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MTF Clint

Study Participant
Posts: 13
Juerg one of your long time friends, Mr Sean Power came down to MTF recently.
He came down to do a cycling test with us. (For those who don't know Sean he is a cyclist so it was only appropriate)
Juerg I know Sean wanted to get your input, and I thought it might be helpful for everybody to see how you would make an assessment from this data. If you get some time please share your thoughts...
ps. There is a RRA at the bottom in the VO2 screenshot, to the right of the RF/VE graph from his step test

Sean Power BIA SS.JPG Sean Power Data SS.PNG 

Sean Power MOXY SS.PNG  Sean Power PF SS.PNGSean Power K4b2 SS.PNG

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Great nice info.
  Once we move them into context  with    some  additional ideas we will have even more  ideas on what we see.
  Here   some  " requests:
  Can you sent me the VO2  numbers  in ml  as well as the raw  MOXY CSV  file.
  Now  here  for the regular reader  some  points  of interest.
 1. Look at the  cardiac hemodynamic  information:
  Live info during a test   done  with a Physio Flow.
Look  at  the  end section of the test  270 / 300 watt.  Look  at HR  and SV  reactions  and  than  compare  to the end result of CO ???
 Second look at the  EF  (  EDV/SV  and   again look at the  end   2  step level.
  Problem with 3 min test is, that we are not sure, whether this really happens  or whether we  would have seen  in a longer step a potential  compensation.
. Now  once we  see the MOXY  data's  closer  we  like to see, what happened  in the  extremity  ( MOXY test area )  at the 270  watt +-  level.
. Is the reduction in ED %  a  reduction in pre-load  due  to a  reduction in blood volume return.
 So we  can look at tHb in MOXY.
.  .  To end of the  Physio flow overview  . Look at the  CCT  ( LVET  x HR )  . He has a   relative low  CCT  34 seconds  in the  critical intensity , which means  his cardiac  system is very happy  supported  with  O2   from a  contraction  time of view.
2. Short look at respiratory  action.  TV  and RF   steady   increase performance indicating  at least   o problem with the  RF  and TV  action. Once we  have the VO2   and than VO2/RRF  we can see  how the O2  transport efficiency   is keeping up. Same for the O2  Pulse.
 Based on that we  can go back to the  NIRS MOXY info  and look at the critical    intensity as well at the question delivery or utilization.
  What the test  shows is, that in 3 min step test  you  do not have optimal information on options   of limiter and compensator.  You will have  nice high watt  info's  and nice  VO2  info's  ( not optimal either  ) and as many look for  watt/ kg  or  for VO2/ kg the results  will be  satisfactory.  We look  not for  any of this but  on where we may see  some limitation coming up, who is the limiter so we  can work on this system  and maintain  the othesr  as well  and not overload compensator  so  that at the end the limiter is still where  he  was and the compensator is  fried  due to overload.

 Summary  Sent VO2  and CSV  file. Thanks 
  Try to get a  5/1/5   going  with all the  toys  you have.
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Here  an add on to the above info.
  It is an example, why we  shift  from a  " classical" 3 min test  to a 5/1/5  idea.
  We  will show much more  ideas, why 5/1/5  as we  can read  much more out of the  1 min rest, than we  ever thought.
  Here some timbits.
a)  take the situation, where you have a certain CO and a certain VE because  of a certain performance. This performance asks  for a  certain VO2 , which is  CO x (a-v) O2 diff .
Now   you suddenly  stop   performance.  What you create is a sudden  stop in ATP demand  from the  working muscles  but you have a lag time of  the reaction of CO  and VE.  Meaning , that the  2  main delivery systems  still deliver  under the intention  to deliver  enough O2   to maintain the performance you just stopped.
 This creates  an "over delivery of O2   which will show up as a  change in SmO2. Now   due to the lag time    we  will see a  drop in CO  and  a change  in VE  after 1 min , as  finally the message  went through , that there is no  activity going  on.
 So as we  suddenly start again we  have now a  too low CO  and a too low VE  fro the performance we  do again. So we  will see a drop in SmO2   due to the need  of using O2  but  we  now take it  from " storage   rather than  for adequate delivery.
  This  trends  will as you soon will learn  give additional info's  on  the way we  "recover.
 Remember  endurance  is  ??? see att.  The  recovery  will give us   much feedback  as well the "restart  on how   the  person reacts  as well the ability  to  create a  "homeostasis"  during the 5 min load.
 We basically have a  "Interval" information   paired  with an endurance information.
 What sounds    strange for the moment will  suddenly make a lot of sense, once we go towards  the information on how  to train  and how to use  MOXY information.
  Short hint:
  We  can use  different interval ideas  with different goals.
 a)  goal  to  improve  the ability  to take O2   from storage   versus  take O2  from delivery. So the rest  in between loads  will be the key to actually change the stimuli  in  different interval ideas.
  So this long story here now ends  with a PP  so you can  already start to see,  how   the 5/1/5    info  shows nicely by what intensity we   can create  with what system still a  flat ( balanced  situation  , and  by what intensity the system may   increase  steady  and never   is able to balance out the need  to be used.  Simply look at the 3 min  and iPAHD  ideas  and  find the  critical intensities  for the different  systems  and or  system  helper  ( RF TV  FEO2 %  )  . This is  by  simply using your    VO2  equipment.
  Once you add  MOXY  to it  and  later PHysio flow  you are  far off the  simple  % idea  of  something  maximal  or  something  with a threshold.  Have fun

MTF Clint

Study Participant
Posts: 13
Alright Juerg I sent you the files you asked for...
As usual you were quick to point out the flaws of the test. In my defense of the 3min step test, if you check the raw VO2 files I sent you from the K4b2 you'll see a critically low battery level. This was my fault since we had a problem with the charging unit itself. That being said, Mr Powers drove 4hrs to come down and test with us, so I decided that a full 3min step test was better than half of a 5min test. Completely my fault, and to make it right plus prove a point I'll invite Mr. Powers back down to do a 5min step test and a 5/1/5 protocol. Then we'll see if the shorter steps really did influence the outcome of the test. (SpO2 data is also contained in the screenshot of the test overview if collected by hand)

In my opinion this is a delivery weakness for Mr Sean, I don't believe we'll disagree on that point. His SpO2% dropped down to 94%, and SmO2% was well below 20%. However, seeing that Sean had a peak CO of 32.3 Liters (which for a 160lb man is quite impressive) and his tHb remained stable throughout the test, I find it hard to believe that this delivery weakness is due to cardiac issues. Stroke Volume, and therefore Cardiac output dropped a bit during the last stage of the test.. but it's been my experience in the past that during the final stage or two of the test they usually begin to move, bounce, bob, weave, or whatever in the saddle as they feel the pain train creeping up on them. This often gives me problems with some of the more sensitive equipment we use...

To your point of cause and effect on this test, perhaps we'll see a different story with a 5/1/5 or 5min step test? Or we may just see a CO of 32L and a VE in the 130's. We know he's capable of moving 200L of air, so 130L should be fairly easy for him. We've certainly seen some big VE numbers in the past (300+Liters or more) but how often do you see an athlete with a Cardiac Output of 40L or more? I know I don't see that very often... In my mind this could be very simple, keep the same 32L of blood per minute being delivered to the muscles he already has, along with 200L of air (instead of 130L) and this would be a 35% increase. That's a big jump, but very attainable as you well know. On the other hand we could ask for a 35% increase from CO which would put us at 43.6L/min. That would be one of the biggest Cardiac Outputs I've ever seen, so certainly not easy to ask for. I understand there are some mobility and efficiency issues here with the added VE, but those seem much more reasonable than increasing CO 35%.

Now maybe the CO really did drop off first, and this in turn caused vasoconstriction and poor delivery. Then again maybe it was a relatively low VE that caused this reaction? I see your point on the 5min step test and couldn't agree more, it's already the test of choice for me (batteries permitting) and I'm on board with the 5/1/5, but this just seems a bit elementary to me at this point that the problem is in the delivery of O2 into the bloodstream that's the problem. Not the delivery of blood to the working muscles, as is evident by the stable tHb reading from the MOXY. Besides that, do you believe we could even expect to see much of an increase in CO from an athlete this developed already? I mean 32L is a solid cardiac output!

My bet is on a delivery weakness due to a respiratory limitation. Time will tell, as I will send out an invite to Mr Powers to come back down and indulge us a bit...
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
So here a behind  feedback on the above  information.
  I got the files and was  moving them into our systems.
As  we are a MOXY  forum here   I like to show  you   what you get or  would do, when you only would  own a MOXY or  2  and no other equipment  like e have above  with VO2  and Physio flow.

Here  pic  1  where we look just at SmO2.  I do not have a start marker  nor  an end marker. What we know is 3 min step tests  and 8  steps. So you  find the end of the test  and go  form there  to have the  full SmO2  info. 
Pic  1 Test    and we look just at SmO2  Try  to make  some " zoning based on SmO2  trends. You can see  at least 3  relative clear trends, despite  the fact , that it was a 3 min step test.

What we miss is an initial  incline  in SmO2 . As we know  by now  without  actual  warm up  we will see in a 5/1/5    inmost cases  an initial  incline in SmO2   and very often as well an incline in tHb.
   In some cases we see no incline in tHb    but  still an incline  in SmO2.
  This is another part, where  "classical"  great theories  may have to be reviewed.  Not thrown out as both the newer  as well the older idea may have some merits.
  The "classical" ideas we all learned    and  the majority of  exercise  physiologist  still use  and believe in  is:
  " based upon August Krogh's observations made nearly a century ago. 'Kroghian' theory holds that only a small fraction of capillaries support red blood cell (RBC) flux in resting muscle, leaving the vast majority to be 'recruited' (i.e. to initiate RBC flux) during contractions,  "

See the  "classical"  picture  we often as well use  but now we   may  think on 2  options  and  have  some better understanding on the second  version  : No increase in tHb   but still an increase in  SmO2.  See    art  as  one  part  to  start a discussion.

Exp Physiol. 2013 Dec;98(12):1645-58. doi: 10.1113/expphysiol.2013.073874. Epub 2013 Aug 30.

Skeletal muscle capillary function: contemporary observations and novel hypotheses.

Poole DC, Copp SW, Ferguson SK, Musch TI.


D. C. Poole: Department of Anatomy and Physiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS 66506-5802, USA.


The capillary bed constitutes a vast surface that facilitates exchange of O2, substrates and metabolites between blood and organs. In contracting skeletal muscle, capillary blood flow and O2 diffusing capacity, as well as O2 flux, may increase two orders of magnitude above resting values. Chronic diseases, such as heart failure and diabetes, and also sepsis impair these processes, leading to compromised energetic, metabolic and, ultimately, contractile function. Among researchers seeking to understand blood-myocyte exchange in health and the basis for dysfunction in disease, there is a fundamental disconnect between microcirculation specialists and many physiologists and physiologist clinicians. While the former observe capillaries and capillary function directly (muscle intravital microscopy), the latter generally use indirect methodologies (e.g. post-mortem tissue analysis, 1-methyl xanthine, contrast-enhanced ultrasound, permeability-surface area product) and interpret their findings based upon August Krogh's observations made nearly a century ago. 'Kroghian' theory holds that only a small fraction of capillaries support red blood cell (RBC) flux in resting muscle, leaving the vast majority to be 'recruited' (i.e. to initiate RBC flux) during contractions, which would constitute the basis for increasing surface area for capillary exchange and reducing capillary-mitochondrial diffusion distances. Experimental techniques each have their strengths and weaknesses, and often the correct or complete answer to a problem emerges from integration across multiple technologies. Today, Krogh's entrenched 'capillary recruitment' hypothesis is challenged by direct observations of capillaries in contracting muscle, which is something that he and his colleagues could not do. Moreover, in the peer-reviewed scientific literature, application of a range of contemporary physiological technologies, including intravital microscopy of contracting muscle, magnetic resonance, near-infrared spectroscopy and phosphorescence quenching, combined with elegant in situ and in vivo models, suggest that the role of the capillary bed, at least in contracting muscle, is subserved without the necessity for de novo capillary recruitment of previously non-flowing capillaries. When viewed within the context of the capillary recruitment hypothesis, this evidence casts serious doubt on the interpretation of those data that are based upon Kroghian theory and indirect methodologies. Thus, today a wealth of evidence calls for a radical revision of blood-muscle exchange theory to one in which most capillaries support RBC flux at rest and, during contractions, capillary surface area is 'recruited' along the length of previously flowing capillaries. This occurs, in part, by elevating capillary haematocrit and extending the length of the capillary available for blood-thecyte exchange (i.e. longitudinal recruitment). Our understanding of blood-indications and substrate/metabolite exchange in health and the mechanistic basis for dysfunction in disease demands no less.


Now  back to  the assessment.
  The SmO2  does give us  some indications and locations
, where we have some  shifts  in  metabolic  reactions to create optimal  energy ( ATP  )  with  O2. The 3 min step test does not give us a lot of informations in  possible ARI  levels  . We have a relative okay info  for STEI  and  FEI, as well as HII.
  Now   second ,you  add the trend in  tHb  ( Blood  flow trend  to SmO2 ). see  pic  3.  We have a relative  "flat "  tHb  till about 1500 than we have an initial increase in  tHb followed by a second  1780  increase in tHb.
  Your    job:
 What  can or would  create an  increase in the  tHb?
  Give some feedback  and than we  go and look at look  at the next stage  to see, whether we  can   just use SmO2    and tHb    for trends or  whether we add Physio flow and  VO2.. Try to find thna a possible reason for limitation of the above performance . Find the weak link.
  Now interesting is to  go back to  Physio flow and respiration  and see, where  SmO2  and tHb  reacts  compared  to VO2  and Physio flow datas. Remember;   VO2  equipment may have  a lag time   as well as Physio  flow if the reason is  peripheral  . If the reason is the  cardiac system we  see no lag time meaning the heart creates the MOXY reaction. If  it is peripheral  than the heart reacts  with a lag.because the peripheral  reaction creates the MOXY picture.
 Lag times in many systems  are  somewhere  5  +-  min.

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