Sign up Latest Topics
 
 
 


Reply
  Author   Comment   Page 2 of 2      Prev   1   2
Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #16 
Daniele, no  problem just was not sure whether we  talked  from the same picture.
 I like to try to think loud again and you come back and add on with   your observations  as well as    critical questions.
 Here  to make it easier the first  graph  of both legs again.
skiing erg RF  ham.jpg 
We  are not  completely sure, whether the start  levels  for both H  and RF  are resting tHb  but let's assume so..
1. When we start we  expect a  muscular compression due to  contraction.
2. As the  delivery system ( cadraic  out put ( HR  x SV ) is   not  yet going  full or  higher, the  compression is the  initial reaction.
  Depending on the cardiac reactions  we  may have  an athlete  reacting more over Frequency  ( so HR  goes up relative fast  ) or over SV  so  HR  increases  slower.
 In both cases  CO increases.
This is a  systemic reaction creating a result on tHb  slighlty delayed.
  ( the delay time depends on the reactions  HR or SV.) but it  may be  somewhere arround 30 second  to 11/2 min till we  reach a higher level of the HR
 Here  2  examples .  one is a  HR  reaction  person, the other is a  Stroke volume reaction person.   can you find  which one is what ?.
Claude HR SV CO.jpg
This  is a Physio flow  information courtesy  Claude  Lavoie  from the univeristy of  Trois Riviere Quebec from a   workshop we did  a few years back..

 The  other possible reaction is  below

carl fact.jpg 
Soas we  overcome teh delay of teh CO  we   hoep to see, that teh CO may overrule teh   muscel compression  and as  such tHb  should during the  next 3 -4  min in this  first stepor  for sure in the next  step with the same load increase  as a sign of  vascularisation reaction  and a  good CO  strenght.
Do we see this in RF  or H.
Than, when we  stop for one minute, the muscular compression is gone  but the lag  time  of CO   will mean  we  still have a systemic higher pressure  which  would   create  an increase  at the one minute rest. Do we see that in H  or RF.
 Last but not least we have  one more   direct reason of an increase in  local tHb reaction.  muscular contraction which  is so strong, that we may create a veneous  occlusion  trend.
 Do we see that in one or the other.
 If we see it  somewhere,  why in this muscle  and what causes it  so fast ?

DanieleM

Development Team Member
Registered:
Posts: 264
 #17 
Lots of interesting stuff as usual.
First the question about HR/SV
hr_sv.jpg 
Here it seems clear that HR is raising a lot on each step while SV is stable at the beginning then drops towards the end, resulting in an overall small drop in CO.
I thought that SV should remain stable...can we say that SV was a limitation for the case above?
Probably this would deserve a specific topic.

Anyway to come back to the skier assessment, some more loud thoughts.
The behaviour of the two muscles is completely different and "out of phase".
If I look at the harmstrings during the load, I can see that tHB keeps dropping during the load:
rf_hs_ski.png  As you wrote we should expect that after a first drop, it should stabilize (vasodilatation due to higher CO to balance muscular compression).
Here, it looks like we have a vasostriction...

In the quadriceps (RF) we have a completely opposite trend.
rf_ski.jpg 
At the start of the load, the normal behaviour should be tHB to drop due to the muscular compression. Here instead it rises very fast at the beginning, then drops when the muscular compression is over.
This could be a typical trend for venous occlusion.
Otherwise there should be some mix combination with other muscles...
The opposite trend should also indicates the need to maintain the blood pressure.

As usual lots of guess and probably mistakes....with the hope to improve [smile]

Daniele

 

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #18 

Daniele  no  you long a go stopped guessing as you start some  critical physiological thinking  and you are    nearly there. (  I am also only nearly there as e  always  get new cases  to see, how individual the whole  physiological reactions  are.
 This   is  what nature is all about, many different options to react  and counteract. This is  why  I have some major problems  to believe, that we  can calculate   physiological reactions . True we  can calculate  anything but ????
 Okay give me  another chance  to     get through this interesting picture  of the cross country erg assessment. here  again  as it may help the overall picture  of the three muscles.
 1. is  Triceps  2 is   RF  and 3    is H
ski erg tHb 2 legs   and one upper body muscle.jpg 
 Okay let's  see.
 tHb reaction.
 Expected reactions.
   and we  always  best look at the start   or at the end  or    and tha's' why we  do a  1 min in between  there  on what happens.
 a)  muscular compression  and tHB  should drop  as   the systemic delivery ( CO  and VE )  are   not  initiated  yet  ( start ) or  dropped in the 1 min rest.
 If the  compression  can be overruled  by CO  than we  may see after an initial drop  a  flattening or   if CO is overruleing  compression a  slightly increase  during the load..
If thisis the case  we  expect when we stop and immediate increase in tHb  as compression is gone    and at least  a  peak  of tHb   to base line but if there  was some vascularisation stimmulation  we  should see  an even higher  peak of tHb than base line.

If  tHb dropes  during the load   than compression may overrrule  and  we  may  add a systemic vasoconstriction to it as well.
 What  do you see  when you stop again ?
Compression   is gone so tHB  has to increase as CO is still high ( Lag ). If there was a  systetmic vasoconstriction ( BP  balance )  we will see a  only  slightly increase in tHb  as we only release compression but  have still systemic vasoconstriction. Depending on the speed of BP recovery  we may see in the one  minute a second  increase trend in tHb.
 If tHb increase  during load  we have as above  an overruleing of a good CO  against the  compression.
 or  we may have a starty of a veneous occlusion  so tHB  will go up due to pooling.
 The difference now is, that when we  stop we do not have  an immediate increase intHb as  when tHb  went up due to CO  high .   and  compression gone. We have now  an initial  drop in tHB  due  to occlusion out flow..
 So  in short look at  H  reaction.  " Normal " reaction at  rest  with tHB increase, indicating  an increase  of tHb due to release  of  muscleconmtraction   now.. Not  optimal   peak tHb  indicating a  still existing vasoconstr
iction trend  due  to
 a) BP  controle

 b)  not rerlaxation of hamstings  completely  at rest.
 If it is BP  control than SmO2  will go up normal to base line  and or above )  if it is  a  still higher  resting  tension than we still need O2  and SmO2  will not increase that much  at rest  so   will often stay below baseline.

c ) quadriceps.
  Look  that    at start  we have  a very short  compression trend in some  starts  but always  an immediate increase in tHB  with  even a plateau  see below  on a close look.

RF  thb  smo2  Very close look    occlusiomall.jpg 

 I will show you later  depending on the discussion an even closer look  but if you look the tHB here  you can see the small up and downs, which   indicates a  higher and lower  compression  as you would expect  in a   motion as he did.

 Below  the reaction of a  world  class cyclist  in the 1 min rest  from a very early  case study we did about  7 years ago  to  look at some specific interventions.
super close look geoff at start after 1 min break.JPG 
 You can actullay see the  RPM  as he starts  loading again.
 The interesting questions we  add than is, is  the  foot  at 6  or 12 .00 position when tHB  goes  up or  down ?? yu as well can see the shift of blood  from T1  to T3  after  an initial  start phase  of  cycling.
 As we have many hundreds  of  cycling assessment we  have a pretty nice trend on what   shows up in a top cyclists  and what  makes the difference between a  top cyclists and a good cyclists.


Now back to quadriceps  In this case we have a  " normal reaction of H  but a  clear problem to maintain  blood flow    towards  the end.
 In the quadriceps  we have  a  very early, but for sure  at the end a very strong  occlusion situation even to an arterial occlusion trend.
  in the triceps. ??
 we have this pictrue  at rest in a  closer look.   .

triecps  systemic  close look.jpg  What  does this indicate ?

Summary.
 In the  erg assessment we see a lot of feedbacks.
 1. This  client  creates a  RF  occlusion,
 he  has a  normal reaction in H  but  towards the  end a reduction in blood flow  due to  compression increase.
.
 Both of this will create a  drop in SV towards the end of  a load  as you can see in the example of trois  riviere case (Physio flow  information.) I showed this once before  from another case, where we  had a  drop in tHB  due to occlusion compression which reduces  back flow of blood to the heart  and as  such  reduces  pre load    and as such  ends up with a lower  SV  and  if possible  an increase in HR  to try to maintain CO. If this is not possible  we have reflex reactions  with a d rop in performance due to  reduction of motor unit recruitments..  So in this case the problem with back flow creates a limitation in CO  and as  such  at rest  he has to balance this with a  reflectoric vasoconstriction and you can see that in the triceps to maintain BP.

 Summary : You can see , that when we  combined  VO2  equipment  and Physioflow  equipment  and NIRS  and  blood assessments like  lactate   and some more, why we  had  more and more our  questions,  that there is no way we can find a  single muscle trend  with MOXY or NIRS  and believe, that this  can be corelated  to a  lactate or  VT  threshold  at all. It has to be looked upon what it is. A live feedback on   what is going on in a team work  like the  body and how they interact  with each other. So in this  ERG  case the question is, whether the erg ACTIVITY IN THIS CLient  LOOKS Like   IT WILL LOOK DURING REAL SKIING or  WHETHEr it MAY LOOK VERY DIFFEREnt.
 iF  IT  IS VERY DIFFEREnt , THAN THERE IS no point TO CREATE A  ZONING BASED on  an   ERG   assessment,BUT RATHER GO OUT  AND SKI.


Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #19 
I got some nice respond  in a  email on the  discussion we have here. In short.
 The explanations make a lot of sense.
 What makes no sense is, that nobody out there   does not use this ideas, if they seem to be so  easy and logic  as they appear.
 Why  does nobody uses this information.?

 First thanks for the nice mail. second  there are many  ideas  out there, who inspired  me  Here  one of a great historical   review   I    got inspired  from to try to find a easy  application (   with  mistakes  if it is  done easy ) but very practical for athletes  coaches  and  patients.
 

 

Skeletal and Cardiac Muscle Blood Flow

Ideas about control of skeletal and cardiac muscle blood flow (1876 –2003): cycles of revision and new vision

Loring B. Rowell

Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, Washington 98195

Rowell, Loring B.

Ideas about control of skeletal and cardiac muscle blood flow  (1876 –2003): cycles of revision and new vision.

J Appl Physiol 97: 384–392, 2004

10.1152/japplphysiol.01220.2003.—
This perspective examines origins of some key ideas central to major issues to be addressed in five subsequent mini-reviews related to Skeletal and Cardiac Muscle Blood Flow. The questions discussed are as follows.

1) What causes vasodilation in skeletal and cardiac muscle and 2) might the mechanisms be the same in both? 

 

3) How important is muscle’s mechanical contribution (via muscle pumping) to muscle blood flow, including its effect on

cardiac output? 

4) Is neural (vasoconstrictor) control of muscle vascular conductance and muscle blood flow significantly blunted in exercise by muscle metabolites and what might be a dominant site of action? 

5) What reflexes initiate neural control of muscle vascular conductance so as to maintain arterial pressure at its baroreflex operating point during dynamic exercise, or is muscle blood flow regulated so as to prevent accumulation of metabolites and an ensuing muscle chemoreflex or both?

Thna a  question back.
 Why in 1968 ( hmm is  it already that far back ) did nobody but Dick Fosbury did the Fosbury Flop ??


" That is to put it mildly. Fosbury's best effort using the western roll was a mere 5ft 4in (1.63m), more than 60cm (23.5in) short of the world record at the time and a height that wouldn't have impressed anyone even in the first half of the 19th century. Given that by the time he stopped growing he stood 6ft 4in tall without jumping at all, there was only one logical conclusion: he was a hopeless high-jumper.
Richard-Fosbury-Jumping-H-008.jpg 

 


Marcel

Development Team Member
Registered:
Posts: 54
 #20 
Juerg help me out here, sorry I need to derail this thread a bit and go back to the start to clarify things for myself, there is almost too much different bits of info and I am trying to digest it all.

A vasoconstriction:

it is the narrowing of the blood vessels, if CO is increased it can overcome the Vasoconstriction.  But is the Vasoconstriction occurring because the Cardiac output is not enough and because it needs to maintain blood pressure or is the narrowing due to the way that the muscles contract and has a direct effect on the blood vessels and now because of the narrowing, CO needs to increase?

If I understand it correctly then Cardiac Output is the factor limiting the performance as the vasoconstriction is the indirect result of not enough blood pressure. So if there is enough CO then we wont have a vasoconstriction?

If we were to use a vasodilator either through nutrition or chemical then the blood would flow easier through the blood vessels but blood pressure and heart rate would need to increase even more to compensate for the low CO so a vasodilator might not be a solution until CO has been addressed.

So in short what I am trying to ask is, is a vasoconstriction a direct result from the activity or a indirect result.

Not sure if I am trying to oversimplify a vasoconstriction.
Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #21 
Marcel great you are coming back on this  because once you can relate  to this reactions you have a fast open book on body  reactions. As you can see above, this questions  are asked  already 1876  and  are ongoing.
One of the main reasons is, that like in many other areas we  try to  make it simple   and that causes  at the end some complications. You can see , that it may be easier  instead of using the work vasoconstriction simply use the idea of  changing blood vessels  diameter.
 Why. Because there are different mechanism  which can create a  change in diameter.
 Again I try to make is  easier.
a)  mechanical   reason. or actual outside compression. One option is muscle contraction, an other option is  simply  positioning , another option is  clothing.
b)reflex  ( example Baroreflex  reaction over  an active now we could use the word  vasoconstriction to change  the diameter.
 The metaboreflex  described  by Dempsey  et all would  be one of this reactions.
c) an actual again vasoconstriction due to metabolites  like hormones . For vasodilatation one of the common  well know  one is Adrenaline.  but there are  different metabolites  ( most likely not all know  yet ) which can create a vasoconstriction.

So I hope this  makes a  case, that the change in tHb  depends  on the balance between reactions, who create a  closing of the blood vessels diameter  versus  reactions  who create an opening of the blood vessel diameter. ?
So in case of  muscle  compression as a mechanical reason, which reduces the diameter  and the increase of blood flow  due to increase in cardiac output,  which  can increase the diameter we have the question on balance. One may overrule the other  and than we have the trend in tHb.

" But is the Vasoconstriction occurring because the Cardiac output is not enough and because it needs to maintain blood pressure or is the narrowing due to the way that the muscles contract and has a direct effect on the blood vessels and now because of the narrowing, CO needs to increase?

The answer or  better the   potential answer is   what is needed  to " survive" the vital systems.
 Most likely the blood pressure has  a higher priority than simply the performance.
 Example. You have a low blood pressure and you stand up too fast you  know what happens. You most likely  will not perform  an activity but wait till the priority  ( BP ) is under control.
 So as you can see it will be a priority list. In  most cases  ( with exception ) on highly trained  people with an incredible vascularisation ) the   risk , tat the CO  can't maintain the blood pressure is  much smaller even if  we have  at the one minute rest a complete relaxation or opening of diameter due to the stop of muscle compression.
 We did  some Spiro tiger   studies  where we  created  a  very high CO22 level so we had a very intense   vasodilatation  and than stopped the exercise  suddenly so we had the systemic vasodilatation  from the CO2   minus  now the muscle compression  plus the still high CO  and  we can create a drop in BP  in any person  and they have to go  fast down on the back including lifting their legs  for a few minutes. So the " surprise reaction of   3 reasoning of opening blood vessels. ( No muscle compression plus high CO  plus high CO2   is  too much   and the  system has to  put you down to concentrate just on one thing  and on one thing only central  blood pressure  for the brain.

So from a total  overload  to no overload  are  very different stages. One of the common one is to separate  upper body  blood circulation from lower body blood circulation so we can see a  vasoconstriction for BP  protection in the arms   but still can keep going  with the legs  as we have  muscle compression there.

So in the case of the erg assessment we see that  in the end stage, where the arms create a delayed  drop in tHb as a BP  protection reaction. where  as the legs follow the  reactions of  muscular contraction. The quadriceps in a double pole motion is always loaded  whether you go up  and or down  so eccentric  and concentric. When we   get tired  we often than change the hip angle  and  with this the hamstrings  activity but the quadriceps   has no chance to really change   contraction even if  we  change the knee angle. We see, that in the  venous  and than arterial occlusion trend  and the   relative normal compression trend in the hamstrings.

If I understand it correctly then Cardiac Output is the factor limiting the performance as the vasoconstriction is the indirect result of not enough blood pressure. So if there is enough CO then we wont have a vasoconstriction?

Yes  and you can see that  during load the muscular compression will support the cardiac output, but as soon the  muscle compression is gone (  end of the race.)  and the cardiac output is still very high  and all the blood vessels  are open  the cardiac output despite it is high can' t maintain the blood pressure  so  we need  either a  reflex  vasoconstriction fast  and if not fast enough you will simply go down on the ground to support the delayed  vasoconstriction with reducing the need  of CO  as you are flat.


If we were to use a vasodilator either through nutrition or chemical then the blood would flow easier through the blood vessels but blood pressure and heart rate would need to increase even more to compensate for the low CO so a vasodilator might not be a solution until CO has been addressed.

Absolutely That's why we need to know the limiter and compensator. That's why we have in altitude  responder  and non responder or we have responder and  non responder when given plasma expander  or EPO in sport.
 If your limitation is the mitochondria density  and blood vessels  and you simply can only turn over so much O2 in the existing mitochondria  you can  give as much  EPO  to move more O2  to the  active muscles  as you like   you still can only convert so much.
 On the other side  like we have in  many sports  an incredible high mitochondria density  so that the utilization ability completely outstrips the  delivery ability than any intervention, who improves deliver  ( like EPO ) will have  an incredible performance improvement
 We tried this over an dover gain with adding additional O2  so when we  do this  on patients  and or  of   beginners we have a very small to no improvement in performance with or without O2. When we  add O2  to people  who have a cardiac  or respiratory limitation so delivery limitation we have  an immediate improvement of performance.
Example. I have a client with a  respiratory limitation like a  simple cold  or a  more serious COPD.  so they have a  delivery problem . I give them a 5/1/5  assessment and add  at the stage , where they decide to quite a higher pO2  they will be able to keep going another stage  easy.

 If  I have  client  with a " chronic " fatigue " diagnosis  and it seems  a   muscular problem  and I  do an assessment  and add pO2    there is no  increase in performance  and or change in the ability to utilize  O2. Same restrictions apply in healthy people   and confirms  the limiter in an easy way.


So in short what I am trying to ask is, is a vasoconstriction a direct result from the activity or a indirect result.

Marcel I think you just made a summary as  I hope I was able to explain that it  can be both but please come back as this are basic  fundamental questions , which to our   advantage  can now be assessed  thanks to MOXY  and we can design training ideas  when  knowing what we lie to improve  and see during the workout, whether it is doing what it suppose  to do.

Small example from last night with a patient. In short great nutritional intervention , incredible  increase in physical activity but  since 2 years no  chance to loose   weight  she  accumulated over time.
 Assessment shows  a hypocpanic respiration with a hug problem to actually desaturation  at all . A  5/1/5  shows a normal tHb  reaction  at the 1 min rest  the SmO2  starts by65 +-  and increase  up to 85 - 90  and stays there  even at the end where she  drops  from the bike.

 So   easy idea. can we shift the  O2  diss curve   and  if yes  can we see a reaction in SmO2  drop as a sign of easier utilization. So we did a  very low intensity workout  and forced upon here a  hypercapnia ( EtCO2  45 - 50 )  and the SmO2  drop( 90 - 92 )  as in any untrained person   form85 - 90 plateaus  to 50 +- So  over the next 6 weeks she will come in  fixes a MOXY  and a SpO2  sensor  and will do this type of workout  and than we will reassess  the situation.

Marcel thanks ffor the great   feedback


Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #22 
here  some  additional  feedback  to try  to respond  to some mails  in this discussion.
 When we  have a mechanical reason of change in diameter  as  explained, we  have often as well an effort involved ( activity )  and as  such we will see if we collect HR a change in CO  due to change in HR ( Not always as I can drop SV  and increase HR  but stay on the same CO )  BUT I can change tHb  and SmO2  by not challenging thee   CO  but still increase  tHb  or decrease tHb as well as Smo2. This are workouts, where I like to stress  some metabolic reactions without challenging the cardiac system. here a nice  in English summary of  option which can influence   diameter besides  mechanical reasons.



Control of Arterioles

http://courses.washington.edu/conj/heart/arterioles.htm


 

Arterioles are the smallest's vessels of the arterial system, with a diameter of about 1/3 millimeter or smaller. There is much smooth muscle in their tunica media, which causes vasocontriction when it contracts, and vasodilation when it relaxes. Such vasoconstriction and vasodilation plays two important roles in the cardiovascular system.

  • controls of distribution of blood flow to different parts of the body

  • determines the total peripheral resistance

    Factors Affecting Arterioles

    First, let's make a list of the most important factors causing vasoconstriction or vasodilation in arterioles.

    LOCAL CHEMICAL FACTORS: In general, as these factors are added to the intersitital fluid in tissues, they cause vasodilation to help match the local blood flow to the local metabolic requirments. These include CO2, H+, K+, adenosine, osmolarity. In each case, increasing levels leads to increased blood flow in the local tissue.

    SYMPATHETIC NERVES: Norepinephrine acting on alpha receptors causes vasoconstriction. This effect in strong in the skin, digestive tract and kidneys. In these organs, normal blood flow greatly surpasses that required to keep the tissues alive. Instead, most of the blood flow serves specific physiological functions in the organs. By contrast, such vasoconstriction does does not occur in the brain or heart, where blood flow serves to keep the cells in these vital organs alive and healthy.

    NON-ADRENERGIC, NON-CHOLINERGIC AUTONOMIC NERVES: Some autonomic nerves do not release norepinephrine or acetylcholine. Instead they release nitric oxide, which is a vasodilator. This is most important in the digestive tract and penis. Also, as described below, nitric oxide can be released in many places from the endothelial cells.

    HORMONES: In the heart, norepinephrine and epinephrine have the same effect since there are only beta receptors. But in blood vessels there can be both alpha receptors, which cause vasoconstriction, and beta-2 receptors, which cause vasodilation. Since epinephrine preferentially activates beta-2 receptors, it can cause vasodilation if there are sufficient beta-2 receptors. This effect is mainly important in skeletal muscles during exercise.

    Two kidney hormones, angiotensin II and vasopressin, are powerful vasoconstrictors. These play an important role in supporting the arterial pressure during serious decreases in the extracellular fluid volume, such as might occur during serious hemorrhage.

    PARACRINES: We have already frequently encountered vasodilation caused by inflammatory paracrines. Another important paracrine, nitric oxide, is released by endothelial cells. Some nitric oxide is released continually and plays a role in regulation, for example, in respiratory physiology. More is also released during inflammation.

    Distribution of Blood Flow

    Now let us see how the above factors control the distribution of blood flow in physiological situations. The structures that normally have the largest changes in blood flow are the skin, the digestive tract and skeletal muscle.

    SKIN: Blood flow to the skin is almost entirely for the purposes of thermoregulation. Very little of the total is required to support the metabolism of the skin cells. Heat is carried by the blood from inside the body to the skin, where it is lost to the atmosphere. Most heat is lost this way, with the only other significant loss of heat occurring through breathing. Sympathetic nerves control the skin arterioles for this purpose, with greater release of norepinephrine causing vasoconstriction. Since under neutral conditions there is some steady sympathetic activity to the skin, reduction of the sympathetic effects allows vasodilation. Unlike many structures, arterioles do not have the dual innervation by both sympathetic and parasympathetic nerves.

    DIGESTIVE TRACT: As with the skin, most of the blood flow to the digestive tract is not for the purpose of supporting the cells of the digestive tract, but rather, of course, to pick up nutrients absorbed in digestion. Again, sympathetic nerves causing vasoconstriction are the dominant factor here. Removable of the sympathetic effect causes vasodilation. Nitric oxide can play a role here too.

    SKELETAL MUSCLE: As a skeletal muscle makes the transition from relaxed to maximum exercise, the blood flow can increase by up to approximately 20 times. There are two factors at work here. At rest, sympathetic nerves constrict the arterioles in muscle. Then as exercise begins, this effect is removed and some vasodilation occurs.

    Epinephrine, acting on beta-2 receptors, also can cause vasodilation in skeletal muscle during exercise.

    But the greatest subsequent vasodilation is due to local chemical factors . These are changes that occur during exercise in the extracellular fluid surrounding skeletal muscle cells. Such changes occur naturally as the cells consume more energy; in other words, the effect occurs automatically as a muscle exercises and only in the specific muscles working. The brain does not need to get involved in trying to adjust blood flow to the correct muscles. It happens automatically through this local mechanism.

     

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #23 
As  so often  I get emails  short  and simple.  " back it up if you may  this statements "
First  for sure, as we  can't afford  to not  try at least to find  studies  supporting the basic  principles of our statements.
 But allow  me  to make a  short statement here.
 Many of this mails use  " statements"  but when ever I ask to   back them up and sent me  some studies  in this directions  , the  emails  stop to come in.
 I think in the  situation like we   move  with NIRS  and MOXY it would be a  fair  discussion, when we  apply the same scrutiny ( healthy critical  questions )  to what we did  in the past and not just what we  may  look to be able to apply in the future. So here some  directions   to show  how  BP  and vasoconstriction as well as  dilatation   work   to  create a  survival ability in BP.
 

Disparity in regional and systemic circulatory capacities: do they affect the regulation of the circulation?

Calbet JA, Joyner MJ.

Author information

  • Department of Physical Education, University of Las Palmas de Gran Canaria, Campus Universitario de Tafira s/n, Las Palmas de Gran Canaria, Spain. lopezcalbet@gmail.com

Abstract

In this review we integrate ideas about regional and systemic circulatory capacities and the balance between skeletal muscle blood flow and cardiac output during heavy exercise in humans. In the first part of the review we discuss issues related to the pumping capacity of the heart and the vasodilator capacity of skeletal muscle. The issue is that skeletal muscle has a vast capacity to vasodilate during exercise [approximately 300 mL (100 g)(-1) min(-1)], but the pumping capacity of the human heart is limited to 20-25 L min(-1) in untrained subjects and approximately 35 L min(-1) in elite endurance athletes. This means that when more than 7-10 kg of muscle is active during heavy exercise, perfusion of the contracting muscles must be limited or mean arterial pressure will fall. In the second part of the review we emphasize that there is an interplay between sympathetic vasoconstriction and metabolic vasodilation that limits blood flow to contracting muscles to maintain mean arterial pressure. Vasoconstriction in larger vessels continues while constriction in smaller vessels is blunted permitting total muscle blood flow to be limited but distributed more optimally. This interplay between sympathetic constriction and metabolic dilation during heavy whole-body exercise is likely responsible for the very high levels of oxygen extraction seen in contracting skeletal muscle. It also explains why infusing vasodilators in the contracting muscles does not increase oxygen uptake in the muscle. Finally, when approximately 80% of cardiac output is directed towards contracting skeletal muscle modest vasoconstriction in the active muscles can evoke marked changes in arterial pressure.

PMID:

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #24 
Here  from a great  source .
 

Are the arms and legs in competition for cardiac output?

Secher NH1, Volianitis S.

Author information

  • 1The Copenhagen Muscle Research Center, Department of Anesthesia, Rigshospitalet, University of Copenhagen, Denmark.

Abstract

Oxygen transport to working skeletal muscles is challenged during whole-body exercise. In general, arm-cranking exercise elicits a maximal oxygen uptake (VO2max) corresponding to approximately 70% of the value reached during leg exercise. However, in arm-trained subjects such as rowers, cross-country skiers, and swimmers, the arm VO2max approaches or surpasses the leg value. Despite this similarity between arm and leg VO2max, when arm exercise is added to leg exercise, VO2max is not markedly elevated, which suggests a central or cardiac limitation. In fact, when intense arm exercise is added to leg exercise, leg blood flow at a given work rate is approximately 10% less than during leg exercise alone. Similarly, when intense leg exercise is added to arm exercise, arm blood flow and muscle oxygenation are reduced by approximately 10%. Such reductions in regional blood flow are mainly attributed to peripheral vasoconstriction induced by the arterial baroreflex to support the prevailing blood pressure. This putative mechanism is also demonstrated when the ability to increase cardiac output is compromised; during exercise, the prevailing blood pressure is established primarily by an increase in cardiac output, but if the contribution of the cardiac output is not sufficient to maintain the preset blood pressure, the arterial baroreflex increases peripheral resistance by augmenting sympathetic activity and restricting blood flow to working skeletal muscles.

 

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #25 
Okay here an answer to a critical  email.
 Our statement.
 We  can change tHb  and SmO2  without  any   changes in the HR    level?
  The implication is, that we  can    workout  n a low level intensity  and  still create tHb  and SmO2  changes  without having to stress the cardiac system.
 Now  first  true  we can't back this one up  with any   current studies  as we may be the only once  doing this  fun ideas.
 Here  from our  own   case studies  some screen shoots. 
1. Normal reaction   as  predicted  in  an  interval  where during load tHb   may drop or   may increase depending  on the type  of activity   and  in  both cases  due to the activity   SmO2  will  drop.

thb smo2 intervall.jpg


This above is the tHb  and SmO2  reaction  in a bike workout. below now  the SmO2 and HR  from the same section

HR smo2 intervall.jpg


So as  expected  an increase in HR   due to increased activity  and a  drop therefor  on SmO2 as well as  tHb

 Below now   from the same athlete a workout, where we  stabilize the HR   but still deoxygenate  and  change the tHb .  so no change in load   but change in   NIRS reactions.
h t b.jpg  hed  line as HR baseline  stable   and the   "interval in the  red square.  a reat  at a higher intensity  ( HR ) at the end where you see the drop in SmO2  on two loads . You can see , where the HR increases . From start to this point   it was always the same load so all tHb  and SmO2  chnages  where  done without   changeing the HR  . This is a   tryout  to see, whether we can use this idea in rehabilitation where we have a HR limitation given  due to medical reasonsIn sport it is used  on days, where I like to rest the cardiac system  but I like to challange  the metabolic system.

Previous Topic | Next Topic
Print
Reply

Quick Navigation:

Easily create a Forum Website with Website Toolbox.

HTML hit counter - Quick-counter.net