycogenolysis] is rapidly activated during intense exercise, and seldom is there near complete reliance on the phosphagen system” (p3)

“When exercise continues longer than for a few seconds, the energy to regenerate ATP is increasingly derived from blood glucose and muscle glycogen stores. This near immediate activation of carbohydrate oxidation after the onset of exercsie is caused by the production of AMP” (p6)

And my favourite:

“The labelling of glycolysis differently based on terms related to the presence or absence of oxygen is inconsistent with the biochemistry of glycolysis”. (p10)

 

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