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Evans

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 #1 
Screen Shot 2015-02-12 at 8.26.55 PM.png Hi everyone. I'm relatively new with the Moxy and I'm posting this up to get the veterans opinion on what is going on. I'm walking this through in my head with my notes and I'm second guessing what I think is going on. Plus, I have some other information about this athlete that I don't know if it is skewing my perception and looking for something that is not there. 

We did a 5/1 test but didn't keep at the same load because of time today. She only had 50 minutes. She has a very good training background, but has recently come under some fatigue related issues under more intensive training. She has done a lot of other assessments (HRV, muscle diagnostics, etc) but everything is coming up clean. She is subjectively great throughout the day, but lately she has been experiencing some fatigue much earlier in her intensive runs than normal.

Any feedback is greatly appreciated. CSV file is attached for those that require/need that.

 
Attached Files
csv TIP_2-12-15.csv (72.81 KB, 64 views)

fitbyfred

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 #2 
Hi, g'morning and thanks for posting.

That's a pretty fit runner you have there--so fun to test and push them?

I have question feedback on the method? Do you think you brought them up too quickly? See the HR jump from sets 2-3.

ARI < 4 mph
SEI = 4 - 6 mph
FEI = 6 - 10+ mph

Evans

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 #3 
Hi Fred.

Based on over 5 month ago treadmill data from the athlete, we felt 10 mph was going to be a good ending point, so we stepped backwards and came up with the step increments,  but also made the adjustments per the live feedback we say with Peripedal and RPE.

One thing immediately that I noticed was her HR response at particular velocities was around 8-12 beats higher than in the past.

She has had a larger (per the athlete) reduction in lower intensive runs in her training diet for awhile now. She feels she needs to do more of that (classic at or right below 2 mmol L intensity) as there has been a bigger distribution of intensive runs happening. 

So even without the testing, there was a suspicion there was too much removal of lower intensive runs on her end  that has attributed her decline.

For her (just by looking at HR data), her heart rate responses for the velocity are (per history) a bit higher like I stated above.

So, the primary reason for the assessment was to gauge to see if we could get any insight on her current fatigue issues.

Thanks.
fitbyfred

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 #4 
Cool. What are your thoughts on the end of assessment recovery response? You didn't include to workload but it seems the athlete wasn't recovering or the load was too much to facilitate recovery?

Do you think a longer single step or (better) a double 5 min step may yield more of the info you were after regarding the SEI status / ability ?
Evans

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 #5 
Hi Fred,

After assessment, she was walking at 2.5 mph.

My initial thoughts are *maybe*. As I stated, I'm relatively new to this type of assessment and technology, so I'm open for suggestions, opinions, facts, etc.

Thanks.
Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #6 
Evan , this is a great great example and we  will be  able  to  get  a lot of   information from your data . Please give  me  a  time  so on the weekend I will   go and  have fun with this.
 It looks you guys  do a great observation job. What is  here resting HR    when she  is on the back in the morning  5 min rest.  and than  she is going up standing  an and than look her  resting HR. What is  her  weight  and height  so we  have an approximate   body   information. I will try (  it is not the gospel  ) to   see, where we  would load  from a  physiological point of view  to stimulate    what systems  and than you can either come  back   and tell us  where she loads  and or just use  our information  to see, whether it makes  sens.
.
Evans

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 #7 
Bodyweight is roughly 122-124 and is around 68 inches tall.

Supine resting heart rate ranges from 53-61. 3 days ago it was 68 (no clue why). HRV testing went great, but RHR was higher than normal.

I think her RHR was a bit higher just standing on the treadmill because she was anxious/excited about testing.
Juerg Feldmann

Fortiori Design LLC
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 #8 
Resting HR in  back position  compared  with resting HR ins standing gives  some indication of SV.
 In back position SV is higher than in standing  so to maintain the same CO  without too much activity you have to increase HR in standing compared  to flat  and as  such you can get some estimation  due to the change.. Resting HR  so much higher can have different reasons. One is  plasma  volume  an done is  RBC  count  and Hct. What is here HCT  and what is here Ferritine level.
 A  change in plasma  volume  or low Hct  can show up in MOXY as a   incredible  fast drop in SmO2  at a start as a sign of   limited delivery   of O2. The limitation can be  due  to low  SV  as well as  due to  low  carrying capacity  of O2. So  whne we  go through your csv  we  can watch  for trend s in that direction.
Evans

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 #9 
Resting HR today: supine: 64
Standing HR today: 92

She normally doesn't train with a HR monitor, and there is only supine HR data from her. So, obviously something is up!

blood work from about 2 weeks ago

Ferritin: 26
Iron, blood: 269 (high)
Iron, saturation: 64 (high)
RBC, count: 4.05 (range, 4-5.20)
Hematocrit: 39
Hemoglobin: 13.1
Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #10 
Sorry  for being behind  but got flooded  from an incredible set of MOXY data  and all are super interesting. It is fun to get  now more and more people   experimenting  and motivate  by many statement s and case  studies  we show  here. A great critical  trend  towards  what we  do  and   what they  did  and this is what  will bring us  forward  towards a new  direction in physiological guided  workouts.
 So here  to get  all in one place the graph  from this case .
evans.jpg

I will show later a closer look  when we use  our   interpretation options. Now important  when we discuss on here is , that  anything I  suggest  is never a  critic   on what  I got sent to me  but just an open opinion  form my side, which often is  wrong   or at least  not really always that great of  an opinion.

So basically  in this direction here.
Red bull expert advice.jpg 

So in  a first  glimpse  on the  data  I was   surprised that  by step 3  ( 6.6  mph  )  and 4 ( 6.5 mph ) there was a  very different HR reactions despite the same load but  a very equal  SmO2  reaction.

 Why  would  we  "deliver"  ( HR  is  apart of a delivery  information as we have HR x SV  = CO ) much more  Blood  and as  such more O2   at the same  load. ?
 Here  what I mean
step 4  and 5 circle.jpg 

Now   the step  3  would be the 6.6 mph  load  and the next step 6.5 mph  load. Now before  we  discuss here further the  initial   idea from my side  is >
 Wowww that is strange.  so did they really repeated in a step test 2  x  the same load  and  why. So my question:
 Is this  real  or  is this a mistake in the graph ?
 If it is real than we have some very  interesting  points  to  look at this reactions.

 Now  to give  some more ideas on here.
 If  this group repeats  a  TIP  and 5 min step test  with  1 min rest is great  than here   how I would adjust the steps..

hr speed  chart.jpg


Last but not least the   interesting  reaction  from resting HR  in back position  and than standing.
 This indicates  an incredible drop in SV  due to change in position  but the drop is   very  big.
 If you look an average blood volume in this    person than you can calculate the SV   in back position and what it ends up in standing. Hard  for me to believe that HRV  would not  show  any reactions in this example  woww  never thought  that.

 

female  blood volume..jpg



  Now to give one more feedback before we go into depth.

dirsc  fast recovery  smo2  thb.jpg
The red  circle  is just taking one section but you can see   the same  or close to the same reaction every time this athlete started the next load.
 You see a  very fast drop in SmO2  and tHb  with a  subsequent recovery  of SmO2  ( exception last step )  and a  subsequent  increase  at the same time in tHb.
 We  see ( no cookbook ) this reactions in   mainly 2  situations in running assessments.
 1. Absolute beginners  first time on a treadmill.

 They  start out   extremely stressed  and the initial  30 - 60 seconds  they run very   un-economic    and stiff till they settle into their   much better stride  feeling.
 Than they jump off and  again have a problem to recover  resp  relax  when standing on the side of a running  treadmill so   not optimal relaxation  so tHb  stays low  as there is still tension in the muscle  and SmO2  will not optimal  rebound  as the tension in the muscles demand  O2   as well  at rest.


2. Second  group as so often  are high performance athletes  with  an incredible  great utilization reaction    at the start of  any load  but a  overload  or over trained ( I like more USP as under performing )   delivery system  so it takes  some time before the delivery kicks  in.
 Delivery  as in   either SV  reaction and or  as in capillarisation reactions.
  We  can create this picture   by   working a lot  ( too much ) in high intensities  so that  delivery limitations  are getting worse  and utilization  have to learn to compensate.
. The majority of  athletes    with this  trend come  form  training i ideas, where we see the still existing   idea  of   " lactate tolerance " training.
 This creates  a  too often to extreme  metabolic  acidosis  and as  such  a dramatically stress on Ca  as  well as Pi    metabolic reactions.
 Some of the well known side effects  off to many metabolic acidosis   loads  are   stress fractures and cardiac  arrhythmia  due to the Ca++     reactions.
.
 If we like to  train  enzymatic    progress  to H +   overload we  can do that  by creating respiratory  acidosis  instead of always    going over  metabolic acidosis.
. . Now  I do not know  in this  case, whether  1  or  2    of the reactions is what causes this interesting  MOXY  pictures. 
 To avoid a flood  of emails  I like to show  one  newer study in this directions.
 Andri  my find  a  much older version  where this  was done  as well. 
 

Effect of metabolic and respiratory acidosis on intracellular calcium in osteoblasts

Kevin K. Frick and David A. Bushinsky

Department of Medicine, Division of Nephrology, University of Rochester School of Medicine and Dentistry, Rochester, New York

Corresponding author.

Address for reprint requests and other correspondence: K. K. Frick, Div. of Nephrology, Dept. of Medicine, Univ. of Rochester School of Medicine and Dentistry, 601 Elmwood Ave., Box 675, Rochester, NY 14642 (e-mail: ude.retsehcoR.CMRU@kcirF_niveK).

Author information â–º Article notes â–º Copyright and License information â–º

Received 2010 Mar 5; Accepted 2010 May 21.

Copyright© 2010 the American Physiological Society

This article has been cited by other articles in PMC.

Go to:

Abstract

In vivo, metabolic acidosis {decreased pH from decreased bicarbonate concentration ([HCO3−])} increases urine calcium (Ca) without increased intestinal Ca absorption, resulting in a loss of bone Ca. Conversely, respiratory acidosis [decreased pH from increased partial pressure of carbon dioxide (Pco2)] does not appreciably alter Ca homeostasis. In cultured bone, chronic metabolic acidosis (Met) significantly increases cell-mediated net Ca efflux while isohydric respiratory acidosis (Resp) does not. The proton receptor, OGR1, appears critical for cell-mediated, metabolic acid-induced bone resorption. Perfusion of primary bone cells or OGR1-transfected Chinese hamster ovary (CHO) cells with Met induces transient peaks of intracellular Ca (Cai). To determine whether Resp increases Cai, as does Met, we imaged Cai in primary cultures of bone cells. pH for Met = 7.07 ([HCO3−] = 11.8 mM) and for Resp = 7.13 (Pco2 = 88.4 mmHg) were similar and lower than neutral (7.41). Both Met and Resp induced a marked, transient increase in Cai in individual bone cells; however, Met stimulated Cai to a greater extent than Resp. We used OGR1-transfected CHO cells to determine whether OGR1 was responsible for the greater increase in Cai in Met than Resp. Both Met and Resp induced a marked, transient increase in Cai in OGR1-transfected CHO cells; however, in these cells Met was not different than Resp. Thus, the greater induction of Cai by Met in primary bone cells is not a function of OGR1 alone, but must involve H+ receptors other than OGR1, or pathways sensitive to Pco2, HCO3−, or total CO2 that modify the effect of H+ in primary bone cells.


 And here the cardiac connection a small piece out of a huge discussion .
 "If you could develop a drug that would bind to the C-terminus and prevent the interaction with calcium or calmodulin, that might keep the sodium channels working normally in spite of the raised intracellular calcium," XY said. "Perhaps you could prevent arrhythmias in the cases where the cell is calcium overloaded – and we suspect ischemic cells are overloaded."  So  hard workouts with tHb drops or occlusions would have something to do  with this. ???
 Ca++  changes can  create  besides biomechanical problems  as well some problem in the delivery system  ( Cardiac  reactions )
 The key of  intervall  workouts is  to    start to undersatnd  that intervall workouts   based on  subjective  timing idea like  30 seconds  all out  or  60 seconds  all out  as well as recovery based on the same    outside non physiological  informations  can  have great  but as well very negative  results.
 As  usual , as long results  show performance improvement we believe in this type of Zoning or training loads. Once something is going  wrong  we are lost  .


Evans

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Posts: 14
 #11 
Great feedback and help, Juerg!

I'll attempt to do another assessment in 4 weeks and I'll post results.

We are going to polarize her training much more and see where we get. I currently don't have away to live train her with Moxy. I'll hopefully get a watch soon.

And the step was 5.5 mph to 6.5, not 6.6 to 6.5. [smile]

Juerg, I see a lot of articles you post here on the forum. It is greatly appreciated.

What are some of your topic articles and/or books to read up more on your current ideas/concepts/theories/beliefs on the training process? I really appreciate your perspective.

Thanks.
Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #12 
Evans , thanks   and thanks  for the feedback on the speed  as it was otherwise  an interesting reaction  I will re  write the graph  but the suggestion on the next  step test  is the same. What I will review is the reactions  accordingly to the   speed information.
 There is one more interesting section I will  add to  and that is the first  and second  step,. The first one was  for sure  walking    and the second step  I am not sure yet   So do not tell as I like to  reassess the  reactions as  walking is a different sport than running  as there are  very different muscle groups  involved. The second  speed is a n ugly speed  as it c could be  done with very fast  walking  but than it would be not very efficient  in many cases( exception speed  walker)  and  if  you run that speed it is  ugly as well as there is a lot  ore eccentric  loading if you go artificially that slow. Will show some nice    numbers  and reactions   when we shift  from walk to run  for  some older  case studies  we did  and I got    40 years back in   school.
So stay tuned. To your last  questions on books  and ideas.
 There  are  hundreds  of incredible great  NIRS  papers  out there  and they  grow  by the day.
 Nevertheless   not  very  many if any  go into the practical applications you can read on the forum here as we  go along. Remember that  many NIRS studies  just start now  to take of  due to  cost of  equipment. A   current so called  Research graded  NIRS is  above 10'000  Cdn  $  and more. So  doing what we do  with sometimes  4    and more  MOXY's on a  subject   would be pushing a  high expensive     study  and   often the  Universities  already  have a problem to buy 2  MOXY's    for some   smaller    studies.
. So    welcome on our  forum  and we  need people like you and many of the regular readers  to allow the practical coach to move ahead  with ithis nteresting technology. As you can see we  are  very open  with a lot mistakes  but some times  some great  ideas   all what we    find and found  over the last  20 years.  and  we  are still far away  from  being  perfect or even good. But what we  for sure believe is that   it is a game changer in individual  programming of  workouts  and rehabilitation  and it is   not  as  complex  as many believe it is  just a different way of  looking  at  clients  rather over their bodies  reactions than over a  calculator.  So  please   come any time back with critical   feed backs   and we all  Can more forward as we all have a   big baggage of  old  classical  ideas  which we have to  learn to integrate  and review  as  we   learn more over new  technology.
DanieleM

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 #13 
Don't know if it is appropriate to post here the results of a completely different workout (it was 7x30'' All Out) but it was performed the day after another high intensity one.
The reaction looks very much similar to what Juerg highlighted at a second option for sharp desaturation.
rip7x.png  
It seems like the previous workout made the delivery system (I would guess cardiac system) fatigued/overloaded (pink circles)


Evans

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 #14 
Hi DanieleM,

Why are you thinking it is a delivery issue (possibly the heart)?

Was the rest passive or active?

I'm speaking out loud here ...

What I see is that immediately SmO2 rises after the termination of the repetition while concurrent lowering of the heart rate.

As heart rate continues to drop, SmO2 begins to fall suggesting muscle is utilizing more than delivered.

Because of the many reasons why heart rate rises and falls, you're assuming that stroke volume is now falling behind even more with the concurrent lowering of HR, thus less delivery, and more consumption?  Also, you see a concurrent lowering of tHb indicating less blood flow to the area ... but wouldn't compression change this as well? Again why I ask about passive or active rest and what were the positions of the legs during this? 

Just trying to learn and see what you vets are looking at.

I'm also wondering, if it is a SV issue, what mechanisms do you feel are most responsible for this? Considering/assuming there is residual fatigue from the day before?
DanieleM

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Posts: 264
 #15 
Hello Evans,

first of all I am not an expert, so my opinion is not necessarily true.

Regarding your question about the workout, I used a very low power at rest.

Why I am thinking there was a delivery problem:
1. at the start of the exercise, so low power but still SmO2 remains very low for a while and it is not increasing as other times.
2. during the rest time of the intervals, I have another graph, same workout, with SmO2 which remains pretty high and slightly drop towards the end of the rest period. In here I see a fast drop. Since the demand was the same, heart rate quite similar, I would assume the drop was due to SV.

Daniele


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