HIIT Protocol Pilot Data

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Roger

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Posted 1469657939	#1

The powerpoint is attached. Attached Files Presentation1.pptx (3.23 MB, 43 views)

ryinc

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Posted 1469738788	#2

Thanks for the interesting webinar.

CraigMahony

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Posted 1469766162	#3

Agreed

Ruud_G

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Posted 1469872022	#4

Adding a graph of the SmO2, tHb, and other measures all together on a time scale which were taken during the HIT test would be informative. It is not in the presentation currently. Furthermore I am wondering how long (i.e. that is just a decision just as 5 min on and 5 min off) the plateaus of on and off were taken? That is. I can do a sprint, recover and see SmO2 go up again. It goes up quickly but I can decide after (say) 20 seconds that it looks like a plateau or after say 30 seconds o it looks like a plateau. Ans did they choose that plateau as being the same level of plateau everytime did they let the plateau level vary? These are all important points which are not mentioned. And how long could the subject sprint for 350 watt? Any increase in TTE or???? My point of plateau on upper level also holds for the lower (desaturated level) I can tell you that this decision can significanly alter the time you can hold on to the exercise. Also of course this influences the type of physiological stimulation!!!!

ryinc

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Posted 1469878048	#5

Ruud i have been thinking about similar ideas as what you write above. I wonder if one of the metrics that will start to develop in this field is the gradient and change in gradient of Sm02. This could be used in future to help define the answers to the questions you are putting forward. E.g. something like when the change in gradient of Sm02 is less than X% for at least Y seconds, then it is considered a "plateau"? Steepness of gradient on load and recovery could be indicative too. Just some ideas....

fitbyfred

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Posted 1469893422 · Edited	#6

Thanks for this good presentation. It certainly matches up with my uses for MOXY in my gym. How about "accessory" muscles rather than "non or less involved" muscles ?

juergfeldmann

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Posted 1469906727 · Edited	#7

To Ruud's great points. Absolutely agree and I like to show hopefully later some of his points as using SmO2 for interval or HIIT alone is on pretty shaky ground to say the least. Top SmO2 plateau as well as bottom SmO2 plateau tell you nothing really other than you are in a delivery and utilization balance. In fact to really push some thoughts. A dropping SmO2 or an increase in SmO2 really only means the % of O2Hb to Hb changed but it really does not mean that we use more or less O2 . This has to be moved together with tHb. and as well with some O2 demand. If I am already " ranting" the set up for looking at priority or non priority muscle is an example how we can create a conclusion by simply avoiding a possible information of priority and non priority muscles. For regular readers following this forum carefully they know, that we need an activity where the cardiac output can not support the huge amount of blood vessels which may have a vasodilatation during a whole body workout. So like many great researchers showed , the Cardiac out put can not maintain the needed BP and a s such the minimal pO2 in the vital systems and as such CG will create vasoconstriction in locomotor muscles which are non priority for the motion. Typical example we showed are swimming , rowing and cross-country skiing. The reaction is very clear and easy to see, between a no priority muscle who increases activity and a non priority muscle who looses blood supply due to protection of BP and a limitation of CO. In the demonstrated cases the arm initial example to see blood shunt was , as they mentioned, for sure no intensity limitation for a CO limitation. Even the second one in a healthy person will not create a CO limitation due to duration as well as due to low muscle mass involvement. In fact the limiter will be very unlikely CO or delivery, but rather a local muscle limitation and as such non need to shift blood from less involved muscles to the overloaded locally fatigued muscle groups. The interesting experiment shows, that when CO is not a limiter, than we do not see a shift of blood or a reduction ( vasoconstriction ) in blood flow in less priority muscles as the BP is well maintained as such base pO2 in vital systems as well. The only limitation is the problem that the needed ATP can not anymore be maintain or produced so to protect the baseline ATP the Brain will reduce motor unit recruitment down to a level where O 2 supply can maintain the needed ATP level and as such we will get a low SmO2 pleatau which is on an individual low intensity level which is an intensity who can be maintained with the available O2 delivery and utilization balance. Perhaps s more later

juergfeldmann

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Posted 1469907926 · Edited	#8

To the point of non involved and involved muscles. The name showed up in studeis done in Japan and other great places in the early 2000 . . Dr. Bellar has absolutely right not a good name and a very poor decision from my side to take it over without thinking. Andri has a much better option as he suggested priority and non priority muscles and we use this in our research and coaching circles now really all the time when we design training plans. The priority is a great word , who shows the picture , whether the body really needs this muscles to survive. You can run or bike easy without upper body in case CO is reaching a limitation so priority to run away is in legs and the option to divert blood to the legs makes sense in this case. Again remember Shift or vasoconstriction in the discussed idea only will take place when there is a CO limitation .In a HIIT there is NOT a shift during the load,in the recovery time as priority muscles will reload before we can afford reloading non priority muscles. This in case in the rest period the delivery is limited. We showed many examples in this direction in the forum. Cases, where the ; load really stopped so no way the no priority muscle was now increasing activity but we see the drop in this muscles as we see an increase in SmO2 in the priority muscles. To ryincs idea n the slope. We id about 10 year back this as an initial idea on TSI % and slope as we have an incredible sophisticated software. We failed but that does not mean it may go so great if people work again on this. Our conclusion was. SmO2 or TSI alone is not an optimal feedback and has to be connected d with tHb and in some cases with HR and RF to stay on simple bio markers. This after we made it very complicated with Physio flow , VO2 blood sampling SEMG and more. So fun to see, hen slowly some institution move again to the steps we did and we see, where they have similar questions and problems as we have and where they make conclusions we did to just find out we where wrong. Fun times as MOXY is more and more accepted. The interpretation is the first step. And we work since a while actual physiological training so this will come up for sure in the next 5 - 10 years. Here a reminder. If we know the history we may avoid many steps which where already done from smart people reinvent the wheel ) and can move forward faster.

DavidBellar

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Posted 1470834854	#9

To the point on vasoconstriction. There is evidence that increased sympathetic outflow during exercise exerts a pressure causing the body to balance blood pressure and cardiac output. Studies on adrenergic blockade have shown this during exercise, though some animal studies where the sympathetic nerves have been severed do not show comparable results. However, alpha adrenergic receptor mediated vasoconstriction has been demonstrated to be attenuated by very modest changes in local environment pH. Based upon the conclusions of some of the best minds in this field ( see Buckwalter and Clifford's review in Ex Sport Sci Review 2001) it is apparent that muscular contractions have a variety of way to attenuate sympathetic vasoconstriction. Therefore if the muscle is "non priority" but still has increased metabolism during the exercise it is likely to produce a local environment capable of attenuating sympathetic vasoconstriction. We have seen that sEMG increases in these "non priority" muscles during cycling, signaling increased contractile activity. I guess to summarize my thoughts: 1) It is not in dispute that sympathetic outflow increases during intense exercise and has the potential to cause vasoconstriction 2) There is evidence that many factors associated with muscle contraction can attenuate this increase 3) In a human with only Moxy it will be very difficult to study the interplay between Sympathetic vasoconstriction/attenuation via activation My question: Since we all agree that using Moxy we can see changes in these non priority muscles can we use this information to tell the coach/trainer something valuable. I.E. does it really matter the underlying cause, if the coach knows that it signals a change in mechanics. Again just my thoughts I don't claim to have all the answers in regard to this topics...

juergfeldmann

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Posted 1470932664 · Edited

#10

Thanks for the nice feedback
Here where it may be interesting to add some more thoughts over the next little while.

My question: Since we all agree that using Moxy we can see changes in these non priority muscles can we use this information to tell the coach/trainer something valuable. I.E. does it really matter the underlying cause, if the coach knows that it signals a change in mechanics. Again just my thoughts I don't claim to have all the answers in regard to this topics...

a) The initial    question for us was many years back, how we can combine and possibly see interactions   with cardiac information's by collecting SV, HR, EF % SVR LVET and so on , than combine this with respiratory feedbacks   like FeO2 % and CO2 reactions as well as how this gas exchange information is influenced by TV and RF and therefor possible change O2 dissociation curve. Than integrating NIRS and   in NIRS using initially a 3    depth feedback   with Portamon to understand possible shift of   Blood   from the surface to the muscle of vica verca . ( we showed some of this   case studies in the forum a while back   and   many years back in the Fact- Canada forum. Than    the old    version of adding SEMG as an additional idea to see,, whether we simply start using   more muscle for an overall performance or not. And as we where really keen in blood values we test factroes like ammonia , lactate   Bicarbonate and more.
One section we very early on had problems was that Physio flow ,NIRS   and SEMG gave us instant live feedback's , where blood tests and VO2 mask test where indirect feedback's.
So as   all can imagine, there was immediately the open questions on the individual time lag in blood values and VO2 values , So the fun part than was to play around with manipulation of VO2   values like TV and RF manipulation including adding O2 or reducing O2.
The result s for us where somewhat intriguing as we very fast had the question n thee actual values of VO2 and Blood values in the filed due to the time lag question. This pushed us to use RF and TV as a immediate feedback and than looked at influencing of cardiac parameters and NIRS parameters.
We did hundreds of test over many years and had the privilege to have    people like Frank Bour    visiting us as to help as well his dad.

So in short the same question as Dr. Bellar has :
can we use this information to tell the coach/trainer something valuable.

This question motivated us to buy anything out there where we could combine    with the goal to see whether any idea would be usable to move back to the grass root   so patients can work with it with a minimal   money investment and an optimal feedback.

I.E. does it really matter the underlying cause,

This was the other most important question
Why. If I have a cardiac patient with a leaking aortic valve, how intense can I   push him to maintain current ability without speeding up the   problem.
If I have a COPD   patient
How   hard can I push his walks to not create a secondary right ventricular problem due to the COPD limitation or a overload of his kidneys.
Or what is the best respiratory workout to balance the chronic overload d of his respiratory mussels. Or how    do I maintain or improve   muscular   situations in a severe leg accident, where I can not load the bone structures for 3   + month.
Sure many coaches will argue   that they do not have this cases.
I would argue you have you simply just do not see it that clear.
So starting with people we knew their limiter clearly we worked our way up to so called healthy people to see, whether we would be able to see similar trends.
Than using the individual approach we have with clear limiter patients and use this training and stimulation ideas on actual healthy people.

This created the idea of Limiter and compensator and the   feedback , that if we do not know the limiter we may overload the compensator.
Again COPD limiter respiration compensator cardiac right ventricle-    sudden problem in the compensator.
Fast forward.
Athlete with a respiratory limitation ( not metaboreflex) so he will compensate with 2.3 DPG and all what shifts O2 disscurve to the right.
Picture great utilization, but poor delivery. Result nothing he simply may reach his performance limitation,   so   some possible answer you reached you genetic limitation, when in fact I as a coach reached my limitation to understand a possible plateau in his current performance.

So
does it really matter the underlying cause,

I believe strongly yes, and that what motivated me   over he last 35 +- years to fins   ways to solve some of this intriguing problems.
Can we do it with NIRS.
Much more than I thought when   we started out combing all of the above feedback's.
The end result starts at the   least important body part which is a non priority muscle as the body can most    afford to reduce   performance there for survival reasons.

So yes what is the underlying cause.
Is it a leg limitation so I try as I can afford to integrate arms to   push the same or short tear a higher performance. As nicely presented in the webinar.
Or is it a cardiac limitation so CO reaches a   limitation ( sleeping giant / Marshall) and we simply can not afford to open    or deliver blood to all the muscles who could help in a higher performance.

So vasoconstriction due to mechanical muscle compression SEMG up or sympathetic vasoconstriction to maintain BP ?
Depending which one will most likely change the stimulation approach.

Or other example.
Long   endurance   load   and now we see a change in SmO2 and tHB after a certain time.
Now it is nice to know what causes the drop.

a) local muscular limitation,
b) respiration fatigue
c) cardiac limitation. Now the easy us e of NIRS combined with HR and in some cases with RF can give a nice indication what is most likely the reason for the change in the NIRS data's in a priority or in a non priority   muscle .
Summary . Initially we found this difference by using all the toys we had and finally started to see, that in most cases (I not all ) we actually only need MOXY or NIRS    and have the answer. So we can go live in the field and correct if we like the reaction or keep the compensator overloading if this is the goal.

I will show possibly on here some cases where we use this and how   as we work daily in this direction.
In 60 min I will do a specific workout in BFR with a severe   injury case and I will ask whether I can show in the evening the live feedback how we control with NIRS the load , the rest and the length of the workout.
Thanks' again for the feedback.

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