Sign up Latest Topics
 
 
 


Reply
  Author   Comment  
juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #1 
I moved this  wingate data collection on the  case study section as it  may be useful  for some  to understand  our  concept  of how we use MOXY  for any  short term loads. In this case it is a wingate  series , but it  is much  more used in our  ideas  of RIP ( recovery intensity profile )  a  assessment idea  we use in team sports  like ice hockey  or  in individual sport like tennis   or in  downhill skiing  to set up an individual program  for  all out  loads  which is more  focused  on the recovery aspect  than on the load aspect  as the recovery is  what counts  in this    sport  much  more often.
 Harre's  old idea  of the  ultimate question. What is  endurance,
 the ability to sustain " fatigue " or the ability  to recover  fast.

 So we  could  talk   for example  about  resisting fatigue  as the question, whether the delivery   of  energy  is the  important  factor    versus   recovering fats , where the utilization  is more important  as delivery is  in many cases  not existing or  of minimal  help  so that in the recovery the reloading of  O2  is the main factor  to see, how much longer we can sustain the   workout  or  race.

 Now this 3  wingate in a row  series  was done    from Roger  and myself with the help  of the USA  army base  from Ft. Bragg. This guys  are incredible  and the result will demonstrate  it.  First as usual  just the SmO2 trends. What I overlapped  already is  the VL  leg muscles  with a  little to non-involved  delta  pars  acromial  muscle. Dark green  leg  VL  light green  delta  muscle

3 x  inv noninv.jpg 
From the start to about short before the 600 time axis  is  a " warm up " they designed  so every athlete  has  to do this warm up.
Than  3  all out loads with a rest in between.

 Now here you see that SmO2    did not dropped  to zero  as we had in the other example  from china.
 One of the  questions we had  form the first  discussion wingate was the " positive " critic, that the literature  shows , that in wingate test  SmO2  values  drop  by 80 +- 12  %. So they argued , that the literature  does not support  their  findings.
 In short the study  they used  was based on  if  I recall properly  8  or  12 samples  where they  had  80 % +- 12  %  fluctuation. Well for us that is a  set of  cases studies  with a  specific  group of athletes . We have hundreds  of this   tests  and  can not offer you  an answer how  the result will be  as we have a fluctuation seen  form  SmO2  down to zero  as in their  case to  minimal  desaturation  of    10 - 15  %.
 Another reason  why I hate  eating in a franchise   restaurant  versus  restaurant  with a unique  chef.  Now in this case it is super interesting to see the reaction   of SmO2  on the non-involved  muscle. What can you see ?
 Now   lets  first look at their  " warm up protocol."
 Again  warm up  is more than just  metabolic    improvement  of  blood flow  and oxygenation. Coordination  and many more  factors  may be a big part of  a sport specific  warm up. So this  doe snot mean  their warm up protocol is not good   The only part we  look here is  how it may have improved  blood flow  and  as well   for  sure  oxygenation.

May favorite  look is  at a biased  graph  so I can see easy and fast and show my  patients, whether they   actually achieved  the  goal of a higher oxygenation.
bias all leg.jpg 
Here the situation of the VL   during warm up  and 3  loads. Bias in our  cases means, that we  artificially  say  all starts  by zero  and we look the relative  changes  from this  point. So in the above case  when red drops  we  immediately use  O2  so that the  start oxygenation level actually drops, so less oxygenation  than  when they  did  nothing.
 So the " warm up " did  not contributed  to  a higher SmO2  level. To be fair   when you look at SmO2   above, than you see, they where already  nicely high. Reason they really did  not stared the warm up  form rest as they  where  already checking saddle highs  and  pedalled a little bit. Therefor  not  an optimal way  of   c discussion the   value of the " warm up "
 What is more interesting is the " recovery ability in the  time  after each all out  load. What  do you think.
 Okay  small help. Below a assessment we  told you about  by Andri  from Swinco on above 3'000 m in Zermatt summer glacier training  with the swiss ski national team  and testing an Olympic  gold medal winner  to see the " recovery  or  " fitness level  between an ACL   post op leg  and a  non operated leg.

here one leg:

bias  l  all.jpg 

 and the other leg

bias  r  all.jpg 


So  you can see e how different this  can be . And than as usual the question: Which one is the operated  leg. and the question. How  do I improve the  situation.
 This pictures  are  for us the main reason , why so many  top athletes  see  a reinjured  of their  leg. Physically , when they tested this athletes the cybex results    where  equal . But performance is not the only part we  have to consider as  physiologically  she  was not optimal rehabilitated.

 Now  I hope this gives a little  bit of  an idea  that we look  Wingate  and loads   as well from a  physiological point of  view  not just  calculated wattages.
 I still have  some  open questions  for myself  how wattage  or  load  in a test can help me to design a program to work on the weakness   and how  do I know based on a wingate  wattage  feedback  besides the wattage  what may  the limitation be ?
 Wattage users  please  help.

 So  after we  had the interesting  nearly shift in "phase " of  SmO2 trends let's look ate  contraction quality reaction  or tHb  trend in this  triple load,


3 x  quad thb smo2 kevin.jpg  By now  most of you are  experts  and  you can explain yourself  what you see in tHb  trends.

 What  do you see and what  does the  increase  in tHb  during the load  and the drop after the load mean.
 So  the  interesting question than is :
 SmO2  was  starting  to drop in the  arm   after the load in the legs  was over ????
 What could that mean  when we look at the situation. that a  wingate test is really  a planned  delivery disaster.. So   besides  dropping thee SmO2  what could we  expect in  the  blood flow  or blood volume situation
 Here the tHb  and SmO2  trend  from the non-involved  muscle. 

3 x  delt kein  thb smo2.jpg

Now  flip  between the smo2 graph  and here  and you see some astonishing reactions.
 What  could cause  this reaction  and why  do we see this in this case. Remember it is not a cook book   and this athlete  has  a very specific  limitation  and that is  why we see this reaction. So a very clear  idea  here   on what he  would have to focus  on to 
  a)  avoid  that  sport does not create  a  health problem   
b )  to actually improve performance.

 That's  where   Ruud an di have a  slightly different  approach. You may recall Ruud' s great points , that as long I see progress  I am happy  and   once  I   do not see progress I may look  at the reassigning closer.
 In many cases  this  may be too late as we  already created  a  health problem  like  right ventricular  cardio myopathy    just  as one  example or   exercise  induced  asthma. I believe strongly when I get this people in my rehab  and we go through their history  of  training  that w e often find the  point , where they started  to over load the compensator    and  the suddenly great  system  is  suddenly  the limiter  but in a bad  way.  So  you see above a very different  possibility  to look  at Wingate  besides the  power feedback.
 The very interesting question IS.
 Is  Wingate  perhaps not an anaerobic  power feedback test  but much rather  an aerobic  information test. We see and  every NIRS  user  will learn that very fast, that  when the nice steady  drop in SmO2  starts  to get into trouble the  performance will drop  or in other words, as soon O2  utilization start to get into trouble  high intensity loads  are in trouble.
 Now  if  we believe  NIRS  is doing what it suppose to  do  and the latest  research  we presented   could be   as well close   but  not the complete truth yet, than this is fun to    follow  for some longer  and more in depth  studies.
 If we believe  NIRS is bogus  and  the  first SATP  CP  glucose  and O2  steps  for segmental  metabolic  use  is true, than you better    follow  your  own different path.

 Here just  for fun an interesting comment. I like this article  as   it is very carefully  written to not  create too much  uproar  as  when you move in the academic  world  you have to  watch  how you formulate  critical  points  to not  rattle the establishment  too much  look at the date  and look when the latest  studies  with this  very highly  ms  time  schedules  where  done.
 

Sports Med. 2001;31(10):725-41.

Energy system interaction and relative contribution during maximal exercise.

Gastin PB.

Author information

Abstract

There are 3 distinct yet closely integrated processes that operate together to satisfy the energy requirements of muscle. The anaerobic energy system is divided into alactic and lactic components, referring to the processes involved in the splitting of the stored phosphagens, ATP and phosphocreatine (PCr), and the nonaerobic breakdown of carbohydrate to lactic acid through glycolysis. The aerobic energy system refers to the combustion of carbohydrates and fats in the presence of oxygen. The anaerobic pathways are capable of regenerating ATP at high rates yet are limited by the amount of energy that can be released in a single bout of intense exercise. In contrast, the aerobic system has an enormous capacity yet is somewhat hampered in its ability to delivery energy quickly. The focus of this review is on the interaction and relative contribution of the energy systems during single bouts of maximal exercise.

 A particular emphasis has been placed on the role of the aerobic energy system during high intensity exercise. Attempts to depict the interaction and relative contribution of the energy systems during maximal exercise first appeared in the 1960s and 1970s.

 While insightful at the time, these representations were based on calculations of anaerobic energy release that now appear questionable. Given repeated reproduction over the years, these early attempts have lead to 2 common misconceptions in the exercise science and coaching professions.

 First, that the energy systems respond to the demands of intense exercise in an almost sequential manner, and secondly, that the aerobic system responds slowly to these energy demands, thereby playing little role in determining performance over short durations.

More recent research suggests that energy is derived from each of the energy-producing pathways during almost all exercise activities. The duration of maximal exercise at which equal contributions are derived from the anaerobic and aerobic energy systems appears to occur between 1 to 2 minutes and most probably around 75 seconds, a time that is considerably earlier than has traditionally been suggested.

 






DanieleM

Development Team Member
Registered:
Posts: 264
 #2 
Very interesting case.
VL seems to have a venous occlusion trend. The slope of Smo2 during the rest interval after the third load is not so good as the first two.
For the non-involved muscle, my explanation for the drop of SmO2 after the load is a possible vasocostriction on the arms in order to allow for more blood to the involved muscles.
Could be this, eventually, a sign of delivery limitation?
juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #3 

Daniel   thanks  for the  feedback. Nothing really to add  as YES.

A  all out  activity  is  always a "planed"  or "unplanned " delivery limitation.
 The sudden  increase in performance like a  sudden sprint  or a n ice hockey player  is on the ice, a tennis player is pushed  far  behind the base line  or  get's  a ball behind and many more cases  are  more or less  forced  delivery limitation situations or  as in a  workout planned   delivery limitations.

 So no matter  what you  train or lie  to do  you will have to deal with this   delivery limitation.
 So as better  you prepare  for this situations.
 a) increase  utilization ability
b) increase " storage capacity of  O2  ( Mb  )
 c)Increase vascularisation
 As  more likely you will have some  clear advantages  in a race situation or  game situation.
 Delivery limitations  means  you  have a limit in O2  intake  but do not forget  you may  have the opposite  form delivery , getting rid  of  CO2  as well as a part of this situation.  So in  activity situations, where  we have this  delivery limitation due to the  sport the key than is  to improve  all the above  as well as  the  recovery  of O2.
 . Now here again the  dilemma.
 If   we belie in the  great classical ideas  of ATP  CrP  glucose  and than O2  so we have to believe in the sequel  anaerobic  alacticid   followed  by  anaerobic  lactic  followed  by aerobic , Than the  recovery situation  would look very different.
 In this case  you  would hope  to recovery  as fast as possible  ATP  as you   depleted  it . Remember the golden cheetah great explanation of  depletion of   the high energy phosphates.
 After  you replenish the depleted  ATP  you than  have somehow to replenish the  now depleted  Cr.P  and  than you still have to handle in the next step the lactate  which is in the system  for up  to one  hour.
So there is some problem here  on how  we  explain the  severe  fast drop in SmO2  (  deoxygenating in the first  30 +-  seconds , when this is all anaerobic.
 Than the next  step is to  try to   explain, how  a  body would react  when ATP is  depleted  and  how in sport we  can avoid a  Rigor   when we deplete  ATP  s well  on how we see very early on ( in the 10 +-  seconds  range a very high  lactate production, when this suppose to start  after  30 +-  seconds

  Here   short section  form a great long paper on 

 historical review  on  anaerobic power.
  The paper is  by :
 

The Measurement of Maximal (Anaerobic) Power Output on a Cycle Ergometer: A Critical Review

1CeRSM, E.A. 2931, Equipe de Physiologie et de Biomécanique du Mouvement, UFR STAPS, Université Paris Ouest Nanterre—La Défense, 200 avenue de la République, 92000 Nanterre, France
2Laboratoire de Physiologie, UFR de Santé, Médecine et Biologie Humaine, Université Paris XIII, Rue Marcel Cachin, 93017 Bobigny Cedex, France

Received 19 November 2012; Accepted 22 June 2013

Academic Editor: José M. Vilar

Muscle biopsies  (You  can see how the  shift takes  place  form lactate at the finger  to  direct  analyzing in the muscle.
 Easier  with  NIRS  to look at  O2  than  lactate  with a biopsy   for most of us. The advantage  here  is that we  have some great indication that  when biopsies s sow a  clear difference than  when we  take lactate  at the finger, that we  at least have  to  ask some critical  question on the value s of  blood  lactate  values  form a finger  during any kind of  activity   with perhaps exception  you  do a MAX LASS  studies  so you have step length of  stable  performance over 10 - 15 min duration. In this cases we have a great  chance, that intracellular  and    finger lactate  sampling  may be stable and  close to a decent    situation. The values will still be very different but at least  stable.
 Same really is true  for all of us  who use  VO2  and RER  and sell this  to our  customers  ass  an indication of  fat  and carb metabolic    changes  or shifts. We    sell the idea , that RER  + RQ  where  as  RQ is the  assessment in the blood  of  O2  and CO2  so  arterial pCO2  and  PO2.
 Than we simply hope that this ratio is the same in the mouth  piece  and  even company sell the equipment  telling us  you  can test RQ. No  way   you assess RER. RER  and RQ  are balanced  or  hopefully closed balanced , when we have a  stable resting position of 6 - 8   and more minutes.  it can be relative stable  under very light   activities  but that's  it. RQ is   most often    not RER  in any current  3   min step test  and RER  is extremely  influenced  by the way we breath and not by the way  we  use  energy. The idea of  breathe  by breath  sounds always incredible accurate  and scientific , when in fact  it is an incredible  variation in this  values  which  can or not  influence the  values we read in the VO2  equipment.  Here just for  fun a breath by breath  inside view  an look at the incredible fluctuation in TV  RF  and therefor  VE  and therefor VO2


breath by breath.jpg 


Muscle biopsies of the quadriceps muscle taken at the end of 10 all-out cycling exercises indicate that lactate production begins earlier than it was previously assumed [58].

You can see the wording " assumed" as  they  did  lactate on the finger  and  lag time   created  the  unreal  seen  when the unseen was  actually real. So  here another historical  reasoning  why we  believed  in anaerobic  alacticid.

This early lactate production is also suggested in the simulation of an all-out 100 m run: the rate of lactate production is high after 5-6 seconds [55]. This increasing production of lactic acid counterbalances the initial muscle alkalosis and pH return to a value close to its initial value around the 10th second in this model [55]. Beyond the 10th second of an all-out test, the glycolytic and aerobic metabolisms provide most of the ATP resynthesis because of the depletion of creatine-phosphate [59].

The lactate concentration at the 30th second of an all-out test was only twice the concentration observed at the 10th second [58]. This lactate concentration lower than expected at 30 seconds could be explained by  a decrease in ATP hydrolysis;  an inhibition of glycolytic enzymes by acidosis;  lactate efflux outside the muscle fibers;  an increasing contribution of the aerobic metabolism. The activities of glycogen phosphorylase and phosphofructokinase are inhibited by acidosis, and the glycolytic rate corresponding to pH at the end of a 30-second all-out test should be approximately 50% lower than at the beginning [47, 60]. There is a lactate efflux outside the muscle fibers during a 30-second all-out test. However, blood lactate at the end of this exercise is much lower than muscle lactate, and several minutes are necessary for equilibration between muscle and blood lactate [6063]. This lactate efflux depends on capillary supply which is more developed around slow fibers [64] and is improved by training.

 Now remember in the meantime  we have  the  equipment ot check it  much  faster in the time  area  of  ms. See  discussion  and info    above.

 So  to finish the thoughts.
  If  we plan a  stimulation based on a physiological plan , so  we hope  we can stimulate a  specific target like the over all target of improving for  example utilization , than we simply  in a  workout avoid  delivery  so we  create a functional  stimulation in the short term  of a  better utilization. There are  many different  workouts  you therefor  can design,  based on experience  and later based on live reactions you will see on a MOXY feedback. The advantage of the live feedback is, that you can see now, whether  the utilization stimulation, which  worked  3  days ago perfect,  still  has the same effect. or whether you have to adjust or change the trigger  for this stimulation. Nice  example is  altitude  training, where we have the first  few  days a respiratory  limitation  and depending on the real limiter in some athletes, this is much less relevant after a few days,  so it is not  anymore the  respiration  situation, which triggers the utilization reaction , but now it would be the delivery limitation  due  to low pO2  and lack of  Hb  or  the cardiac  system per see  with a too low  CO  for certain intensities.
 As long we  do not look  for limitation and compensation, we  will have  as well in the future  the answer.
 Well there are  high altitude responders  and non responders. I  do not think that this is the case, there are  athletes  who benefit  from altitude  due to the limitation they currently have  and  so others do not  benefit  (  so   do  not respond ) because the stimulation  altitude  creates  does not improve their  limiter  at all , in fact may even overload it  further.
 Responder  or non responder  is much rather  a  lack of our understanding  of  explaining  why  it works  in some  and why  not in others.


 Summary:
 If NIRS  works  we have a very  nice  option now  to get  a  fast direct feedback on the potential new idea of  the timing  of metabolic reactions. It is the first time  where you and I  on the street  have a live  direct feedback  and can see,  what I have to change if I like to create a  certain physiological stimulation. I  can instead of  training with a performance train with a live physiological feedback  to achieve the  goal I have  set out  to achieve, no matter whether it is a health related  goal or a performance goal.  I hope this shows  you even  nicer, where our  big dilemma  was a few  years back  when technology  allowed us  to question current classical believes.

 Where we wrong?  YES.  is that bad   NO 
it is  the natural  progress  we hope to make    with  the increased  understanding in what is going on  due  to improved  technology. So nothing wrong  with what we  did  as long we recognize  where we  can improve.
  Daniele  thanks  for your  short    and great feedback.

  A  last  thought. If we see in whole body athletes the above reaction, we have  to change training ideas. If this happens in an ice hockey player or a basket ball player  or a tennis player , we  therefor loose performance in  the upper body in the above case  so still running fast, skating fast,  but loosing the game  due  to lack of upper body performance.


juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #4 
Thanks  for the many feed backs on this  fascinating topic  and the interesting questions on the aerobe  and anaerobic discussions.
. Many are  from coaches  from sports  like tennis  and  team sports.
Not surprising, as it fundamentally changes the way we look at  ideas  of individual designed  trainings.
I  may later  be back on this  development  and  the  way we  may depart  from all out  loads  to achieve  certain stimmulat5ions  to some  more targeted stimulation  with the same end results  but somewhat better  control and protection of  " side effects'  which  are more common in all out  workouts.

 One  question was the placement of the second  MOXY. If  we  talk about a  non-involved muscle , than  this is not optimal. This is  why the cook  books  not work. We    have   rarely  any muscles, which  are non-involved  so yes  much better would be the term  less involved muscle.
In a sport like tennis  or  figure skating , as there where the most feed backs, there  are  most often  all muscles somehow involved in  more or less a high intensity workout  or  race or competition..
 So  what we look is  to have  one moxy on a lower  body muscle  which we assume is heavily involved  and one on a upper body muscle  which  can be as well heavily involved.( Some additional ideas  will come later)
 In  sports , where a big   or  a great % of  total muscles  are involved  we  will see often the dilemma  , that the  O2  demand, which  comes  from the high %  of the total muscle group involved, is  so big , that the delivery  has a real  problem. But not just the delivery itself , but the  priority  of the body  on where it is  absolutely  important  to  supply sufficient  O2. This  moves  us back to our  simple idea of the energy hierarchies  or pyramid  we showed many times.
 Vital systems  will have always priority    and loco motor  muscles  therefor  have to take   the first " cut" in O2  supply.
 If they still would " steel " O2  from vital  systems  than we have the different protections  ( reflexes ) which  will  avoid this.
 2  of the   reactions  ( most likely many more )  are nicely  traceable  with NIRS  when we look  how they  react  and therefor create  trends in SmO2  and tHb.
 1. metaboreflex ( Dempsey  et all )  where we have a  limitation  set by the respiration system  and the protection is the vasoconstriction to the  locomotor  muscles in case  O2 is limited in delivery.

 The reduction in blood flow  will as well reduce the amount of  O 2 moving to the loco motor  muscles. This  is what we see in  sports like tennis  and  figure skating where sometimes suddenly   "unexplained "  technical mistakes , like not optimal DNA  patterns  in the motion show  up. The respiration or better the diaphram is really the ultimate  core muscle  and as  such in case of  overload, the respiration ( O2 in  and CO2)  out  will overrule his  duty  for core stability  and you  start  loosing efficient technique  as   the core stability is less vital than the gas  exchange. 

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.

 

Diaphragm Recruitment during Nonrespiratory Activities

 

FADI AL-BILBEISI and F. DENNIS McCOOL

 

Departments of Medicine, Brown University Medical School, and Memorial Hospital of Rhode Island, Pawtucket, Rhode Island

 
 There are  many more great studies  on the core involvement of the  diaphragm  and it throws the interesting discussion out  , how smart it is  to train the rectus  abdominals  so hard, when he has no actual  function in the core stability  at all. Another interesting  classical  idea  which may have to be  reviewed    once in a  while.


 Now  id  we unload  respiratory  work  than we  will have  an improvement of  oxygenation in the loco motor  muscles.
 So   what we  can  do is to fix the second moxy on a  movement  but as well  respiratory involved  muscle under heavy load. One  of the  possible location is the upper trapezius muscle  or  the sternocleidomastoid.
 They  are  involved in upper body movement  but as well  in  extreme  inspiratory    work  as  so called  auxiliary muscles. So that  could be  a possible location  for  the second moxy  as we have no additional feedback on possible  respiratory limitations.
 There  are great  studies  done  with unloading  respiratory  work and they indicate  due to the  result  that  respiration  can  be a potential limiter even in healthy  people.
Here  one  of the studies  I like to read.

Thorax. 2008 Oct;63(10):910-5. doi: 10.1136/thx.2007.090167. Epub 2008 May 20.

Respiratory muscle unloading improves leg muscle oxygenation during exercise in patients with COPD.

Borghi-Silva A1, Oliveira CC, Carrascosa C, Maia J, Berton DC, Queiroga F Jr, Ferreira EM, Almeida DR, Nery LE, Neder JA.

Author information

  • 1Pulmonary Function and Clinical Exercise Physiology Unit, Division of Respiratory Diseases, Department of Medicine, Federal University of São Paulo (UNIFESP), São Paulo, Brazil.

Abstract

BACKGROUND:

Respiratory muscle unloading during exercise could improve locomotor muscle oxygenation by increasing oxygen delivery (higher cardiac output and/or arterial oxygen content) in patients with chronic obstructive pulmonary disease (COPD).

METHODS:

Sixteen non-hypoxaemic men (forced expiratory volume in 1 s 42.2 (13.9)% predicted) undertook, on different days, two constant work rate (70-80% peak) exercise tests receiving proportional assisted ventilation (PAV) or sham ventilation. Relative changes (Delta%) in deoxyhaemoglobin (HHb), oxyhaemoglobin (O(2)Hb), tissue oxygenation index (TOI) and total haemoglobin (Hb(tot)) in the vastus lateralis muscle were measured by near-infrared spectroscopy. In order to estimate oxygen delivery (Do(2)est, l/min), cardiac output and oxygen saturation (Spo(2)) were continuously monitored by impedance cardiography and pulse oximetry, respectively.

RESULTS:

Exercise tolerance (Tlim) and oxygen uptake were increased with PAV compared with sham ventilation. In contrast, end-exercise blood lactate/Tlim and leg effort/Tlim ratios were lower with PAV (p<0.05). There were no between-treatment differences in cardiac output and Spo(2) either at submaximal exercise or at Tlim (ie, Do(2)est remained unchanged with PAV; p>0.05). Leg muscle oxygenation, however, was significantly enhanced with PAV as the exercise-related decrease in Delta(O(2)Hb)% was lessened and TOI was improved; moreover, Delta(Hb(tot))%, an index of local blood volume, was increased compared with sham ventilation (p<0.01).

CONCLUSIONS:

Respiratory muscle unloading during high-intensity exercise can improve peripheral muscle oxygenation despite unaltered systemic Do(2 )in patients with advanced COPD. These findings might indicate that a fraction of the available cardiac output had been redirected from ventilatory to appendicular muscles as a consequence of respiratory muscle unloading.

 I will be back showing you  omr the discuss triple  wingate some additional thoughts  and  how the delivery  can  come withing the locomoror  system  if  ddelivery  from the " outside" is  inefficient  or  blocked.




juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #5 

Now  here some additional feedbacks  , when looking  at  high  short term intensity  versus  a longer  timed  VO2  max test.
 Again as  the current terminology suggest.
 Wingate = anaerobic  power  and information on the anaerobic  system
 VO2  max    as  a  feedback on maximal  O2  used  form  how ever used it  at that moment..

 Now  a  30 second all out   or in this case  a   Wingate  load is a planned  delivery limitation. We just never looked  at it this way.
 The time   option in 30 seconds  to allow all the physiological systems  which are integrated in  energy delivery  and  possibly utilization  are  overwhelmed  and some may simply have no chance  to  ever  be a part of the possible delivery.
So  as we had on the one  website the   information, that we take  what we have stored or  is in the  area, where the action takes  place  and where we  need the energy  sources.
 What is missing in the  established  ideas is the O2  which is  stored  as well.
 Now  when we look  at some data's  of  a  wingate versus a  VO2 max test  than it could look like that.

hr.jpg 
Now  if  you allow us  to look the data's  from our  point of view  than we  have :
 a) a much higher O2  use  from the area in the 30 second  all out  compared  to the   VO2.
 That does not mean we used more O2  but it means, that due  to the delivery problem  we  have to use  as much as possible  as long  as possible  from the  O2  which is in the  area  and hope  for a speedy involvement of  the  stimulated  delivery.
If the  performance  or better the muscular contraction  force in the  30 seconds  is  extremely high  so we may  produce an   art. occlusion, than the hope is gone  anyway.
Otherwise  we  have a b venous occlusion  which means  still some hope  for delivery  but some disadvantages  on getting rid of  H +  and  CO2.
In any case  we have a  very high integration of  O2  and   for all MOXT Y users,   look at  open minded  when you do something like this  and you will see, that as soon you see the SmO2  drop  to " hesitate"  you know the end  of  performance is  close    for this  muscle or  at least  the performance will drop down to an intensity , where the  O2  delivery  and  utilization may  be in balance  to maintain ATP  homeostasis . So you may see a  drop  ( sharp )  drop  and  finally a  flat  SmO2. Now  look at  performance  and  for  all SEMG users look at SEMG  activity  and  you have  an interesting answer.
 True  not what we learned  but what  you see.

b) look at the maximal workload . wingate  versus  VO2  max  What  do you think that  would indicate ?
c) lactate. Now y this study  did  not indicate  how  and   when they took lactate   . If they took it immediately at the end of  each test , than the 10. mmol lactate in the wingate test is very surprising  and I never  saw a  value  after  30 seconds  all out  like  that immediately after    30 second.  As  we showed it can go up. I  can see  this value  in after  load   sampling but  nice would be than  to show the full trend   as it may be  different or they where  just  "lucky" to have a close to the same   value.
 If  it is  as we can see the same , than  based on the old theory  of anaerobic  an aerobic  the VO2  max  would crate the same  amount  of anaerobic  lactate production like the  " anaerobic   wingate  test " ???? That sounds like an interesting  thought  does it.?

d)  HR  comparison. If  we  accept  HR  as a part off Cardiac output  as CO = HR  x SV, than we  could argue that CO  was  lower  in the wingate  than in the VO2 max  and CO is a part of  the delivery system.
e) Fatigue index.  Well if  anaerobic  or lactate is a  reason of  fatigue  the lactate values  would contradict this  information.  ?? The second  though is, that  when I give time  for  many system  to be involved   it  just  may be that the " fatigue  index  may in fact be different.


f) There where no VO2  data's  which is strange  e, as we have VO2  info's   in wingate  test as well. The  values   are just very different.
 Where do you expect the  VO 2 values  may be ? Now  what  "conclusion"  would we  make  when just looking  at VO2  data's  and not   at the NIRS feedback. ?

 Last  what is interesting is , that they   did not collected  or at least  did not looked  at  the respiration  per see. So  fun would  be to see  RF  TV  and as  such VE  but as well CO2  and O2   values.

 Now  some would argue  that for  30 seconds  you do not  have to breath  so   it is  anaerobic  as you do not  breath O2  in ???

  Could be  an interesting topic  but  much  more fun  could be that you try  a  Wingate  and  you are not  allowed  to breath ? Or  doe a  VO2  max test   and in the   last  or  some of the last  steps  you  are not allowed  to breath  for 30 seconds. Try  have  fun  and check the reaction  of  MOXY    as you do this   small individual  case study. Now  here the last part bin this case  look  the interesting reaction  form the MOXY on the arm and see, that the reaction actually  was exactly the opposite  form the leg muscle.

noninv wing.jpg 
WU  = warm up
R = rest
L = load
CD =  cool down Green is SmO2 trend in  delta  muscle in our  Wingate triple load Yellow  /brown is tHb  in the same muscle. 
 so when we overlap  SmO2  it is   even nicer  to see.
3 x  inv noninv.jpg 





Previous Topic | Next Topic
Print
Reply

Quick Navigation:

Easily create a Forum Website with Website Toolbox.

HTML hit counter - Quick-counter.net