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Roger

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 #1 
David Bellar sent this over as a follow up on the Summit discussion around whether the Deltoid should be considered "non-involved", "minimally involved", or something else during a cycling assessment.


We got busy this morning and decided to add an EMG data capture to a 20min cycle at 65% Vo2 max with a Moxy on the anterior deltoid.  I attached the resultant data.  The EMG signal is expressed as a % of Maximum Voluntary Isometric Contraction (%MVIC) which was acquired prior to baseline.  The first data points on the chart are the MVIC signal and hyperemia on the Moxy post contraction.  
 
The chart clearly shows that over the course of even this level of exercise the muscle activity in the anterior deltoid rises quite dramatically.  This is what we were talking about at the summit, thought the muscle doesn’t ‘look’ that involved it is obviously quite active.  I would guess at this point that if we had used an EMG in the slideboard exercise demo from the summit, we would have captured very robust activation.  
 
Anyway just wanted to share our little result from this morning.
 
Dave B.

Bellar.jpg 

MTF Carter

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 #2 
Thanks for the update. I have NIRS data as well on all the opposite legs of healthy and PAD patients that did our supine plantar flexion exercise study. Essentially SmO2 in the non-exercising limb stayed flat. The only time SmO2 changed was if the participant was flexing their leg to the metronome or if our ultrasonographer hit the NIRS with the probe. Thus, our data from 0.5 kg to 7.0 kg at 20 contractions per min. suggest that there is not a shunting of blood occurring in the opposite leg in PAD or healthy participants. 

One way I have increases SmO2 (n=2) is using the drug isoproterenol to rase HR. This drug also lowers peripheral resistance. note that there is not much of a change in tHb (not the big 0.5 to 1.0 g/dL changes we saw with the LBNP tank) yet this is a big vasodilation. The patients tend to get flush red and they report the force of contraction in their chest feels greater along with increased HR. SmO2 is up but not my much.

Subject 1 Healthy
Screen Shot 2016-05-17 at 5.47.10 PM.png  
Subject 2 Healthy 
Screen Shot 2016-05-17 at 5.47.23 PM.png  
I wanted to include this image of a PAD patient with bilateral iliac disease. This is what many of our PAD patients look like. On the left you can see the distal aorta completely stops. The arteries are fed by small collateral vessels however as you can see a large part of both iliac arteries are completely occluded. Luckily they were abel to insert guide wires across the lesions and deploy 2 stents opening both vessels. Unfortunately in many cases the downstream effects have already started to effect the microcirculation. So many patients that get stents find that it doesn't improve walking times and symptoms return.

Screen Shot 2016-05-17 at 11.01.56 AM.png   
So you can see how this would reduce SmO2 greatly. Look at all the collaterals in PAD... they just can't get the job done. 

Thanks for letting us present our data at the Moxy Summit and we look forward to using the Moxy in our future studies as it has worked very well for us. 

Carter

juergfeldmann

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 #3 
Nice info  from both  posts.
 The  SEMG  would be fun to have done on what we use  as a minimal involved muscle  part of the delta muscle.
 The pars lateralis  resp  the pars  , which mainly is involved in the first  40 - 60 degrees of   gleno humeral abduction. The anterior   pars or pars  claviculare  of the  delta is a  strong  helper in  glenohumeral  elevation  together  with the long biceps  head. So  no wonder in any  cycling activity  this muscle will be involved quite a bit.
 We use  always  pars acromialis  of the delta muscle  for  upper body minimal involved muscles  activity  and  than it as well depends on the  position of the  upper body. If you go in a  aero  position with relative  narrow  arm position  so  strong  adduction involvement  and you fatigue  you may see a  surprising  activity  when  it is getting harder  at the   delta pars  acromialis  as well. Have to  check  my  old  datas  but we did  many years back an 8 channel  SEMG  where we  divided the delta into  4 sections  and as well added  biceps  triceps  lattisimus  and  teres major to the position.
 So if you have a multichannel  SEMG  try  this and see  how it looks in your case studies. Than as so often make it on different people with different upper body  size  but on the same   bike handle bar length  and see   what  come sup  than. Can we  create a cook book.
juergfeldmann

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 #4 
2 more  thoughts.
 1. When ever you use  NIRS  combined  with  SEMG  use  more the tHb  reaction  in combination with SmO2  and  SEMG  activity and look how  tHb reacts in comparison with increase in  SEMG  activity
2. When you look at SEMG  activity and SmO2/ tHb
 look what is  the resting  SEMG  activity  as a  start   base line as you did  but as well look what is a full contraction  isometric  activity level   of the  muscle  and whether you can create a tHb  trend reaction  form out flow  to venous occlusion and  perhaps even arterial occlusion but  more interesting actually  whether we  create a vasodilatation despite a  increase in  SEMG  activity  so  CO overrules  contraction force 

 and here just for  fun the  non cook book situation I  was talking about.
geoff barry wicks.jpg 
Can you see what I mean  In front  Geoff Kabush  and behind Barry Wicks

Now   let's look another  case.

geoff MTB.png 
or look many cases


group geoff.jpg

Andri

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 #5 

Thanks Roger, Thanks David. Maybe we need to change or define terms better. Something we discussed at the conference. Perhaps better than non-involved is calling the deltoid non-priority muscle; I am looking forward to Davids comment on this. The reason I say this, and the reason I still think mounting a Moxy on the deltoid for a cyclist is nicely presented in the abstract below. I have seen a lot of data by Holmberg among others; including Rowell's Sleeping Giant. What happens in the upper body is related to what happens in the lower body, even if it is as simple as vasodilation and blood pressure response. 




J Physiol. 2004 Jul 1;558(Pt 1):319-31. Epub 2004 Apr 30.

Maximal muscular vascular conductances during whole body upright exercise in humans.

Abstract

That muscular blood flow may reach 2.5 l kg(-1) min(-1) in the quadriceps muscle has led to the suggestion that muscular vascular conductance must be restrained during whole body exercise to avoid hypotension. The main aim of this study was to determine the maximal arm and leg muscle vascular conductances (VC) during leg and arm exercise, to find out if the maximal muscular vasodilatory response is restrained during maximal combined arm and leg exercise. Six Swedish elite cross-country skiers, age (mean +/-s.e.m.) 24 +/- 2 years, height 180 +/- 2 cm, weight 74 +/- 2 kg, and maximal oxygen uptake (VO(2,max)) 5.1 +/- 0.1 l min(-1) participated in the study. Femoral and subclavian vein blood flows, intra-arterial blood pressure, cardiac output, as well as blood gases in the femoral and subclavian vein, right atrium and femoral artery were determined during skiing (roller skis) at approximately 76% of VO(2,max) and at VO(2,max) with different techniques: diagonal stride (combined arm and leg exercise), double poling (predominantly arm exercise) and leg skiing (predominantly leg exercise). During submaximal exercise cardiac output (26-27 l min(-1)), mean blood pressure (MAP) (approximately 87 mmHg), systemic VC, systemic oxygen delivery and pulmonary VO2(approximately 4 l min(-1)) attained similar values regardless of exercise mode. The distribution of cardiac output was modified depending on the musculature engaged in the exercise. There was a close relationship between VC and VO2 in arms (r= 0.99, P < 0.001) and legs (r= 0.98, P < 0.05). Peak arm VC (63.7 +/- 5.6 ml min(-1) mmHg(-1)) was attained during double poling, while peak leg VC was reached at maximal exercise with the diagonal technique (109.8 +/- 11.5 ml min(-1) mmHg(-1)) when arm VC was 38.8 +/- 5.7 ml min(-1) mmHg(-1). If during maximal exercise arms and legs had been vasodilated to the observed maximal levels then mean arterial pressure would have dropped at least to 75-77 mmHg in our experimental conditions. It is concluded that skeletal muscle vascular conductance is restrained during whole body exercise in the upright position to avoid hypotension.

juergfeldmann

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 #6 
I will be back later on this depending how the  discussion evolves.
. Key words. PNF  ( proprioceptive neuromuscular facilitation). or some  would name it DNA pattern for  dynamic natural activation  or  in Europe it is better known as  Spiral motions. I work  daily on this  with stroke patients  where this is very interesting  to follow  through, but it is  essential in any movement  including sport.
 In reality there is no  muscle  non involved  so yes Andri is right  to  change the name.
 This is where it is fun  as when ever  we try to make it simple  we have to  agree, that it is not simple  and when ever we make it more interesting and more inclusive, people  call for a cook book.
 This is  what makes it all fun.
The use  of SEMG  and  SmO2  as we have in the above picture  has  some limitation. We  can have a  flat  stable SmO2  %  but  that does not reflect the  situation, whether we  use more O2  than we deliver  or   deliver more than we use. It has to be in context  with tHb  reaction.
 Stable  SmO2  and a dropping tHb  can mean what?
 Stable SmO2  and increase in tHb  can mean  what?
As well  when using SEMG  it is fun to  mount a second electrode  at the antagonistic  position to see  whether it is an actual motion picture  or a  stabilization activity. This  than would bring us  to the terms  muscular  dysbalance  or  muscular dysharmonie  when looking in a PNF  pattern.
DavidBellar

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 #7 
The work by Saltin's group really demonstrated that systemic blood flow was controlled during whole body exercise to maintain MAP.  The showed a difference between isolated muscle activity vs whole body.  The studies (including the most recent review paper by Calbet 2012 Journal of Physiology) are mostly focused on this topic.  There is some evidence for central mechanisms causing vasodilation in contralateral limbs, but as far as I am aware the effects are not large and it is intensity dependent.  

The notion that sympathetic vasoconstriction in completely inactive muscle might help with delivery of Q to working muscle has been around for a while but the evidence is old (1967 - Stranded and Shepherd) to the best of my knowledge.  

Regardless,  if a muscle is at all active it would be unlikely to vasoconstrict.   Given the complexity of human locomotion on foot or bike or skate almost all muscles in the body are 'involved' and thus unlikely candidates for vasoconstriction.  My feeling is that the results are more consistent with changing techniques as fatigue sets in and the body seeks other ways to continue to promote motion.  (Maybe talking point here would be so separate muscles into prime mover, synergist and support muscle and look for uses of the data from each)

Again, these are my thoughts and I have not done an extensive literature review in this area.  However, I have done a great deal of EMG work and I can tell you that during any complex human movement it is incredibly difficult to find a muscle that is not active, some are more active than other but none are likely to not be in need of increased metabolism. 


juergfeldmann

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 #8 
I need some help here.
I do not see, where there is a discussion on here as we have discussed this direction so many times.
1. Absolutely agree there is never a situation during most complex activities like running skiing and so on, where we have nonon involved muscles. So the term is terrible but was used to make it simple or easier, but as we see this does often not work.

2. Yes any initial activities, where the cardiac out put has no problem to maintain central blood pressure will create a vasodilatation( as shown in many topics) so in minimal involved muscles where the muscle contraction is low the vasodilatation effect will always overrule as long central blood pressure can be maintained. Look as well he many graphs we showed where we can see that.
In major involved muscles we will have initial when we do not stimulate Cardiac output but start cold the muscular contraction will overrule the for the moment too low CO and we see an initial drop in tHb . If the CO can be increased than there is the question between muscle contraction and blood pressure form the CO. depending on this situation we have all three options of tHb. This reaction i a big part of a 5/1/5 interpretation on possible cardiac out put limitation and easy to show with a Physio flow.
We did this hundreds of times many years back when we started combining NIRS SEMG and Physioflow. So I assume David is doing the same great work .

If we reach some specific limitations like respiratory metaboreflex reactions, than we see a constriction ( See Dempsey et all )
Many ties shown n this forum as well.
If we have an actual respiratory limitation in VE we as mentioned will see a vasodilatation due to the CO2 effect in the systemic system.
Again a big part of the 5/1/5 interpretation options and to verify this you combine NIRS and VO2 equipment

Again this reactions are as David mentioned not new at all. They go the first time discussed in Gaskell 1896 I think but will dig back and find the paper to show again here .
Another fun way to look how reactions and blood-pressure are going hand in hand so vasoconstriction and to muscle compression or o due to blood pressure protection. Do workouts on an inversion table and do the same workout once up right once horizontal and once head down. Same weights same muscle groups some physical set up.
look at reactions and if you have a physioflow and VO2 and SEMG combine them and do his . Sent the feedback as this is what we did many years back when we had all this questions many of the readers come up so great critical questions. The answers can be discussed theoretically or can be done as an experiment. The problem ,the theory often gets trampled by the experiment and by individual reactions.

In top endurance trained athlete the is a high risk of the sleeping giant reactions and tHb often has to drop ( resp blood pressure has to be ov beserved. bets time to ssess thsi is at the end of a race of cross-country skiwr , when they collapse as the sudden end of the race wht a hugh vasodilatation effect and the sudden stop o muscelcontraction simply overwhelms the ability of teh C and BP drops and skier drops to at leats not have to work agains gravity. Srry typos patient is waiting cheer greta discussion
DavidBellar

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 #9 
I agree some of this discussion is one of terminology.  While I understand the need to have easy to understand terms, it is also important to make sure they are correct.  I think we all agree that the term non-involved is not accurate.  My fear is that continued use of this term will limit the credibility of people talking about the use of the sensors.  This will be more true among the most educated of users, who may also be the most influential.  

In terms of vasodilation/vasoconstriction I will post some more 'pilot' data from our lab in the the next couple of days.  

On another note:
We have a hard time using the Physioflow (or similar impedance based measures),  there are too many papers that demonstrate the device over estimates during exercise and demonstrates poor bland-altman agreement with pathology.  I was involved with a study that looked at the reliability of its use in acute cold exposure and it worked, but probably only a a change from baseline measure.  


juergfeldmann

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 #10 

I agree some of this discussion is one of terminology.  While I understand the need to have easy to understand terms, it is also important to make sure they are correct.  I think we all agree that the term non-involved is not accurate.  My fear is that continued use of this term will limit the credibility of people talking about the use of the sensors.  This will be more true among the most educated of users, who may also be the most influential.  

Absolutely agree and welcome in the  club of  finding a solution   to  explain complex  ideas  easy.
 I will come back on this topic  when we may have some respond  on Max lass and LT and how  come that this tipoc  is  made so simple whne there is  little  accepted research available at  all.  2. I was  wrong  with 1896  the   first discussion was 1877 and followed by many great papers  after that. 1996  was the incredible  discovery  by Friedrich Miescher on the effect of CO2  on inflammatory  processes  and  O2  diss curve reactions when using it as a physiological tool
 Here a part of that paper  revised  1962


SD 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.

3.We have a hard time using the Physioflow (or similar impedance based measures),  there are too many papers that demonstrate the device over estimates during exercise and demonstrates poor bland-altman agreement with pathology.  I was involved with a study that looked at the reliability of its use in acute cold exposure and it worked, but probably only a a change from baseline measure.  

For  us in Physio  flow is more the ability to repeat  the  measurement  so we look at a  trend rather  than absolute values.
I  go  from the assumption, that you use   or used Physio flow  for  some of  the comparisosns.
 Therefor    most  who followed our  discussions  on the fact forum  many years  back know that  Physio flow  is  NOT  comparable  with
or similar impedance based measures.
It uses  the impedance  ideas but  is a morphological   technology  to estimate  the  cardiac hemodynamic.
 The  person  to discuss this is Frank  Bour  and in case there is  some interest in this technology  I can   contact  with Frank and see, whether he  can give some closer ideas on  the  equipment. We had Frank in Boulder  during a  MOXY  seminar  where he  nicely showed the technology  and its  options.


4. In terms of vasodilation/vasoconstriction I will post some more 'pilot' data from our lab in the the next couple of days.  
 That  would be incredible  generous  and wow   what a great  chance  or  basic  forum like this  Thanks  so much!!!

juergfeldmann

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 #11 
First thanks for this great input.We or I need to make a correction as there was a clear mistake  when we  started to use  NON involved muscle as apart of our ideas.
 So let's  find a better term like for example non priority muscle or not essential involved muscle or  ????
 Improtnat to have a good term to avoid what we created in the past as a mess where we have terms lie O2 deficit and or like anaerobe in combination with sport and so on.
 Will be back on this later as it is a great step forward form David to clear this terms.

Second I like to split the discussion on blood flow in user friendly coaching related   discussion on how to use tHb  trends  for physiological workout designs  and in a   " researcher' based  discussion, where we  unlikely will find consent, as we find as many studies, as we like to often contradict the  former study.
 It starts with the whole idea of blood flow and capillary recruitment we discussed in depth on this forum  from the classical Krogh idea to some newer options. So let's see and I look forward to a very interesting  discussion.
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