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kptrzk

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 #1 
Did a few short (5min or less) intervals yesterday using SmO2% as guide for time on and recovery. Something stood as out as odd - after stopping the work interval, SmO2% dropped steeply for a few moments then recovers steeply. See image below. Have any of you experienced this or have any understanding of why this occurs?

Thanks,

10.7.19 Intervals.jpg

tristan

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 #2 
I suspect a repository problem, it is definitely some sort of systemic issue. This is one of those situations where the repository data from a gas analyser is very useful.

Otherwise pay attention to what is happening to your breathing pattern during the session to pick up more clues.
jankubes

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 #3 
This happen usually when you go full gas, so the body, muscle, need even after interval finish more oxygen. I have experienced during my workouts, how low it goes. But if you stop workout with no additional O2 requirement (such as jogging) you are fine. just stop and wait until SmO2 rises.... you will be fine.
Kim

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 #4 
I read this as a delay in SmO2 rebound, which is a pulmonary limitation. Have you tried breath work? 
ryinc

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 #5 
Very interesting...and this is what makes Moxy so fascinating.

Could i just make a few observations with respect to the respiratory interpretation:
  •  Normally the respiratory limitation being referred to (build up of C02 causing dissociation curve to shift right) would result in a delay in Sm02 rebounding. Here we are observing a sharp drop in Sm02, and the slope is much steeper immediately after the interval than just before the end of the interval - why would Sm02 drop more quickly when demand falls
  • With the respiratory limitation we might expect to see maximum recovery Sm02 decline as the intervals progress. Not sure if we see this very clearly, maybe a little bit.
  • With the respiratory limitation the C02, and vasodilation effect would build up, and so might expect to see tHb levels rising across intervals. I am not sure there is very clear evidence across intervals (tHB increases within the interval but not so much across intervals).
  • lastly the tHb rises very quickly at the onset of recovery which points to possible local  effects.
Just as an example of alternative interpretations:
  • is it not possible that at the end of the interval, for some reason there is a very momentary but very strong contraction on the muscle being measured causing an occlusion effect, causing a rise in Thb and a drop in Sm02. You might expect to see tHb not rise as quickly after such an effect (i.e. once the pooling effect is released), but possibly this is 'masked" because tHb is strongly increasing anyway because muscle compression from the more general interval is gone so there is a strong tHb flow.
  • Is it possible that after the interval, desaturated blood on the venous side flows "backwards" into the muscle (e.g. due to a poor functioning valve on the venous side/and or gravity effects) causing tHb to increase but Sm02 to fall?
See for example the following https://www.jobst.com/mainnavigation/leg-health/veins-valves.html

"Healthy legs have veins with smooth, elastic walls that are perfectly designed to adapt to the changes in pressure within a vein. Veins have valves that keep blood moving in one direction: back toward the heart. As the leg muscles are activated, the venous valves open to allow one-way flow in the direction of the heart. When the muscles relax, the valves close to stop any back-flow.

But if the walls of a vein have been damaged by varicosis or thrombosis, the vein may dilate and the valves fail to close properly. When valves fail to work properly, blood flows backward into the veins."

I'm not suggesting respiratory limitations are necessarily the wrong interpretation here, just pointing out that maybe worth exploring/making sure not to eliminate other possibilities too quickly.

Running the same workout with Moxy on non-priority muscle might help to identify whether systemic or local.
jankubes

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 #6 
Hi,

this "Running the same workout with Moxy on non-priority muscle might help to identify whether systemic or local" seems to be good idea.

I am using moxy for over a year, daily, training, racing. got better result than racing even with powermeter on bike.

For example I know, how long I can run full speed from my steady state (AE) SmO2 until total ex. 😉

In addition my FEV, FVC etc. are quite good, due to using POWERbreathe several years :-). 
tristan

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 #7 
The main reason I suggested a repository issue is the exceptionally long tHB "peaks" in the rest intervals. Especially the 2nd rest interval. That tHB peak is really abnormal, how it levels out like that for almost 3 minutes. It makes me think that the CO2 must be hanging around instead of being exhaled.

So a breathing pattern problem rather than just respiratory insufficiency. Also why does the the 2nd rest period have such an unusual tHB pattern yet the rest periods before and after have more normal peaks, even if the peaks are suspiciously wide. It suggests to me that the athlete is doing "something" at the end of the active part of the interval. For example breathing in a deep controlled manner during the active part of the interval and but returning to a disordered repository pattern during the rest. Or perhaps even something like EILO which is kicking in when the athlete relaxes.

There is also the possibility that there is something wrong with the data. I have had an incident with similar, but more extreme tHB behaviour. It was a once off and characteristics like complete saturation made it clear that the data was faulty.


kptrzk

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 #8 
Interesting to hear the responses. I do very controlled breathing through these sets. In through the nose slowly and a forceful exhale through the mouth. Once breath rate increases I will take in air through mouth and nose and out through mouth.

Here is an hour long interval I did last night avg 340 (threshold approx 390). The same dip in SmO2 occurs after the workload is ceased. Any insights gathered from a longer working session? Thanks!
10.8.19 wout.jpg 

MoxyPhysiology

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 #9 
Thanks to everyone for their insightful comments on this post!

@kptrzk, my initial observations are as follows:

1) Throughout your intervals (both above and below threshold) there is a slow but significant increase in tHb, which indicates that a venous occlusion is present, this just means that your muscle is contracting hard enough to limit outflow of blood from the muscle.

2) The intervals that were completed in the first graph were above threshold, indicating a higher reliance on non-aerobic metabolism (glycolysis and creatine phosphate), therefore, it is possible, that a large amount of CO2 was building up in the microvasculature causing vasodilation, as well as shifting the oxy hemoglobin curve to the right (oxygen doesn't bind as well) this could lead to lower global oxygen binding immediately following the interval (you could measure this by pulse oximeter), so while you might be increasing blood volume to the muscle, the effect of CO2 may outweigh this causing a further drop in oxygen as the mitochondria continues to use oxygen to replenish non-aerobic stores. 

3) For the second graph, while there is a small dip in SmO2 after the cessation of exercise this could an artifact of movement or another confounder. I think that if you wanted to test it again, you would have to do some more intervals above threshold and see how things respond. If there is a tendency for this to happen, you could consider increasing your respiratory rate during your intervals to blow off more CO2.
ryinc

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 #10 
Thanks MoxyPhysiology. I am not sure i understand point 2. At the start of an interval it is argued we see a drop in smo2 because local ("non aerobic") oxygen stores at the muscle are used. I struggle then to understand why we would see a drop in Smo2 when these same stores are replenished. I.e. if its measuring "crediting" this oxygen at the start before the interval, it should also be "crediting" in the reading in the replenishment?

Hope i am explaining myself ok.

Also why a faster rate of drop in Smo2 in replenishment than when the load is there? Surely overall oxygen demand is MUCh higher with the load on, than the demand of the replenishment (and we know delivery of oxygen would not have materially changed in a short phase)
MoxyPhysiology

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 #11 
@ryinc yes at the beginning of exercise we see the steep drop in SmO2 as local oxygen levels are depressed in response to exercise because the heart cannot deliver enough oxygen via the blood right away. Point 2 was mostly speculation. But to try and explain better. After the intervals are completed, the mitochondria need to continue to utilize oxygen in order to replenish (rephosphorylate) non-aerobic stores, potentially causing a further depression in oxygen saturation (as the mitochondria continue to consume O2). While heart rate has increased (allowing more blood to be delivered), the deleterious effects of a build up in CO2 may be interfering with the amount of bound oxygen that is getting to the muscle leading to a net decrease in SmO2. This is the idea behind post exercise oxygen consumption (epoc) but now we are essentially seeing it in real-time at the level of the muscle. 

Hopefully this makes more sense. 
kptrzk

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 #12 
Just to add a bit more data... Over the last 2 Mondays I've done similar sets -

Monday 1 (11/18) 10x35s @600w

Monday 2 (11/25) 10x40s @600w

Side-by-side graph below (11/25 on left 11/18 on right)

Comparison SMO2 Drop.png 
The same SmO2 drop as in the original post occurred in week 1 but the SmO2 recovery was very different in week 2.... Any thoughts? Could it be an adaptation? as MoxyPhysiologist said it could be CO2 build up and now the body has learned how to remove more efficiently?

Have there been any Moxy case studies to observe the body's adaptations?

Thanks

MoxyPhysiology

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 #13 
@kptrzk, cool data! It does appear that on your second workout you were recovering more quickly, while doing even more work. There could be a number of different things occurring that would change these SmO2 curves. The first is that you could have been more recovered, better hydrated, etc. which could facilitate the same SmO2 drops, but faster SmO2 recovery. You could indeed be adapting, but that is very hard to tell and I do not know of any clinical research/case study that has actually looked at this. If anyone does have examples I would love to see them! 

I would be interested to see what would happen based on repeating this workout a few more times over the course of the next few weeks. 
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