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sebo2000

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 #1 

We are going away next week on vacation, I’m not sure if I will have chance to visit the forum, I hope I will, but I’m not sure, I will be collecting Moxy data while practicing my double pulling technique, or rather learning it [smile]

 

I decided I will leave another puzzle for you to play. It is kind of very unfair and in my opinion impossible to guess, yet you never know, Moxy KungFu is super strong here [smile]

 

2 Moxy monitors, one was right VL and second left Deltoid

 

SMo2 , tHb (darker colors) – Right VL

SMo2 -2 tHb-2 (light colors) – Left Deltoid

 

I’m also attaching csv data from both Moxy sensors.

 

To get you started: I didn’t use any compression bands or socks etc.

And to make you feel better and not afraid to share your opinion. I totally do not understand and can’t explain what happen in lap 3 and lap 5. I hope I will have good understanding what happened by the time we are done, same as in the case of compression socks.

workout2.jpg 

 
Attached Files
csv Moxy_30_Jan_2017_Left_Deltoid.csv (25.98 KB, 4 views)
csv Moxy_30_Jan_2017_Right_VL.csv (26.83 KB, 3 views)

ryinc

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 #2 
Thanks Sebo these are fun! Will do some "homework" and come back with guesses!
ryinc

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 #3 
Hmmm big chance of going totally wrong here, but i will share my thinking even at the risk of being completely wrong!

Ok let's start with the VL priority muscle. Lap 2 and Lap 4 have decreasing Sm02 and increasing tHb.

VL traces.png 

This could indicate:

  • A right shift of the dissociation curve either through respiratory system limiter or through a planned respiratory manipulation (C02 causing vasodilation causing tHb to rise, and Sm02 drops because of a reduction in the affinity for oxygen)
  • A venous occlusion either through muscle strength limiter or a planned manipulation
Now if it was a 5-1-5, we would know that at the end of 5 minutes it would be a recovery and we could use that to help decide which of the above options it may be. If Sm02 rises, and tHb drops that would hint towards an occlusion, if Sm02 rises more slowly and Thb rises immediately that would indicate the dissociation curve. We don't know for sure that there was a break at the end of lap 2. Nevertheless it is still useful to have a look. We see at the start of lap 3 (and lap 5 after lap 4) that tHb drops rapidly and Sm02 rises. This seems to point to the occlusion being more likely, and that laps 3 and lap 5 were a recovery/light load.

We can try to validate this in two other ways:
  1. We can have a look the non-involved muscle - we would expect to see a drop in Sm02 on the non-involved during lap 2 and lap 4 if it was a respiratory curve shift. We don't see that. It seems to be rising in both cases.D traces.png   
  2. We can have a look at the bias graph of laps 2 and 4 for the VL muscle. Here we can see the amplitude for HHB does rise above the amplitude for 02Hb (see the mirror image to see this easily). This therefore seems to be confirm that there are occlusions on lap 2 (first graph below) and lap 4 (second graph below) for the VL muscle.Bias VL Interval (Lap 2).png  Bias VL Interval (Lap 4).png 
Ok now moving onto the non-priority muscle: The first interesting observation is that in laps 2 and 4 there is a wave trend. In lap 4 the amplitude seems to reduce over time. Presumably this is some form of vasoconstriction/vasodilation over-under reactions that converge to stability. Here is the graph again.
D traces.png 

Then the next interesting trend is the rapid increase in tHb in laps 3 and 5. These coincide with the drops in tHB on the VL at 3 and 5. If you look at a bias graph for non-priority muscle you can see that these spikes are caused more by a rise in 02Hb than a rise in HHb. see below (again mirror images help to show this).

Bias D.png 
The last interesting piece is that when the tHb shoots up on the non-priority, it shoots up then drops slightly. On the VL, on the release of the occlusion it drops, then has a small spike and drops again. Clearly there is some kind of systemic bloodflow reaction going on here.

tHb traces.png 

So what does this all mean. I really don't know. It is clear that the tHb of the VL and non-priority muscle are closely linked and the body is directing it as required.
  1. Hypothesis 1: the non-priority muscle vasoconstriction completely releases when the occlusion at the VL is released, allowing blood to flow more freely?
  2. Hypothesis 2: Somehow when the occlusion is released, a much greater bloodflow returns to the heart, which then spikes bloodflow into the non-priority. 



bobbyjobling

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 #4 
A play with gravity force?
ryinc

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 #5 
Thats out the box thinking!
sebo2000

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 #6 

Hi Guys,

 We just came back from our ski trip, sorry for not giving some more hints sooner, we had access to the internet, but I was so tired each day I was going directly to bed [smile] I have new level of respect to all cross country skiers… Super humans.

 Going back to my puzzle:

 Wow even without any details you guys almost got it!

 Bobby please collaborate [smile] you are very close and on the right track, but people might think I went to the moon or invented antigravity device [smile]

 Ryan yes, systemic blood flow reaction 100%, caused by…

 Many times we are saying we should not be looking at the “absolute” numbers, but in this case this was one of the clues: Lap 1 was calibration lap, notice my VL SmO2 about 60, then never goes down below that number… Similar with deltoid we never see Smo2 decreasing even for a moment. I honestly didn’t do much if anything at all, besides having my eyes open and listening to some tunes [smile]

 Rayan, I’m still learning to analyze bias graphs; by any chance do you still have file showing lap 2 from VL, could you post it here? So this graph shows very slight increase of HHb over 5 min time is that correct? If yes, then Moxy can show really very fine difference, incredible!

Here is me on CX trail, honestly I would say it is impossible to do 5-1-5 on the trail, but we all have seen XCskier data showing perfect increase in HR steps…My HR 125, perceived exertion 10/10, I could not even see any data during exercise as it is impossible to look at the watch and ski[smile]
I had every muscle working except those that should be working..., my technique was absolutely bad, regardless it was super fun as my daughter and wife were also learning. 



IMG_2409.JPG      


bobbyjobling

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 #7 
[rofl]

I have to say that Ryinc explanation helped me with my conclusion without some of his points I would have missed it, see image below and stick man body position. Pink area = transition to next pose.
But I haven't done a test on deltoid  

3054612.jpg 

ryinc

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 #8 
Sebo not sure i have the file, when i have some time i will create a little excel based bias grapher for you.

To answer your question, In lap 2 and 4 VL graphs what we see (slightly) is:
Positive Change in HHb>Negative Change in 02Hb.

Where the "change" is measured from their values from the chosen fixed bias point, e.g. start of interval.

I simply create a mirror image so that you can see it more easily as sometimes the differences are slight.

For example in occlusions, the blood is pooling but the HHb will increase slightly more than 02hb will reduce because its deoxygenated blood that is pooling. I assume that there is some kind of similar type of effect going on here, related to whatever you did!
.
.
sebo2000

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 #9 
I'm totally blown away by the knowledge of forum members here, this was really hard puzzle without any details at all! 


Here is me during that exercise (pics below) , I used my very unused inversion table, I did not do anything during between position changes, just kept my eyes open [smile]

I'm very surprised Moxy was able to detect VL work while standing up, I have to admit during the test I felt my VL is not totally relaxed since I was standing, and I was wondering if that slight "work" will be detected and how. It was actually detected in the from of increased HHb, I'm very impressed.

There is something I do not understand:

Lap 3 and 5: (upside down)

VL tHb decreases and Smo2 increases we do have more O2Hb in VL.
on Deltoid tHb increases but that also causes increase of Smo2? Opposite tHb trend from VL, but causes the same Smo2 trend? Biased graph below shows increased O2Hb on Deltoid and when looking at VL it also shows increased O2Hb? How come?

It almost looks like we are getting increased O2Hb on VL and deltoid when in upside down position, or I'm not looking at the charts properly? If that is the case and O2Hb increases in both places, wouldn't that be ideal "recovery" position instead of all fancy socks and pumped sleeves "devices" etc.



Lap 2,4,6 (normal state)

IMG_2502.JPG 




lap 3,5 (workout[smile]

IMG_2504.JPG 


ryinc

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 #10 
Sebo, on the VL upside down is it possible that standing upright the muscle was being utilised a bit but when upside down it has basically zero utilisation. In such a case tHb might drop but 02Hb might still increase? Also i think perhaps the 02hb increase might depend on the point from which you start your bias?

Example, say thb = 12, and hhb =9 and. o2hb = 3. Then say thb goes to 11.8, hhb goes to 8 02hb = 3.8. Even though thb down, smo2 and 02hb would be up.
sebo2000

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Posts: 227
 #11 
Hi Ryan,

Looking at VL Lap 3,5 O2Hb increases by a lot and HHb decreases a lot (HHb and O2Hb chart in Golden Cheetah) almost like blood shift would cause very good oxygenation on my VL, I have no clue about cardiovascular system, could this be venous blood shift causing increase in O2Hb, but then the same venous blood shift should increase HHb on deltoid but that is not the case?









ryinc

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 #12 
Sebo the venous blood from VL would not go straight to the deltoid. It would return to the heart. The increase in thb on deltoid is "other" blood, in the arterial rather than venous system. Not sure i understand your question?

I am definitely not knowledgeable about cardiac system either!
sebo2000

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 #13 
Venous blood would go back to the heart I get it, same as in the case of compression socks.

I understand that decreased tHb on VL and increased Deltoid tHb is caused by position change and blood shift to the upper body while I'm upside down.

I will try to rephrase the question:

Why decreased tHb on VL increases SmO2 and at the same time increased tHb on deltoid also increases SmO2. (Increase in deltoid could be explained by more arterial blood in that position)




bobbyjobling

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 #14 
One reason for smO2 increasing and tHb decreasing when inverted might be due to blood flow velocity going up. The pressure difference in & out of the capillary is greater due gravity helping with the venues return, the mean pressure within the capillary is reduced so tHb will go down.
Opposite will happen to the deltoid
sebo2000

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Posts: 227
 #15 
So if we see reverse position helping with venous return on our VL, and we also observe tHb increase on deltoid due to increase of arterial blood, I'm assuming since heart is in upper body and now we have upper body reversed we will have increased arterial pressure in our reverted upper body...

Having said all that, I have to say reversed position is really awesome for recovery, I'm not sure how it affects all small arteries in our brain and what affect it has on them, but from muscle perspective, that is win win position? Can somebody argue otherwise? (I'm editing this post to add: awesome recovery position for cyclists [smile] 

Is anyone here practicing reverse daily recovery? 

People spend big bucks on recovery shoes with pumps etc, massive complicated systems, that seem to help with just that: venous return and all they have to do is simple head stand...

I think I'm gonna use my table a lot more now [smile]







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