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sebo2000

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 #1 

On the weekend we did 5-1 run assessment with one of my friends, I didn’t see him for a long time, he said he started to run, but noticed his HR spikes quite a lot initially, and sometimes when he runs a cross the street he feels dizzy for a moment, and he feels his HR goes up by a lot very quickly.

 We started very easy, since treadmill only had speed control in miles, we did following speeds:

 

Lap 1 - just standing on the treadmill, after putting the shoes on etc.

Lap 2 – 3 mph

Lap 4 - 3.5 mph

Lap 6 – 3.5 mph

Lap 8 – 4mph

Lap 10 – 4.5 mph (fast walk)

Lap 12 – 5mph slow run from now on

Lap 14 – 5.5mph

Lap 16 – 6.5mph

Lap 18 – 7.5mph

 

Moxy on right VL and Left Medial Deltoid, we also monitored SpO2. During one minute stops we stop completely in the same position standing up still, not moving.

 

We didn’t have time for 5-1-5 but I wanted to get very low speeds. Before the test he said when he starts running his HR is usually HR170 in just few minutes then it drops down. (He is just recreational runner, not an athlete, but that felt like he has broken HR monitor [smile]

 

Interestingly enough HR while standing 75HR, then he starts to walk and his HR quickly goes up to 130HR, during first rest his tHb goes up, but SmO2 drops in both cases Deltoid and VL.

Lap # 4 same behavior but HR goes up to about HR121, during rest exactly the same behavior tHb up SmO2 down.

 

In lap #6 HR normalizes and drops to 85bpm, almost looks like some adjustment in Stroke Volume, but I’m surprised it happens at very slow walk.

 

What surprises me is SmO2 behavior during rests, it actually drops each time, while tHb increases, this looks like some kind of serious Arterial Occlusion, HHB increases during rests while O2Hb decreases? Since tHb still increases during rests this does not look like Venous Occlusion.

Each rest has very similar pattern indicating we did assessment properly and this is actual reaction. Lap – 9, Lap – 11, Lap 13, Lap – 15, Lap 17

 

Initial rest laps have very pronounced tHb increases but with downtrend pattern, we can observe that on both Moxy sensors, then tHb is not increasing that much on VL but does not spike at all on Deltoid, it does not look like respiratory problem, but some very strange Cardiac behavior. HR increases and drops quickly indicating healthy “pump”, but plumbing looks clogged? (I know this is not medical term) each time when new start interval SmO2 spikes back for a moment CO kicks in, and pushes more arterial blood, then muscle uses the O2 and it equalize SmO2 during the run portion.

This looks strange, because I have never seen similar patterns, any comments would be really appreciated. Initial tHb on VL is very high.

Sp02 data confirms initial low SpO2 trend (94-95%) while walking first and second lap, then only increases.




OlszSmo2.jpg 
spo2.jpg 


 
Attached Files
xlsx 5-1-5 Run TO VL Delt HR.xlsx (212.64 KB, 3 views)

juergfeldmann

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 #2 
Will give it a closer  look very intriguing   information.
 Did  you  guys   had   HRV  feedback  from the HR  as well.

What is  his  resting BP  and did  he had a  EKG  done lately ?  Thna we   he stopped the 1 min  was he jumping  one leg  left and  one leg right on the side of  the still running treadmill or  did  you actually stopped the treadmill ? When he  jumped  to the side  was he   still holding ion the side  rail or   was he  standing  without  holding ?
sebo2000

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 #3 
Thanks Juerg,

We didn't do HRV, he said he felt good, and was recovered, he runs 2 times a week 30 min each time, so nothing big, very recreational activity, last time he run 3 days ago. I told him to be fresh for this assessment.

During stops we actually stopped the treadmill completely, full stop, he was standing on both legs equally, hands down, didn't hold anything. I didn't ask for EKG, but his data really looks strange, he looked good during the run, but honestly he looked better mid assessment and at the end that at the begging, at the begging looked kinda paled.








juergfeldmann

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 #4 
If  you stopped  the treadmill  to a  complete  stop how long  does this  takes in seconds.
Was  he holding the side rails  as  it slowed  down and  than  let go  or was he always  holding the  side rails.?
How as his  breathing  reactions    during the walk  run and than  during  the stop phase.
 Where  you  checks  SpO2   you as well have   pulse  rate.  was the pulse  rate  equal  HR  from the chest belt   to ensure  proper  SpO2  readings. ?
Gunnar

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 #5 
I've had problems with a Suunto watch giving me also HR values at around 180 bpm at the beginning of runs. The real heart rate was considerably lower and I can not even get to 180 bpm in real... 
Maybe he has a similar problem with his heart rate monitor?
sebo2000

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 #6 
He never hold the rail, first 6 sections was walk from slow to very fast, then run, didn't hold the rail at all. takes about 10 seconds from pressing stop button to complete treadmill stop.
We only check the pulse and SpO2 HR reading initially during first 4-5 walk sections, and it was the same as HR strap, we didn't check later during runs. I have to adjust my meter to record pulse.

sebo2000

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 #7 
Gunnar I'm quite positive HR was correct, I use this strap myself and it is correct, plus we matched it with SpO2 meter at the begging, first 4 sections.
Plus he noticed the same during his runs, his HR goes way up at the begging then goes down.
juergfeldmann

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 #8 
If  we have  HR  and pulse  rate  identically  than we have a relative  good feedback that the HR was most likely what  you guys  saw. If  we have interference than HR  is often off  and  pulse rate is  still okay  so  that's  where  SpO2  and HR  is an  interesting combination to have   once in  while during assessments.  There is a limitation in  SpO2  sensors  or in any   pulse rte  feedback. ( Occlusion trends)  so we loose the pulse  rate. So  all the wrist monitors   working on pulse rate  will have problems    in sports like  MTB  or  climbing or  cross country skiing where we  may have a  high activity of  forearm  muscles.
 Than   SpO2  sensors  are not   very accurate   as  soon  you have additional  motion  so  during running much less likely to have optimal readings compared  to walking.
ryinc

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 #9 
I dont want to be alarmist but is it possible that there is some.kind of arrhythmia/af that occurs at the start of the assessment which then goes back into synch later? I would suggest having it checked out properly.
ryinc

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 #10 
Possibly extremely low blood pressure at rest?
ryinc

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 #11 

Sebo, had a closer look at the 1 min breaks with bias graph. Definitely, the HHb increases by more than 02Hb decreases implying that there is some HHb pooling (see one example below). Now if this was only occurring on the VL muscle, I would have bet that this is some kind “technique”/mechanical reaction that caused the pattern. What is absolutely fascinating is that you see the same thing on the Deltoid muscle – hinting that it is systemic.

Occ.png 

I am not sure that it is an arterial occlusion though, because in that case would we not see tHb flatten out, but Sm02 continue to drop? (Or in bias view HHb continues to rise, stay flat, and 02Hb continues to drop sharply since it will be the supply side that gets cut off). Instead we see Sm02 flatten out (or recover) at some point, suggesting a slight release of a venous occlusion perhaps rather than the arterial occlusion being created?

You can also see that the HR on recovery is quite erratic – not a nice smooth downwards trend.

So to me it seems that the various mechanisms within the body that function together to control blood pressure are perhaps out of synch with each other – for example perhaps the vasoconstriction is so strong that it actually causes an occlusion reaction on recovery, then the HR responds slightly relieves the occlusion slightly, Sm02 recovers slightly etc. This might also explain the early HR reaction, where HR reacts abnormally to perhaps compensate for something else that is not working properly in terms of blood pressure management?

Even if this is possibly what is going on, it is still not clear to me, is it because of low blood pressure, some kind of cardiac issue, some kind of vasodilation/vasoconstriction issue, or is it simply that these things are not working well together.

Very interested to hear thoughts from those with better physiology knowledge.


sebo2000

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 #12 

I touched base with my friend today and right from the bat I asked:

 Dude, what is happening, tell me everything… He goes: so you actually saw it? (I got him at this point)

I said sure, tell me everything.

Year ago, he stated to feel really bad during his runs especially at the beginning, went to the doctor they have checked him out and immediately asked him to install stents 50%-60%-95% block, so he got two stents installed, he is still on aspirin, brilintaz, l-lysine, Proline, L-arginine, CoQ10. Vit C

Initially he did Edata and phosphatidylcholine for 3 months twice a week. This looks like genetic gift from his mother side. High lp(a) 1300

That explains the strange Moxy readings. Does anyone have data examples from similar case?

juergfeldmann

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 #13 
look at  our  master  chef  ryinc

 What is absolutely fascinating is that you see the same thing on the Deltoid muscle – hinting that
it is systemic.


Tachycardia at  a  start of  activity  can be   benign  or  malign  will  come back later.

rinc
I am not sure that it is an arterial occlusion though, because in that case would we not see tHb flatten out, but Sm02 continue to drop? 

 Deliver  limitation SmO2  drops. The  similar trend  like in venous  occlusion  when there is a  problem  with respiration  and cardiac  partnership  and  SpO2  was  most likely  as well. Test your  HRV  and play  with respiration and look what happens  to HRV. If there is not  an optimal  contraction of  the heart.
 Will try to  get a  case   picture of  what happens in  this case  most likely   in the heart with some physio flow pictures.  have  to dig in my mess. 
  As well will check  some otehr trends we see in cardiac  limitation  clients  and athletes. 
 In this case we now know hat it was for sure a cardiac limitation so go back and look  the  graphs

.ryinc

So to me it seems that the various mechanisms within the body that function together to control blood pressure are perhaps out of synch with each other 

ryinc,
when  do you open you gourmet  restaurant ?  great great  fun to read  all you guys loud  thinking.

  Shy  question.
 Is there  somewhere a  forum out there  with this  quality of  loud  thinking. That  does not mean we are  right,  but  at least we  try to make some physiological sense from data  collected  with a  very simple small but genius   equipment  NIRS/ MOXY. 
 Can you see, why this is  so much  more  fascinating than using a  calculator and a  formula  to    make some   statistical  speculations. ?

Thanks to  all  for the  fun  feedback  and  great  discussions.

sebo2000

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 #14 
Just speculating (thinking out loud), I'm puzzled with 2 things:

1. Initial HR spike in first 2 sets.
2. 1 min rests SmO2 behavior.

a1. Can this be caused by blood thinners he is on, initial delivery limitation to about 105bpm when system is warmed up and delivering enough O2, additionally his blood work shows he is low on Iron, he could have additional issues with O2 binding.

a2. His arteries are blocked, not sure how much, but blocked for sure, so reduction in arteriolar diameter will increase vascular resistance and decrease blood flow (during recovery it will happen really quick), changes in arteriolar diameter are primary mechanism our body is using to regulate blood flow.
I read somewhere that 10% increase in vessel diameter will increase blood flow by 46%, only imagine opposite situation.
When he stops, HR drops CO drops, delivery is limited and smo2 drops very quickly, then when he starts we do see spike as system is trying to compensate. Now due to partial blockage, system is trying to "sync" and it does it, but with all the erratic symptoms described by Ryan.







ryinc

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 #15 
Sebo, could it be the opposite? The stents have unnaturally opened the circulatory system, and vasodilation/vasoconstriction is in effect taken away as a means to control blood pressure (i.e. the diameter of the vessels is more "fixed" after the stent). Therefore at the beginning of the workout, the circulatory system in a sense is too "open" and HR  has to try to react urgently to maintain blood pressure. Further into the workout, it normalises and the diameter of the vessels is closer to what it would be in the case of a fully dilated vessel would by in that intensity in any case due to vasodilation and SV has also had time to increase so less reliance is placed solely on HR to maintain the BP.

As an analogy, i imagine it as a fire hose - if the stream of water coming out of the hose is not strong enough, the pressure in the hose needs to be increased. This can either be done by (a) squeezing the hose (vasoconstriction) or (b) by opening up the tap supplying the hose (cardiac output). A "normal" person would use both in conjunction i would imagine (i.e. vasoconstriction/vasodilation plus cardiac output reaction). A person with a stent might not have option (a) as easily available so they have to react through option (b).
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