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Development Team Member
Posts: 1,501
Now  , when we look at the nice difference in  this  2 graphs  than  you an see, that we  can use  this  in a very early stage in a  " warm up "  . This isi what we discussed far back  one  with Daniele  and  how  to adjust  daily  the  workout idea, deepening on your goal  you ave set. 

 Now  you have 2  options.
  1.The practical coaching  option to find individual  graphs  for you or  you  client.
2. Discuss  the  situation and graphs    theoretically through to find   possible limiters  and compensators. This option  is  fun and fascinating, but  needs a lot  of physiological back grounds  and connection  from different  systems.

 I prefer  option one  in coaching and when working  with athletes  and or clients.

 So here how option one is done.
 In the  case above Rynic  did  two different   workouts  or  was in 2 different physical/ physiological  conditions..
 The result  you see above.
Now you like to establish a  "  personal " finger print"  on how  your  NIRS graphs looks , depending on what system was  or is overlapped,  so you can decide  to  give it more recovery time  or keep it   overloaded or what ever you plan.

So  as a cook book. 
 a ) you establish  the individual  graph ( reaction  [wink]    when  respiration is overloaded.
b)  you establish  the graph  you  know  cardiac is  overloaded
 c) you establish the graph   after you overloaded a   muscle group in your  sport  so in cycling for example your legs.

Now  that is  easy  as  you or your  coach is doing this  eveyr day  wen you pan a  training  or workout.
 So  simply overload  your respiration  only  an than assess  and you see how  your  NIRS graphs looks.  Than on an other day  overload  your muscular systems  only and see how  your graph  shows  up.  Or  overload  your  cardiac systems  only and see the  same.
 The key is  not  to overload  all systems  as  you than have no clear picture. So one system  at a time  and avoid  the overload  of  compensators.  You as well an do this  with coordination  and  what ever  you believe will show up in a  specific feedback very early in an assessment.

Once  you than have the graph as  above  you  than  go  and  make  an interpretation. We will do this  in this situation later  with his  2  datas.   BUT  the  practical options as  explained above is much easier as it needs  less physiological combination  it is straight forward.


Development Team Member
Posts: 369
Juerg, thanks for the insight.

In creating individual graphs per person, even though you say it is easy i am not actually sure how you would overload cardio system without respiratory and respiratory overload without cardio involvement? Is there any form of direction you could give here. Would the workouts to overload a specific system be cycling based workout or off the bike?

No problem if you are not able to answer due to venturing into training discussion.



Development Team Member
Posts: 1,501
hmm not  sure  , whether I understand  BUT . if  you  bike   you  eitehr  simply go out  and biek  wiht feeling  and hope you get better.
 You have a training plan  which means  you  or  your coach  have a  goal ion what they like to achieve not just in being better  by pushing  more wattage but  by improving  for exampel  your muscular  strength or your    bike efficiency  or  your  bike specific  respiratory  demand in upright  or in aero position  or  your  cardiac  performance by increasing  cardiac out  put. At least that what i learned  40 years back  at the university. Training  has a target  you  plan it you assess  and you readjust. So  I assume  for cycling  the task is  easy  as there  are many training books  out there on how  to improve.
I assume that's  why people  pay  for a coach or a training plan as they hope to target  their limitation to improve. So look at training peaks  and other great site4s  like golden cheetah  an  incredible great  source  for  cycling and tracking performance and progress . Than  use  their ideas on   muscular loads,  or respiratory loads  and so on  and see the  reactions in  performance  and physiological  reactions.
 Many great  cycling books  and bible s out there to  use  as guide  for training ideas  and therefor  assessment to  track  reactions after the load.

Development Team Member
Posts: 1,501
next up  will be a  theoretical  interpretation of the  2  great  graphs  we have. BUT  we need all your brains. o  I will ask  a lot  and we see   what possible answers  we can get.

Development Team Member
Posts: 369
Juerg on the previous point, the problem is that many of the traditional training ideas stress multiple systems at the same time. For example i am not aware of workouts or guides training bibles that clearly explain how to stress or overload respiratory system without stressing cardiac system or vice versa. So you might see a reaction the next day but you still don't know what was overloaded. Isolating muscular overload i think is maybe easier.

Thanks for the insights so far, looking forward to next part of the discussion.

Development Team Member
Posts: 1,501
hhmm   that is interesting. If  we do a  tennis  training program we  plan for example  to do a  specific  idea like  service  and  avoid  an overload of the cardiac system. If we plan to  do a  cross country training on skis  we may plan  to do just a cardiac  overload  with some technical skills  versus  for example a  leg  workout  with muscular overload. If we do a  swimming workout  we may plan a respiratory  overload   for  desaturation. If we  do an ice hockey  circuit on  the ice  we may have a respiratory overload  station  followed  by  muscular  leg overload  and so on.
 if we do a rowing workout  we may like to work on stroke rates  as high as possible  with a minimal  load on a cardiac  reactions.
 That  same is possible in cycling and there  are many great cycling coaches   out there  who should  be able to give you  some   feedbacks on that. 

Development Team Member
Posts: 1,501
Okay let's  have  some fun thoughts on the theoretical  information we have from this  2  workouts.
Here  the  tHb  once more  where I like to start.

fat  non fat  tHb overlapp.jpg

bove the  2  workouts. One  was " classified  as  ' Fatigued  "  and one as  less fatigued  or   better recovered.
Now  tHb is  an indirect feedback on Blood  volume  and some    say  about  blood  flow.
 tHb  can be influenced  from  physical  forces like  muscular  contraction  force  (  compression )  or  from  gravity  so position of an extremity, from outside forces ( pressure ) like  compression  socks  on  stockings  or   from  circular  fixations on an extremity as we see in some NIRS  devices.
 We  have  systemic reactions like vasoconstriction in the  often discussed  BP  protection or  dilatation  due to energy demand  or  due to CO2  levels  or  the inside   - outside  fight between muscular  compression and  cardiac out pout pressure.
So  let's  take the first  0 - 600  section.
We have the now  common feedback,  that  when we start " cold " we have a  delay of  
the  delivery  team   CO  and VE  and therefor  the   battle between  muscular contraction  force  tHb  down  and  CO  force. tHB  up  is    for the moment towards  the muscle force. Now  whether  we have a fatigued  or a  rested situation, the  same  wattage  will ask  for a very similar contraction force. So  we can assume  ( always  exceptions )  that we may recruit  similar amount of motor units.  ( Now   again  exception  if we have sever  muscular fatigue )
 Now  similar   muscular   pressure  may create a similar  drop in tHb.
 Than  the  CO reaction     may be  similar as well so increase in CO  ( HR x  SV )  will create a counter  pressure  so tHb  can increase.
This is the case  when we have a similar  CO  due to similar  HR  and similar  SV

  0 - 600 thb overlapp.jpg

f the  cardiac  output  reacts   better and faster and high  ( HR  and SV )  than we  may see a faster increase in tHB.
Now  let's  see what the  HR  did  as a  small window  for CO

monfat fat  HR.jpg 
What  do you think ?  Now look again the full  graph.

fat  non fat  tHb overlapp and circles.jpg 

Look the  difference  between HR in the different loads  and  than the tHB  difference  . What  can you see ?

 Now   the biggest difference is the reaction in the one min rest.
 In one  case we see a  very nice increase in tHb  and in the other little increase  actually an initial  drop.

see a closer look  in  one  section.

thb one rest  section.jpg

hat  creates  the  tHb reaction  in the  1 min rest   what could be the cause of this.?
  So lets  stop here  with  a  thought.
 1 What may be  the limiter in one case  and if   this is the limiter  how  would  SmO2  react  accordingly to the   job  of  the limiter.?


Development Team Member
Posts: 178
Hi Ryan

A possibility to stress the respiratory system without as much stress on the cardiac system may be to train with an 'Elevation training Mask', It is supposed to simulate altitude training but I read somewhere that is really just restricts the volume of air you can breath in so is basically a version of breathing resistance training. Not sure as I have never used it myself.

As for how to stress the cardiac system without stressing the respiratory system I am not sure.

Development Team Member
Posts: 1,501
Elevation training Mask',  it will actually  stress the cardiac  system very hard and you are  limited on time as well. 

Development Team Member
Posts: 217
Spirotiger should be able to stress the respiratory system with minimal influence on CO.
Or waterboarding .....

To juerg question: PB regulation on the fatigued day graph is not as efficient. Maybe reduced blood volume or HR contractability or high blood flow resistance.
SMO2 will increase during rest period but the slope of this increase is reduced. If respiratory is OK then SMO2 will rise as soon as the muscular load is reduced

Development Team Member
Posts: 1,501
Bobby  good  feedback.
 So  we see in tHb  that one  day  the  ability  to actually increase tHb was reduced, in fact   in the one minute  rest, where we  would expect  that tHb  goes up  due to  still high CO  and VE  ( lag time )  we see an actual drop in  tHb. So   the   CG  does not allow a  vasodilatation win  due to muscle compression  gone. What  does the  CG  tries  to protect.
 Now next  question I  always  ask  is ,  doe we have   between this  2   workouts a information towards   delivery limitation on  one  day  and not a delivery limitation. So by the same wattage if we have a delivery limitation we still would need   the  similar  amount  of  O2.
see below , Which green SmO2  belongs to what  tHb  graph.

fat  non fat  smo2 overlapp.jpg

ow three main  question on  delivery limitation ( if  it is a delivery limitation on one  day :
 respiration limitation
 Cardiac   limitation.
muscular  vascular limitation.

Next  we  ask : How  would we expect a  respiration limitation to look like 
 Remember 2  options  a) an  actual  metaboreflex  where  locomotor  muscle  steel O2  from the vital  organs
 or an actual  respiration limitation due to a limited ability   of  the VE  volume.

If  it is  a cardiac limitation  so  CO   is too week  to maintain the basic   central BP  what  would we see  and  from CO  what  small feedback  do we have   (  HR ) 
 What will the HR show  to many surprises  in the one minute  rest period ?


Development Team Member
Posts: 369
Juerg thanks, i am enjoying the case particularly because one of the areas i find hard in the interpretations is differentiating delivery side limiters.

I have a few questions/requests

You said in relation to the respiratory limitation "  actual  metaboreflex  where locomotor  muscle  steel O2  from the vital  organs  or an actual  respiration limitation due to a limited ability   of  the VE  volume." I am not sure that i understand metaboreflexes 100%. Could you confirm the following is correct or make the corrections:
For a respiratory metaboreflex, the respiratory muscle is fatigued, the result is that there is vasoconstriction in other parts of the body to direct bloodflow to the lungs. When the compression is released on a priority muscle in activity (e.g. at the start of a 1 min break),  there is a potential BP problem and so there will be vasoconstriction? 

Am i correct that this is different to the situation when priority muscles "steal" blood from non-priority muscles - that is something else not referred to as a metaboreflex?

If the above is correct, then i assume that a fatigued respiratory system is likely to show up as vasoconstriction type reactions? Where the respiration is a limited ability of VE volume, then i assume that what we would see is a build up of C02 (tHB up) and right shift of the dissociation curve)?

Weak cardiac output that is not strong enough to maintain BP, i would imagine that we would also see a vasoconstriction reaction?

The question then becomes how do we seperate this from respiratory metaboreflex reactions?

I am assuming that a muscular vascular limitation will present as an occlusion? In this case, the tHb drop on rest will be immediate, whereas a vasoconstriction/BP related reaction will have a lag time? More or less how many seconds (or range of seconds) would a vasoconstriction reaction take vs occlusion?

Please, please, please could you post a picture (Sm02 and THb) of a case using only 1 Moxy and HR on the priority muscle, for each situation:
- Respiratory limitation (metaboreflex)
- Respiratory limitation (VE volume)
- Cardiac limitation
- Muscular vascular limitation

Hopefully it will help me (and others) to finally differentiate each of these, particularly metaboreflex vs cardiac vs muscular vascular limitation.


Development Team Member
Posts: 1,501
good  point  and here a  start

The as always  fascinating   part is  the  years back  where this  was discussed and the  lag time we have in established  circles  to look at least this new ideas and critically moved  them into classical ideas  or  delete  some classical ideas as they have a hard  time to still fit in new directions.

Robin Hood for the
lungs? A respiratory metaboreflex that ‘steals’ blood flow from locomotor muscles


In this issue of The Journal of Physiology, Dempsey and colleagues (Sheel et al. 2001) contribute another key chapter in their ongoing series of elegant investigations on novel interactions involving the respiratory muscles, autonomic nervous system and cardiovascular regulation in humans. Earlier, they demonstrated that manipulation of the work of breathing during maximal exercise resulted in marked changes in locomotor muscle blood flow, cardiac output and both whole-body and active limb oxygen uptake (Harms et al. 19971998). They also established the remarkable metabolic costs of supporting respiratory muscle function during maximal exercise, requiring up to 16 % of the cardiac output (Harms et al. 1998). Importantly, the reduced locomotor muscle blood flow and vascular conductance in the elevated work of breathing condition was associated with augmented noradrenaline (norepinephrine) spillover from the active limbs, suggesting enhanced sympathetic vasoconstriction (Harms et al. 1997). These physiological effects of the work of breathing have important functional consequences, as demonstrated by an ∼15 % improvement in endurance performance with respiratory muscle unloading (Harms et al. 2000).

The next generation of experiments attempted to establish the mechanisms underlying these fascinating physiological connections. In a paper recently published in this journal (St Croix et al. 2000), high-resistance, prolonged duty cycle breathing at rest, resulting in respiratory muscle fatigue, evoked an increase in leg muscle sympathetic nerve activity (MSNA) that was independent of central respiratory motor output, indicating a reflex origin. Moreover, the temporal nature of the response (MSNA was unchanged during the initial 1–2 min of the fatiguing task but increased progressively thereafter) was characteristic of a slower-developing muscle metaboreflex (chemoreflex), rather than a mechanoreflex stimulated by force development (which would be expected to evoke sympathoexcitation at the start of contractions).

The present article by Sheel et al. (2001) represents a critical extension of this work by establishing that this presumed respiratory muscle-limb reflex has the ability, at least under resting conditions, to reduce significantly limb blood flow and vascular conductance. Thus, together with previous observations (St Croix et al. 2000), the present contribution provides compelling evidence for the existence of a metaboreflex, with its origin in the respiratory muscles, that can modulate limb perfusion via stimulation of sympathetic nervous system vasoconstrictor neurones (Fig. 1).

Figure 1
Respiratory muscle ‘metaboreflex’

Teleologically, this reflex may have as its fundamental goal the protection of oxygen delivery to the respiratory muscles, thus ensuring the ability to maintain pulmonary ventilation, proper regulation of arterial blood gases and pH and overall organismic homeostasis. Presumably, as the ‘vital organ’ responsible for supporting pulmonary function, perfusion of the respiratory muscles, particularly during physiological states in which there is competition for cardiac output such as heavy submaximal and maximal exercise, has priority over the locomotor muscles. This subservience of active limb blood flow may be similar to that previously established for the arterial baroreflex during large-muscle dynamic exercise (Rowell, 1997). Specifically, under conditions in which wide-spread vasodilatation has occurred, thus threatening the maintenance of systemic vascular resistance and arterial blood pressure, arterial baroreflex deactivation (unloading) will produce a strong reflex sympathetic vasoconstriction targeted, at least in part, at the active limbs. This vasoconstrictor drive can be sufficiently strong as to produce vasoconstriction in working locomotor muscles, thus ensuring the maintenance of arterial perfusion pressure.

As with any developing drama, several unanswered questions remain. For example what is the influence, if any, of this reflex during normal in vivo exercise? Can the reflex explain the physiological consequences of the work of breathing in limiting maximal aerobic capacity (maximal oxygen uptake) and human performance? Is the reflex active during moderate, submaximal aerobic exercise performed for health and fitness purposes in non-athletic adults? If so, at what intensity of exercise, level of pulmonary ventilation, etc., is the reflex engaged? Perhaps the reflex is tonically active in patients with clinical disorders associated with chronic elevations in the work of breathing (e.g. congestive heart failure or chronic obstructive lung disease)? Can the conditions under which this metaboreflex is triggered be modified by training of the respiratory muscles? Finally, does the ‘stealing’ work both ways? That is, can active limb metaboreflexes act to redirect blood flow away from respiratory muscles to the locomotor muscles, thus potentially compromising pulmonary function during heavy submaximal and maximal exercise?

As with our favourite page-turning suspense novel, we look forward to the answers to these and other questions in the next intriguing instalment of this series.


Development Team Member
Posts: 369
Juerg thanks i had read that abstraxt before om another tgread but was not sure if i was understanding it correctly.

Development Team Member
Posts: 1,501

I  can  as  so often explained  not  show a cookbook  but  what I will keep trying is  to explain how  the different systems  are often closely interacting  and than NIRS interpretations  can  help  to sort this  out.
 Again the easiest  way is to   do a  workout  (training) where you plan  specific  overload and see how  you react. In  your case of the 2  workouts
You can see that one  was a great example of a  " fatigued"  or not yet recovered cardiac system.  I will show over the weekend more examples    and  I have some fun  once  form different cross country ski assessment  with multiple  reactions in the same athlete to show  how  this  interacts.
it as well shows  nicely  the limitation when we use  one  single MOXY only.

 please could you post a picture (Sm02 and THb) of a case using only 1 Moxy and HR on the priority muscle, for each situation:
- Respiratory limitation (metaboreflex)
Respiratory  and cardiac  limitation , where we  create reflex  defensive  reactions
 ( respiration  with  a  vasoconstriction  to limit blood flow  to the  extremity muscles  to   protect O2  delivery  to teh respiratory muscles  or  cardiac limitation like  BP  protection   or more  will reduce motor unit recruitment  and with this  the O2  demand

Now  the   problem is that  assessments  and as such tests  are "Brainless",
 meaning  that we  force a  certain performance on a  person  and  eitehr he  can do it or he  quits. there is no such thing like simply keep running   as fats as possible with the current available energy  delivery  ability, like we  woudl  do in a survival mode. I  do   all my assessments  without performance  load  fixed  I  let   clients  do the  steps  and  they drop not know  what they push and I see for exampel on a bike, that they   still push  "hard " but really drop performance steady  they  just  subjectively believe  they maintain performance.  On a tread, mill I have  anon motorized  treadmill so they  can keep  running but  may actually slow  down , but think they are still going all out.

Now  the second  part is:
  You see changes   during the load  if  the performance can not  be maintained or  we see reaction   in the 1 min rest  or  after  a load  when we get rid  of the muscular O2  demand.

- Respiratory limitation (VE volume)
Respiratory limitation can be without  problem of  O2  delivery to  the repsiratroy muscles  like in a metaboreflex  but you simply demand a higher VE  from your  respiration due t o a very high CO2  production, but you  are  limited  with the volume  due to  chest expansion  for example. Easy  to produce  on a bike   .Sit upright  and than go in an aero position  and you  have the difference. Now     do this in different intensities and you can see  by what intensity  upright  still allow  you to get rid  of CO2  and  when  you start to create a performance problem  due to  the reduction in VE  due to aero positioning. Thna  you  look at live  NIRS  reactions on a priority  muscle and  or on a  non priority muscles  and you have your individual   finger print on this problem.

Cardiac limitation
- Muscular vascular limitation  More later as  I just have to start  working here  with clients
 Will show  some fun examples  for  training  on  interpretation.

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