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Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #1 
I got a  hint  from a  reader to  try to start a separate    feedback on respiration an training  as it is hard  to find in the tour   de France  ideas.
 So here  where we stand  starting from that discussion:
 

Endurance training of respiratory muscles improves cycling performance in fit young cyclists.

Author information

Abstract

BACKGROUND:

Whether or not isolated endurance training of the respiratory muscles improves whole-body endurance exercise performance is controversial, with some studies reporting enhancements of 50% or more, and others reporting no change. Twenty fit (VO2 max 56.0 ml/kg/min), experienced cyclists were randomly assigned to three groups. The experimental group (n = 10) trained their respiratory muscles via 20, 45 min sessions of hyperpnea. The placebo group (n = 4) underwent "sham" training (20, 5 min sessions), and the control group (n = 6) did no training.

RESULTS:

After training, the experimental group increased their respiratory muscle endurance capacity by 12%. Performance on a bicycle time trial test designed to last about 40 min improved by 4.7% (9 of 10 subjects showed improvement). There were no test-re-test improvements in either respiratory muscle or bicycle exercise endurance performance in the placebo group, nor in the control group. After training, the experimental group had significantly higher ventilatory output and VO2, and lower PCO2, during constant work-rate exercise; the placebo and control groups did not show these changes. The perceived respiratory effort was unchanged in spite of the higher ventilation rate after training.

CONCLUSIONS:

The results suggest that respiratory muscle endurance training improves cycling performance in fit, experienced cyclists. The relative hyperventilation with no change in respiratory effort sensations suggest that respiratory muscle training allows subjects to tolerate the higher exercise ventilatory response without more dyspnea. Whether or not this can explain the enhanced performance is unknown.





































































































































Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #2 
Yes there  are some  very intriguing ideas and studies  done, who   look  outside the BOX  when looking at cycling performance.
 One nice one was done  in Maastrich  NL  with the Rabobank  group some years back.
 In  short: They where looking  where there  still is a difference between professional  road cyclists  and the amateur  road cyclist.
 The test  all classical parameter  from VO2  max  and  CP  and so on  an still did not found a  clear  difference  , which may explain the   still clear  performance gap.
 Not  true  they found some intriguing reactions.

2. Breathing pattern

Once more, Lucia and colleagues are the only researchers that have studied differences in

breathing pattern between professional and elite amateur road cyclists (37). Breathing pattern

in endurance athletes refers to parameters such as respiratory minute ventilation (VE in l/min),

tidal volume (Vt), breathing frequency and the ventilatory equivalent for oxygen (and carbon

dioxide). Chapter 2.1 elaborates on the parameters VE, Vt and breathing frequency, followed

by the ventilatory equivalent for oxygen in chapter 2.2.

2.1 Minute ventilation, tidal volume and breathing frequency

In general, during incremental exercise, minute ventilation increases due to both an increase

in Vt and breathing frequency (46). At high exercise intensities, however, a tachypnoeic

breathing pattern develops, in such a way that the rise in minute ventilation is mainly caused

by an increase in breathing frequency, where tidal volume shows a plateau (27). On the

contrary, some research has shown that training may result in a larger tidal volume and a

lower breathing frequency, the so-called lack of a tachypnoeic shift (37).

The study by Lucia on differences in breathing pattern between professional and elite amateur

road cyclists (37) shows that minute ventilation is significantly higher in amateur cyclists at

absolute submaximal exercise intensities (300, 350 and 400 watt). However, when VE is

compared at the point where lactate starts to accumulate (where professionals had a

significantly higher power output), VE is significantly higher in professionals (44), suggesting

that this group has a greater ability to perform better at high intensities. Furthermore,

breathing frequency is significantly higher in amateur cyclists during submaximal and

maximal exercise intensity (37), suggesting that these riders exhibit a tachypnoeic shift at

high intensities. Also remarkable is the significantly lower tidal volume at maximal intensity

in the amateur cyclists, where these riders show a plateau in tidal volume (figure 3).

The differences in both Vt and breathing frequency cannot be attributed to anthropometric

factors, but are probably due to the more demanding years of training and competition, carried

out by the professionals. Lucia accounts the lack of tachypnoeic shift in the professional

cyclists to metabolic factors and to an attenuated mechanical feedback from the lungs and

 

the lungs for a longer time, resulting in a higher oxygen extraction from the inhaled air (46).

Thus, the higher breathing efficiency of professional cyclists could partly explain their higher

level of performance.

 The main problem  is  what  we  discuss so many time.
 Researcher  who do not know the history will find the same  result  again , or  make the same  wrong conclusions  as others  did many years back.
 This findings  are not new  at all. Dempsey / Boutellier/ Spengler  to name some of the great researchers in that field ,  documented  this many many years before.
 We, as a  small group ,  developped many years  back  the assessment ideas  where this is all involved,

 Se  below the section  of a  5/1/5  assessment looking just at respiration
Courtesy  of Andrea  and Cesare  from Ticino Switzerland

resp info ex.jpg 


Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #3 
Here  two practical daily  examples  on how  respiration is used  to achieve  some  physiological specific  stimulation's.

 . 1. Systemic  deoxygenation  to maintain  the  ability  for low SmO2  ( or  ability  to deoxygenate easier ) This   can be used  in high performance athletes  who can't  work  or load hard    for examples  the legs  due to injury  or due to  already overloaded    muscles  caused  by metabolic acidosis  workouts.
.
 Below a  deoxygention  workout  with minimal  load  as  an example systemic  deoxy all three.jpg 

 The load between 3000 - 3300  is a 5 min load  of 400 watts.
 The 2  loads  after 3600  are  loads  with  100 watts. The deoxygenation is created  over a respiratory  manipulation in this case.

 Now below the opposite. The goal is  to avoid deoxygenation  to create a hypoxic   situation due to   destroying an optimal bio availability of  oxygen. This  can be used  to stimulate different  reactions  for red blood cell  development  for example , but as  well for some  structural changes  in this athletes delivery  systems. The number in  green and black you see  are  EtCO2  numbers  in mmHg tested over a  capnometer.



tri  thb smo2  last three.jpg p[lus  co2.jpg

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #4 
respiration and performance.
 This is  a very interesting discussion, as there is a big split between the different researcher who  show that respiration can be a limitation and the   groups  who  argue  respiration is never a limitation.
 Once you start to integrate  NIRS / MOXY into your assessment tools  but even more fun into your live feedback workout  routine  you may  make  up your own mind.
 There is a  lot  of  fun experiments  you can play with  and see, how your body  or your athletes  or clients  body reacts, when you play  with thee respiration.
 The first  really easy  experiment is  simple  and straight for a ward.
 Mount a MOXY  on any muscle  on your body  like biceps  or what ever.
 Relax  and see what the resting SmO2   and  tHb  are.
 Than  breathe  for  a few minutes ( depending  how much you change  CO2  hypocapnic , meaning you  hyperventilate. Now  as in many activities you can train this so  you will have  not  always the same reactions  on SmO2  when you compare  with different people.
 What   may be the SmO2  reaction in this experiment.

 Now  go back to relaxed  respiration  for a few minutes    and than do the opposite. Breath hypercapnic so hold breath as long as possible  or breath super shallow  so  you  keep lot's  of  air in your  body.
 What    do you expect to see  in SmO2  trend.
  Last but not least  what causes this   often seen reactions ?


 Why  do we do this fun games. Well one reason is, that you see why  we fundamentally  differ  when we  look at results in many cases  compared to  the   assumptions  and  suggestion often offered  by the  research group.
  Here  an example  with respiration .
 

Eur J Appl Physiol. 2007 Dec;101(6):761-70. Epub 2007 Sep 15.

Inspiratory muscle training improves cycling time-trial performance and anaerobic work capacity but not critical power.

Johnson MA1, Sharpe GR, Brown PI.

Author information

Abstract

We examined whether inspiratory muscle training (IMT) improved cycling time-trial performance and changed the relationship between limit work (W (lim)) and limit time (T (lim)), which is described by the parameters critical power (CP) and anaerobic work capacity (AWC). Eighteen male cyclists were assigned to either a pressure-threshold IMT or sham hypoxic-training placebo (PLC) group. Prior to and following a 6 week intervention subjects completed a 25-km cycling time-trial and three constant-power tests to establish the W (lim)-T (lim) relationship. Constant-power tests were prescribed to elicit exercise intolerance within 3-10 (Ex1), 10-20 (Ex2), and 20-30 (Ex3) min. Maximal inspiratory mouth pressure increased by (mean +/- SD) 17.1 +/- 12.2% following IMT (P < 0.01) and was accompanied by a 2.66 +/- 2.51% improvement in 25-km time-trial performance (P < 0.05); there were no changes following PLC. Constant-power cycling endurance was unchanged following PLC, as was CP (pre vs. post: 249 +/- 32 vs. 250 +/- 32 W) and AWC (30.7 +/- 12.7 vs. 30.1 +/- 12.5 kJ). Following IMT Ex1 and Ex3 cycling endurance improved by 18.3 +/- 15.1 and 15.3 +/- 19.1% (P < 0.05), respectively, CP was unchanged (264 +/- 62 vs. 263 +/- 61 W), but AWC increased from 24.8 +/- 5.6 to 29.0 +/- 8.4 kJ (P < 0.05). In conclusion, these data provide novel evidence that improvements in constant-power and cycling time-trial performance following IMT in cyclists may be explained, in part, by an increase in AWC.

 

1. inspiratory muscle improves cycling time-trial
 
This is a great statement  and fits into our ideas, that  respiration can be a LIMITER  and as  such if that is the case and we  work on improving the limiter we  can improve  overall performance.

 Now  we  work on respiratory  specifc  workouts  since  over 15  years  and have the privilege  to  be very involved  with a  Swiss group  who  developed  the only  normocapnic hyperpnoea  training equipment.

Now  therefor  it is  easy to be biased  and argue that  who ever will train  with this will improve  performance.
 Reality is, that this is not  at all the case.
 If  your respiration is  not the LIMITER, than you will see  little  to no  improvement  and in fact , if your  respiration is  already  a compensator  and you add an additional overload  to the  system you may actually loose performance  as you overload the  compensator  and as  such loos this ability during a race  and or a  workout.
 The biggest problem is , as we often see, that many athletes  and coaches really do not know  what the limiter is  and as  such  loos the control on  who  will get stressed  and who may be overloaded  .

So there are cases we had, where the inspiratory  muscles  are  very well trained, but the VC( Vital capacity)  did  not improved  at all. Reason, to rigid  costovertebral joints  and thoracic  spine. The lungs  can only increase volume, when they are  able to increase    and for that the rip cage  has to be more flexible. So you can increase VC  by  doing a very specific  thoracic  and costovertebral ROM  training.
 This brings us  to the next  part  in the interpretation for the  above study.

2.  critical power (CP) and anaerobic work capacity (AWC

CP . We believe  and see, that  we can have different people  with the same or  basically the same CP  but  with very different reason  why the CP is where it is.
 You can have athletes  where the respiration as a limiter will create the  level of the CP. Than you can have athletes, where the muscle strength  combined  with the cardiac output create the same level in CP.

 In the athlete  with the respiratory limitation the  utilization ability ( better deoxygenating  so very low SmO2  will be the compensator.
 The  athlete with the  muscle strength limitation will create a  venous occlusion trend  and   if the cardiac system is  string / compensator  he  can create a CP  which is very different than when the cardiac  system is not that great  so the  venous occlusion  will create a drop in SV  due to less  back flow and lower pre load  and now the limitation  moves as well into the cardiac system.
  In case one ,respiratory limitation, the  training of IM  will most likely show a very nice progress.
 In the second case  less likely a progress  as a  specific  strength training  would make  more  sense.

Now the fact, that CP  did not changed  but the TT  end time change  shows, that there was  something developed, which allowed to  stay longer in the O2  delivery  stage.
 Now  improvement of  respiration  is not always a result of more O2  going in , but in many more cases  an improvement of  CO2  getting out.
 So I would argue , that not at all did Anaerobic  work rate improved  due to the IM training but rather that aerobic efficiency  got a boost  due to the ability to  get rid  of CO2  and  maintain much longer a balanced  H +  and as  such  longer the ability  to  use O2  . So O2  intake  and  CO  output where balanced  and the athlete stayed  normocapnic  and therefor  good  loading  and good  utilization as O2  Diss curve  stayed  neutral.

Would have been very easy  to look at this live  with NIRS  and  a capnometer  and  we  would have an answer  rather than a suggestion based on a  potential theory.

 Now that is the" annoying"  situation with  equipment you see result live. They may go against  what I like to believe  and sell  and as  such   are not very nice  to be used as we need than to change the theory to the  facts  , which is not always that easy to  do.

 Like the  situation in many athletes , where they in an anaerobic  test like the Wingate test  drop or utilize  O2   to a much lower level , than  they  are able to  do in a top aerobic test a VO2  max  test ????

Just a different view   to look at the same results.
Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #5 
Thanks  for this  mail  and I like to answer on here.
 Question was  on the buffering of  H +
 Kidney's versus respiration.
Both help but under  load the  blood flow in the  kidney's is not optimal  so less  help  and too slow  for a fast responds in trying to keep  H + balanced  as long as possible. Below  2 great  pics  who  show you  the connection.
 
 1. Blood  flow   under load  and rest and change in blood distribution   followed by a  a simple but great graph  on H  +  buffer    ideas.

blood redistribution at rest and exercising.jpg

buffer H =.jpg 





So in practical terms.
 If your  VE in any activity is 140 L/ min  an this is the   most you can move, than  you  have a limitation in cases, where the H +  production  and therefor the CO2   elimination   asks  for a  VE  of  160 L / min.

 The lack of respiratory ability  to get rid  of the  20 Liter will create a accumulation of CO2  and as  such a  shift of the O2  dissociation curve to the right. This will  improve  for a shorty moment O2  utilization 9 SmO2  drops, it may improve  for a short moment   blood flow  due to  vasodilatator  help of a  higher CO2  / tHb  up  but on the other side  will reduce the ability  to move  O2  from  lungs to the blood. ( EIAH  signs  with a lower SpO2  level.
 By training your respiratory system you are  able to  reach  160 L VE or more  and you  therefor  can stay longer in a  H + balance.
 So the key is  to simulate this situation  with respiratory  training  and one  nice  way  is normocapnic  ( Stable  CO2  in acceptable range) hyperpnoe. Extremely fast  and hard  respiration. ( not  to be confused  with hyper ventilation.)

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