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Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #1 
Last night I was in my barn treating a swollen eye  of one of  my  newborn  goat babies  and watching  some Olympic  high lights from the 2  days before.
 As a  Swiss and Canadian  it is fun to see how in this 2  countries   performance sport is handled  very different. One  part is the  near  size different in population and size, when you  see, that Switzerland  is  somewhat Vancouver Island. The other part is the very different approach to innovation  and  coaching approaches,  with the individual approach clearly  in the for front in Switzerland  compared  to the institutional  cook book approach in Canada. 
 I had  some  chuckles    during a super interview  with the silver medalist in men figure skating  and  at the same time reading a n article  form a small Swiss news paper on the gold medal winner in  women  downhill.
  The    female  gold medal winner  , a great athlete  but for sure not  favorite  to win the gold  has  a very interesting approach  thanks to some  connections.
 See  Art 1.    and  pictures    talk  more than  many words.

The  gold medal favorite  in the men  figure skating  had  an incredible great Olympics  as well  but had a very different task on hand     in his program
  Where I like to  give you some  ideas  to think through as this 2  example  could not be  more  extreme  apart from where we  sit today  in the  physiology between " classical " ideas and    new different approaches.

Here  the interview in physiological perspective.
  1. Immediately after the  program  coming  form the ice  the skater  was  asked  some questions.
 During his   interview  he  steady had  to cough  and  breath  short hard  bursts.  Every  track and field athlete  as well as  every 500 - 1500 m speed skater  knows this  coughing .  A  physiological reaction  to get rid  of CO2, .
  So  an indication , that the event produced  a lot  of  CO  due to   a big part of O2 independent  energy production.
 One  way to buffer  fast is over respiration.

Any of this skaters  will be in a   respiratory  limit  at the end of their  skate.
  So  in the evening interview   the skater did  an incredible  step by step  analyzing  what  he did  and what went through his  head.
  a) start . He    was breathing  very deep  and slow  before  going on the ice  and in preparation to start his program.
 Not  many  but the once  who ever  assessed what    deep breathing without  load is doing  knows  what happens.
  CO2  is released   ( hyper ventilation)  O2  Dias curve top the left  and great loading but poor  unloading to the working muscles..
b ) start of the program. Great start  with  a  quadruple   and triple  combination.
  great    all moves well.  Incredible effort  and  who ever used  a nirs in a figure skater knows what happened in his legs during the jump combination
. c) short recovery  with  some dancing  sections planned in.  His instruction was  to breath deep  .  Now the difference between  deep breathing without  activity ( start )  and deep breathing  with a   huge load of  CO2   waiting to be released  after the effort is very different..
 Now the deep breathing will   keep the CO2  in  and  shift the O2  diss curve to the right, meaning bad loading , ( which now  would be needed )    but great deloading , which  is not needed  at all at this stage.
. Result  a   steady and  very low  SmO2  level , pushing some critical  physiological  feedback  to the brain into  low critical levels..
d)  so  very low  O2   situation  to get ready for the next   jump combination.
. Risk of energy problem  and   result  was a  great   take of  but a  not as great landing  with hand touch on the ice.
. . So  extreme effort  with an additional need to get rid  of CO2.
 So instruction again  between the jumps  deep breathing.     and so on.  Result  not that great third  jump combination  and  at that time his  CO2   must have been so high, that  he had no choice  but start to  breath  not deeper  but CO2 forced him to breath faster.
  and  very fast  and    for sure drop of TV. Only goal  was to get rid  of CO2. ( H + ).
  the now overwhelming  activity and need  from the respiration system took his  main core muscle out of  action  ( Diaphragm )  and you can  see the  problem after that with any   combination  and or jumps  where he would have needed  core stability.

 The  interesting part than was  the question, what  "physiological " test they do  to    see, what is going on.
 The answer.  We sue HR  and  see, that  it will be low  100 +-  in the dance section where we breath deep  and up  to 180 +-  in the  jump sections..
 The low HR    is  a nice feedback to see, that the deep breathing was very effective.   Deep breathing will lower your HR  and  as well will increase your CO2   which can as well be shown  when using lactat5e as markers  as  the lactate  will drop under deep breathing compared  with fast breathing.
 As the common idea  still is here , that lactate is  not good  it was great to   have it lowered  in the   relaxed  sections.
 Or , as many athletes  will learn  form coaches, you have to get rid of the lactate in the cool down.????
  End result a great  silver medal  from a great athlete  guided  by a very different physiological  theory , than  what    was done in the  great downhill skier. You  can   judge  and  go through the   physiological   information.
  The question is  unseen real  or unreal seen. The other question is:
  The Swiss   skate federation   uses  some   interesting tools  with  some introduction from Andri in Switzerland.. The skiers  seem to do this somewhat longer.
  What for sure will change  as usual after Olympics is the approach  from  countries who where not that successful   and the fear  for changes  of countries  who where successful.
 Att 2  is a  O2 Hb case study  from  an athlete  with  deep and  fast breathing you  can figure out  what may be what.?
  Att three is a case study   where the red  graph shows  a   one leg load  like in a figure skating  situation, but we did not allow to get rid of CO2  and  the athlete had  to  quite  to " survive'  The blue line is  an instruction  what he can achieve  in a  longer need  for oad  when  manipulation a great  trained respiratory system
  Last  is a great  info  on core stability  and respiration.

Exercise-induced respiratory muscle fatigue: implications for performance

+ Author Affiliations

1Centre for Sports Medicine and Human Performance, Brunel University, Uxbridge; and 2Respiratory Muscle Laboratory, Royal Brompton Hospital, and National Heart and Lung Institute, London, United Kingdom
Address for reprint requests and other correspondence: L. M. Romer, Centre for Sports Medicine and Human Performance, Brunel Univ., Uxbridge UB8 3PH, United Kingdom (e-mail: lee.romer@brunel.ac.uk)

Next Section

Abstract

It is commonly held that the respiratory system has ample capacity relative to the demand for maximal O2 and CO2 transport in healthy humans exercising near sea level. However, this situation may not apply during heavy-intensity, sustained exercise where exercise may encroach on the capacity of the respiratory system. Nerve stimulation techniques have provided objective evidence that the diaphragm and abdominal muscles are susceptible to fatigue with heavy, sustained exercise. The fatigue appears to be due to elevated levels of respiratory muscle work combined with an increased competition for blood flow with limb locomotor muscles. When respiratory muscles are prefatigued using voluntary respiratory maneuvers, time to exhaustion during subsequent exercise is decreased. Partially unloading the respiratory muscles during heavy exercise using low-density gas mixtures or mechanical ventilation can prevent exercise-induced diaphragm fatigue and increase exercise time to exhaustion. Collectively, these findings suggest that respiratory muscle fatigue may be involved in limiting exercise tolerance or that other factors, including alterations in the sensation of dyspnea or mechanical load, may be important. The major consequence of respiratory muscle fatigue is an increased sympathetic vasoconstrictor outflow to working skeletal muscle through a respiratory muscle metaboreflex, thereby reducing limb blood flow and increasing the severity of exercise-induced locomotor muscle fatigue. An increase in limb locomotor muscle fatigue may play a pivotal role in determining exercise tolerance through a direct effect on muscle force output and a feedback effect on effort perception, causing reduced motor output to the working limb muscles.


Contraction of the human diaphragm during rapid

 

postural adjustments

 

 

 

P. W. Hodges *, J. E. Butler, D. K. McKenzie and S. C. Gandevia t

 

Prince of Wales Medical Research Institute, Sydney, Australia and *Faculty of Health

 

Science, The University of Queensland, Brisbane, Australia

 

 

 

1. The response of the diaphragm to the postural perturbation produced by rapid flexion of the

 

shoulder to a visual stimulus was evaluated in standing subjects. Gastric, oesophageal and

 

transdiaphragmatic pressures were measured together with intramuscular and oesophageal

 

recordings of electromyographic activity (EMG) in the diaphragm. To assess the mechanics

 

of contraction of the diaphragm, dynamic changes in the length of the diaphragm were

 

measured with ultrasonography.

 

2. With rapid flexion of the shoulder in response to a visual stimulus, EMG activity in the

 

costal and crural diaphragm occurred about 20 ms prior to the onset of deltoid EMG. This

 

anticipatory contraction occurred irrespective of the phase of respiration in which arm

 

movement began. The onset of diaphragm EMG coincided with that of transversus

 

abdominis.

 

3. Gastric and transdiaphragmatic pressures increased in association with the rapid arm

 

flexion by 13X8 + 1X9 (mean+ S.E.M.) and 13X5 + 1X8 cmH2O, respectively. The increases

 

occurred 49 + 4 ms after the onset of diaphragm EMG, but preceded the onset of movement

 

of the limb by 63 + 7 ms.

 

4. Ultrasonographic measurements revealed that the costal diaphragm shortened and then

 

lengthened progressively during the increase in transdiaphragmatic pressure.

 

 

 

5. This study provides definitive evidence that the human diaphragm is involved in the control

 

of postural stability during sudden voluntary movement of the limbs.



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Nkrause

Development Team Member
Registered:
Posts: 49
 #2 
Thanks Juerg! Great post with lots of info to digest
Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #3 
Let's  get    back into a different world  of looking at performance.
  I had  an other chuckle  today afternoon in my barn.
 You can see, once you have a farm you have time  to watch  Olympics.
 A  very special  channel   has this really great and nice  intermezzo  called SCIENCE  says.
  So just before the cross country relay  the  Science info  showed  up.  It made  sense, that they talked  about energy use of the different  physiological systems  and   there was  no question the VO2  max  would come up . And  yesssssssssssss it did.
 The summary was even that great, that they argued , that the guy with the highest VO2  max  really would win the race.
 So my question  as a simple goat farmer :
.  Why  would  they do a race, when every athlete just could have sent in the VO2  max test  information  and than they could have  had a  game of cards  before the  medal ceremony, instead of  working so hard  to try  to win a race.
In fact  , why  do we  have a difference even under the  few best skiers  in a race  despite  the  more or less same VO2  max result. We  discussed this  since  the 1970  .  One of  the newer  examples  was the " famous " lance Armstrong  new York Marathon  ,  as they compared   Tergat's  VO2  max  of  85    with  the same 85  VO2  max  tested on Lance.  The  race result  was  pretty close  as the VO2 max  would suggest.
  Tergat  was only 1  hour  faster  ( just over  2 h  for the win  ) compared  with  Lance  who was just under 3  hours  including some  pharmacological help  perhaps ).  Lance   must  have lost    somewhere some VO2  max  values   going to the start line ?????

Well lets' go slow here:
  Science   has a very different  idea  today on VO2 max.
  Look at  att.  and you can see, the  actual more than 50%  of so called all out tests  never show a VO2  max  result ( plateau ) but just a tested  VO2  peak.
 The once  , who where classified  as VO2  max   not even  showed a plateau  but  had to full fill some  points  to be accepted  as a plateau???.


 Okay now  back to the race.
 The commentator   where great, One  a former  national team coach  and the   support a  former  gold medal winner in Cross country skiing.
 So no questions  experts  in their  own  rights.

 Great  comment  and  lively   info  from the skier.
  In the third  section the Finnish  skier was  taking over in second position   and skied  out very hard  and  nice  looking   By  km 6.5  - 7    we had this great  close  shot  coming up the hill  and if you looked  carefully  you could see, how he  just lost  VO2  max  from his performance. In fact you could see, how his respiration was  completely off  ( possibly swallowed on VO2  max ) ,  and a bout  100 m later his technique fell completely apart. Now here the difference on how we look to how  VO2  max  works.
  My tale was.  Wowww  he  has a problem either  with delivery  tHb  would drop in a MOXY  or  he has a problem  with utilization.
  Different physiological scenario.
  VO2  max is easy  he  kept going   a certain %  and it did not work ed out .
 MOXY :
  he started  super fast to try to bridge to the   athlete in front.
  High intensity would show up as a  dropping SmO2   as he used more O2  than delivered.
  No problem as this happens  to  every one  at the start moment.
  Now  problem 2  he  did not  reduced speed early enough so the demand of O2  went  up  even more.
 The sudden start created   besides a good O2  use SmO2  drops ( not a O2  deficit )  as well an integration of  O2 independent energy supply.  Result  an increase in lactate due to the   use  of glucose   but as well an increase  of H +  due to O2 independent activity.
Lactate was nice, it helped  him to move  H +  out of the  cell ( MCT 1  )  and   than he  was able to release  H +  and reuse  lactate.  Problem. The increase in H +    had  to be buffered as well so CO2  went  up  an this increase his respiratory demand.
  Depending on his  respiratory fitness he w as  able to sustain for a while the load  but finally  something gave in:
 Either  he  pushed the respiration to its limit  so  he  could not get  rid of CO2  anymore (  hypercapnia )  SpO2  drops ,  and he would  allow a better  use of O2   ( SmO2  drops )  If  he  already was low  on SmO2  he would have a feedback to the Brain  pO2  getting low . metaboreflex  and cardiac reflex  which would create  either a vasoconstriction or a  reduced   motor unit  recruitment or  possibly bot,
 Result   give up  core muscle ( diaphragm )  so technique falls  apart  and less motor unit  recruitment  so   speed completely collapsed.
 Why . Well still same VO2  max  result  but   the body is on survival mode  rather than interesting in skiing  and  as he was  or  is healthy   his ECGM  simply   shut him down to   save  vital organs
  The out come  of  Science  says   and commentator  was.
  The lactic acid  just  stopped him.
 Perhaps  the lactate  at least  helped  him to go somewhat longer than  if  he  had no lactate.
 The lactic  acid  seems  to be  in  cross country skiers  every 4  years   and it never  got tested  as we  can't stop the athlete;et  during the race.
 I did  some test during racing  many years back and I never found lactic acid in the athletes body.  as I never was  able to  test  for lactic  acid in the finger just for lactate only.
 Again  a  reason why we have so much  different ideas compared  what people learn and see on a TV  from Science. says. Have fun looking  the next race  with Science  view  and with goat framers  ideas.


The influence of PaO2, pH and SaO2 on maximal oxygen uptake.

Nielsen HB, Madsen P, Svendsen LB, Roach RC, Secher NH.

Author information

  • Copenhagen Muscle Research Centre, Department of Anaesthesia, Rigshospitalet, University of Copenhagen, Denmark.

Abstract

Influence of arterial oxygen pressure (PaO2) and pH on haemoglobin saturation (SaO2) and in turn on O2 uptake (VO2) was evaluated during ergometer rowing (156, 276 and 376 W; VO2max, 5.0 L min-1; n = 11). During low intensity exercise, neither pH nor SaO2 were affected significantly. In response to the higher work intensities, ventilations (VE) of 129 +/- 10 and 155 +/- 8 L min-1 enhanced the end tidal PO2 (PETO2) to the same extent (117 +/- 2 mmHg), but PaO2 became reduced (from 102 +/- 2 to 78 +/- 2 and 81 +/- 3 mmHg, respectively). As pH decreased during maximal exercise (7.14 +/- 0.02 vs. 7.30 +/- 0.02), SaO2 also became lower (92.9 +/- 0.7 vs. 95.1 +/- 0.1%) and arterial O2 content (CaO2) was 202 +/- 3 mL L-1. An inspired O2 fraction (F1O2) of 0.30 (n = 8) did not affect VE, but increased PETO2 and PaO2 to 175 +/- 4 and 164 +/- 5 mmHg and the PETO2-PaO2 difference was reduced (21 +/- 4 vs. 36 +/- 4 mmHg). pH did not change when compared with normoxia and SaO2 remained within 1% of the level at rest in hyperoxia (99 +/- 0.1%). Thus, CaO2 and VO2max increased to 212 +/- 3 mL L-1 and 5.7 +/- 0.2 L min-1, respectively. The reduced PaO2 became of importance for SaO2 when a low pH ( H +  accumulation  respiration could hold  balance , our  comment  )inhibited the affinity of O2 to haemoglobin. An increased F1O2 reduced the gradient over the alveolar-arterial membrane, maintained haemoglobin saturation despite the reduction in pH and resulted in increases of the arterial oxygen content and uptake.

PMID:

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Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #4 

Another story from the barn.
Jorisen ter Mors,  a story   and a name  most of you never heard of  and most of you will have already forgotten if you  heard  of it.
  It is an interesting story  for me  as it takes  place in a sport  I was  growing up with  ( Speed skating ) As a  former  speed skater and  Swiss national team member aiming  for the Innsbruck Olympic)  I was  daily involved in speed skating.  Davos  my birth place  had  at that time the worlds  fastest  400 m natural ice track  and no wonder the  world  ( including the dutch )  where living  literally in my parents house.
So  prior  to the Olympics  I always watch , where my generation of  Friends   ( now in coaching are in Holland  and it was fun to see one  specific name  showing up  in  a very  unusual combination.
  A  extraordinary   out of the BOX  brain   trying  what never   was tried  before . Training a girl  to co0mpete  in the 1500 Short track and long track    .
 So  two days ago she competed in the short track 1500 m  , three  times   on the same day  an the next  day  she won  the  gold in long track 1500 m  with an Olympic record. ???
  For  all the more out of the box thinking people , try to  get back  and  look for the following   sections.
 
"warm " up"     action  or  better lack of  " cool down "  in between the   three races  and  after the    gold medal race.  Compare this  with  even the  athletes  from the same team.
. Remember some  discussion on " cool " down to get rid  of  lactic  acid ???  and    some  possible other options.
 Remember the goal  for a warm up  we set  versus  the " classical'  Idea of a warm up.
  If you combine all of this , add a MOXY  to the picture  ( or  if you are  from Holland  a  local  Portamon  information )  and  you may get in conflict  with many classical   ideas.

The Dutch   actually  made a very great study in Maastich University . I showed it a  few times n this forum as well.
 In short . They where looking  at the difference between professional  cyclists  and  top  amateur cyclists .
 Their  question was.
 What separates  this 2  categories  physiologically.
  Here  what  was not different.
 VO2  max values  where all the same  as well as lactate values.  There was no difference between this parameters  in the  two categories.
  So why the difference in performance. Remember the Science  says  Canadian version   of VO2    and  performance prediction.
  The dutch  study  found  one  major  difference  and it was in the   dynamic  of  respiration  by looking  at VE  and how VE was  produced.
  If  the in their next study  add MOXY, than they   will be able to see, how the VE  directly influences  Oxygen bio availability  and  delivery pattern  (tHb ). So we  have in the practical world  more and more indication, that  the performance  just may be  controlled by a  main center ( let's  name it ECGM)  and the key is  to fond out  what is needed  to survive )
 Summary.
 Th easiest way to find out,  whethere we start to get into a survival problem is  to test the place, where we  first  can give up  O2  delivery  without risk of  not being able to survive.
 This would be the muscle.
 You  even can go further and really test  a muscle, which is not  desperately needed in the sport.
 Example speed skating.
.
 Mount a moxy on the inside  upper arm (  delta muscle )  as it is  used very limited  to  avoid using O2  in an  extremity , which is  not  very helpfull  in the most part of the race,.
.  Here what you will see.
  The first  hint   of getting into trouble  will show up in the delta muscle.
 MOXY will show  2  reactions.
 1. Drop in tHb  and d drop in SmO2 . This despite the fact, that the muscle is passive  and  not used   very intense  or at all.
  Meaning:   as the  O2  use in a  resting muscle is stable   we  can assume , that a drop in SmO2  is not due to O2  use  but rather due to  not delivering O2  to this muscle.   The body is doing this by  constriction of the blood vessels.
 So we have a tHb  drop and a SmO2  drop.
 This  just short before we  have a  limitation for the main muscles.
 So before  the body gives up the  leg work  it will try  to redirect  O2  and blood to the area   where it is needed , leg  muscles.
.
 If  the O2  consumption  is  still far above and beyond, what the   vital organs  can allow ( Steeling blood  from vital  organs  , sleeping Giant  Marshall 1967 )  than we will have a  ECGM reaction over  reduced  motor unit recruitment  as well as  vasoconstriction over  respiratory metaboreflex.
  The race is over. Look at the Canadian  and USA  skaters . all   lost "  due to a very different  approach in   technique, which on this ice  will create a   tHb  drop due to  muscle contraction  due to to long gliding  on a  not very gliding  ice. Lots'  to think in the barn  and fun to keep watching.  Open your mind  to see from two angels  " classical "  unreal seen  and  MOXY's  unseen real.
 What would you prefer,  having direct access to information live  or reading the news paper the next day.
 MOXY  and you are there. VO2  lactate    you read the   newspaper

Happy feeding.


Nkrause

Development Team Member
Registered:
Posts: 49
 #5 
Hi Juerg, is this the study you're referring to? Just want to make sure that I'm reading the right one. 
Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #6 
N  I can't open the link  you sent for the study  so  for  all interested  in the study  and ready    to red it  with 2  brains  " classical" ideas versus  what we do here  here the  full  paper.
Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #7 
Well  , I got  quite a few  emails  concerning my  crazy take on the Canadian skater  and his respiratory    situation.
  The  majority  come all with our  " educated"  point, that respiration is never a limiting factor  and that SpO2  never  drops in sport in a healthy   athlete. The  Main   "educated"  answer is , that we never reach MMV  in any activity in sport.
  After over 25 years  of discussion this  it is   time  to  say :  well if that is  so  so be it.
 . Nevertheless  I got  as of yet no  e mail back on the question:
 How  did you  measured  the MMV ? So please help.?
 
  For the people  still in between  the  idea  that it is never  and our  idea, that  it  can be a limiter  here  a short review  .
 

Exercise-induced respiratory muscle fatigue: implications for performance

1.   Lee M. Romer1 and

2.   Michael I. Polkey2

+ Author Affiliations

1.    1Centre for Sports Medicine and Human Performance, Brunel University, Uxbridge; and 2Respiratory Muscle Laboratory, Royal Brompton Hospital, and National Heart and Lung Institute, London, United Kingdom

1.    Address for reprint requests and other correspondence: L. M. Romer, Centre for Sports Medicine and Human Performance, Brunel Univ., Uxbridge UB8 3PH, United Kingdom (e-mail: lee.romer@brunel.ac.uk)

Next Section

Abstract

It is commonly held that the respiratory system has ample capacity relative to the demand for maximal O2 and CO2 transport in healthy humans exercising near sea level. However, this situation may not apply during heavy-intensity, sustained exercise where exercise may encroach on the capacity of the respiratory system. Nerve stimulation techniques have provided objective evidence that the diaphragm and abdominal muscles are susceptible to fatigue with heavy, sustained exercise. The fatigue appears to be due to elevated levels of respiratory muscle work combined with an increased competition for blood flow with limb locomotor muscles. When respiratory muscles are prefatigued using voluntary respiratory maneuvers, time to exhaustion during subsequent exercise is decreased. Partially unloading the respiratory muscles during heavy exercise using low-density gas mixtures or mechanical ventilation can prevent exercise-induced diaphragm fatigue and increase exercise time to exhaustion. Collectively, these findings suggest that respiratory muscle fatigue may be involved in limiting exercise tolerance or that other factors, including alterations in the sensation of dyspnea or mechanical load, may be important. The major consequence of respiratory muscle fatigue is an increased sympathetic vasoconstrictor outflow to working skeletal muscle through a respiratory muscle metaboreflex, thereby reducing limb blood flow and increasing the severity of exercise-induced locomotor muscle fatigue. An increase in limb locomotor muscle fatigue may play a pivotal role in determining exercise tolerance through a direct effect on muscle force output and a feedback effect on effort perception, causing reduced motor output to the working limb muscles.

Att  shows  you even more.

 And in case it just may  be that teh  inspriartory muscel ( diaphragm ) may  be abel to get tried  here  from anotehr source:
 

J Physiol. 1997 Dec 1;505 ( Pt 2):539-48.

Contraction of the human diaphragm during rapid postural adjustments.

Hodges PW, Butler JE, McKenzie DK, Gandevia SC.

Source

Prince of Wales Medical Research Institute, Sydney, Australia.

Abstract

1. The response of the diaphragm to the postural perturbation produced by rapid flexion of the shoulder to a visual stimulus was evaluated in standing subjects. Gastric, oesophageal and transdiaphragmatic pressures were measured together with intramuscular and oesophageal recordings of electromyographic activity (EMG) in the diaphragm. To assess the mechanics of contraction of the diaphragm, dynamic changes in the length of the diaphragm were measured with ultrasonography. 2. With rapid flexion of the shoulder in response to a visual stimulus, EMG activity in the costal and crural diaphragm occurred about 20 ms prior to the onset of deltoid EMG. This anticipatory contraction occurred irrespective of the phase of respiration in which arm movement began. The onset of diaphragm EMG coincided with that of transversus abdominis. 3. Gastric and transdiaphragmatic pressures increased in association with the rapid arm flexion by 13.8 +/- 1.9 (mean +/- S.E.M.) and 13.5 +/- 1.8 cmH2O, respectively. The increases occurred 49 +/- 4 ms after the onset of diaphragm EMG, but preceded the onset of movement of the limb by 63 +/- 7 ms. 4. Ultrasonographic measurements revealed that the costal diaphragm shortened and then lengthened progressively during the increase in transdiaphragmatic pressure. 5. This study provides definitive evidence that the human diaphragm is involved in the control of postural stability during sudden voluntary movement of the limbs.

Or here:
 

Postural and respiratory functions of the pelvic floor muscles.

Hodges PW, Sapsford R, Pengel LH.

Source

Division of Physiotherapy, the University of Queensland, Brisbane, Queensland, Australia. p.hodges@uq.edu.au

Abstract

AIMS:

Due to their contribution to modulation of intra-abdominal pressure (IAP) and stiffness of the sacroiliac joints, the pelvic floor muscles (PFM) have been argued to provide a contribution to control of the lumbar spine and pelvis. Furthermore, as IAP is modulated during respiration this is likely to be accompanied by changes in PFM activity.

METHODS:

In order to evaluate the postural and respiratory function of the PFM, recordings of anal and vaginal electromyographic activity (EMG) were made with surface electrodes during single and repetitive arm movements that challenge the stability of the spine. EMG recordings were also made during respiratory tasks: quiet breathing and breathing with increased dead-space to induce hypercapnoea.

RESULTS:

EMG activity of the PFM was increased in advance of deltoid muscle activity as a component of the pre-programmed anticipatory postural activity. This activity was independent of the direction of arm movement. During repetitive movements, PFM EMG was tonic with phasic bursts at the frequency of arm movement. This activity was related to the peak acceleration of the arm, and therefore the amplitude of the reactive forces imposed on the spine. Respiratory activity was observed for the anal and vaginal EMG and was primarily expiratory. When subjects moved the arm repetitively while breathing, PFM EMG was primarily modulated in association with arm movement with little respiratory modulation.

CONCLUSIONS:

This study provides evidence that the PFM contribute to both postural and respiratory functions.

And here one more  about  SpO2   and arterial desaturation.  (  As well implcation on shift of  the O2  diss curve  and therefor the utilization of  O2  ( bio availablity )  and  whith MOXY    is a  great  gadget  to get this all together in a n easy way in the field. .

Arterial desaturation during exercise in man: implication for O2 uptake and work capacity.

 

Nielsen HB.

 

Author information

 

  • The Copenhagen Muscle Research Centre Department of Anaesthesia, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. h.bay@dadlnet.dk

 

Abstract

 

Exercise-induced arterial hypoxaemia is defined as a reduction in the arterial O2 pressure (PaO2) by more than 1 kPa and/or a haemoglobin O2 saturation (SaO2) below 95%. With blood gas analyses ideally reported at the actual body temperature, desaturation is a consistent finding during maximal ergometer rowing. Arterial desaturation is most pronounced at the end of a maximal exercise bout, whereas the reduction in PaO2 is established from the onset of exercise. Exercise-induced arterial hypoxaemia is multifactorial. The ability to maintain a high alveolar O2 pressure (PAO2) is critical for blood oxygenation and this appears to be difficult in large individuals. A large lung capacity and, in turn, diffusion capacity seem to protect PaO2. A widening of the PAO2-PaO2 difference does indicate that a diffusion limitation, a ventilation-perfusion mismatch and/or a shunt influence the transport of O2 from alveoli to the pulmonary capillaries. An inspired O2 fraction of 0.30 reduces the widened PAO2-PaO2 difference by 75% and prevents a reduction of PaO2 and SaO2. With a marked increase in cardiac output, diffusion limitation combined with a fast transit time dominates the O2 transport problem. Furthermore, a postexercise reduction in pulmonary diffusion capacity suggests that the alveolo-capillary membrane is affected. An antioxidant attenuates oxidative burst by neutrophilic granulocytes, but it does not affect PaO2, SaO2 or O2 uptake (VO2), and the ventilatory response to maximal exercise also remains the same. It is proposed, though, that increased concentration of certain cytokines correlates to exercise-induced hypoxaemia as cytokines stimulate mast cells and basophilic granulocytes to degranulate histamine. The basophil count increases during maximal rowing. Equally, histamine release is associated with hypoxaemia and when the release of histamine is prevented, the reduction in PaO2 is attenuated. During maximal exercise, an extreme lactate spill-over to blood allows pH decrease to below 7.1 and according to the O2 dissociation curve this is critical for SaO2. When infusion of sodium bicarbonate maintains a stable blood buffer capacity, acidosis is attenuated and SaO2 increases from 89% to 95%. This enables exercise capacity to increase, an effect also seen when O2 supplementation to inspired air restores arterial oxygenation. In that case, exercise capacity increases less than can be explained by VO2 and CaO2. Furthermore, the change in muscle oxygenation during maximal exercise is not affected when hyperoxia and sodium bicarbonate attenuate desaturation. It is proposed that other organs benefit from enhanced O2 availability, and especially the brain appears to increase its oxygenation during maximal exercise with hyperoxia. 



 But that is it now on respiration.
 Summary :
  If you believe  respiration is never a limitation good  for you.
 If  you think it could be  in some cases a limitation  good  for  you.
  Remember it took the british  Admirality only 250 years  to accept the fact  that Vit C  may be helpfu if  you stayedn many days  on  the sea.
 . "classical "  exercise physiology   still has  another 150 years time  to possibly accept the fact, that Respiration  can be a limiter.
. By the way, how long  did it took the catholic  church to accept  Galileos    point that the world is not the center of the universe. ???


Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #8 
Winter  Olympics  2018
 Utopia  or reality ?
  We are working  here   n a  reality  as we use it  already  for  sports like ice hockey  but as well for many other ideas.
  2018  you will have  as a coach the following options in an ice hockey game.
  a)  You  will see, that your key player simply is  too overloaded " fatigued"  and he    can;t  bring anymore  performance on the  ice.
 So you better let him rest  one more shift   before sending him out on the ice.
  b)  yous see that    a player simply does not give   his all out effort  so you  bench him and take a player    m,mentally ready to go all out    to move on his place.


 When you where watching today's game  for the Bronce medal you  had  this feeling :
 Either   the USA player where  so  " fatigued"  they simply  where not able to push anymore . or  they  where    not anymore motivated  after their   loss  in the game for the gold or  silver medal  against Canada.
.  A  small device n their legs  would have given the coach this answer:
 Fatigue  or motivation..
 In both cases  you will have a reduce  motor unit recruitment  and very  distinct  reaction in the working muscles.

  So  2018 the coaches   will have a lap top  on the bench  with direct feedback  to the  athletes physiological reactions on load  and recovery.  The decision  how fast to change for shifts  and whether yous send  a player back on the  ice  will be  much more objectively  than just  believing in names    and   statical numbers.
  Here a preview  for people looking for an advanced exercise physiological options.
  The  pic  one is  an overall view of three ice hockey shifts  during a game.
   . The first shift was  in a perfect  state of  all out ability . The third  shift  was  either   fatigue  or  no  motivation.   No matter what  but in both cases  you  can keep the player on the bench  and replace him  with a player who will show up with the first picture.
  att 2  and 3  and 4  show all three shifts  and you can   see, what we mean.  Cheers  and  have fun  to look towards  2018

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