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Juerg Feldmann

Fortiori Design LLC
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 #1 
In strength training but as well as in interval sports  and  in any  workout, where we  push high intensity the open question is   still:
 Active versus passive recovery in between  sets  and or loads.
 So here  some loud thinking

  1. Originally we all learned  and believed  and got educated that the reason of fatigue  is lactate or lactic acid.
Therefor we  where  testing  active versus passive recovery in  or  with the level of lactate disappearance.

So we  test  lactate  at the  start of  a load  , at the beginning of a load  and than  somewhere later. If the lactate  was lower  after an active intervention  we  agreed, that this is good  and  active  recovery  clearly drops the lactate level faster  and lower, than  passive recovery  ( doing nothing )

 Here  one  of many typical  studies   "proving " this point .
 

J Sports Sci Med. 2006 Mar 1;5(1):97-105. eCollection 2006.

Effects of Active Recovery on Lactate Concentration, Heart Rate and RPE in Climbing.

Draper N1, Bird EL, Coleman I, Hodgson C.

Author information

  • 1Centre for Adventure Science Research, University of Chichester , Chichester, West Sussex, UK.

Abstract

The performance advantage of active rather than passive recovery during subsequent trials for repeated high intensity short-term exercise is well documented. Research findings suggest that shorter periods of active recovery, than traditionally employed, can be prescribed and still retain performance benefits over passive recoveries in successive exercise trials. The aim of this study was to examine the benefits of a short duration active recovery for repeat climbing trials. Ten recreational climbers volunteered for the study. In this randomly assigned crossover study each climber completed five two-minute climbing trails before a two minute active or passive recovery. This was followed by a one and a half minute passive refocusing period for all climbers before the subsequent climbing trial. Heart rate was monitored continuously, RPE immediately post climbing and fingertip capillary blood samples collected during each refocusing phase. There was a non-significant difference between active and passive recoveries for heart rate during climbing. After the active phase climbers had higher heart rates than when following the passive recovery protocol, however, by the end of the refocusing phase the active recovery protocol led to lower heart rates than for the entirely passive recovery. There was a significant difference between active and passive recovery conditions in lactate concentration (F(1,9) = 18.79, p = 0.002) and RPE (F(1,9) = 6.51, p = 0.031). Lactate concentration and RPE were lower across all five climbing trials for the active recovery protocol. After active recovery climbers started the next trial with a lower arterial lactate concentration than for a passive recovery and indicated lower RPE scores at the end of each climb. The refocusing period following active recovery allowed climbers heart rates to return to a lower level at the start of the next climb than for the passive recovery condition. Key PointsThe three and half minute recovery strategy employed in this study did not allow sufficient time for complete recovery for either the active or passive conditions.The active condition appeared to allow for a more complete recovery after each climbing trial than did the passive recovery.Lactate concentrations and RPE were lower for the active recovery.The use of larger and or alternative muscle groups in the active recovery may benefit lactate clearance.The use of a refocusing passive phase at the end of the active recovery may provide a useful and more ecologically valid mechanism for recovery in an applied sporting context.

Now  they start very interesting
 : The performance advantage of active rather than passive recovery during subsequent trials for repeated high intensity short-term exercise is well documented. Research findings suggest that shorter periods of active recovery, than traditionally employed, can be prescribed and still retain performance benefits over passive recoveries in successive exercise trials.

Than they "prove " their point :
There was a significant difference between active and passive recovery conditions in lactate concentration (F(1,9) = 18.79, p = 0.002) and RPE (F(1,9) = 6.51, p = 0.031). Lactate concentration and RPE were lower across all five climbing trials for the active recovery protocol. After active recovery climbers started the next trial with a lower arterial lactate concentration than for a passive recovery and indicated lower RPE scores at the end of each climb


 and they  end  with the clear  statement :
active recovery may benefit lactate clearance.



Question:
 If  we  since the late 1980  know  and  may even accept the fact, that lactate is NOT the reson of  fatigue  and that in fact it may be a very beneficial  metabolic  product    for many   functions.  ( Buffer  of  H +  ) energy shuttle   and  refuelling of energy storage, than  why  would we use it    as a marker    and like to get rid of it by keep moving so we need more energy  and we will look for a very efficient  energy certainly in between  hard loads  and intervalls..


Question:
 Why  is lactate  lower  and   dissapears  faster   in an active    recovery versus a passive recovery ?.


  Why  do we  feel better when we  do an active recovery despite the fact that we  burn  a great energy source  for nothing really.
  How about the option, that when we  bang stop  we  stop or reduce drammatically the respiratroy  function and with it the cardiac  function.
  We  will therefor reduce VE  by a  few times  compared  to  active recovery.
  Perhaps the reson  why we feel better after  an all out  workout  or load is, because we have to  try  as  fast as possible to balance pH    and H +    dysbalance  and by  keeping moving we maintain a much higher VE  than when resting. Nevertheless  immediatly after an all out  load  we  often just do one thing .
Breathing.
Rowing-FISA-Junior-WRC-2010004536.jpg 

Should they not immediatly  row  to get rid  of the lactate ?
 What  do they do  there anyway ?

  Look at the  after lactate  trend.  They shoud feel great  and get much worse  5 - 10 min down the road (  down the boat )  as the lactate actually is getting much higher.

  lactate post.jpg 
See the timing.


 Question.  Is the  lower   pecieved  feeling    in a passive recovery  perhaps , because we have  much less balanced  out the pH  and H + .Is the high lactate  perhaps  not already a sign , that  lactate did  its job  and moved  H +  from the intracellular  level into the blood stream.
 Who is next to help cleaning up the now release H + in the blood stream ?
 If  lactate is not a  "waste " product , why would  we  get rid  of it.  What is  a  possible  " waste " product w  may like to get rid of?
  Here    for your eastern bunny reading, as  there  are very  few easter bunnies who actually stretch before they get hunted  nor  do they stretch  when they are in a save  location and survived nor  do they  actually  cool down to get rid  of the lactic  acid.  But  what they for sure  do is  intense    breathing to get rid  of  something???

COMPONENTS OF CELLULAR PROTON PRODUCTION, BUFFERING, AND REMOVAL

 

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 + .

 

Respiration/Expiration

abcd.jpg 


And  here one of teh rare  stduies  who may in fact   have  teh answer, when you read carefully.
  So  there si no such thing liek passive recovery  but we  coudl make a  differecne between  moving   extremity  muscels  to  burn unnessesary    energy sources  and teh ability to use a  perfect trained respiratory system to remove CO2  to help some part of teh  balance of  H + .

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 unevenness and relative hyperventilation that are observed when cool-down exercise is not performed.

 

 

stretchin  mail man.png   




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