Here some additional insight view in a discussion with a very advanced training and coaching group. The case is the one we discuss above. form the PP.
see in red below some additional thoughts
Subject: Re: P’s Moxy results
Date: Sun, 12 Jul 2015 10:00:08 -0700
Juerg and Andri,
I thought I was following your logic, and your descriptions, until you laid another level of complexity on top, so I just wanted to confirm the conclusions you have given, to ensure I am understanding your train of thought…
I can see the difference in tHb reactions between first and last recovery period on your "world-class cyclist" example.
Summary…early in testing after lower loads, the tHb recovers quickly, almost exactly with the SmO2. However, after higher loads, the trend reverses, and we see a drop in tHb even though SmO2 recovers.
There are 2 common situations, where tHB drops when we make the one minute break or in general when we suddenly stop :
muscular activity stops so does the demand of O2 / Delivery meaning CO and VE still are high due to lag time so delivery of O2 is up and that gives us the increase in SmO2.
If at that moment the respiratory muscular system is in trouble, so we may have a lot of CO2 remaining in the system and lungs, than we have a systemic reaction still. This means in the in minute rest the tHb will go higher than usual. ( No muscle compression still high CO and now additional vasodilatation due to CO2 still high.
As soon we are normocapnic again the tHb in the rest will actually drop a little bit due to now less vasodilatation as CO2 is normal. In this case we as well have a delayed systemic SmO2 reaction. What you will see is that when you stop tHb will go up immediately as explained above lack of compression CO up and CO2 up.
But due to the O2 disscurve on the right you will still see a low SpO2 ( EIAH) and a ongoing drop in SmO2 due to still optimal deloading of O2 but lack of loading and then with a lag time as soon normocapnic an increase in SmO2 at the rest period. See picture of a workout where we triggered this situation. att 1
This study was done by Mary Ann Kelly PS 2015
Muscular contraction stops so there goes the compression. This is an example of a systemic reaction on O2. Now the example
I sent you is an example of Marshal's sleeping giant idea 1967.
And later picked up by Holmgren in his work on cross country skiers. att 2 and 3 arm blood flow alone or leg blood flow alone but arm plus leg cannot be covered so there is a vasoconstriction somewhere with less priorities. That’s when MOXY in a non-involved section will give feedback.
So when we have an occlusion trend and CO is good enough and we stop we have a mechanical release of compression and an immediate drop in tHb as an occlusion outflow., or an immediate increase in tHB as a relaxation of compression and CO takes over.
If we have a BP reflex reaction than as we stop we have a short delay of the reflex so we have a flat tHb so same level but no additional inflow but a start of BP reflex reaction with than if successful vasoconstriction than with lag time of 10 - 15 seconds we see a drop in tHb
Question: Are you (and the attached article) suggesting this is a result of the body trying to support BP, through vasonconstriction, because there is a limitation of CO? In the case of PW, we think this is a reflection of limitation in SV, because we see a rising HR.
Yes see above Holmberg
In PW situation we do not have a lag time so we see a mechanical tHb reaction. So not a limitation of CO for the whole systemic reaction as he still seem to be able to maintain BP. (would be confirmed or not with a non-involved muscle reaction. See att cross country triceps reactions. This is at the end of a cross-country assessment the reaction in the one minute rest in the triceps as a systemic delayed tHb reaction for BP protection. In PW's case he has a muscular occlusion trend which reduces pre load and therefore to maintain CO he has to increase HR as SV will drop.
See tricpes reflex vasoconstriction in a cross country skiier .
This datas are form Roger form a assessment he did with a crosscountry skier and a ski erg
This is from Holmberg as well as the next one .
The " fight " for blood volume is lost as CO is too low . so BP is priority.
This is where MOXY on a less involevd muscle or in rowing orCrosscountry skiing comes in at the upper body area.
Question: With a 6 day stage race coming up in two weeks, and a long career ahead of him, we could suggest…
1) Adding a few sessions of SV work to try to help overcome this perceived weakness in the short term.
To maintain or even improve SV and use the 6 days race as a SV workout the best is over plasma volume reqctions in the daily post race nutrition. Talk with your nutritional specilist on how to do that.
2) Do some specific maximal strength work to help reduce the muscle tension on capillary beds.
Yes intramuscular strength sets every 3 rd or 4 th day and you should load till you see an arterial occlusion on the screen.
1) Continue to focus on both capillarization and SV as the two main structural elements in his training program.
Yes as in structural development you will need first always capillarsiation before we see an increase as well in mitochondria density. Density. Key word angiogenesis and the different options which are discussed.
Question: Is there any way to use Moxy and HR data in combination to assess the best means of increasing SV through training?
We have played with the ideas a few times, looking for maximal tHb at varying intensities and different cadences, and it seems to be possible when using Peripedal software. Are there any other recommendations you can suggest for in the field work on SV?
Yes besides seeing live reactions over Physio flow the next best option is to look at tHb reactions in combination with HR and respiratory interventions.
see last att. an experiment we did to see how we can influence SV during a step test.
Have a great season Juerg