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HallvardN

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 #1 
Hey!
This is a printout from a IPAHD test, done in classical technique uphill cross country rollerskiing. We had a little too much turbulence on the vastus lateralis Moxy, we did a quick retest and the trend seems right even tough the graph looks a little messy. A really surprising result with this athlete, a former cross country runner and now a national team cross country female athlete. Very high SmO2 and very low stroke volume compared to the value we see in running(up to 150-160 maxium compared too 100+- maximum on rollerskis). Interesting is also that this athlete perform better on snow compared to rollerskiing on tarmac, and it would be fun to test her on snow as well in the future. A general trend in cross country skiing is that the more muscular athletes compete better on tarmac than on snow, perhaps because they have more use for their well developed muscular systems in this kind of terrain.

Definilty some aspects to work on for this athlete in the future. Discuss

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Roger

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 #2 
Hi Hallvard,

Can you post the .csv file from the Moxy?  The data look unusually noisy so I want to take a look at it.

Thanks!

Roger
HallvardN

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 #3 
Here is the csv files!

 
Attached Files
csv Britsen_riviera_bein.csv (33.20 KB, 44 views)
csv Britsen_riviera_overkropp.csv (47.04 KB, 37 views)

HallvardN

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 #4 
In the test i showed the tape wasn't too good on the vastus lateralis and we strapped it harder on the two last 5 minutes, you can see the signal quality was better in the last segment of the test. 

In general it looks like the graph from the upper body is a little bit more "messy" than from the lower body, perhaps from more disturbance or muscular occlusion. Here is a print out from another test, this is done with two IPAHD style , but in cross country skiing terrain with upphills, downhills, flats on a completely different athlete.

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Juerg Feldmann

Fortiori Design LLC
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 #5 
I have some problem opening your cvs excel sheet is there another way  that roger can sent me this info Thanks.
Juerg Feldmann

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 #6 

Great info. Hallvard  can you sent from the last MOXY you show on here the excel file to Roger and Roger than to me so I can work  with it.
 I will first finish the started discussion and than move over to this one.
 Here a question.
 1. Can you make with the   girl ( runner  now cross country skier with the SmO2  of 90 a simple triceps workout  either on a  pulley system classical   triceps workout or with an elastic as a   double pull workout . I like to see, how far she actually can desaturated when  just using triceps.
 This will give us  some very interesting trends and info's.
2.. When we  talk about limiter , than we mean a limitation of further  increase in the performance. Example CO or VE.
 Now  a cardiac system , who compensate   can compensate with 2 ( 3 ) options.
 possibly more .
 a) HR  as HR x SV = CO
b)  SV see above
 c) both can go up  till to the end of a test.
d) LVET increase and therefor HR x LVET = CCT increase
e) Deoxygenation  ability of the cardiac muscle.
 As  such we have in our  original idea of VO2 max - CO x a-v O2 diff.  an add on  to do.
 Now a plateau in VE or CO does not mean it is a limiter , as it may be , that a higher CO  simply does not make sense as only so much O2 can be used from the  loaded muscle.
 . Step  1  with MOXY.  tHb  flat or dropping .
 Step 2 with MOXY SmO2 trend  overall and inside  the double step.
 Now you  have some initial indication :
 1. Delivery limitation
 2.  Local muscular limitation
I will show you later than how you can use the beauty of an "IPAHD" to actually  test already during the assessment certain limitation or compensation.

HallvardN

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 #7 
Here is the csv files from the two last test i posted. I have more tests done results as well and will put them in the Moxy folder. 

Could arrange a triceps test with this athlete in a couple of days and could make a test with a more "double poling specialist" as well so you could see some different responses. 

 
Attached Files
csv Vetle_bein.csv (60.51 KB, 36 views)
csv Vetle_overkropp.csv (68.67 KB, 33 views)

HallvardN

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 #8 
Now we have done a little bit of playing/testing with the female cross country athlete. Under double poling only she got down to a SmO2 of 80 %, meaning 10 % lower than during whole body cross country skiing. She had pretty much the same trend here as in whole body exercise, meaning that the intensity had relatively small impact on Smo2 that was stable for all intensities except for rest where it was lower. 

This is not the general trend tough. For many of our other skiers the trend is that they can desaturate similar or even more during arms only exercise, down to 15-25 % easy. Interesting is it that we have tested a number of these gays during double poling with the physioflow and even tough the use of the available oxygen is good the cardiac output values are much lower than during whole body or legs only work. So the question is: what is the reason for this? Muscular occlusion, limited number of blood vessels and capillaries, anatomical factors etc. And interesting for the discussed female athlete; we doesn't she show the same trend despite many years of endurance training?

Many interesting questions

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Juerg Feldmann

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 #9 
First of all thanks for the great feedback and sharing of data's.
It shows what we see since many many years. There is no such thing like a cookbook and I always have to smile, when I see studies where at the end we have to come up with a conclusion and the conclusion is based on statistic and the statistic is based on 6  subjects.
Hard to believe , that this is a accepted as a study  as it is in the best case scenario a 6 person case study summary.
 The data you sent here are great, as it confirms what we see and opens the same questions  you guys have and we have here..
 A few points we have to discuss and look further.
1. Point you make on occlusion.
. When we start using NIRS ( MOXY) we have to look  at the difference between an actual occlusion   and what I call a compression.
. When we look at occlusion pictures than we  always will see a :  1. Increase in tHb ( venous occlusion )  or a stable tHb  arterial occlusion.
 In  the test we do we will have under the MOXY ( test area) initially always a compression, meaning a drop in tHb.. So we have to look at this trends and than add the information of SmO2 and if needed O2Hb and HHb.
 In a occlusion test, where we are not active we will see.
 1. Venous occlusion.  tHb up and normally O2Hb  and HHb up and depending on the activity just before the occlusion test   SmO2 with different reactions but normally up. ( Hb diff is interesting to use as well.
2. In the arterial occlusion you will see tHb flat stable  and HHb up and O2Hb down and therefor SmO2 down as well..


 Now to the lower  CO or SV when looking at upper and lower body.
 The theory in some books suggest , that SV will increase initially and the will create a plateau.
 In our many years of testing we  can't confirm this at all.
 We not even can make a fixed statement. What we see is everything.
  SV  increases  from the beginning till to the end of the test.
 Or  SV increases and than plateaus
 or SV increases and than somewhere closer to the end drops.
 There are many different reasons for this reactions.
Any fixed conclusion  will often be thrown out but are existing.
 When we test  lower and upper body  separate workouts, than we see  often SV higher , when testing lower body only  compared with upper body.
 In fact we had cases, where SV  when biking a steady increase, but when testing on a hand cycle  it actually drop towards the end.

 A lot may have to do with the so called Pre load  ( Return of blood to the heart.
 In leg trained people like cyclists, we see that the trend in T1 and T3 in the upper body is very different, than in the leg. This indicates a shift of blood from or to the surface area and as such a change in  blood return as well.
 We see this when we test in warm or hot situation, how the TSI can go the opposite way  than SmO2. If we change muscle activity we as well will see shift in  blood circulation from one are to the other in the muscle ( surface to depth for example.
  See the test here and look at T1  ( narrow thin line  and T3 deeper  layer , Thick line. Just look at picture only as decide, where you see a shift of circulation .
Pic  1
 PIC 2 is the overview of this test   from a cardiac hemodynamic point of view.
What  would be fun to look is :
 The cross country girl with the low SmO2 drop when using  whole body workout than only a small drop when arm use only but still as a > endurance load.
 
Here what you try. Let here do :
 1. A real local triceps  workout as a dumbbell kick back or on a pulley system elbows tugged in and local load and see how far  you can deload  SmO2   in a localized  workout.
 2. Than do the same workout  and make a triceps occlusion  and than do the reps so you have a fixed tHb due to the occlusion above the triceps and see the desaturation reaction.
 3. Than you do the same double pull test you did already but  you manipulate CO2  by doing a double pull for 5 minute with supper fast respiration .Get rid of CO2 done too 22 and lower EtCO2. , than normal respiration respiration Et CO2 35 +
 and than hypercapnic respiration  EtCO2 45 + and look at SmO2 trend.. Timing and level.
 This than will help us to design a workout idea to see, whether  we can change the trend  of SmO2 .
 Now I will add an additional  chain of thoughts in the next thread to show you how interesting MOXY may be once we get used on a different thinking pattern.
 Here in short. MOXY SmO2 trend may in fact help to understand the overall VO2 picture. ? See next info page.

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Juerg Feldmann

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 #10 
Okay let's get to a very interesting question.
 1. Classically we argue, that VO2 max will be a prediction of performance ?
 Meaning :
 VO2 max = CO x A-V O2 diff.
 Old story  well know, but :
 Is it still accepted. Many critical voices out there finally, who at least ask the question, whether this is true.
 1967 remember Dal Monte.
 Pic 1. What may limit VO2 n this 2 athletes with  different activities.
What is the conclusion out of that.
 VO2 test for a runner on a bike. for a biker on a treadmill for a swimmer on a bike. for a runner in the pool , for an ice hockey player on a bike.
 Perhaps :
 VO2 has top be tested in the sport  we do ??
 So  :
 VO2 predicts the performance.
 How about the PERFORMANCE ( activity  ability ) may  demand  a VO2 ?

 Now old pic 2  VO2 as the result of  the whole bodies demand or use of O2
 Now pic 3. Factors, who influence VO2


Now look at all the point VO2 can be influence.
 Could it be, that it is not the VO2 who deiced the  performance, but activity  you do , who may influence or use some of the different factors contributing to the VO2 use.
 Take the runner during a run and during a kayak erg. Could it just be, that local limitations of his upper body may decide the VO2 reaction and as such do not tell us anything other, that when using warms he can't  n use as much VO2  out of different reason.
 Why would the  cardiac system has to beat 190 times and  crate a huge cardiac output, when only so much blood can move into the upper body and only so much mitochondria  can convert O2 into energy needed.
 Now  where  does MOXY comes in.
 a) A- V O2 difference is perhaps  related to SmO2 change. ?

 Respiration  and change in CO2 levels shifts O2 Diss curve. So SmO2 will change due to change in respiratory  reactions. ?
 Will  the muscle pump and muscle contraction change tHb and as such blood volume return to the heart and as such SV ?
 Once you start looking  at the  reactions for the different systems ( respiration and cardiac reactions and metabolic trends and you overlap it with the SmO2  ( MOXY ) information, you will start to see, how they actually interact  with each other.
 MOXY has an immediate reaction ( locally ) and  the other s may have the same timing or a  lag  in time due to the way we test it.  ( VO2 is an indirect info on what happened in the muscle  and a direct info on what happens in the  lungs.
 Now  look at ideas from other bigger names and give it some thoughts.

 Now look at the  three last pics , combine the above questions  with what you see there and try  to understand how MOXY information can support many of the open questions on where and what  activity will decide the VO2 use .

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Juerg Feldmann

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 #11 
Here an add on to MOXY and SmO2. When you  do testing in whole body sports like rowing , cross-country and so on  and you try to separate upper  and lower body in a test than look at VO2 trends and SmO2 trends. Interesting will be when you look at possible " plateaus" in lower or upper body.
 If we talk that there is a VO2 Max and that there will be a plateau.
 Why do we see in cases like upper and lower body sports , when separated that we  may see a higher VO2 without  plateau reached in the lower body but we may see a clear plateau  at a much lower VO2 max when testing the upper body.
Perhaps VO2 may be dependent on the activity rather the activity on VO2. The VO2 may not at all predict performance but the performance may  produce a certain VO2.
 In case some factors may improve ( Respiration more efficient, coordination more efficient, Cardiac  work more efficient. A - v diff changes and so on. VO2 may in fact drop at a given performance .
 ???
Summary:
 When we look at limiter and compensator we always have to keep the whole  physiological reaction in front of us. A drop in SV does not  mean automatically a cardiac limitation It can be that there is no need for this high SV or it may be the SV drops due to a limitation of blood volume return due to a  vasoconstriction ( tHb drop ) the thB  drop can be caused because of different reasons.
 1 ' Mechanical reason ( pressure ) respiratory reason ( metaboreflex ) and other possibilities.
 This is the reason , why  we take as many information's as possible and overlap  at the IP ( Interest points ) the information from the different physiological systems , Than you look timing , possible lag time  and reactions under the different systems. Who or what influences at what time and to what kind of a degree.

Simple example.
 IPAHD   : You see  at a certain stage a "plateau  of the cardiac output.  Different options. HR plateau and SV plateau. HR increase and SV drop  SV increase and HR drop (very specific cases )
 Now you  repeat the second stage  with the same load  and you add simply to the leg work on the bike some upper body activity. This triggers a higher demand of O2 and if the cardiac system still can increase CO it will do that without problem despite the same load  as now it made sense to ad more CO to the demand from the body.
 If you have an athlete , who is not train on a bike , like an ice hockey player than you very often can increase CO and VO2 by adding this activity. If you make a classical VO2 test you simply have the limit of his legs and VO2 results do not reflect the full picture.
 In fact , if in an ice hockey player in a VO2 test we see a VO2 plateau  than we often see as well a MOXY SmO2 plateau , indicating the lack of extracting more O2  form the tested leg and as such one main user of O2 is on its limit , creating a VO2 plateau but not a VO2 max plateau. You add now upper body work to it  than SmO2 stays in the leg the same but CO and VO2 will increase.

In essence. VO2 max testing on a bike with an ice hockey player is great for the people who test as it makes good money but it is of absolute minimal information for what ever workout the coach will plan for this  team member. ( exception : You like to change the ice hockey player to be a better cyclists )
Juerg Feldmann

Fortiori Design LLC
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 #12 
Here a similar example as we got from Norway.
 It is a test  where we have one MOXY on the  vastus lateralis  left side and one on the delta pars acromialis left side.
 It is a " warm up" section as you can see well , followed bu a loading section of fix load. The intensity we took is an intensity , where we just see a  "stable SmO2 level ( Balance  O2 intake and demand )
 As you can see , the start  drops as so often SmO2  and interestingly enough not just in the active  vastus lateralis but as well in the inactive Delta muscle.
 Both trends then increase  to stabilize ( Homeostasis)..
 What we did than is to see, what would happen if we load a very short moment the delta muscle with additional activity. You will easy find where we did this.
 as you can see the O2 demand increased and the SmO2 dropped.
 As soon we stopped this the  balance was achieved very fast.
 This  was a pretest to a set of additional  task we try out, in cases like we had  from Norway with the girl and a super high  SmO2 in the upper body.
 The question there is :
- Is she simply not activating the triceps enough  to desaturate more?
- Is she not able to desaturate due to vasuclarisation and or muscle fiber constellation.
Or some additional questions like respiration, O2 Diss curve and influence of respiration in a whole body situation.
 Change of vasuclarisation to balance BP and so on.
So the question here would be :
 If she will be able due to intention to s desaturate more on the upper body ( meaning SmO2 drop ) will the overall VO2 readings change  and in what direction.

Is the combination of VO2 trends with SmO2 trends a very new and interesting tool to understand the different interventions we try with different workouts.
 Is a so called "lactate " tolerance workout doing what, when looking at O2 trends
 And again the question , whether an absolute watt/ kg value we may achieve in a Wingate test really telling the same  if we have to athletes with the same value.
 Could it be possible that one reaches this result due to an incredible great desaturation of Hb  ( Dropping SmO2 and this all the way with no SmO2 plateau.
 and the other one may very early on reach a SmO2 plateau  and than has the ability to work O2 independent much better due to different option to maintain H + balance and or  bigger  or better ability of ATP and CP drop ?
 Which one , as we have the same watt/ kg result has really the better " anaerobic " power ? and why ?
Here the pic overlap[ from the delta case study  compared with the vastus lateralis

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HallvardN

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 #13 
Thank you for the input Juerg. You are really putting forward some really interesting ideas here now!

We lost our female guinea pig now for a national team camp in the Alps so we will not be able to test her again before we get our own Moxy. It's fun too see how wrong conclusions we can make based on just general knowledge and feeling. We were at least 99 % sure that this well developed athlete had a great muscular system after so many years of training. So the question for us now is: how do we change the training to make her muscles more effective? The last three years this athlete has had a general program with a lot of high intensity and training around lactate balance point or whatever term we use for a intensity than can be sunstained for 1 hour + The first thing we have done is to tune her program down to a more traditional low intensity program and trying to see if more hours of structural endurance training and better recovery from less intensive training can make a difference the next months. What is interesting is that the high SmO2 trend don't just involve her upper body, but also her lower body that is stable around 80-85 % despite increased effort. This is tested in rollerskiing, cycling running and is always the same.

The testing with occlusion, local endurance and different forms of breathing is really interesting and I will do some testing with another athlete tomorrow before I send the Moxys back to Andri. I started to read trough the studies I found about blood restricted training and was amazed by how many studies that has been done in this field, especially in strength athletes. Looks like this is a field with some interesting possibilities. 

Did some playing/testing on myself with 150 mmHg and 200mmHg occlusion during low intensity cycling today(together with a doctor as I was way to afraid to do this on myself without any kind of supervision). What was interesting was the stable SmO2 and increasing Thb at both pressures. Could this be a potent stimuli for increased capillarization or make increased concentration of signal molecules and potentially greater stimuli as some studies suggests, even for endurance? We had a little hard time to make a real arterial occlusion on the legs with our equipment during exercise. Think we need some better cuffs as those weused was not too good. It is perhaps easier on the arms as the muscles generally is a little bit smaller.(maybe harder on the bodybuilder you gays are working with ).

Here is one of the interesting studies I found:

Blood flow restriction enhances post-resistance exercise angiogenic gene expression.

Source

Department of Aging and Geriatric Research, University of Florida, Gainesville, FL 32607, USA.

Abstract

PURPOSE:

The objective of this study is to evaluate the effects of blood flow restriction (BFR) on muscle oxygenation during low-intensity resistance exercise as well as postexercise expression of molecules related to physiological angiogenesis.

METHODS:

Using a randomized cross-over design, six apparently healthy young adults (22 ± 1 yr) performed 120 unilateral knee extensions at 40% of 1 repetition maximum with and without BFR (CNTRL). Near-infrared spectroscopy was used to measure oxygenation of the vastus lateralis during exercise. Serum and muscle expression of Post-Resistance vascular endothelial growth factor (VEGF) were determined preexercise, 4 h postexercise, and 24 h postexercise. Transcript (mRNA) expression of VEGF and other angiogenic genes was also determined.

RESULTS:

BFR increased muscle hemoglobin (Hb) concentrations during exercise (14.4 ± 1.6 vs. 0.9 ± 1.6, P = 0.002), driven largely by an increase in deoxygenated Hb (11.0 ± 2.5 vs. 0.5 ± 1.1, P = 0.030). BFR also increased (P < 0.05) transcript expression of VEGF, VEGF-R2, hypoxia-inducible factor 1 alpha, inducible nitric oxide synthase (NOS), and neuronal NOS. The most dramatic change in response to BFR was an increase in VEGF mRNA at 4 h postexercise (4.1 ± 0.6 vs. 0.6 ± 0.2-fold change, P = 0.028). Compared with control, transcript expression of endothelial NOS, serum VEGF, or muscle protein expression of VEGF was not altered in response to BFR (P > 0.05).

CONCLUSION:

Acute BFR increases postexercise expression of mRNA related to skeletal muscle angiogenesis, plausibly in response to changes in muscle Hb concentrations. 
Juerg Feldmann

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 #14 
Great info.
Here 2 things to add.
 First.
 Upper body developed incredible in the  last 1/2 century in many  whole body sports including Cross country skiing.
Pic 1
Pic 2  here a nice example, that since we test with VO2  nothing happened and it maybe time to try to add some new ideas like NIRS ( MOXY ) as well as physioflow to the classical VO2 use to get  more questions and possibly more answers.  And there are some answers for O2 use  between upper and lower body.

To the occl;usion test. They are tricky. If you not are fast enough you will have an increase in tHb and than if complete a plateau.
 If you do not  close completely you will see  first a  occlusion reaction with tHb up as a sign of a venous occlusion pressure followed suddenly  with a tHb plateau but because the veneous occlusion is leaking  and not because you close completely off.
 The actual reaction will be seen in SmO2 reaction.
 If you have total occlusion you will get no new O2  so O2 Hb will drop  and HHb will go up. The speed depends on the O2 use in the occluded area.
 And SmO2  will drop.
 If you have an incomplete occlusion you will see as mentioned first a tHb increase and than a flat tHb  followed with depending on the O2 use a stable SmO2  or any option possible.
   Will be fun to see some of this ideas   in practical application. 
Picture from Holmberg Ostersund

HallvardN

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 #15 
The NIRS testing in double poling, arms only, have opened some new questions for us. In some athletes the SMO2 stays high and the blood volume increases with increasing intensity as a classical situation where the central organs are compensating for limited muscular oxygen abilities with increased blood flow. Despite this some athletes show massive desaturation(even more than in the legs) and flat/decreasing Thb trend despite lower SV and HR and less stress for the breathing system. As Juerg has pointed out the difference could be a result reduced venous return or blood flow trough different layers at different intensities.

The question for us is how to to develop athletes with different strengths and limitations. Could it be that some athletes need to work on developing capillaries with relative hypoxia to improve oxygen efficiency and that some athletes need to focus more on developing bigger blood vessels to increase total blood flow with more mechanical/shear stress or better flow resulting from decreased relative muscular force. 
Can different "crazy" training interventions with intensity, breathing or different forms of occlusion trigger the wanted development in athletes that has done years of classical endurance and has reached a developmental plateau.

Would be happy to get some critical input on this and how you gays think we could develop muscular abilities even more with smart use of NIRS. Here a little interesting study I that could open the question for the of need of different approaches for different forms of development.

Arteriogenesis versus angiogenesis: similarities and differences.

Source

Max-Planck-Institute for Heart & Lung Research, Parkstrasse 1, 61231 Bad Nauheim, Germany. m.heil@kerckhoff.mpg.de

Abstract

Cardiovascular diseases account for more than half of total mortality before the age of 75 in industrialized countries. To develop therapies promoting the compensatory growth of blood vessels could be superior to palliative surgical interventions. Therefore, much effort has been put into investigating underlying mechanisms. Depending on the initial trigger, growth of blood vessels in adult organisms proceeds via two major processes, angiogenesis and arteriogenesis. While angiogenesis is induced by hypoxia and results in new capillaries, arteriogenesis is induced by physical forces, most importantly fluid shear stress. Consequently, chronically elevated fluid shear stress was found to be the strongest trigger under experimental conditions. Arteriogenesis describes the remodelling of pre-existing arterio-arteriolar anastomoses to completely developed and functional arteries. In both growth processes, enlargement of vascular wall structures was proposed to be covered by proliferation of existing wall cells. Recently, increasing evidence emerges, implicating a pivotal role for circulating cells, above all blood monocytes, in vascular growth processes. Since it has been shown that monocytes/ macrophage release a cocktail of chemokines, growth factors and proteases involved in vascular growth, their contribution seems to be of a paracrine fashion. A similar role is currently discussed for various populations of bone-marrow derived stem cells and endothelial progenitors. In contrast, the initial hypothesis that these cells -after undergoing a (trans-)differentiation- contribute by a structural integration into the growing vessel wall, is increasingly challenged.

 
 
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