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juergfeldmann

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 #1 

We just finished a very intense  few weeks with a great EXPO and presentation of MOXY at the annual  congress for strength and conditioning coaches in Las Vegas.
Not only very hot weather but very hot discussion and super interested feedbacks and contacts.
 Many of the great coaches  had very fast the concept going , that we have to  move to the next level and train  with physiological feedback information rather than with mathematical % ideas , 5 finger count  or fixed time for recovery.

The direct t feedback AS YOU WOK OUT  FOR LOAD CONTROL AND  REST DURATION AS WELL AS OVERALL SETS  WAS AN EASY SELL FOR COACHES OPNE TO TE IDEA, THTA o2 IS USED  FOR ENERGY PRODUCTION  AND THIS EVEN IN SHORT STRENGHT LOAD IDEAS.

The fact that you can run 4  or  more people on a screen in your weight room  ad some fascinating discussions as a result.
  The presentation of the wasp system for team sports or for bigger gyms as well. We now can cover easy a hockey field or  soccer field for assessments and training.
 So we look forward to a fast expansion of MOXY use in the personal coaching and team sports.

The second fun part was a spontaneous demonstration of an endurance assessment on a  watt bike on the wood way booth.
 With MOXY you have a small pocket with you  and it takes 2 min to set up anywhere a  full endurance assessment.
 Here the discussion and some thoughts we presented to the person we tested.
 Any  reader is welcome  to give us feedbacks and comments  to our  word document we sent to this client.

















 
Attached Files
docx word_document_vegas_test.docx (389.88 KB, 77 views)

Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #2 
Thanks  for the feedbacks.
  Here for the  general reader :
  1. First I will   see, whether we  can start a thread here  for  just ideas like this case studies  with interesting trends  and open questions  but deeper thoughts.

 Here again for the general reader  and insight  look into  an very open  discussion we have  with some very open thinking people. Any idea is   welcome and  we try to back them up with  already existing research or  we have to do our own little  case studeis to see what we may be able to understand closer  and  or not  at all  as of yet.
 Here a  great feedback  from the european groups  SWINCO ( Switzerland  with some thoughts )
  " Hi Guys
 
I wanted to talk about this, as I think we all feel measuring upper and lower body at the same time will give us more information.
 
The great physiological reaction of a healthy system. The system reflex situation of metabolic transfer. In this case of O2 from non-involved area to areas, where it is needed and can be used.
 
Two thought on this as well is, instead of talking about an O2 transfer; do we think that O2 actually moves out of arms for example into the legs, likely it is a change in delivery.
 
Firstly, this may be a reflection of a central governor reflex (metaboreflex), in that it would make much more sense that if you were to start limiting oxygen supply to peripheral muscles in order to protect central function you would first start by limiting oxygen supply to peripheral muscles that do not need the oxygen. In this way we see tHB drop and then as an automatic consequence smO2 drops because less is being delivery, but the same amount is still being used. In other words for example, a respiratory metaboreflex would first start a vasoconstriction during cycling in the upper body in order to maintain respiratory function and attempting to maintain cycling power. Once this is complete, lower body vasoconstriction will start if energy supply to the respiratory muscles is further impeded.
 
Secondly, we need to consider ideas of lactate shuttle and glycogen shunt. Once we start increasing glycolysis beyond the mitochondrial capacity increased LDH reaction, (lactate values), will potentially increase oxygen demand in non-active muscles that will attempt to restore glycogen in working muscles by burning lactate as energy. This may also be a factor in decreasing upper body smO2.
 
 
Just some talking points.   and here  his add on :
 "
I wanted to add one more point about the zoning, as we have talked about this and thought about this lots. How to we decide zoning, and represent these decisions rationally with consistency and physiological basis. Take a look at this section below and I will give my thoughts.
 
STEI is the balanced approach of metabolic delivery and utilization.
FEI is the intensity, where the body needs to compensate as we reach a limitation in the weakest link
 
Juerg nicely shows how HR is no longer balanced from the first part of the binary step to the second part, and logically looks at this as a biomarker for change, in the sense of limitation or compensation. I agree. But I think there is a discussion to be had at creating STEI and FEI zones. Using this imbalance as a marker between the zones is good, and may be simple to apply. However, If you determine the STEI zone in this example as shown, perhaps his base training would be too intense, assuming his smo2 reacts this way every time (this is why sing moxy as a training monitor would be beneficial, no assuming). Perhaps not, but taking a look at some papers like the one I attached there is a relationship between O2 availability, and high O2 availability, and oxidative phosphorylation. In other words if you want to train mitochondrial function you had better make sure plenty of oxygen is around. Now, I already know what Juerg is going to say and I agree, there is a difference between o2 availability and actual o2 bioavailability. Yes, having oxygen does not mean it is used or useable, and a lower smo2 may actually yield a higher cellular po2 and therefore still better oxidative phosphorylation. However, I would say, perhaps being a little careful, that it is more likely that having a high SmO2, indicating, likely, a high arterial po2 as shown in the paper, will yield the best oxidative phosphorylation training results (I could be very wrong), especially, and likely only for, long duration trainings. This would mean there is an intersection between maximum smo2 and maximum performance that would be the sweet sport for oxidative phosphorylation training, with a potential smo2 drift over time. Back to practical application if you give a guy his STEI zone as in the example Juerg gave, he will likely always train at the high end of this zone and would, if, if, I am correct be too intense for optimal oxidative phosphorylation training.
 
 
Again just some thoughts. And possible adjustments for our training guides.
cheers
Andri

As a potential " control" element,. whether we have  bioavailability  or whether we just   O2  delivery you always can use respiration.
. Play with  reducing in this stage the respiration  to half the RF  by trying to keep Tv  about equal;  and thna  do this  for about 3 - 5 min  than  go the opposite  with double RF  and keep  TV the same.
What do you see : Use HRV  SpO2  and  MOXY  as  feedback information.
 What do you expect  and what do you see,  and  what would that  give uss  on additional information ?

Here  as well the  att  from Andri

Hyperoxia decreases muscle glycogenolysis, lactate production, and lactate

efflux during steady-state exercise

Trent Stellingwerff,

 

1 Paul J. LeBlanc,2 Melanie G. Hollidge,3

George J. F. Heigenhauser,

 

3 and Lawrence L. Spriet1

1

 

Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph;

2

 

Department of Physical Education and Kinesiology, Brock University, St. Catharines;

and

3Department of Medicine, McMaster University, Hamilton, Ontario, Canada

Submitted 14 October 2005; accepted in final form 5 January 2006

Stellingwerff, Trent, Paul J. LeBlanc, Melanie G. Hollidge,

George J. F. Heigenhauser, and Lawrence L. Spriet.

Hyperoxia

decreases muscle glycogenolysis, lactate production, and lactate

efflux during steady-state exercise.

 

Am J Physiol Endocrinol Metab

290: E1180 –E1190, 2006. First published January 10, 2006;

doi:10.1152/ajpendo.00499.2005.—The aim of this study was to

determine whether the decreased muscle and blood lactate during

exercise with hyperoxia (60% inspired O

 

2) vs. room air is due to

decreased muscle glycogenolysis, leading to decreased pyruvate

and lactate production and efflux. We measured pyruvate oxidation

via PDH, muscle pyruvate and lactate accumulation, and lactate

and pyruvate efflux to estimate total pyruvate and lactate production

during exercise. We hypothesized that 60% O

 

2 would decrease

muscle glycogenolysis, resulting in decreased pyruvate and lactate

contents, leading to decreased muscle pyruvate and lactate release

with no change in PDH activity. Seven active male subjects cycled

for 40 min at 70% V˙

 

O2 peak on two occasions when breathing 21 or

60% O

 

2. Arterial and femoral venous blood samples and blood

flow measurements were obtained throughout exercise, and muscle

biopsies were taken at rest and after 10, 20, and 40 min of exercise.

Hyperoxia had no effect on leg O

 

2 delivery, O2 uptake, or RQ

during exercise. Muscle glycogenolysis was reduced by 16% with

hyperoxia (267

 

 19 vs. 317  21 mmol/kg dry wt), translating

into a significant, 15% reduction in total pyruvate production over

the 40-min exercise period. Decreased pyruvate production during

hyperoxia had no effect on PDH activity (pyruvate oxidation) but

significantly decreased lactate accumulation (60%: 22.6

 

 6.4 vs.

21%: 31.3

 

 8.7 mmol/kg dry wt), lactate efflux, and total lactate

production over 40 min of cycling. Decreased glycogenolysis in

hyperoxia was related to an 44% lower epinephrine concentration

and an attenuated accumulation of potent phosphorylase

activators ADP

 

f and AMPf during exercise. Greater phosphorylation

potential during hyperoxia was related to a significantly

diminished rate of PCr utilization. The tighter metabolic match

between pyruvate production and oxidation resulted in a decrease

in total lactate production and efflux over 40 min of exercise during

hyperoxia.

carbohydrate oxidation; glycogen; pyruvate dehydrogenase activity;

blood flow; arterial-venous measurements; oxidative and substra

Now the fun part is, that we  can create a short term " natural" hyperoxia"  with playing with respiration in the STEI  or  very short in the FEI  intensity.
  Here what you do. You go into the FEI intensity  till you create the " famous " MAXLASS.
  So you may have a   great intensity with a stable  lactate of somewhere between 3 - 6 mmol depending on the athlete.
 Than you   go and create a  shift of the O2 Diss curve  by going  voluntarily  hyper capnic  and than you check the lactate trend..
 Or you can go STEI intensity   no lactate  go hypocapnic    for 3 - 5 min check lactate and go back to normo or better hypercapnic  and check lactate.
 The  hyperoxia is  given by  change in O2 disscurve  and therefor the bioavailability.
 I will search for some  own case studies I did  15 years back  with  a O2  generater  to see the changes in lactate  and the influence on the " lactate threshold " due to change in  O2  bioavailablity.

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #3 
Some short mails  I got.
 Straight forward  and easy to answer.
  Q:  Is there in fact research out there ( accepted)  who actually supports your crazy ideas on vasoconstriction and delivery and demand ideas.
  A:  1. What means accepted.  Is accepted because it is published  or accepted because of the position of the author  (Smile.)
  Here a more serious answer  . There are   hundreds  of accepted  studies  out there.  So I basically randomly open  my   study  folder and take any of them  . Here  one.
 

Noninvasively determined muscle oxygen saturation is an early indicator

of central hypovolemia in humans

Babs R. Soller,1 Ye Yang,1 Olusola O. Soyemi,1 Kathy L. Ryan,2 Caroline A. Rickards,2 J. Matthias Walz,1

Stephen O. Heard,1 and Victor A. Convertino2

1Department of Anesthesiology, University of Massachusetts Medical School, Worcester, Massachusetts; and 2U. S. Army

Institute of Surgical Research, Fort Sam Houston, Texas

Submitted 5 June 2007; accepted in final form 13 November 2007

Soller BR, Yang Y, Soyemi OO, Ryan KL, Rickards CA, Walz

JM, Heard SO, Convertino VA.

 Noninvasively determined muscle

oxygen saturation is an early indicator of central hypovolemia in humans. J Appl Physiol 104: 475–481, 2008. First published November

15, 2007; doi:10.1152/japplphysiol.00600.2007.—Ten healthy human volunteers were subjected to progressive lower body negative pressure (LBNP) to the onset of cardiovascular collapse to compare the response of noninvasively determined skin and fat corrected deep muscle oxygen saturation (SmO2) and pH to standard hemodynamic parameters for early detection of imminent hemodynamic instability. Muscle SmO2 and pH were determined with a novel near infrared

spectroscopic (NIRS) technique. Heart rate (HR) was measured continuously via ECG, and arterial blood pressure (BP) and stroke volume (SV) were obtained noninvasively via Finometer and impedance cardiography on a beat-to-beat basis. SmO2 and SV were significantly decreased during the first LBNP level (_15 mmHg), whereas HR and BP were late indicators of impending cardiovascular collapse. SmO2 declined in parallel with SV and inversely with total peripheral resistance, suggesting, in this model, that mO2 is an early indicator of a reduction in oxygen delivery through vasoconstriction. Muscle pH decreased later, suggesting an imbalance between delivery and demand.

 Spectroscopic determination of SmO2 is noninvasive and continuous, providing an early indication of impending cardiovascular

collapse resulting from progressive reduction in central blood volume. tissue oxygen; near infrared spectroscopy; physiological monitoring

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #4 
Personal loud thinking  on the above info:
" that SmO2 is an early indicator of a reduction in oxygen delivery through vasoconstriction. Muscle pH decreased later, suggesting an imbalance between delivery and demand.
Early indicator means  what we  in a very basic intro in  MOXY try to get over to coaches.
Vasoconstriction  can be nicely traced over  tHb as an indicator of blood flow /volume
pH decrease later as an indicator that drop in SmO2   can mean that  pH may change but  later   and as well it can mean that pH  does not change later because SmO2  drops  and therefor  there is  still O2 used . if the  "time ' is too long than we may need O2 independent help for   proper ATP production but if the time is   " short " than the drop in SmO2  was a  sign of a O2  dependent coverage of the energy demand.
 That's why we  not simply can use the trend in SmO2  as a equal trend in lactate   or  similar O2 independent energy substrate use.

Remember  what MOXY /NIRS  is . A direct info with the advantage of  "direct" versus indirect  info like VO2   or  Lactate  with the time lag  and as such the loss of information from the real direct moment to the unreal indirect moment.
moxy idea.jpg 

Here for the once who like the  whole overview  from our case study as a more philosophical explanation but it helps to understand, why we look at the whole team and not  on one single marker.
The Vegas meeting showed us  with every single client, how they start to  smile, once they  give themselves time to look at the overall picture.
 Why strength coaches suddenly start to understand that O2  is as well important  in their   sport.

ryinc

Development Team Member
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Posts: 360
 #5 
I am trying to build my understanding and working through the case studies to learn as much as i can from the forum....so apologies for digging up old threads (and apologies that there will probably be more to come). While the conclusions of some of the case studies might be obvious to some, they are not always clear to me and i am sometimes left wondering whether i understood or not.

Jeurg, firstly thanks for the nicely laid out case.

Readers not familiar with the case, should read the attachment posted in the first post by Jeurg. However, for this post i want to move immediately to the end. The case finished with the following graph and questions:
Involved vs Non-involved.jpg 
Look at tHb trend in arms and non-involved legs (sidenote i actually think there was a mistake and it was supposed to say non-involved arms and involved legs???- i am assuming that it was incorrectly stated).  Than go back to CO = HR x SV

Is the HR increase due to SV plateau or  drop  so limitation of the cardiac system or is it a compensatory reaction?


My thoughts/questions 
  • There seems to be a clear shift of blood from non-priority to priority ("non-involved" vs "involved") muscle from about 2400 on.
  • Presumably the body starts running into trouble about here, HR increases but this is not sufficient so also starts redirecting flow between priority and non-priority muscles?
  • If this was a respiratory metaboreflex, then i think we should be seeing blood in both involved and non-involved muscles drop (since the blood would be being directed to respiratory muscles?). We don't seem to see this, since it goes up in one muscle but down on the other - am i understanding correctly?
  • I am not sure i understand why the tHb is reducing on the priority but increasing on the non-priority in the first part of the assessment. In particular the recovery trend of tHb in the rest periods (during the loads the downward trend of tHb on the involved might make  sense because of compression). Can someone explain this to me?
So in conclusion - there is a cardiac limitation (SV plateau), HR tries to compensate but is a weak compensator and almost immediately is itself ineffective. The body needs another compensator and tries to move blood around?

Would appreciate people steering my thoughts into the right direction if the above is not correct.

bobbyjobling

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Posts: 211
 #6 
Some thoughts:
THb reduction especially in the rest phase in the involved muscle at the start of the assessment could be also due to a greater efficiency in recirculating the blood back to the heart. One component of thb we don't talk about much is velocity or flowers rate.

On the non-priority muscle this flow rate could be less due to higher return flow resistance, tHb would increase as per CO output, eventually blood pressure control will restrict blood flow in.

We need to see SmO2 [smile]
juergfeldmann

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 #7 
Great  points  and I like  just in between clients  to start  with   for me the  nicest  one.
 I am not sure i understand why the tHb is reducing on the priority but increasing on the non-priority in the first part of the assessment

Before  the 2400 point

 We  create in the legs a  muscle contraction  which will reduce  tHb and as the load is not very hard  we  have a  higher  compression  from muscle  than a  vasodilatation  from cardiac output  and  other  options. Now  the cardiac output still goes up  and HR is a  small  feedback on this  reaction.
 In the   low priority muscle we  will have   no muscle contraction but  a higher CO  and  CO  will be  stringer  than the  minimal  muscle compression in arms  and  as CO is NOT  a limitation in this  intensity we will see a dilatation in  arms (  non compression but higher CO )   where in the legs  we  have muscle contraction  higher  than CO ) Hope  this makes  some  sens.
We than  reach a   relative balanced situation (  circle) where  we  have a higher CO  again  but possible  close to   getting  to its limitation.
 So  in the legs, where we have a higher  muscle compression  and we let go in the one minute rest we will create a huge inflow  and have a huge  vasodilatation effect.
 As we approach CO limitation  this  simply  can not open up   in the one  minute as before  and we  would loose BP.
 But it really does not make sense  to  not  " recover " in the   priority muscle  so you can see the shift   that in the less priority muscle  the  recovery  tHb  starts  dropping not just  during load  but as well in the recovery..
 Now  this could be  due  to  involvement of this  delta pars acromialis. ( as  in the webinar  shown  by  Dr. Bellar. Different options  to  show   whether it is   volume shift  or  just  additional involvement.
 a) VO2 peak . What  will happen  with VO2 peak if it is a   blood volume shift versus a additional  involvement of  arms ?
b)  with SEMG   on legs  and arms. What will happen in the a rm SEMG  and what in the leg  SEMG
c)  physioflow. What  will we see in  SV  and HR ( CO ) if  it is a shift   of blood versus an integration of  arm muscles in the performance.
d) SVR  ( systemic vascular resistance)  or in our  case tHb reaction.

If  we  stop suddenly a very hard load, we i will loose  muscle compression immediately  and as  such a  kind of a support of BP over mechanical  help. The big risk of loosing BP is  the sudden lack of muscle compression in the legs  as we have there as well the  highest dilatation  effect.
 Now as we  stop suddenly we  will have   low  muscle compression but high CO  and possibly as well     higher  than  baseline CO2 as an additional vasodilatation.  So  the expected reaction  if CO  would be  sufficient  to minati8n BP    would be, that we see in the legs a  sharp  increase or  shoot up  of tHb as  we open up  the   blood vessels in the legs.
 The same will as well happen in the  arms.. This incredible increase in opening up  a space  for blood volume will have a terrible effect on the  BP  for the brain  and most athletes  know  that after a very hard load  they feel a short moment dizzy  and like to   lay down or often do that.
In this case we had a  small  uncomfortable feeling but than it  he was okay as he balanced  out  the  BP  help  with a   vasoconstriction  in legs  extremely  and in arms  somewhat look at the extreme tHb  drop  despite   no  activity  just sitting on the bike. in his leg  basically  down to a level he  had  during loads. In the  arms a   overshoot  with  than  a short  small vasoconstriction.

The   other points  like the one on the metaboreflex  is absolutely correct.
 Add on  many   do not have a  respiratory metaboreflex,  but simply a weak respiratory muscle system  than the reaction would look very different . How  would it look  like ?
  The  seen reaction is a great example and you can observe it  any time  at the beginning of a  step test  that when CO is strong enough  you will see in low priority muscles  an increase in tHB  and  in SmO2 , where in priority muscles  due to a low  start CO  you see a  drop in tHb  as  muscle compression is  higher than  CO but the delivered amount  of O2  is   far enough to  maintain  ATP  and pO2  level so no need to panic  and  try  to open up  blood vessels by inefficiency push more  form  CO. On the other side  if  we see this  normally happen  and  we  made a  very intense  cardiac  workout  we see the next day in the   " getting ready  for a  new  workout, that  the non priority muscle  doe snot show  this increase in tHb  and  SmO2  because we already  have a close to limitation cardiac  demand.   This is  one  way we  know  the cardiac  stimulation from yesterday  was  success full  but the recovery incomplete  so we  will change perhaps  the planned  workout we had  for today as we see we  can not count of a  decent support   from CO  today.  This is exactly  why we  not follow a plan  but we follow  physiological reactions  with physiological guided  workouts.
 No such thing like  5  reps  with a fixed wattage  as FTP  today  with a weak cardiac  system may be  very very different than  when we  made the FTP  test in a  fully recovered stage.


bobbyjobling

Development Team Member
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 #8 
Sorry Juerg if this is a stupid question [frown] or if you have already answered it, but can you explain this for me:

Muscular compression of the priority muscles reduces tHb within it and during rest periods tHb increases. On the non-priority muscle, why on the rest period we don't see a reduction of tHb as the rush of blood returns to the priority muscles? It should look graphicle opposite
juergfeldmann

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Posts: 1,501
 #9 
Good point.
 Remember, that  the " shift " of  blood  or v  blood volume is only in action, when the cardiac output is not able to sustain BP. So   in the  stop  period , where we get rid of   muscle compression  and therefore  due to the lag time  of CO  the  rush of blood in the muscles increase, we   will see a " cardiac " weakness, when we  have not enough  pressure  to maintain  the  central BP  and than we will have a  vasoconstriction. This  can be  anywhere but is most  often , where it is most efficient. The   upper body   blood  flow  may be in  bikers  or  for sure in runners  much smaller than the huge  capillary  network in legs  so a  release in muscle compression   in the legs  will " suck " a lot of blood in the   now open vasodliatated   leg region and we will see a  vasoconstriction there.
 This vasoconstriction can be very local  depending on  the situation.

We have  some great example s from cross-country skiing  , where  your point is well taken  as we see  the drop in tHb in the  arm muscles  when we  hit a CO limitation.   There is a  great point  in Dr. Bellars  webinar, where he  shows , that many MOXY users see a drop in SmO2  and    sometimes in tHb in nonpriority muscle.
 That is  absolutely  right and that is   what we look for. The question only is ,  what   causes  this  drop in SmO2  and tHb, when do we see it   and  than we  can make some  interpretation on what   or   where a limitation  in that  moment is. There are many  individual access, where in some it  is veyr easy to see   and in others  we have to add some additional feedback or ideas  to it like HR  RF  to name some easy to use  bio markers

Here some   interesting topics  looking at this  direction. As you can see 1877  the topic  was already in discussion !!!!!
 

J. Physiol. (1963), 166, pp. 120-135

Blood FLOW THROUGH ACTIVE AND INACTIVE MUSCLES OF THE FOREARM DURING SUSTAINED HAND-GRIP CONTRACTIONS

BY P. W. HUMPHREYS AsD A. R. LIND

From the National Coal Board Physiology Research

Branch, Department of Human Anatomy, University of Oxford

(Received 4 July 1962)

Despite the vasodilatation which occurs in a muscle during contraction,the full exploitation of this physiological response is hindered by the mechanical compression of the vessels by the contracting muscle (Gaskell, 1877), and its function is presumably thereby impaired. The continuous

mechanical compression of the blood vessels through the active muscle has been generally accepted as the cause of the early onset of fatigue during sustained contractions; the validity of this view may be judged from the values of intramuscular pressure, of 150-300 mm Hg, determined during

maximal isometric contractions of frog muscle (Hill, 1948) and of rabbit muscle (Mazella, 1954). Grant (1938) and Barcroft & Dornhorst (1949) found small increases in the blood flowing through the muscles during both sustained and rhythmic contractions, while in a previous report from this laboratory Clarke, Hellon & Lind (1958) showed that at a tension of 1/3 maximal the increase of blood flow during contractions was greater as muscle temperature increased and could, in fact, be substantial.

Some more  updated  studies but really  no t new.

Are the arms and legs in competition for cardiac output?

Secher NH, Volianitis S.

Source

The 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.

PMID:

17019302

[PubMed - indexed for MEDLINE]

 

Than another nice  one

Acta Physiol Scand. 1998 Mar;162(3):421-36.

Skeletal muscle blood flow in humans and its regulation during exercise.

Saltin B1, Rådegran G, Koskolou MD, Roach RC.

Author information

  • 1The Copenhagen Muscle Research Centre, Rigshospitalet, Tagensvei, Denmark.

Abstract

Regional limb blood flow has been measured with dilution techniques (cardio-green or thermodilution) and ultrasound Doppler. When applied to the femoral artery and vein at rest and during dynamical exercise these methods give similar reproducible results. The blood flow in the femoral artery is approximately 0.3 L min(-1) at rest and increases linearly with dynamical knee-extensor exercise as a function of the power output to 6-10 L min[-1] (Q= 1.94 + 0.07 load). Considering the size of the knee-extensor muscles, perfusion during peak effort may amount to 2-3 L kg(-1) min(-1), i.e. approximately 100-fold elevation from rest. The onset of hyperaemia is very fast at the start of exercise with T 1/2 of 2-10 s related to the power output with the muscle pump bringing about the very first increase in blood flow. A steady level is reached within approximately 10-150 s of exercise. At all exercise intensities the blood flow fluctuates primarily due to the variation in intramuscular pressure, resulting in a phase shift with the pulse pressure as a superimposed minor influence. Among the many vasoactive compounds likely to contribute to the vasodilation after the first contraction adenosine is a primary candidate as it can be demonstrated to (1) cause a change in limb blood flow when infused i.a., that is similar in time and magnitude as observed in exercise, and (2) become elevated in the interstitial space (microdialysis technique) during exercise to levels inducing vasodilation. NO appears less likely since NOS blockade with L-NMMA causing a reduced blood flow at rest and during recovery, it has no effect during exercise. Muscle contraction causes with some delay (60 s) an elevation in muscle sympathetic nerve activity (MSNA), related to the exercise intensity. The compounds produced in the contracting muscle activating the group IIl-IV sensory nerves (the muscle reflex) are unknown. In small muscle group exercise an elevation in MSNA may not cause vasoconstriction (functional sympatholysis). The mechanism for functional sympatholysis is still unknown.

However, when engaging a large fraction of the muscle mass more intensely during exercise, the MSNA has an important functional role in maintaining blood pressure by limiting blood flow also to exercising muscles.

 Than here one   you can combine  with a  case  we showed on  inversion   reaction.
 

Noninvasively determined muscle oxygen saturation is an early indicator of central hypovolemia in humans

 

Babs R. Soller,1 Ye Yang,1 Olusola O. Soyemi,1 Kathy L. Ryan,2 Caroline A. Rickards,2 J. Matthias Walz,1 Stephen O. Heard,1 and Victor A. Convertino2

 

1Department of Anesthesiology, University of Massachusetts Medical School, Worcester, Massachusetts; and 2U. S. Army Institute of Surgical Research, Fort Sam Houston, Texas

 

Submitted 5 June 2007 ; accepted in final form 13 November 2007

 

ABSTRACT

 

Ten healthy human volunteers were subjected to progressive lower body negative pressure (LBNP) to the onset of cardiovascular collapse to compare the response of noninvasively determined skin and fat corrected deep muscle oxygen saturation (SmO2) and pH to standard hemodynamic parameters for early detection of imminent hemodynamic instability. Muscle SmO2 and pH were determined with a novel near infrared spectroscopic (NIRS) technique. Heart rate (HR) was measured continuously via ECG, and arterial blood pressure (BP) and stroke volume (SV) were obtained noninvasively via Finometer and impedance cardiography on a beat-to-beat basis. SmO2 and SV were significantly decreased during the first LBNP level (–15 mmHg), whereas HR and BP were late indicators of impending cardiovascular collapse. SmO2 declined in parallel with SV and inversely with total peripheral resistance, suggesting, in this model, that SmO2 is an early indicator of a reduction in oxygen delivery through vasoconstriction. Muscle pH decreased later, suggesting an imbalance between delivery and demand. Spectroscopic determination of SmO2 is noninvasive and continuous, providing an early indication of impending cardiovascular collapse resulting from progressive reduction in central blood volume.

 

 

and here one  from this group   doing many great studies.

 

Cardiac output, and leg and arm blood flow during

 

incremental exercise to exhaustion on the cycle ergometer

 

Jose A. L. Calbet (1,2), Jose Gonzalez-Alonso (2), Jörn W. Helge (2,3),

 

Hans Søndergaard (2), Thor Munch-Andersen (2), Robert Boushel (3,4), Bengt Saltin (2)

 

(1) Department of Physical Education. University of Las Palmas de Gran Canaria, Spain

 

(2) The Copenhagen Muscle Research Centre, Rigshospitalet, 2200 Copenhagen N,

 

Denmark.

 

(3) Department of Biomedical Sciences, Panum Institute, 2200 Copenhagen N,

 

Denmark.

 

(4) Department of Exercise Science, Concordia University, Montreal, Quebec, CanadaJ.A.L. Calbet

 

 

 

 

 

Abstract

 

To determine central and peripheral haemodynamic responses to upright leg cycling

 

exercise, nine physically active males underwent measurements of arterial blood

 

pressure and gases, as well as femoral and subclavian vein blood flows and gases during

 

incremental exercise to exhaustion (Wmax). Cardiac output (CO) and leg blood flow

 

(BF) increased in parallel with exercise intensity. In contrast, arm BF remained at 0.8

 

l.min-1 during submaximal exercise, increasing to 1.2±0.2 l.min-1, at maximal exercise

 

(P<0.05), when arm O2 extraction reached 73±3%. The leg received a greater

 

percentage of the CO with exercise intensity, reaching a value close to 70% at 64% of

 

Wmax, which was maintained until exhaustion. The percentage of CO perfusing the

 

trunk decreased with exercise intensity to 21% at Wmax, i.e. to ~ 5.5 l.min-1. For a

 

given local VO2 leg vascular conductance (VC) was 5-6 fold higher than arm VC,

 

despite marked haemoglobin de-oxygenation in the subclavian vein. At peak exercise

 

arm VC was not significantly different than at rest. Leg VO2 represented around 84% of

 

the whole body VO2 at intensities ranging from 38 to 100 % of Wmax. Arm VO2

 

contributed between 7 and 10% to the whole body VO2. From 20 to 100% of Wmax, the

 

trunk VO2 (including the gluteus muscles) represented between 14-15% of the whole

 

body VO2. In summary, vasoconstrictor signals efficiently oppose the vasodilatory

 

metabolites in the arms suggesting that during whole body exercise in the upright

 

position blood flow is differentially regulated in the upper and lower extremities.

 

 

And here the one  I mentioned  where  there is no problem  when we  have a   muscle copmpression  and lower flow as long the intensity is  not   high .
 

  1. Low blood flow at onset of moderate-intensity exercise does not limit muscleoxygenuptake.

PubMed

Nyberg, Michael; Mortensen, Stefan P; Saltin, Bengt; Hellsten, Ylva; Bangsbo, Jens

2010-03-01

The effect of low blood flow at onset of moderate-intensity exercise on the rate of rise in muscle oxygen uptake was examined. Seven male subjects performed a 3.5-min one-legged knee-extensor exercise bout (24 +/- 1 W, mean +/- SD) without (Con) and with (double blockade; DB) arterial infusion of inhibitors of nitric oxide synthase (N(G)-monomethyl-l-arginine) and cyclooxygenase (indomethacin) to inhibit the synthesis of nitric oxide and prostanoids, respectively. Leg blood flow and leg oxygen delivery throughout exercise was 25-50% lower (P < 0.05) in DB compared with Con. Leg oxygen extraction (arteriovenous O(2) difference) was higher (P < 0.05) in DB than in Con (5 s: 127 +/- 3 vs. 56 +/- 4 ml/l), and leg oxygen uptake was not different between Con and DB during exercise. The difference between leg oxygen delivery and leg oxygen uptake was smaller (P < 0.05) during exercise in DB than in Con (5 s: 59 +/- 12 vs. 262 +/- 39 ml/min). The present data demonstrate that muscle blood flow and oxygen delivery can be markedly reduced without affecting muscle oxygen uptake in the initial phase of moderate-intensity exercise, suggesting that blood flow does not limit muscle oxygen uptake at the onset of exercise. Additionally, prostanoids and/or nitric oxide appear to play important roles in elevating skeletal muscle blood flow in the initial phase of exercise. PMID:20089709

 

There are many many more  studies  supporting this interesting idea  and  again  is helping us  to close the gap  between science  and practical application.




ryinc

Development Team Member
Registered:
Posts: 360
 #10 
Now this could be due to involvement of this delta pars acromialis. ( as in the webinar shown by Dr. Bellar. Different options to show whether it is volume shift or just additional involvement.
a) VO2 peak . What will happen with VO2 peak if it is a blood volume shift versus a additional involvement of arms ?
b) with SEMG on legs and arms. What will happen in the a rm SEMG and what in the leg SEMG
c) physioflow. What will we see in SV and HR ( CO ) if it is a shift of blood versus an integration of arm muscles in the performance.
d) SVR ( systemic vascular resistance) or in our case tHb reaction.

Question a) if it is additional involvement, i think VO2 would increase without a significant increase in performance.
b) i suppose SEMG will.show activity if arms actually getting involved
C) i suppose if it was arms actually involved HR and SV would increase?
D) Not sure what SVR actually measures and but presumably if blood.is being shifted around it is being done so with vasoconstriction and this would show up, but i am not sure how this compare to what the measuremenr looks like when there is compression from arms getting more involved.
bobbyjobling

Development Team Member
Registered:
Posts: 211
 #11 
Thanks Juerg, I will study the papers over the weekend [smile]
juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #12 
Will be back later  just short some  feedback.

 Now this could be due to involvement of this delta pars acromialis. ( as in the webinar shown by Dr. Bellar. Different options to show whether it is volume shift or just additional involvement.

There was a difference in non priority muscle  placement in the webinar.
 They decided  to  place a MOXY  on the  delta pars  anterior.
 Here in  very basic words
. We place it in  cycling assessments on the  delta  pars  acromialis.
 This   section of the delta muscle   can  help in  abduction of your arm and  its  activation is from neutral zero position to  about 60 +- degree abduction  the most involved one.
 The opposite or  antagonistic muscle  would do  adduction.
 So  when you  create  handle placement where, in case you start to  get upper body more involved like to  avoid a delta pars  acromialis  involvement  you  look for an internal rotation adduction  muscular chain reaction. To   achieve this  we have a 45 +- degree  gleno humeral IR   position on  full extended  elbows.
 For  people  with SEMG  they easy can see minimal  activity in triceps biceps  due to the  full elbow extension  and  slightly increase  activity in pectorals(  subscapularis is hard  to  assess with SEMG   as well some  activity  in  lattisimus.
 The antagonistic  muscles  show   just  base line  resting EMG  activity.
 Now  we do not have    perfect feedback   from the  webinar. What we know is  that the MOXY  and SEMG  where placed on the anterior pars of the delta. This part is involved in glenohumeral flexion together  with   the long biceps  head  and  more in this muscle chain. We do not know  whether the  athlete   was sitting upright  and had   elbow extension or whether he  was in a more  "aero position.
 We  do not know whether  was holding in pronation position on the handle bar  or in the   drop position or  in neutral   shoulder position on the brakes.
 We  do not know, whether he changed  position as the  time went on.
 We  do not know  whether they as well had a  SEMG on the leg muscle  to see  SEMG  activity in combination  with SmO2  and tHb.

To  than look  what causes  the SmO2  tHb  change in a  minimal priority muscle   we  as mentioned used initially  CO VO2, SEMG  and NIRS  and NIRS in 3   depth levels to see, whether perhaps  the  drop or change in TSI %  may be  due to  body temperature  regulation.
  The reason  for  this  and why  we think it matters   what  happens in non priority  muscles is exactly  that we are able   to not move in the dark  and  try and error but know  what  is going on. This is why we sue  NIRS.

You look  for in  simple  terms three main reaction. in non priority muscles reactions.

a) non reaction  in the nonpriority muscles which than  can be used  for  physiological training ideas
b) increase in activity in  non priority muscles , which than  agai8n helps  to correct or  control the   planned physiological  direction.
d) a blood volume shift   towards  the  priority muscle. which is a very important  feedback depending on your physiological stimulation goal.

 So   when Dr. Bellar   writes, that MOXY user in the field see SmO2  and tHb reactions in the nonpriority  muscles , than he makes a very  great point.
 This is  exactly  why  you actually  have a live feedback  from NIRS  as this reactions guide  you  or tell you , whether you  are on your physiological target or  not.

So  in the  webinar example. they  could see  with SEMG  but  as well with  NIRS, when this athlete started  to integrate  his delta  anterior  part in the activity.

 This is than used  either  for  technical workouts, where you may concentrate more  on legs  and n not like to involve  upper body. or it   can be used  for a cardiac stimulation  if you know the cardiac systems not pushed  hard  and so on.

 So I assume  they used as well VO2  and cardiac  out put info in this case study  and had  therefor information whether the   athlete  had a cardiac limitation  or whether he had a respiratory  limitation  and   based on the VO2 , SEMG  and CO reaction  they than make   make a conclusion whether  the  delta pars  anterior   was  more involved  or not.  Last   when you  look at the muscle chain   on holding on the handle bar in different positions  than you can see, whether it is easier  or less easy to involve a muscle in an all out  effort.


 second. RYINC Thanks  for your  feedback
 Mail me your contact  to factquestions@hotmail.com. I like to  sent you an  in depth feedback on your  answers  with some additional thoughts , because they  go far to   deep on the forum and contain  some VO2  and lactate feedback  and I promised  to  Ruud  and  another   reader  just to focus  on NIRS , but in this case   I  have to  move back  to    move forward.
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