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Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #1 
I was watching a UCI world cup race on TV and some " expert" from the cycling world where helping the commentator to get an inside view in the  cycling world and its problems.
So every  second word during the ongoing sprint event was the explanation on how the lactic acid is slowing the guy down and why he would sit on the roller after the load to get rid of the lactic acid otherwise   he will still have the lactic acid in his system the following day for the road race.????

Here some  question.
 or speculations.
 If  and only IF we  may start to accept the fact, that lactate may not be the cause of fatigiue butjjust a great biomarker of some metabolic  reactions during a load or even without a load ( see sepsis) and if we accept, that lactate could be recyceld and  used for further energy supply than  we  at least have to  discuss the possibility , that " cooling " down  may have an other reason to be justyfied  than reducing " lactcic acid."
 Yes if we " cool down" the post  load  lactate  numbers  are clearly lower. Why? how about the possibility , that moving may need further energy and the possibility , that this energy may come from recycling lactate ?
 So a drop in lactate after cool down is  a sign  that we used energy but  most liklely not a sign of a better recovery.
 What causes the drop in performance and what  has to be a part of recovery.
?
 If  there is ( can be discussed) a peripheral metabolicc reason of some reduction in performance  due to  drop in   motor units recruitment or due to vasoconstriction, than we  can accept as a part of the idea, that H +  could be a part of the reason of loss of performance with a feedback loop  for " survival ".( pH balance)
 There are different ways we can get rid of H + and one of them is over respiration.
 The question  is, whether active recovery in between sprints may in fact be beneficial or whether perhpas just trying to get rid of H +  may be the way to go.
 Here what  may happen. H + increase will increase CO2 levels and drop pH levels. This shifts the  O2 Diss curve to the  right allowing a  better deoxygenation. So during an active recovery we   will see  a less optimal  ability to get rid of CO2  as we still   have to produce  energy so we may see a  bigger drop in SmO2  with active recovery versus passive recovery. When we add to passive recovery some additional respiratory interventions we  may see a  much faster SmO2 recovery   and much more interesting reactions..
 Here a nice study, who  looks at  SmO2 and the influence on active and passive recovery. It  does not tell us the result of the performance  after both and it does not  combined respiratory reactions as a part of the balance of CO2 in the system. But it is  one more interesting study you will be abel to do on your own and get the answers as soon you use MOXY for assessments as well as during workouts and for interval workout designs.
 
 
Int J Sports Med. 2009 Jun;30(6):418-25. doi: 10.1055/s-0028-1105933. Epub 2009 May 12.

Muscle deoxygenation during repeated sprint running: Effect of active vs. passive recovery.

Source

Faculté des sciences du sport, Laboratoire de Recherche: Adaptations Physiologiques à L'Exercice et Réadaptation à I'Effort, Amiens, France. martin.buchheit@u-picardie.fr

Abstract

The purpose of this study was to compare the effect of active (AR) versus passive recovery (PR) on muscle deoxygenation during short repeated maximal running. Ten male team sport athletes (26.9+/-3.7y) performed 6 repeated maximal 4-s sprints interspersed with 21 s of either AR (2 m.s (-1)) or PR (standing) on a non-motorized treadmill. Mean running speed (AvSp (mean)), percentage speed decrement (Sp%Dec), oxygen uptake (V O (2)), deoxyhemoglobin (HHb) and blood lactate ([La] (b)) were computed for each recovery condition. Compared to PR, AvSp (mean) was lower (3.79+/-0.28 vs. 4.09+/-0.32m.s (-1); P<0.001) and Sp%Dec higher (7.2+/-3.7 vs. 3.2+/-0.1.3%; P<0.001) for AR. Mean V O (2) (3.64+/-0.44 vs. 2.91+/-0.47L.min (-1), P<0.001), HHb (94.4+/-16.8 vs. 83.4+/-4.8% of HHb during the first sprint, P=0.02) and [La] (b) (13.5+/-2.5 vs. 12.7+/-2.2 mmol.l (-1), P=0.03) were significantly higher during AR compared to PR. In conclusion, during run-based repeated sprinting, AR was associated with reduced repeated sprint ability and higher muscle deoxygenation.
 

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