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