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Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #1 
Happy new year to all of  you.
 I am  a lot behind  with answering  many many mails  I got  over the last few  weeks. Sorry  will  pick up one by one  and try  to give you  feed backs.
 Sometimes  good once  often  more questions.
 I am running behind  here as well.
  So  we had  one great summary  from Nkrause . ( can't remember n what topic   so I  try to pick up the   answer, resp  some more feedback on here.
  As I can recall his  summary  was  short and sweat :
 Something like that.
. Cooling  down  or  active movement  in between intervals  would  take energy   and we  take the energy  by using lactate ()  great energy source).
 As  such we  would take energy away, who  either  could be stored  or  could be used  for  more vital organs  who use  lactate  as a  source  of energy in desperate   situation.
  So  it  does not make sense to cool down  from . an energy point of view.
 Goal is to balance pH  and   therefor  CO2  levels    to be able to have decent normal  situations in the muscle cells  to be ready  for the next load.

My  add on was, that the drop in lactate  during active recovery  is not a sign of  good recovery or good col down  but rather a sign of  the use  of lactate as an energy source, and as  such   cool down lactates     do  tell nothing really about recovery.

The question  I often get back is than:
 Why  in top athletes  lactate drops  faster than in beginner. Is this not a sign of faster recovery ?
 Now you answer this  question  why in top athletes  lactate drops  faster.


Now the risky part is, that people now take  a respiration   device   to  try  to get ride of the CO2    without  using  lactate.
  Problem.
 Your respiratory device needs the ability  to allow you to breath  so that you actually move towards hypocapnia  or  hyper ventilation but you have to avoid  getting dizzy  due to  hyperventilation.
 Meaning, that I need a  certain amount of time to balance the CO2  and therefor I have to be able to breath a certain amount of time   slightly in the hypocapnic  stage  so I  can do that without  getting really  too hypocapnic..
  Second  part is the  question what  or how  I have to  "cool " down    for respiration but as well for cardiac  systems  and not just looking at the metabolic reactions.
 Here 2  article  who  stress this point.
  But first  active passive recovery as a  review  followed  y  resp  and cardiac  view.

Abstract
CHOI, D., K. J. COLE, B. H. GOODPASTER, W. J. FINK, and D. L. COSTILL. Effect of passive and active recovery on the re synthesis of muscle glycogen. Med. Sci. Sports Exerc., Vol. 26, No. 8, pp. 992-996, 1994. The purpose of this investigation was to determine the effect of passive and active recovery on the re synthesis of muscle glycogen after high-intensity cycle crgometer exercise in untrained subjects. In a cross-over design, six college-aged males performed three, 1-min exercise bouts at approximately 130% VO2max with a 4-min rest period between each work bout. The exercise protocol for each trial was identical, while the recovery following exercise was either active (30 min at 40-50% VO2max, 30-min seated rest) or passive (60-min seated rest). Initial muscle glycogen values averaged 144.2 +/- 3.8 mmol-kg-1 w.w. for the active trial and 158.7 +/- 8.0 mmol-kg1 w.w. for the passive trial. Corresponding immediate post exercise glycogen contents were 97.7 +/- 5.4 and 106.8 +/- 4.7 mmol-kg-1 w.w., respectively. These differences between treatments were not significant. However, mean muscle glycogen after 60 min of passive recovery increased 15.0 +/- 4.9 mmol-kg-1 w.w., whereas it decreased 6.3 +/- 3.7 mmol-kg-1 w.w., following the 60 min active recovery protocol (P < 0.05). Also, the decrease in blood lactate concentration during active recovery was greater than during passive recovery and significantly different at 10 and 30 min of the recovery period (P < 0.05).
These data suggest that the use of passive recovery following intense exercise results in a greater amount of muscle glycogen re synthesis than active recovery over the same duration


Using a specific  respiratory device  could solve the problem of the H +  resp  CO2  dys balance  .

What about  cool  down of the respiratory system.

Effects of 'cool-down' during exercise recovery on cardiopulmonary systems in patients with coronary artery disease.
Koyama Y, Koike A, Yajima T, Kano H, Marumo F, Hiroe M.

The Second Department of Internal Medicine, Tokyo Medical and Dental University, Japan.

The effects of 'cool-down' during exercise recovery on cardiovascular and respiratory systems have not been fully clarified. The recovery of respiratory gasses was compared in cardiac patients after maximal exercise during which subjects either performed a cool-down or rested. Twenty-one patients (61+/-10 years) with coronary artery disease performed 2 symptom-limited incremental exercise tests on a cycle ergometer: one with a cool-down and the other without during recovery from the maximal exercise test. Expired gasses were analyzed on a breath-by-breath basis throughout the test and for 6min of recovery. Without a cool-down, the ventilatory equivalent for O2 (VE/O2) increased dramatically during recovery compared with the resting values or those of peak exercise: 44.5+/-7.7 at rest, 44.0+/-10.6 at peak exercise and 63.3+/-14.5 after 2min of recovery. End-tidal PO2 (P(ET)O2) also increased significantly during recovery. However, the overshoot phenomenon of these variables was attenuated when cool-down exercise was performed during recovery. The high ratio of VE/VO2 reflects ventilation perfusion (VA/Q) unevenness and P(ET)O2 is an index of arterial PO2.
Thus, it is suggested that cool-down exercise during recovery after maximal exercise testing provides beneficial effects on the respiratory system by decreasing the VA/Q

Now  when  we know , that a  big part of the EPOC  is due to O2  use  from the respiratopry system, which is NOT in a O2  Deficit  but  needs  post exercise  O2   to keep going in an elevated  activity, till  acid  based  levels  are back to normal.

So  question agan is  whether the out of balance  acid  situation like H +  but as well other   situations like Ca++  and P keep the bodies activity above  start VO2  levels.
  Again not as a re-pay  of O2 deficit, but  due to a  re- establishment of  homeostasis.
  If  we  can speed up this by  controlled respiratory interventions  either increase CO2  or decrease CO2  levels  we  can speed up recovery time  but as well gain  rebuilding time.


Now  what about the cardiac system ?

OL.13th;NO.;PAGE.89-92(1998)
Figure&Table&Reference;FIG.1, REF.14
Pub. Country;Japan
Language;Japanese
Abstract;To examine the influence of cool-down exercise on cardiac recovery after moderate exercise, we measured heart rate(HR), stroke volume(SV), and cardiac output(CO) in five young, healthy untrained male subjects in a sitting position before, during, and after 10min of exercise corresponding to 68% of maximal oxygen uptake (VO2, max). The recovery from exercise was evaluated separately under the following two conditions: complete rest for 10min(passive recovery); and cycling at 28% VO2, max for 7min followed by 3min of rest(partially active recovery). HR during passive recovery decreased rapidly during the first 120s and decreased gradually thereafter. A similar decrease in HR was observed during the first 7min of the partially active recovery condition. However, after 7min of cycling, its HR decreased remarkably, resulting in a lower average HR at rest following active recovery compared to that following passive recovery. SV during active recovery was maintained at a level similar to that during the prior heavier exercise. In contrast, SV during passive recovery decreased to a level significantly below the pre-exercise level. CO during active recovery was higher than that during passive recovery. We conclude that cool-down exercise during recovery from moderate exercise enhances the rate of recovery of HR and facilitates venous return, resulting in the protection against the post-exercise pooling of venous blood. (author abst.)

  Add  on as quesrtion.
  Respiration  with deep controlled  respiration creates  a  blood return to the heart.

MOXY  will give you feedback over tHb  on potential pooling  . So you can    use gravity  and respiration to avoid this and  relax the cardiac system.
  SV in standing is  lower than in prone position or on the back.



Jiri Dostal

Development Team Member
Registered:
Posts: 51
 #2 
Attached is our poster we had in ACSM congress in 2013.
Short summary - lactate removal has significat interpersonal variability, with no correlation to VO2max and other measured parameter in the test! This is in contrary what was published before in a small groups of 5-10 athletes.

We have repeated these tests this year, with the same group of athletes, and guess what.... the trends for individual athletes were the same. We do not have the numbers calculated yet, but the slow removal remained slow, and fast guy keeps fast speed of removal.

Jiri

 
Attached Files
pdf PosterPresentations.com-36x72-Template-V4.pdf (627.98 KB, 50 views)

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #3 
Thanks so much this is a great paper.
 Here a  thought.
 Repeat  with at least one   person with a clear  trend in lactate removal the same load  and or test but let him breath very different  in the after load.
  . Than train the same person  for  8 - 12  weeks  with Spiro Tiger   ( I can help with setting up the program. I would need a  simple " classical  VO2  max test  and form this test the VE  and RF information  only.    Than  we repeat the same load  and  check the  change in possible lactate removal.. In many cases  you will see  a possible change in the lactate removal  immediately  if you load  all the same people but force them to do very different respiratory after loads   not just let them breath.   There are different options on what you can do..  Thanks again  and if you do one or the other   game  as I suggested please share the info and trends.
 Her a another hint to play with . Push  an athlete to the so called ( but not existing MAXLASS  ) intensity.
 Now keep a MOXY on his leg  and you should have a relative stable SmO2.  Now   let this be stable  for 5 min.    no specific respiration. After  5 min let the person breath double as  fast RF as he did  before  for  if possible 5 min look at  SmO2  trend  and test lactate , than go back to  " normal  and test again after 5 min   and than go to  half the speed  respiration and test  and look always SmO2  and  lactate trend.  Think O2  disscurve shifting.  Cheers Juerg
Jiri Dostal

Development Team Member
Registered:
Posts: 51
 #4 
Thanks Juerg! Will do both ideas. I will talk to the team general manager and we will arrange someting. It will just take some time, probably during  the Olympic Games break.
I will send you the results from the tests once I know, who will be the one to be tested.

Thx a lot

J.
Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #5 

Update.

Jiri  is super busy  sending me great results  form some preliminary testing. Once  we understand  better what we  do    we  most likely will give you much more ideas. I already used some ideas  from his great work  on this forum.
 Problem as usual  that  we get many many great  info's  who create  many interesting questions.  I will try to discuss them  with  Jiri's group  and see, what we  get out of it.
  I like  to add some more   fuel to the fire of  " cooling down"
  I lie to show  you some  small abstracts  from studies  arguing  for  " cooling  down"  and like to add some questions to it.
 The regular reader will be able to understand the questions, some  may be  confused, that  we have the question,  whether it is  smart to get rid  of  lactic  acid, when it is not there in the first place  and   if  we only have lactate  there, , and we accept the  new  ideas on lactate ( since 1985  +- ) , why  we still use this as  an argument  for cooling down. ????



One study published in Medicine & Science in Sports and Exercise (1) found that active recovery immediately after the event encourages recovery and reduces muscle lactate levels faster than complete rest. After hard intervals, one group rested completely while a second group exercised at 30 percent intensity between intervals. The active group reduced blood lactate levels faster and could achieve a higher power output throughout the workout.

A third study found active recovery encouraged lactic acid removal and and helped speed recovery. (3) The general theory is that low-intensity activity assists blood circulation which, in turn, helps remove lactic acid from the muscle. Low-intensity active recovery appears to significantly reduce accumulated blood lactate and speed muscle recovery. However, all agree that more study is necessary to establish a clear answer regarding the best way to recover from activity.

How  about the possibility , that  “ lactic acid “  was  faster  lowered, because they may have used  it  as a fuel  as it may be the most efficient  way  to  maintain ATP levels  and in the same time  stop using   fuel  which is still stored.

  How about the option, that  active recovery may have maintained  the delivery systems  liek CO  and VE on a higher level, which needs   as well energy  and  lactate  may be a good  energy source  for this system.

  And how about the possibility that the   activity after  a load kept the respiration on a higher level  and therefore  helped  to balance  CO2 levels  faster  and easier, than   doing nothing.

  How  about the option to try to keep the lactate for refuelling by  NOT  moving but on the other hand  keep  VE    and CO  up over respiration  for H +   CO2 balance. 

  This is just a question. ???

 

 

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