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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
This is a great discussion  and as  mentioned before, who really is  an expert in the first place ??? (Smile )
 Here  some simple  practical ideas.
 Cardiac  and respiratory  system  react  very  similar.
 Cardiac  is a pump  moving liquid. Respiration  lung /diaphragm " is a pump moving  air.
So  Cardiac  work is  a kind of used  as CO ( Cardiac out put in L/min ) CO  = HR  x  SV
Respiration work is a kind of used as VE  is ( amount of  air  ventilated   as in L/min?  VE  = RF x TV

 So  RF  and HR  is the  rate  per minute  and is often in connection with coordination.
 So if you do a very high respiratory coordination workout  or you do a very high HR  coordination workout you will see often    after the workout a problem in this  two  areas. Problem  is sometimes to  reach a high HR  and problem  to actually  have a high respiratory  frequency.
  If you do a volume  workout like big air volume,so   big tidal volume,   and you do a  cardiac  volume workout  you will often see the opposite : easier to reach high HR  and easier  to reach high respiratory frequency.
 This does not mean  high CO  and High VE .
 This is a reason  why ventilatory threshold  can be , but is not  always  LT  or vica Versa.
  for people using  VT   = LT.
 In fact if  respiration is the limiter than the trend in lactate  is going up as we reach the  discussed idea  of  VT.
 This makes sense  as now the  body has to start compensating  and we see many  different   values going up. lactate, blood sugar  , epinephrine,  nor-epinephrine  and   others. So how many  " thresholds "  do we like to use ?????
 If  respiration is  in good shape  and not the limiter, than  VE  will create  " threshold" but  lactate not  ????. Now  this as well will change  SmO2  and tHb reactions  and  now  we have  some problems by  assuming that  NIRS  can give a lactate threshold information ???
 We  for  sure will get back   with all this great discussions.
  Now back to Evans  case  first  and it may shed  some light to the Daniele  and Evans  points.
 as the volumes  may  drop more than the frequencies  can compensate.

 So  resting respiratory rate  as well as  resting  HR  can help to get some initial reactions in the morning on an athlete  when we look at his information. See  Evans feedback on HR in back position and in standing.
 Here a small help  to understand   connections between  SV  and  HR.

SV CO HR in different position.jpg 
 Can we use   HRV ?  HRV can change  due to respiratory fatigue  and not  only due to cardiac  reactions. There are many respiratory reactions influencing HRV.
 Now  I will get  later back to the great discussion on here, how we  can a little  more  guess   whether we have a   delivery   and or a  utilization limitation in any workout you may do  daily.
 We  do what I call " a calibration  " warm up "  and than a resting calibration  1 min rest  to decide  , whether I will go a head with the planned  workout  or whether I will readjust the idea  or  the goal depending on the bodies   current reaction.

smo2  thb  all.jpg 
I added  to Evans case some  circles  and some lines to  show you some ideas. For fast thinkers  or restless readers the circle   have to be  connected in the thinking process.
  The start  and the end of  an assessment can have  one  thing in common. ??? What is it ?
  Now  let's  focus first on the 2  first loads  2.8 mph  and  4.0 mph

 2.8  is    for most people  too slow  to  run  and  nice to walk. So I assume  in this case this was  a  walking  step.
  No2  4.0 is  somewhat tricky. It is  actually still possible to walk  but may  create some ugly coordination problems  when walking is not your sport ( speed  walking ).  So you mat y run but  running 4 mph   can be very ugly as well as it is  too slow to actually lean  and use  your center of gravity to have a great  economic  ruin .
 So  what we create is a fight between  economy  and  stress.

 If you look at this closer  it will look like this.
walk  and run.jpg 

Gehen means  walking , Laufen  means  running. You can see in this case the critical   speed  , where one is   more or less economic ??

Now  as  VO2  is  the summary for a  whole team we look  at the cardiac, respiratory  and locomotor   systems  who all  need O2   .We  where interested to see, how this may change in delivery  and utilization  aspects.
 So here a example of many case.
 You guess    how many sets    where  walking and when   this client change to  running.

Here  we start  with  NIRS.
 The  thick  line  color   is the  deeper level so more likely  deep in the muscle  trend  versus the skinny   lines are   surface  feed backs  so more likley  skin feedback.

ipahd 2.JPG

Now let's look at  cardiac  respond
pf overall picture - Copy.jpg

Left blue top is HR. middle top is SV right top is CO
left bottom is EF % middle bottom is LVET in ms and right bottom is SVR 

Now    " classical  " feedback on VO2 in this case.

vo2 fm.JPG 

Now  as mentioned, VO2  has limited information  so  let's look at  respiratory trends  like RF  VE  and therefor VE. Last but not least take VO2  = CO  x  A-V O2  diffference.
 So look at the cardiac reactions  and  at the  NIRS reactions rather than VO2.
 Why :

vo2   co  hr sv overveiw.jpg

VO2  and  ecgm.jpg

So here to complete the picture  from the respiratory  reactions point of view.
 Than you go back to Evans  case  and  try to figure out,whether  4.0 mph  was a walk or a run step.

Have  fun.  I will be back and go back to baseline to make  the so often  demanded  " cook book " . You can see why  to be a chef is  nicer  but harder to compete   against " franchise "  where you use   a simple Formula  and all tasts  the same.


Development Team Member
Posts: 14
Screen Shot 2015-02-20 at 8.30.38 PM.pngAthlete is feeling better. She has continued to train, but today was one of the first workouts back with the Moxy. She had a continuous run today, and she performed it on the treadmill. We did not have LIVE moxy coming in, but we just took her TIP and estimated a good speed/HR "zone" for her. I just received the Garmin 920XT -- excited for the Connect IQ app!

Based on her TIP, this profile looks NOTHING like I would have guessed. I wouldn't have guessed her SmO2 values would be registering nearly 90%. Her HR as well was noted to be lower as well. 

Before the 40 minutes, there was a gradual dynamic warm-up. She then placed the Moxy on, and she did 5 minutes of walking at 3.0 mph then proceeded into the run.

We instructed her to stay between 5-6 mph (per TIP), and heart rate between 140-155.

The sprints did not cause a the magnitude of SmO2 change I would have predicted.

Also, she actively rested at 3.0 mph for 1:30 between sprints.

Just updating the group. If anyone has any comments, I'm always interested!

Attached is the CSV file if you need it.

Attached Files
csv 2-20-15-MD.csv (60.13 KB, 29 views)

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Evans  will be back tomorrow  and thanks for this  great data sets.
 I  have to  go through some data  from a big team today  but will be back tomorrow. Just very  short  as I never can hold back  and look at the csv  information.
  First  the TIP  actually  confirms  what we  would expect    nice  and great.
  step 4  and 5 circle.jpg  You can see based n the TIP the only  section where she was  stable  ( homeostasis  was in  load  43  and 4  so by  5.6  - 6.5  mph.
 So  6  mph  is pretty much in between.
 The HR  here  at  5.6  was  150 +-. The HR  in the  6.5  level  was much higher  but that is not unusual as it was a  5 min step test  so not  enough time  for  vascularisation and cardiac  reactions to actually see, what is the optimal    CO  ( HR  and SV as the  steps  shows  you the tHb reaction, where she has a  very   extreme drop when starting  but than  after   45 +- sec starts  to  get going  with an increase in tHb in each single step. So giving her system more time  shows a  great opening of the tHb    numbers.
 So  the SmO23  numbers   really confirm the  TIP  level that  the 6 mph is a STEI intensity. or even    slightly close to ARI STEI.
 The sprints as well confirm her tip  really nicely.
 We argued in the tip a  delivery problem so fast  and immediate  need of O2    before the lag time of the delivery  kicks  in.
 Now  after her 40 min run, what did she  for sure got  going  very nicely ( delivery systems  optimal CO  and optimal  vasuclarisation so the 20 seconds  load  where done  with a   very efficient  delivery  support so  little need to  for utilization. The  sprints  show a problem with H +   release  due to a weak  respiratory ability to get rid  of  CO2. Here just short the pick of  one sprint  at a a closer look. sprint  12.5.jpg    Summary.
 The TIP  pretty much  confirms  all what we see in a really nice  way. So not sure , what the expectations  where    but would; be  fun to know Cheers Juerg


Development Team Member
Posts: 14
Hi Jeurg,

Thanks again for the great feedback.

i wasn't expecting such high SmO2 values based on her TIP at those speeds. I understand the argument for stating she had a lagged delivery system as that made sense per the TIP. But perhaps that was because her cardiac system was overloaded and masked her cardiac's true ability. 

The supine/standing HR responses give some indication of this.

So, yesterday, from what you're saying, it seems the delivery and utilization is setup and operating well, but when things intensify she lacks on the respiratory side.

I'm going to throw in the towel and admit I have no idea how your interpreting there is a respiratory issue with the sprints. I would appreciate any insight on this interpretation.

As always, thanks!

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Do not throw in the towel  as we are not  fighting here at all  (Smile ).
 First  to the  much higher SmO2  than you may have expected.
 The 6 mph  speed is  for here  most likely  a nice  relaxed  run. So  it may be  in a  TIP where you run all the time  an intensity  at the   change  for ARI  to STEI. meaning that we  have all the time a  higher  delivery than we need  so there is  an ongoing load  if we do not change speed  till we reach a  maximal level she can load  which as you can see is very high.
 This  in combination with the highest  possible thb  would be the key  for  an optimal " warm up "  program. ???
 Now  bad    question but I like to keep this  fire burning. In the traditional way on how  you and me  are  coaching or testing, how  would you see what we see  with MOXY. How  would you decide  what is the  optimal " warm up " procedure  form a metabolic point of view  ( I do not talk  about the whole   neurological pattern  for intra  and inter muscular coordination  and so on, just simply  " gas tank " optimal  O2  loading  and optimal blood flow. ???' It that not  a  potential fascinating step forward  with all the care full interpretations  we always have to  do ???
 How  can we deliver this feedback when we use   MAXLASS  or  % of max HR  or speed  at 4 mmol lactate  or  %  of VO2 . If we  ask  critically  all this questions  by looking  at MOXY  we have  to fair  and ask the same questions  on what we use  till now.  It is all about  fair sport  isn't it ??? 

So  first question.

I'm going to throw in the towel and admit I have no idea how your interpreting there is a respiratory issue with the sprints. I would appreciate any insight on this interpretation.

 Tell us  how you  use this 6  sprints  to find out  what you may have stimulated  and what was limiting her further  performance.
 Why 20 seconds  sprint  and why this speeds. ?
 For the regular readers.
 Please : This is a test  whether I am able to move  the message over. Why do we see in his 20  sec load  , that she has a respiratory limitation  at the end of the sprint  and what would we see, when this  would be not the case  so   20 sec load would not  challenge  her respiration ? if  not I did  another bad  job  and have to  try to be better.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Small hint to the above  question.
 post 12.14.14.
 Now include in this :
CO2  reaction on  blood vessels  as well as O2  disscurve shift  due to  CO2  and you can create a graph  with SmO2  and tHb where we can see, that  respiration is not a limitation. How  would a graph like this look like ? Take into the account, if you use a capno meter, the lag  time  or if you use VO2  equipment. MOXY feedback has a  direct information with a very small lag time ) , but  any face mask assessment  ,whether it is   with a VO2  equipment or  with  a  capno meter  for EtCO2  has a lag time, including the risk  that if the  steps  are too short   EtCO2  is not Pa  or PA  CO2  at all.
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Okay  I may have to  throw a towel. I am sweating hoping  for a feedback on my challenge.
 here a last hint before I have to  tell myself  that I did not a great job  so there is  still some confusion out there  so have to try again.
 So here the small additional hint. It is a  set similar to the one  we have  from that middle distance runner  with 6  runs over 20 seconds  with 3  same speed  followed by 3  faster loads.
 Go  back and look the SmO2  trend  and  the tHb  reaction. Now  compare here. This is  an ice hockey workout  and you can see   that the  one set shows  a limitation due to respiration  and the rest where okay.
 Courtesy  Brain Kozak  of Next level coaching.
jump pum,p moxy set.jpg
 and here  when we look  all information's  but  at the end  you will be able to see HHb  and O2Hb    when you have SmO2  and tHb in front of you as they  all  come  from the same .

jump pump moxy trend.jpg 

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Here a long delayed response  to Evans  nice case study of the runner  and the 6  x  20 sec   "interval". I had a  great one by one  idea  exchange  with Evans  and I like to try to make a summary here of some ideas we exchanges  concerning a respiratory limitation  in this 20 sec  runs . I hope Evans  may come in  and correct  where I  am    not clear on it  or  comes back  with some additional  thoughts  questions  and critics.
 02/21 is the very close look  at the  runners 20 sec  run. Now important is  to see the difference between a  sport , where I cold turkey  can just stop like on an elliptical, or  on a rowing  equipment or  on a stepper or  actually even on a treadmill . where  in the field in running I  simply  slow  down   before I stop. (  reminds me   to go back to a  question Daniele  sent  in one  forum , where he highlighted  some SmO2  trends in the " recovery " phase . Have to search for it.)

okay 02/21 or the last set in the  loads  of Brian's  ice hockey example. Same situation.
tHb ( trend in blood flow  / volume :  we have a  good indication, where the  runner   ended  the  20 seconds ( Well we have  the time ) but even without the time  we  can see, where the tHb  after a drop due to  overrule of contraction compression  starts  to  increase  due  to less contraction compression..
 This indicates  a  slower  run or lower performance. 
Question , : Why do we know    ( if we would not have the 20 seconds  time . )  that this increase is NOT a venous occlusion trend ?
So as we  see a reduction in speed  and therefor  assume there is as well a reduction in energy demand    we would assume , that SmO2  should increase  as well  at the same time  or a  very  small lag time. See the  first  few  loads in the Ice hockey case.
Yes there is a  small time lag  on SmO2  or MOXY data's  but ( roger  can correct  me )   I  would see that in the range  of  3+- seconds.  only  and not in the range we see here  of  15 +  seconds.

 So  what happens. In this short  relative  hard loads we  have an immediate  demand for a  lot  of energy  and all availed options  are getting into action. Nevertheless  we  have a  higher utilization , than delivery  and as  such  we  have the need  to  balance H +  if we like to  keep going for somewhat  longer.
 Different options  and two  we often discuss is  lactate as a  a buffer option ( So not the reason of  fatigue  but the reason of  being able to sustain  a  little bit longer.
 As second  option is the release of CO2  over  expiration.
 Both options  can be trained relative  easy.
. So  if we  can't  release  enough CO2     we have a shift of the  O2  diss curve to the right. This allows   for a better release  of O2  from the blood to the cell but    makes it  harder  to load  O2  from the lungs to the  blood ( EIAH)
Now  a high CO2  has  some other reactions   who can come into place  locally . Vasodilatation of  systemic  blood vessels.
 So in our  case  we have a reduction in muscle compression  due to  end  of the 20 second  load , but we have a  right shift  of O2  disscurve  so  perfect release of  O2  and not as perfect load of  O2,  and a  vasodilatation  due to high CO2. This creates  a   reaction as we see. As  son the respiration  has balanced out  the CO2  we will have  a  fast  incline  of SmO2  and a  better load of  O2  again.
 Now  you can see how a  great trained respiratory system  can  help in changing this situation.
 This  is  super critical in sports like Tennis  for  example. Who ever saw  the  Game in Acapulco  Harrison Ryan  against  David  Ferrer    knows  what I am talking about. After the first step  you had a  young  Harrison   starting to breath with his " shoulder'  > Complete overloaded  diaphragm  and therefor  a  heck off a problem to  ever reload  the  main muscles. So legs  kept going but  his  serve  and his  hits  where complete  gone.
 Serves went  al into the net due to   abdominal  normal strength  and lack of  core stability over the diaphragm   so all pull down. Less arm extension due to overload of  upper trapezius,  scaleni  and sterno  muscles  and you could see that perfectly in the close  up shots.
 So shorter   hit   2  - 3  m before baseline  so  Ferrer  could stop  in    and  dramatically shorten the   time of  the  hits  , which created  an even bigger problem  for Ryan  and so on.
 Remember the diaphragm is the main core  muscle   and    has  tow  jobs  core stability  and respiratory  balance  CO2    in this case nearly more important  then  O2. Survival reflex  will tell him . I  do not care  , whether you play tennis  so core is  of no urgency  for me  but I really care  about you in case you  stop breathing  so  better  keep that going.
 Summary. Respiratory   limitation  is  an often overlooked  situation. Reason: we all learn respiration  is never  a limiting  factor  in healthy  people. We better learn to think twice.
 An average   ice hockey player  of an NHL  team (  personal  test information  of  a  full NHL  team tested  at a  university has  an average  VE (L/Min ) for 150  +- 30 L.
 A  respiratory trained athlete    has a  VE  of  250 + 50 L in  basically  any case  where we trained athletes over the last  20 years.
 Are they better player . Possibly not  , do they recover better  YES  for sure  so they  do not play better  because of that but they  maintain  longer the best they can play as   core stability is maintained  and reloading  is  much faster so   less  risk  of  starting to use upper body areas to compensate  for lack of  delivery or in this case out  delivery of CO2  with their upper body.
  Here  for  some more researched  base  readers  some   additional information   form timing on gas  restoration  in the lungs  and cell to   some indication, what happens  when the respiratory system may  in fact  start to be a limitation.

 I will start a new  page  as it is too long   to sent it here of  so  keep reading  some of the examples.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530

Fatiguing inspiratory muscle work causes reflex reduction

in resting leg blood flow in humans

A. William Sheel, P. Alexander Derchak, Barbara J. Morgan *,

David F. Pegelow, Anthony J. Jacques and Jerome A. Dempsey

Department of Population Health Sciences, John Rankin Laboratory of Pulmonary

Medicine and * Department of Surgery, University of Wisconsin-Madison, Madison,


(Received 20 April 2001; accepted after revision 12 July 2001)


1. We recently showed that fatigue of the inspiratory muscles via voluntary efforts caused a time-dependent increase in limb muscle sympathetic nerve activity (MSNA) (St Croix et al. 2000). We now asked whether limb muscle vasoconstriction and reduction in limb blood flow also accompany inspiratory muscle fatigue.

You can use a MOXY and a Spiro Tiger and test this out.


2. In six healthy human subjects at rest, we measured leg blood flow («QL) in the femoral artery with Doppler ultrasound techniques and calculated limb vascular resistance (LVR) while subjects performed two types of fatiguing inspiratory work to the point of task failure (310 min). Subjects inspired primarily with their diaphragm through a resistor, generating (i) 60 % maximal inspiratory mouth pressure (PM) and a prolonged duty cycle (TI/TTOT = 0.7);

and (ii) 60 % maximal PM and a TI/TTOT of 0.4. The first type of exercise caused prolonged ischaemia of the diaphragm during each inspiration. The second type fatigued the diaphragm with briefer periods of ischaemia using a shorter duty cycle and a higher frequency of contraction. End-tidal PCO2 was maintained by increasing the inspired CO2 fraction (FI,CO2) as needed.

That  is  exactly  what you do  with a Spiro Tiger  , so no CO2  tank needed  just  simply a  Spiro tiegr  and  you go.

Both trials caused a 2540 % reduction in diaphragm force production in response to bilateral phrenic nerve stimulation.


3. «QL and LVR were unchanged during the first minute of the fatigue trials in most subjects; however, «QL subsequently decreased (_30 %) and LVR increased (5060 %) relative to control in a time-dependent manner. This effect was present by 2 min in all subjects. During recovery, the observed changes dissipated quickly (< 30 s). Mean arterial pressure (MAP; +413 mmHg)

and heart rate (+1620 beats min_1) increased during fatiguing diaphragm contractions.

4. When central inspiratory motor output was increased for 2 min without diaphragm fatigue by increasing either inspiratory force output (95 % of maximal inspiratory pressure (MIP)) or inspiratory flow rate (5 w eupnoea), «QL, MAP and LVR were unchanged; although continuing the high force output trials for 3 min did cause a relatively small but significant increase in LVR and a reduction in «QL.


5. When the breathing pattern of the fatiguing trials was mimicked with no added resistance, LVR was reduced and «QL increased significantly; these changes were attributed to the negative feedback effects on MSNA from augmented tidal volume.


6. Voluntary increases in inspiratory effort, in the absence of diaphragm fatigue, had no effect on «QL and LVR, whereas the two types of diaphragm-fatiguing trials elicited decreases in «QL and increases in LVR. We attribute these changes to a metaboreflex originating in the diaphragm. Diaphragm and forearm muscle fatigue showed very similar time-dependent effects on LVR and «QL. is consistent with the idea of a metaboreflex that increases sympathetic vasoconstrictor outflow. Furthermore, increased sympathetic outflow to, or vasoconstriction in, selected vascular beds has been elicited in anaesthetized

animals by electrical (Szulczyk et al. 1988; Offner et al. 1992) or chemical (Hussain et al. 1991) stimulation of phrenic afferent fibres.


We now asked whether respiratory muscle fatigue in humans would also have functional consequences in the form of vasoconstriction and reduced blood flow in the resting limb.

 In addition, we addressed the cardiovascular consequences of augmented central respiratory motor output, per se, and determined to what extent the cardiovascular effects of inspiratory muscle fatigue paralleled those during fatigue of the forearm muscles. We believe these proposed reflexes from the respiratory

muscles may influence blood flow distribution during exercise (Harmset al. 1997, 1998; Wetter, 1999


The cause of metabolic acidosis is not merely proton release, but an imbalance between the rate of proton release and the rate of proton buffering and removal. As previously shown from fundamental biochemistry, proton release occurs from glycolysis and ATP hydrolysis. However, there is not an immediate decrease in cellular pH due to the capacity and multiple components of cell proton buffering and removal (Table 5). The intracellular buffering system, which includes amino acids, proteins, Pi, HCO3−, creatine phosphate (CrP) hydrolysis, and lactate production, binds or consumes H+ to protect the cell against intracellular proton accumulation. Protons are also removed from the cytosol via mitochondrial transport, sarcolemmal transport (lactate−/H+ symporters, Na+/H+ exchangers), and a bicarbonate-dependent exchanger (HCO3−/Cl−) (Fig. 13). Such membrane exchange systems are crucial for the influence of the strong ion difference approach at understanding acid-base regulation during metabolic acidosis (5, 26). However, when the rate of H+ production exceeds the rate or the capacity to buffer or remove protons from skeletal muscle, metabolic acidosis ensues. It is important to note that lactate production acts as both a buffering system, by consuming H+, and a proton remover, by transporting H+ across the sarcolemma, to protect the cell against metabolic acidosis.

Once it is in the blood we  have one  great ability  to  get rid  of H + .



Respiratory training  / Spiro Tiger


Juerg Feldmann

Fortiori Design LLC
Posts: 1,530

Inspiratory muscles experience fatigue faster than the calf muscles during treadmill marching

Renana Perlovitcha, Amit Gefena, David Elada, Anat Ratnovskyab, Mordechai R. Kramerb, Pinchas Halpernc





Department of Biomedical Engineering, Faculty of Engineering, Tel Aviv University, Tel Aviv 69978, Israel


Pulmonary Institute, Rabin Medical Center (Belinson Kampus), Israel




Department of Emergency Medicine, Tel Aviv Medical Center, Israel

Accepted 17 August 2006. Available online 24 August 2006. 


The possibility that respiratory muscles may fatigue during extreme physical activity and thereby become a limiting factor leading to exhaustion is debated in the literature. The aim of this study was to determine whether treadmill marching exercise induces respiratory muscle fatigue, and to compare the extent and rate of respiratory muscle fatigue to those of the calf musculature. To identify muscle fatigue, surface electromyographic (EMG) signals of the inspiratory (sternomastoid, external intercostals), expiratory (rectus abdominis and external oblique) and calf (gastrocnemius lateralis) muscles were measured during a treadmill march of 2 km at a constant velocity of 8 km/h. The extent of fatigue was assessed by determining the increase in root-mean-square (RMS) of EMG over time, and the rate of fatigue was assessed from the slope of the EMG RMS versus time curve. Results indicated that (i) the inspiratory and calf muscles are the ones experiencing the most dominant fatigue during treadmill marching, (ii) the rate of fatigue of each muscle group was monotonic between the initial and terminal phases of exercise, and (iii) the inspiratory muscles fatigue significantly faster than the calf at the terminal phase of exercise, and are likely to fatigue faster during the initial exercise as well. Accordingly, this study supports the hypothesis that fatigue of the inspiratory muscles may be a limiting factor during exercise


Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Here  some more interesting readings for coaches facing athletes with respiratory limitation.

Related trends in locomotor and respiratory muscle oxygenation during exercise.

Legrand R1Marles APrieur FLazzari SBlondel NMucci P.

Author information

  • 1Laboratory of Human Movement Studies, Faculty of Sports Sciences and Physical Education, Lille University, Lille, France.



    We investigated the potential effect of respiratory muscle work on leg muscle oxygenation without artificial intervention in non-endurance-trained young subjects and searched for the range of intensity when this effect could occur.


    We simultaneously monitored accessory respiratory and leg muscle oxygenation patterns with near-infrared spectroscopy (NIRS) in 15 healthy young men performing maximal incremental exercise on a cycle ergometer. Pulmonary gas exchange was measured. The respiratory compensation point (RCP) was determined. Oxygenation (RMO2) and blood volume (RMBV) of the serratus anterior (accessory respiratory muscle) and of the vastus lateralis (LegO2 and LegBV) were monitored with NIRS. The breakdown point of accessory respiratory muscle oxygenation (BPRMO2) and the accelerated (BP1LegO2) and attenuated fall (BP2LegO2) in leg muscle oxygenation were detected.


    BPRMO2 occurred at approximately 85% .VO2max and was related to RCP (r = 0.88, P < 0.001). BP2LegO2 appeared at approximately 83% .VO2max and was related to RCP (r = 0.57, P < 0.05) and with BPRMO2 (r = 0.64, P = 0.01). From BP2LegO2 to maximal exercise, LegBV was significantly reduced (P < 0.05).


    In active subjects exercising at heavy exercise intensities, we observed that the appearance of the accelerated drop in accessory respiratory muscle oxygenation-associated with high ventilatory level-was related with the attenuated fall in leg muscle oxygenation detected with near-infrared spectroscopy. This suggests that the high oxygen requirement of respiratory muscle leads to limited oxygen use by loco motor muscles as demonstrated in endurance-trained subjects. The phenomenon observed was associated with reduced leg blood volume, supporting the occurrence of leg vasoconstriction. Below is a case study from  Jiri as one  of over 500 studies. The lower graph of the peripedal is a  MOXY info  from intercostal muscles. The upper  as I can remember is a  leg muscle  MOXY  info.  Look at the recovery  reaction of SmO2. Jiris  group  with   Martin together run In prag one of the most advanced  sport testing  institution   and test all different  sports


    And below  just to give some more  additional info

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Had some  interesting feed backs on this   discussion.
 . The   point was, that  if  NIRS/ MOXY is a direct feedback  and we see  at the end of  a  very hard  load  the picture  as explained, meaning, that we take O2  form the storage local area  and that the CO2  will shift O2  disscurve to the right, than in a lag  time  we  should see a   drop in VO2  intake  in the same workout  with the expected   lag time. meaning we have a decrease in VO2   in this situation.
 This is a great  feedback  and  yes   you will see  that .
 This is one of the reasons   why we like the  trend information  from MOXY.
Here  an independent study  form a group  without MOXY  and  using our  old  classical    equipment  like VO2. 

Decrease in Oxygen Uptake at the End of a

High-Intensity Submaximal Running in Humans

S. Perrey1

R. Candau2

G. Y. Millet3

F. Borrani2

J. D. Rouillon1


1 Laboratoire des Sciences du Sport, UFR STAPS, Besanc¸ on, France

2 Laboratoire Sport, Sant>, D>veloppement, Montpellier, France

3 Groupe Analyse du Mouvement, UFR STAPS, Dijon, France

Corresponding Author

Dr. S. Perrey · Facult> des sciences du sport · UPRES EA 2991 · 700 av du pic saint loup ·

34090 Montpellier · France ·

Phone: +33 04 67 41 57 54 · Fax: +33 04 67 41 57 50 · E-Mail:

Accepted after revision: October 6, 2001


Int J Sports Med 2002; 23: 298–304 H Georg Thieme Verlag Stuttgart · New York · ISSN 0172-4622


The purpose of the present study was to examine oxygen consumption

(V˙ O2) kinetics during severe-intensity running exercise

through a four-phase model that considered a decrease in

O2 at the end of the exercise in light of previous research in

which this decrease was only noticed. After determination of

maximal oxygen consumption (V˙ O2max), thirteen highly trained

males performed a square-wave running to exhaustion at ~95%

ofV˙ O2max on a level treadmill.V˙ O2 and ventilatory gas exchange

variables were determined breath-by-breath. Computerised

non-linear regression techniques incorporating exponential and

linear terms were used to describe V˙ O2 and ventilatory gas exchange

variable responses. In contrast with the classical 3-component

model that describes the increase in V˙ O2 for severe-intensity

exercise, we observed a 4th phase characterised by a significant

decrease in V˙ O2 before exhaustion (slope of V˙ O2-time

relationship significantly different from a zero value, p < 0.01) in

7 out of 13 subjects. Following a time delay of 31 O 44 s after the

decrease inV˙ O2, a significant decrease of minute ventilation (V˙ E)

was present for 6 of the 7 subjects (p < 0.02). During the exercise

for the subjects who decreasedV˙ E, a reduction of 288 O 169 ml in

tidal volume was associated with an increase of 10.2 O 2.4 min–1

in breathing frequency. These data suggest that the respiratory

system might be stressed more for some endurance-trained athletes.
My  add on :What they  forget  to look as well is , that the reduction in TV  increases the  dead space  and as  such  it is much  more difficult  to get rid  of CO2. The lag time  they observed is the time needed  for   balance  of  gas exchange.

The specific link between reducedV˙ O2 and reducedV˙ E remains

to be explored.

Key words

Oxygen uptake kinetics ·V˙ O2 slow component · breathing pattern

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