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.
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.
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 ?
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.