Thanks will look at closer over the weekend, as the curves look very familiar.
One of the first questions we had, when we created the same reactions a few years back was:
Definition of occlusion and more important: Expected reactions in theory on occlusion.
As mentioned in the reply before, it is crucial to forget the picture we have form scientific test, where we create an occlusion without any activity behind the occlusion.
Here the questions.
1. If I create an occlusion than I have two possible occlusions.
a) Always first a venous occlusion followed by , if enough pressure is applied ,an arterial occlusion. See the two classical pictures. See att one of the main problem is the speed of the application of an occlusion.
A normal BP cuff is simply too slow so you will have always some left over as the pressure increases from a Venous occlusion followed by an arterial occlusion.
See 3 tests done by three different groups and only one achieved a proper result. The one from Andri Feldmann (Msc University Bern) in his work. If you look close enough you can see which one it is. Now when studying occlusion, than we look at trend in tHb as indirect information on possible blood flow under certain conditions.
If we create or apply pressure for a venous occlusion than we have still intake in the occluded area over the arterial system on blood so tHb will increase.
If we have zero activity in the tested area we still have a certain amount of O2 use but less O2 use than we get O2 in. So O2Hb will increase as a sign of more intakes, than use of O2.
But we as well will still have a resting muscle activity, using O2 and developing therefor HHb so HHb will increase .
Now if we apply more pressure, than we stop not just outflow in the tested area, but as well inflow. So the blood volume and with it the tHb in the tested area will not change anymore.
In case of a rapid arterial occlusion application the tHb will barely change, just simply will stay stable. In case of a too slow application of the occlusion tHb will first increase somewhat and than will stay stable.
In case of an " inactive" occlusion application we simply only have the resting O2 demand of the cells in the occluded area and as such , depending on the O2 demand will see a drop in O2 Hb ( red ) due to O2 needs ) and therefore an increase in HHb due to increase of deoxygenated red blood cells. the discussion here is open on how far we can drop O2Hb. Can it go to zero and if yes what is the risk of it. Does the body defend pO2 and how good an how long and if we would reach pO2 of zero what would happen. ? The other open questions we have is the fact, that we not only have information on haemoglobin loading or deloading of O2, but as well of the myoglobin level. So drop in O2 always can be a drop of O2 on Hb and O2 on Mb..
Now so far this is what we may expect on occlusion under resting conditions.
The situations changes rapidly, if we do the same test and apply an occlusion under different conditions,.
a) Immediately after a heavy workout. What changes is the situation of the applied or produced EPOC. Now we have an occlusion but as well a possible much higher resting O2 demand.
So you will see a very different picture.
Than b) apply an occlusion and at the same time keep the muscle activated like we have in the test above.
Now we have again a new interesting task on hand,
1. An actual occlusion would keep tHb stable?
So what we see is not an occlusion or:
it is an occlusion with a compression.
What does that mean?
As we create an occlusion we stop tHb increase or decrease and it suppose to be stable
. Now under activity we most often will not create an occlusion but a compression. See tHb reactions . on the many IPAHR picture we showed here already..
The initial start of a bike (pedal stroke) always creates a muscular compression in the tested area and therefore we will see a drop in tHb.
Now the question could be. – If we push down initially we will see a drop in tHb but on a lower intensity we will see a decompression, where tHb will increase again.
Now when we make a compression due to a position we may see an increase in tHb due to a short term venous compression??? So what would we expect during a pedal stroke tHb dropping when we push from 12 – 6.00 or tHb increasing when we pull from 6 to 12.00.
I moved that questions many months back to some cycling experts and the answers I got back from some had many speculations involved but none was actually close to what we actually see, when looking much closer. The rest did not had any opinion, despite writing and giving lot’s of “expert advices “
The most interesting findings we made here is, that the actual bike fitting situation can exactly reverse the tHb picture due to the change in position. . The question than arrives, what may be the better position physiologically.MOXY / NIRS in fact may change the way we may fit sport equipment and may increase the idea, that physiological factors may be sometimes as much important as physical factors like aerodynamic . Again possible a compromise or a closer look on durations of the activity will make some different decisions out o these ideas.
Here 2 pics from 2 world class athletes during a IPAHR. Of a cycling 360 degree movement. You can actually see the RPM they had during this load.
\ Now depending on the intensity of the pedal stroke we will see a “decompression” phase to adjust ( create a homeostasis of the needed power we have to apply to maintain the wattage load we have put on). This means that in the decompression phase tHb will increase.
This could make or create confusion with the situation that we could argue: tHb increase is a sign of a venous occlusion. Here are some of the tricky and fun parts of the interpretations of the MOXY ( NIRS ) data’s and that's where we work since over 5 years to get a hand on.( and still working on it)
Now if we go back to the information’s we have and results from our great example from Norway.
a) An actual occlusion will show a stable tHb. So the drop in tHb would be a compression during an occlusion.
Meaning, that under the moxy (test areas) due to the activity the muscles created a mechanical compression, reducing therefore the blood volume (tHb ).
Now due to the fact, that in the distal section of the occlusion the tHb (blood volume will stay stable, the question will arise on where the blood volume is pushed to, when the tHb under the MOXY ( test area is reduced due to the compression of the muscles???
So what we did, once we had teh same open question as we have here a few years back (Have to find the data’s as I often move them somewhere and than forget where.
I used for example different sites on the muscle ( Vastus lateralis , medialis hamstrings group but as well gastrocnemius , to see, whether I would have a decrease in one area tHb drop and an increase in another area tHb does up during an occlusion.
The easier way to do it is on your arm. Make an art. occlusion proximal of the short biceps head.
Than make an activity, where you try to only involve forearm muscles and not biceps or visa versa.
Have one test unit on biceps and one on the finger flexor muscle groups.
. The result is super interesting.
This type of test could be named hybrid.
Why. We have in vitro and in vivo tests.
Now people thinking in terms of existence of a central governor may easy understand, why one testing idea or scientific approach lacks one main issue.
The feedback loop from and to the working muscles, and therefore the influence of the Central governor.
. So here what I did before I started to see, that the central governor or for us the ECGM (extended central governor idea may have some interesting truth. It is exactly what the Norwegian group is doing.
Create an occlusion and than an activity in the occluded area. Here the thoughts and you may find teh answers .
Hybrid between in vitro and in vivo.
In the occluded body part we will still have a metabolic reaction like increase in CO2 decrease in O2 *( o2 Hb change and HHb change, but as well an increase in H + for example).
The problem or the beauty is, that we have no interference with new blood coming n so the tHb would or will stay stable. The muscle activities may shift blood from one area to the other but in any case O2 will drop ( O2HB will drop ) and HHb will increase.
The question is, whether the blood moving in and out of the contracted area is changing O2 content and how due to compression and decompression.
When we look what a compression makes on the venous blood vessels and what may happened in the arteriole than there are many speculations possible.
The fact remains, that we still have a connection to the CG.
The problem is, that the change in CO2 for example or in H + for example may give a feedback to the CG to increase respiratory activity. Now if that happens, the problem is, that the increased activity will not change the situation in the occluded area due to the problem of occlusion. So we have an in vivo in vitro situation. An area who not reacts to the CG and a CG who reacts to the reactions in this area.
Hmmm does that make sense in Swenglish. ???
If and only if. The CG or ECGM is working , than we should see an increase in respiratory activity despite the fact, that there is no connection in blood circulation to the occluded area.
The CG respond (increase in respiration can’t solve or try to compensate in the occluded area as CO2 and with it H + is not able to be balanced.
. Now the increase locally on CO2 and as well of H + will shift the O2 diss curve and we would expect a further drop in O2 Hb than we often see.
Why is that not happening.
. On the other side we can take lactate on that side and have by the same load a very different picture.
The main problem with lactate is, that we cannot occlude long enough to see the actual real lactate value as it still lags behind.
What we can see is a relative high SmO2 value in many cases as we see in this group.
The reaction we see is very similar as we have here and it may give us some very interesting answers on the fibre constellation of an athlete.
The occlusion activity experiment shows for us an interesting key to the idea of the ECGM and hwy there is a very dangerous idea to make conclusion from in vitro to in vivo experiments and visa versa as the CG may have changed result very strongly if the reactions created by the CG could have made or create an influence on the metabolic reaction in the tested area.
Last but not least a small brain workout.
Last pic is a pedal stoke inside view at a load of 300 watt. Think occlusion , compression and blood volume shift. Your ideas now for the weekend.