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Dr Matt

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 #1 

Apologies for long post.

Wondering if the brains trust can critique my reading of Moxy data. Im a Mechanical Engineer so the inner working of the body is not my area of expertise, but I have spent a while reading this forum and trying to understand and I think my results indicate the following is going on

  • Well developed mitochondria concentration in quad muscles from years of racing and interval training leading to….
  • Restricted blood flow to quad muscle by crushing the blood supply leading to…
  • Drop in SMo2 as quad utilize all available oxygen from available blood flow, SMo2 dropping well below 30% leading to…..
  • Increase in H+ and Co2 leading to…..
  • The need to increase breathing rate trying to expel Co2 leading to….
  • Blood flow diversion from upper body to lower body more and more to diaphragm as load increases (respiratory metaboreflex) leading to….
  • Respiratory muscle fatigue from working harder leading to….
  • A further drop in available blood to working muscles leading to…
  • A downward spiral and ultimate failure – RIP.

If that is correct data interpretation then the solution is to improve respiratory endurance (buy a Spirotiger) and increase my heart stroke volume if possible by doing the work out noted a number of times on this site (ride at a power level just below the point where the non involved muscle ThB starts to drop). Is that a correct interpretation of the data or have I missed the mark? 

Thanks for reading, more detailed information below.

********
I have used the Moxy on many 5-1-5 tests, interval sessions, general riding and time trials. But I want to focus on two 5-1-5 tests I conducted where I had access to two Moxy sensors. I didn’t do the 8th interval in both tests as I got the data I wanted. The quad data is typical of what I see with ThB basically flat no matter the load and SMo2 data going down to 5% or less before I blow up. Burning quads is a feeling I know well and I think I now understand why.

Test 1 – Based on the many posts I have read about measuring a non working muscle to view diversion of blood flow - On road bike on trainer, riding on drop bars entire test. Moxy on right quad VL held in place with bib shorts and Moxy on right bicep held in place with strapping tape (no compression applied). At end of interval 1 left leg down, end interval 2 right leg down and so forth. 

Quad Bicep.png

Test 2 – Based on posts I have seen suggesting in well developed cyclists the hamstring is a better muscle to measure for a cyclist - On road bike on trainer, riding on drop bars entire test. Moxy on right quad VL held in place with bib shorts and Moxy on left hamstring rectus femoris held in place with bib shorts (picked left to avoid any issues of NIRS light contamination). At end of interval 1 left leg down, end interval 2 right leg down and so forth.

Quad Hamstring.png 

Combo plot of Test 1 & Test 2 data
smo2 thb.png 
In the excel file attached also included are two other 5-1-5 tests where I have right VL measurement only. The SMo2 response on my quad is fairly consistent, there are some variations in quad ThB. I did not control my cadence very well across the tests, I need to improve that to remove variability. 

******************

Bit about myself. Long time cyclist 15 years +, coming from a downhill mountain biking background using flat pedals, then cross country mountain biking with flat pedals, a little bit of track riding but recently almost 100% road cycling for about 5 years with last 2 years focusing specifically on time trials. Actual power numbers are about 385w for 20min and 335w for an 1 hr. In time trials my 1 hour normalised power is about 355w, I can get my 20min NP over 400w.

My bike position on both the TT and road bike is forward, low and aggressive. I am quad and glute dominant cyclist. For pedal stroke I would say I am a masher on the down stroke. I have problems with Hamstrings cramping in hard races over 2.5 hours, does not impact criterium or TT riding. I have been told my hamstrings are very weak, the comment is “My hamstrings lift less weight than middle aged woman recovering from knee surgery”.

I suspect breathing is a limiter. I have tried exercises contained in the book “Oxygen Advantage” and I struggle to do breath holds of 20 seconds. I definitely am a mouth breather when power gets up to Z3 or above. When I get to load 8 or 9 in the 5-1-5 tests im puffing like a steam train. I think I would benefit from using a Spirotiger but I can’t 100% pickup clear evidence of this in my data, don’t want to spend money on it if I don’t have to and something else is the issue.

I also have a left to right power imbalance based on my Power2Max of around 47-48 left to 53-52 right.

 SMo2 Observations
  • SMo2 quad – Fast o2 drop, it looks like I have no problem unloading the o2 and utilising it. Homeostasis reached for each load step (the absolute value of SMo2 reaches just over 10% - my experience is under very heavy loads I can get to 5% or less). I think this implies I have no utilisation problem in my quad and the issue is delivery related. I can burn any oxygen I can deliver. I think the target for SMo2 is above 30%? So at these utilisation rates I am producing a lot of h+ and Co2 shifting the disassociation curve to the right (??)
  • SMo2 bicep – Homeostasis never reached, infact, the ending SMo2 level for each load is decreasing over time, but it rebounds back to 90% when load removed. Why is the re-oxygenation of blood much higher in bicep when compared to the quads and hamstrings? Is this because its not a working muscle? Closer to heart?  Again there does not appear to be issues with releasing oxygen.
  • SMo2 hamstring –SMo2 in the quad drop fast and reach homeostasis but it drops slower in hamstring – I think this is related to the blood flow into the hamstring. Load step 7 is interesting, the SMo2 is still dropping by end of the load. It is still higher than that in the quad though. Indicates I have a delivery problem at higher loads. Could a drop to very low SMo2 levels trigger the cramps on longer races???? I have tried salt tabs / hydration etc and none of that works.

ThB Observations

  • ThB quad – Blood flow very flat for quad. The blood flow to the quad just does not seem to change meaningfully under any load or recovery. Is this a sign of weak CO or sign of vasoconstriction, possibly due to highly developed mitochondria concentration in quad?? (long time cyclist, lots of interval training). I think it is the 2nd? So that is good from muscular point of view, but I need to improve blood flow (increase SV?) or SMo2 delivery (need to increase stickiness of oxygen to haemoglobin??)
  • ThB bicep - Much different story for bicep, blood flow clearly moving from upper body to “somewhere”. When the load is removed and HR recovers the blood flow returns quickly but drains out slowly. ThB trend is down overall.  
  • ThB hamstring – When load is applied there looks to be a sharp restriction to blood flow, probably due to muscle compression? Then reaches some level of homeostasis after time as CO overcomes this constriction (increasing HR)? This impacts SMo2 response in the muscle.  Given Hamstring is a working muscle shouldn’t the rise in ThB be faster than indicated, is this a sign of a weak hamstring muscle? The response of this working muscle is clearly different from the quad.   
  • Is blood flow being diverted to respiratory system? – I think the ThB comparison chart is interesting. It looks like initially the upper body blood flow is being diverted to the hamstrings and then remainder into the quads. At higher power not all the blood flow is getting to the legs, my assumption is this missing blood flow is being diverted into the respiratory system? I think this is indicating I need to improve the respiratory muscles in order to free this blood flow for the working leg muscles.  

Heart Rate Observations

  • Stroke volume – Heart rate drops back to same level after 2 identical power intervals, suggests for same CO the SV of heart is stable. But is the SV enough?
  • Heart rate homeostasis – Reaches homeostasis during intervals 1-4, from 5 onwards clearly drifting upwards

Cardio Output Observations

  • Based on assumption of stroke volume not diminishing, then if HR is up then cardiovascular output is up and looks ok in general, as in the SV is not decreasing?
  • But I think trying to increase the SV needs to be a long term goal to overcome the vasoconstriction in my quads, is that a correct interpretation of the data? Somehow my cardio system needs to overcome the vasoconstriction in the quads.

Respiratory System Observations

  • It looks like blood is being diverted to respiratory system from upper body around the time the CO system gets maxed and HR starts to drift upwards (from load 5 onwards)
  • I think the low SMo2 levels in the quads gives an indication that the respiratory system ends up being overloaded trying to remove excess Co2 from the system.

 

 


CraigMahony

Development Team Member
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Posts: 169
 #2 
Hi Dr Matt

Welcome. Firstly, I would modify your assessment procedure a bit. I noticed that your VL working SmO2 never goes above your starting resting value. So I think you may have started the assessment at too high an intensity. Your Hamstring SmO2 goes up higher so that indicates that the hamstrings are not working hard yet, but VL appears to be so.

Secondly, I would still tape the moxy onto your leg rather than just let your bike shorts keep it in place. There is better tape than strapping tape to use to do that.

Thirdly, you alternated which leg was in the 12 o'clock position. This changes the trend. You can see that with your VL on the second and third time you had LD, your tHb declined during the rest period whereas it increased or stayed the same when you did RD during rest. We look for trends like increasing tHb during rest intervals, etc, so changing position of your legs makes this more difficult.

Regarding your Bicep SmO2, it definitely reduces during the harder work periods. However, I find that the non priority muscle SmO2 recovery is delayed if the drop was caused by blood shift to the priority muscles. Possibly you started using your biceps during the harder intervals, or at least were not relaxing them. I would be interested to hear from Sebo on this and any other cyclists.

So, do you have a respiratory limitation. I am not sure. One thing we would look for is a rising tHb during the rest intervals. Possibly you do have this in your VL, but changing your legs has made this inconclusive. You seem to have a slightly increasing working tHb in your VL so it is possible you have a respiratory limitation. Alternatively it might just be a muscular compression that is causing a restriction in blood flow out. You can definitely see in you graph of Oxy and deoxy tHb that the deoxy Thb increases a lot in the last few intervals.

Other thoughts.
  • Your hamstrings appear to do little work in the first 4 intervals and are in the Oxy Zone. Then they seem to skip the Balanced Zone and go straight to the Deoxy Zone. So they either need strengthening or perhaps a better coordination in the cycling pedal stroke.
  • In your last interval your VL still seems to be in the balanced zone, although the hamstrings appear to be struggling.
  • It appears that your VL never gets a high delivery of O2, ie SmO2 is never high. This might be due to your placement of the Moxy. This is also why I would be interested in seeing what happens when you start at a lower intensity, to see if in fact it can go higher.

I think another test will help clear things up. A second opinion other than my own would be a good idea as well.
Dr Matt

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Posts: 14
 #3 
Thanks Craig, great feedback for us newbies. Appreciated.

No problem, can do another test in next 24 hours. Been an easy week of cycling this week so will be fresh.

Moxy sensor on right VL and right bicep ok? What kind of starting power, 50w? Load increment between steps, 75w okay? If Moxy is on right VL do you want right or left leg down at 1min recovery? I arrived at the previous method by following the instructions I read saying to alternate left/right leg and starting power was picked by Moxy Garmin app, no issue to change.

On the trainer I was riding in a racing style position to try and simulate the correct responses, my bike setup is low for aero. See attached, i am front rider. I could try and sit up and unload bicep as much as possible for 5-1-1 test if that would help. Sensor mounting as per attached picture.

Attached Images
Click image for larger version - Name: sensor position.jpg, Views: 43, Size: 179.98 KB  Click image for larger version - Name: riding position.jpg, Views: 40, Size: 238.64 KB 

CraigMahony

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Posts: 169
 #4 
Well you could trial the medial deltoid for the non priority muscle. I have my leg with the Moxy on it in the 6 o'clock position, but that is just me. If you get different readings with your leg up v leg down then that potentially shows something. In your case it does seem to.

Maybe rather than doing another assessment, try in your warmup to go slowly and see how high you can get your SmO2 to go. I find that if I start slow enough my SmO2 will rise, then a little harder and it might rise some more. See how much you can gradually increase until the SmO2 levels start to decline. You can then note work out how low your first level should be in a 5-1-5 assessment to be in the AREI Zone / Oxy Zone. You should be able to get your SmO2 to rise significantly above your initial resting / calibration period.




Dr Matt

Development Team Member
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Posts: 14
 #5 
Had some data issues with HR and Moxy sensor at start. Decided not to dig too deep at end and pulled pin. Data looks a bit noisy. Moxy on right VL and left bicep. Right leg down each 1min rest.

515.png

CraigMahony

Development Team Member
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Posts: 169
 #6 
Looking only at the VL, just prior to pedaling your SmO2 is 54. The highest it gets to during work intervals is 59. So you are in the Oxy Zone only until and including the first two double loads, ie the 4th interval. The fact that your SmO2 rises to only 59 from a start of 54 indicates to me the possibility of an insufficient oxygen supply. However, your SmO2 level gets to much higher levels in your DL. The SmO2 levels also keep rising in the DL after the VL SmO2 levels start dropping. So I do not think Cardiac Output is the main limiter.

The tHb on most rest periods shows a drop before usually increasing. In the earlier loads it increases to above working values but in the harder work loads it sometimes only came back to working values, ie not above. During the harder work periods tHb increases slightly. This can be due to vasodilation or venous blood flow restriction or both. As you have drops at the start of many of the rest periods I suspect their is some venous outflow restriction occurring due to muscle compression. This does not discount that there may also be vasodilation as well. The vasodilation maybe an indicator of excess CO2 this a respiratory problem.

I think the main problem is a lack of O2 supply. I think it may come from a lack of capillaries in the VL as opposed to Cardiac Output. Either that or you are very tense when you ride and the muscle tension reduces the blood flow into the muscle. I would be interested in what other think.
ryinc

Development Team Member
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Posts: 355
 #7 
Dr Matt,

Welcome to the forum and thanks for posting your data. I have not worked through data in detail but did want to make a couple of points.

I don't think biceps are a "non-involved" muscle. Medial Deltoid would be better as Craig suggested. Also the Rectus Femoris muscle is actually one of the quad muscles not hamstrings as mentioned in your post. I am not sure if you had the Moxy on the hamstrings and called it Rectus Femoris or the other way around.

Then on your summary - I don't think mitochondrial density would lead to restricted blood flow. The blood flow would be a function of vascularisation (local blood delivery), cardiac output strength and muscle strength.

With extremely well developed mitochondria you would also potentially see sharper drops at the start of the interval (no delivery but utilisation) and then much higher Sm02 rebounds (delivery but no utilisation).

One idea to test whether the bicep (or medial deltoid) is distributing blood vs actually getting more involved is to hardly grip the handlebar with the arm that the moxy is on. If you are certain you are not using the muscle and still observe the shift in THb then you have your answer that it is blood flow distribution.


Quote:
  • Well developed mitochondria concentration in quad muscles from years of racing and interval training leading to….
  • Restricted blood flow to quad muscle by crushing the blood supply leading to…
  • Drop in SMo2 as quad utilize all available oxygen from available blood flow, SMo2 dropping well below 30% leading to…..
  • Increase in H+ and Co2 leading to…..
  • The need to increase breathing rate trying to expel Co2 leading to….
  • Blood flow diversion from upper body to lower body more and more to diaphragm as load increases (respiratory metaboreflex) leading to….
  • Respiratory muscle fatigue from working harder leading to….
  • A further drop in available blood to working muscles leading to…
  • A downward spiral and ultimate failure – RIP.

Dr Matt

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Registered:
Posts: 14
 #8 
Thanks again Craig & Ryan. I will ponder your input over the coming days.

Yes Ryinc, you are right I mislabeled the muscle, it was on the Hamstring muscle (biceps femoris). I will re-run the same 5-1-5 test protocol with the 2nd Moxy sensor on the Medial Deltoid, will try to make sure I dont have any sensor or measurement issues this time.



Dr Matt

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Posts: 14
 #9 
Ran the 5-1-5 test again with a Moxy on Right Quad and Left Deltiod.

515 16_07.png 

Data cleaner than previous test from Bicep.

Its a bit hard to not grip the bar for 1.5 hours, I tried to stay as relaxed as possible. The ThB and SMo2 trend of the Deltoid has that inverted U shape.

Still looks to me like blood being shifted from upper to somewhere lower, possibly the respiratory system as per my previous comment.


ryinc

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Posts: 355
 #10 
Hi Dr Matt

Nice data. I would go along with your  blood redistribution interpretation, but even with the new data I leaning towards cardiac rather than respiratory limitation. 

Not normally a zoning fan for Moxy data - but here it shows quite nicely the concept that at loads something between load steps 3 and 4 is where the limiter (whether respiratory, cardiac or something else) starts to need some help...so in your case i think you could quite nicely use this feedback to control workouts.

Regards
Ryan


Dr Matt

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Posts: 14
 #11 
Thanks Ryan and Craig. Its clear how hard data interpretation is if expert users come to different answers on the same data.

Craig - I think the main problem is a lack of O2 supply. I think it may come from a lack of capillaries in the VL as opposed to Cardiac Output.
Ryan - But even with the new data I leaning towards cardiac rather than respiratory limitation.

Is this because of the difficulty in identifying Cardio as per Juerg's comments?

http://forum.moxymonitor.com/post/finding-the-limiter-7188765
In a brainless step test - including our own 5/1/5   we  can't really see optimal the   limiter  if  it is the cardiac system.

So having thought about it over night I reflected on all comments so far.

I find that the non priority muscle SmO2 recovery is delayed if the drop was caused by blood shift to the priority muscle

This is the zoom in of last double load step, I can see the delayed SMo2 response in priority and non priority muscles indicating a blood shift from non-priority to priority muscle groups.

SMo2 shift.png 
ThB.png 

So, do you have a respiratory limitation. I am not sure. One thing we would look for is a rising tHb during the rest intervals.

ThB rising is non priority but not in priority. So SMo2 is indicating a blood shift is occuring but its not going to the quads. Reflecting on Chris's comment.

Alternatively it might just be a muscular compression that is causing a restriction in blood flow out.

I do see that the non priority muscle ThB rises during the rest period and drop during periods of load. But the quad ThB doesn't change much when there is compression or no compression? Why doesn't the ThB change?

Juerg - http://forum.moxymonitor.com/post/finding-the-limiter-7188765 In  very  great  endurance trained athletes cyclists, the body got  thanks to  incredible great  training  so  good  in vascularisation density as well as mitochondrial density, that the delivery systems  like cardio pulmonary systems  simply has no chance  to   delivery the   O2  which could  be used in all the muscles.  So the CO is  simply   to weak to maintain blood pressure in all the    circulation  and still have a sufficient  one  for the central system.

Ryan - Then on your summary - I don't think mitochondrial density would lead to restricted blood flow. The blood flow would be a function of vascularisation (local blood delivery), cardiac output strength and muscle strength. With extremely well developed mitochondria you would also potentially see sharper drops at the start of the interval (no delivery but utilisation) and then much higher Sm02 rebounds (delivery but no utilisation).


When I first started with the Moxy (and the reason I borrowed a second Moxy to test the theory) my initial hypothesis was the flat ThB profile in my quad against a rising HR could indicate a weak CO due to a reducing SV as the intensity gets harder (CO=HR*SV)? But the other muscles responses have thrown me as the ThB increases and decreases in other muscles. I feel like I have come full circle and my understanding is no less confused  [confused]

So is the following a better interpretation?
  • Well developed quad muscles (high vascularisation concentration??) leading to….
  • Restricted blood flow to quad muscle due to a weak cardio ouput (first limiter, possibility due to decreasing stroke volume??) leading to…
  • Drop in SMo2 as quads utilize all available oxygen from available blood flow, SMo2 dropping well below 30% leading to…..
  • Increase in H+ and Co2 leading to…..
  • The need to increase breathing rate trying to expel Co2 leading to….
  • Blood flow diversion from upper body to lower body more and more to diaphragm as load increases (respiratory metaboreflex) leading to….
  • Respiratory muscle fatigue from working harder (second limiter) leading to….
  • A further drop in available blood to working muscles leading to…
  • A downward spiral and ultimate failure – RIP.
?????

ryinc

Development Team Member
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Posts: 355
 #12 

Hi Dr Matt

Yes, i agree that most the interpretations are really hard, but this is also what makes this fun - it is not 100% clear what the answer is.

I am not an "expert" user as you put it - most of us on here are just different levels of amateur [wink].  So be careful to discard your own views of what is going on in an interpretation – sometimes you might find you are the one that is right, and others’ interpretation is wrong.

Even though there are differences in the interpretation of the case here, also consider some of the commonality - nobody is saying that muscle oxidative capacity or utilisation is the limiter here - so in my view, even if the limiter itself can't be pinpointed, eliminating what the limiter is not can be a potential huge step forward.

Just to respond to some of the points and add additional perspectives on the thinking – (the idea here is to stimulate the discussion and build on thoughts rather than convince that one set of thoughts are more valid than another):

  • The reasons I have a different view about the local delivery being the limiter are the following :

(1)    my understanding is that mitochondrial density development would normally follow vascularisation development – i.e. it would seem unusual to be able to de-saturate quite low but poor capillary development. (e.g. refer to http://forum.moxymonitor.com/post/bike-515-8486620?highlight=gunnar&pid=1295624218 )

(2)    I am thinking of extreme cases. If cardiac output was very strong, but there were limited capillaries to push blood through, what trend would I expect to see on THb during rest periods when compression is removed on the working muscle vs if there was extremely weak cardiac output but a very well developed capillary bed. What might we observe when the compression on the muscle is released? (General caveat here is that THb trends on VL might be influenced by your leg position during resting periods so the impact of this should be explored).

  • Look at your heart rate data. What happens to HR, compared to the prior load steps, at the same/similar point at which blood is potentially being redirected and what could this indicate?
  • You quoted “One thing we would look for is a rising tHb during the rest intervals.”,  To be clear, what I am talking about here is rising peak THb values. So on the working muscle we don’t really see big changes between the internal and rest THb (peak THb’s almost don’t exist on the working). On the non-priority the peak THb values, if anything, appear to be declining.
  • I think in just about any athlete in a 5-1-5, there is always going to be an increase in C02, and the respiratory rate and tidal volume are going to increase, the lungs bloodflow requirements will increase and by the end of the assessment breathing will be more “strained”, but this is true even when respiratory system might not be the limiter (the same as you would always/almost always see a heart rate increase, but that doesn’t necessarily make cardiac output the limiter).
  • I think on your summary. I would be cautious to make the call of x leads to y, leads to z. There are some things we can hypothesize from the data, but I’m not sure that all of the statements and interactions of the statements of such a detailed and hard defined interpretation are clearly and easily supported. I’m not saying that they are wrong, I’m just not sure what the observations are that would give us clear confidence that they are correct. 
CraigMahony

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Posts: 169
 #13 
Dr Matt

I also am no expert. 
Regarding your new set of data I would make the following comments.

If we looked only at you VL moxy and disregarded the fact that you had a second one on you DL I would have said you had a Cardiac Output limitation as your working SmO2 starts deflecting downwards after the first pair of intervals. Your resting peak SmO2 starts deflecting after the second pair of intervals. However, we see that the DL working SmO2 does not deflect downwards until after the fourth pair of intervals. If Cardiac Output was the limiter I believe the DL SmO2 would start dropping prior to the VL SmO2 as oxygenated blood would be redirected to the working muscle. So I think there is another limiter before the Cardiac Output limiter (or probably compensator) is reached.

The fact that SmO2 initially at rest is low and that working levels rise only a small amount above this leads me to believe there is a shortage of O2 to the working muscle. Initially, I though it was due to a lack of capillarization in the muscles not allowing blood to get in sufficent quantities to get in. However, in your oxy/deoxy graph, your deoxy level is already higher than oxy at rest before you start the first workload. To me this is unusual. So I wonder if there is any restriction. Are you wearing compression shorts? Is your VL actually relaxed when resting? I think this is the key to what is going on.

After the second pair of intervals the O2Hb levels, both working and resting start to decline. Whereas the HHb (deoxy) levels, both working and resting start to increase. I would normally put this down to a respiratory limitation as your blood may not be fully replentished with O2 due to excess CO2. However, the fact that your HHb level is greater than your O2Hb level at calibration makes me unsure.
Dr Matt

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Posts: 14
 #14 
Thanks guys. ANyone who knows more than me is an expert :-)

Standard cycling shorts are worn, I wouldn't say they are compression shorts. But...... I do notice that when I remove the Moxy sensor and light shield after a workout I can clearly see the horizontal indentations of the light shield, I can even see where the NIRS emitters were. So its being held firmly against the skin. The sensor worn on the Hamstring was also under the shorts and didn't seem to display the same trend. Inserting thought thought, I will test it on quads without shorts over the top next time to be sure.

I dont have a good understanding why ThB blood flow would not change under increasing HR & CO. Its almost like something is restricting the cross sectional area of the delivery systems veins/capplieries directly inversely to CO. Initially I thought it might be muscle compression forces, but then after thinking about your comments last few days I should get a quick increase after the load is removed if that was the case and that does not happen. Not sure what other mechanisms could do that? 
 
CraigMahony

Development Team Member
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Posts: 169
 #15 
Have you looked at the bike fit moxy webinar? That might have some clues.

What happens if you sit in a more upright position instead of an aero position? I am wondering if it is your actual position that is causing a blood flow restriction.
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