A+A (AXE) alactic, really?

[Paotle]

Hi everyone,
It is obvious that training of <4 seconds mainly uses PCr pathway which is alactic. However, my past experience as a sprinter and lactate testing done on me at the time showed that even a small number of intervals with very short sprints (3-5 seconds) with 3-5' rests caused high lactate peaks >20mmol /L.
I came across this post (see below) from Hakan Andersson an elite sprinting coach who shows that 3*4*60m/3'/10' caused a lactate surge similar to what I had experienced on efforts of 5-6 seconds.
Two reminders:
1. The (critical) lactate threshold is at 4mmol/L. The data shown here on "alactic sprints" with nearly complete rest are a massive lactate production (20mmol/L) similar to very high intensity intervals of 4 minutes.
2. these workouts are supposed to be much less lactic than what the Strongfirst system advocates.

Although these are good level sprinters who necessarily produce a lot of lactate, this still shows that there is no such thing as alactic effort and that even a few short (<7 seconds) repeats with long rest produce massive lactate.

Have some of you done lactate testing during A+A? How were your datas?


Best,
Paotle

 

[Xene]

I would love to hear what Pavel has to say about this! @Pavel

 

[Bauer]

Hi everyone,
It is obvious that training of <4 seconds mainly uses PCr pathway which is alactic. However, my past experience as a sprinter and lactate testing done on me at the time showed that even a small number of intervals with very short sprints (3-5 seconds) with 3-5' rests caused high lactate peaks >20mmol /L.
I came across this post (see below) from Hakan Andersson an elite sprinting coach who shows that 3*4*60m/3'/10' caused a lactate surge similar to what I had experienced on efforts of 5-6 seconds.
Two reminders:
1. The (critical) lactate threshold is at 4mmol/L. The data shown here on "alactic sprints" with nearly complete rest are a massive lactate production (20mmol/L) similar to very high intensity intervals of 4 minutes.
2. these workouts are supposed to be much less lactic than what the Strongfirst system advocates.

Although these are good level sprinters who necessarily produce a lot of lactate, this still shows that there is no such thing as alactic effort and that even a few short (<7 seconds) repeats with long rest produce massive lactate.

Have some of you done lactate testing during A+A? How were your datas?


Best,
Paotle


View attachment 22834


View attachment 22836

I haven't tested anything.

This is probably based on 100% effort sprinting.

AXE is 80% power and uses micro rests. This is one of the reasons why Hand to Hand Swings and enjoying the float are recommended.

Q&D, however, uses higher effort, cuts the float/lockout short, and has less complete recovery built in.

 

[Paotle]

I haven't tested anything.

This is probably based on 100% effort sprinting.

AXE is 80% power and uses micro rests. This is one of the reasons why Hand to Hand Swings and enjoying the float are recommended.

Q&D, however, uses higher effort, cuts the float/lockout short, and has less complete recovery built in.

The response of Chris Sauer in the tweet above (10m fly with 35m lead-in) isn't full effort. It's 35m relaxed acceleration with 10m (less than 1 second) of maxspeed.
AXE and even A+A is in my opinion far, far more glycolytic as such sprints. The sprinting we are talking about, is effort lasting 3-6 seconds with 3min rest. AXE effort is longer and with 3x shorter rests.

 

[SteveR]

At the risk of sounding unknowedgable, isn't the at least one of the main purposes of A+A training to improve the aerobic capabilities to clean up the waste produced by the initial <= 15 sec burst? If so, then it would seem that whatever the waste is technically comprised of doesn't matter. Long live A+A.

 

[psmith]

Man, I gotta buy a lactate meter.

 

[Paotle]

At the risk of sounding unknowedgable, isn't the at least one of the main purposes of A+A training to improve the aerobic capabilities to clean up the waste produced by the initial <= 15 sec burst? If so, then it would seem that whatever the waste is technically comprised of doesn't matter. Long live A+A.

I'm not questioning the effectiveness of A+A training. I just question the name "alactic", when it is still a highly lactic form of training (more than Z2 aerobic training and even Z3 (tempo). I remember very well that I had a lactate of 20 mmol/L doing exercises of less than 6 seconds with 3' of rest in between (taken in laboratory and multiple times during track training). I wasn't out of breath at all and didn't feel any burn or other "stop sign", HR was back to 60-70bpm before next sprint, but the data is there: I was bathing in acid. And it was the same for my training companions.
I wasn't an elite sprinter (10.9x on 100m at 17yo), but my data is similar to elites at that level.

It is known that elite sprinters are aerobically deficient and produce enormous levels of lactate, even more than "healthy" (not overweight or with a CVD or metabolic disease), but inactive/ sedentary people. This is linked, among other things, to their high proportion of IIX fibers.

 

[Luwuwu]

This picture is from Kettlebell AXE. It actually tells us a very important message, that in a way we do not really have THREE energy systems, we have ONE energy system which consists of 3 different parts. It can be observed that all 3 parts are working together from the very beginning of the effort. The difference lies on the proportions of each one to the whole. From 0 to 10 seconds the CP swiftly gets exhausted and glycolysis quickly climb up. So it seems to me that it is absolutely reasonable a lactate surge can be detected even at the first few seconds of the effort. Therefore, not entirely alactic.
But then again, IMO, I think what we are trying to do with AXE or A+A is "as much alactic as possible, and as little acid as possible". There are no contradictions.

 

[North Coast Miller]

I'm not questioning the effectiveness of A+A training. I just question the name "alactic", when it is still a highly lactic form of training (more than Z2 aerobic training and even Z3 (tempo). I remember very well that I had a lactate of 20 mmol/L doing exercises of less than 6 seconds with 3' of rest in between (taken in laboratory and multiple times during track training). I wasn't out of breath at all and didn't feel any burn or other "stop sign", HR was back to 60-70bpm before next sprint, but the data is there: I was bathing in acid. And it was the same for my training companions.
I wasn't an elite sprinter (10.9x on 100m at 17yo), but my data is similar to elites at that level.

It is known that elite sprinters are aerobically deficient and produce enormous levels of lactate, even more than "healthy" (not overweight or with a CVD or metabolic disease), but inactive/ sedentary people. This is linked, among other things, to their high proportion of IIX fibers.

Tabata's research demonstrated that high effort with long rest did not yield much aerobic improvement - sprint protocol. This maybe falls in with a relative lack of mitochondrial biogenesis observed in many powerlifters.

Paradoxically perhaps, by keeping effort slightly below 100% and using shorter rests (his trademark 20:10) one improves anaerobic and aerobic efficiency in roughly equal measure.

The details of much of the adaptive response re to energy systems is not understood by me. I tend to look at training strategy by structure to outcome rather than metabolic theory that I can neither verify or test. If it works, it works.

 

[North Coast Miller]

This picture is from Kettlebell AXE. It actually tells us a very important message, that in a way we do not really have THREE energy systems, we have ONE energy system which consists of 3 different parts. It can be observed that all 3 parts are working together from the very beginning of the effort. The difference lies on the proportions of each one to the whole. From 0 to 10 seconds the CP swiftly gets exhausted and glycolysis quickly climb up. So it seems to me that it is absolutely reasonable a lactate surge can be detected even at the first few seconds of the effort. Therefore, not entirely alactic.
View attachment 22838But then again, IMO, I think what we are trying to do with AXE or A+A is "as much alactic as possible, and as little acid as possible". There are no contradictions.

Good points.
Also need to point out that while most lactate will be consumed system wide, a lot of it will be converted back to glycogen in the liver - it won't be burned up locally by muscle working in a reduced output mode.

 

[TobyC]

From my understanding, A+A training allows for some lactate generation but then aerobic recovery from the short, intense efforts, as opposed to crossfit style where the efforts are more extended and don’t allow for aerobic recovery, but just more lactate production.

 

[Paotle]

Thank you for your answers. Great insights. I know very well the studies and theory behind that.

But we 're getting off topic which was why efforts of <6 seconds with 3' rest produced as much or even more lactate than longer anaerobic/glycolytic intervalls (minutes...) with little rest. And second, that stop signs are poorly correlated with lactate in such cases.

 

[james_1127]

I don't think anyone would argue that lactate isn't present, but A+A is supposed to reduce/minimize the amount & by pass the negative impact of acid baths... I wonder what the reading would look like if the rest was more condensed and it was more of a smoker type session

 

[Paotle]

I don't think anyone would argue that lactate isn't present, but A+A is supposed to reduce/minimize the amount & by pass the negative impact of acid baths... I wonder what the reading would look like if the rest was more condensed and it was more of a smoker type session

18mmol/L is massive! It isn't a little bit acid. Tempo/Z3/lactate threshold running (not LISS) produces way less than 18mmol/L. It's more 4mmol/L. The datas from those <6 sprints/3 minute rest indicates 2-3 times more lactate production than a 1500m all-out to death effort (see paper attached).

I'm not sure you're realizing what 18mmol/L is. It 4 times HIGHER than the lactate/second ventilatory threshold. You're not minimizing anything when you reach such levels!

 

[offwidth]

Man, I gotta buy a lactate meter.

They aren’t all that expensive. And you can also share the cost with some training partners if you have any.

 

[North Coast Miller]

Thank you for your answers. Great insights. I know very well the studies and theory behind that.

But we 're getting off topic which was why efforts of <6 seconds with 3' rest produced as much or even more lactate than longer anaerobic/glycolytic intervalls (minutes...) with little rest. And second, that stop signs are poorly correlated with lactate in such cases.

I'd hazard a guess that the machinery simply isn't using much pyruvate or fat, the pyruvate gets fermented to lactate.

The effort magnitude is such that some type 2 fuel is sourced from glycolysis, but very little is being consumed by type 1 fibers except to rephosphorylate CrP as surplus ATP becomes available. There will be a lot of circulating lactate and very little demand.

Hence the outcome observed by Tabata...

 

[Adachi]

Thank you for your answers. Great insights. I know very well the studies and theory behind that.

But we 're getting off topic which was why efforts of <6 seconds with 3' rest produced as much or even more lactate than longer anaerobic/glycolytic intervalls (minutes...) with little rest. And second, that stop signs are poorly correlated with lactate in such cases.

I suppose there are a couple phenomenological questions I'd have to ask, to aim more specifically at the work rest ratios, and consequent blood lactate....

What can be said about the rapidity of steps in a sprinters stride? I would submit this density of work is much higher than swings or snatches . which, for me in particular, seems to average about 1 contraction per 2 seconds at the low end and 1 contraction per 1.5s at the high end of frequency. How many contractions does a sprinters legs suffer in a near maximal sprint?

I appreciate the raw lactate data provided above . And I guess I would have to ask about what we're seeing here ...

It would seem that other non-sprinting protocols have lesser lactate consequences.

A short excerpt from the strong endurance manual.



Maybe I have some more particular questions about the particulars of Volkov et al, 2000.

And fwiw , as far as I can tell, in the strong endurance paradigm, it would seem that the concern over lactate is actually a secondary proxy for the primary concern over hydrogen ion accumulation. But, this is my own interpretation.

---

From S&S 2.0


I ponder a bit about what this means for submaximal sprints, as discussed in the beginning of this thread.

---

From Q&D

15 minute rests and up? Verily sprinting has very high consequences indeed.

 

[Xene]

Thank you for your answers. Great insights. I know very well the studies and theory behind that.

But we 're getting off topic which was why efforts of <6 seconds with 3' rest produced as much or even more lactate than longer anaerobic/glycolytic intervalls (minutes...) with little rest. And second, that stop signs are poorly correlated with lactate in such cases.

I admire your knowledge and your persistence. As we all don‘t know the exact science it would be a nice question directly for Pavel. Maybe this can be asked at a Strong Endurance seminar or someone of the SF leaders who also know the science can jump in here (@Brett Jones @Fabio Zonin ). I am also looking forward to seeing a conclusion in here!

 

[Georgiaoutdoors]

What can be said about the rapidity of steps in a sprinters stride? I would submit this density of work is much higher than swings or snatches . which, for me in particular, seems to average about 1 contraction per 2 seconds at the low end and 1 contraction per 1.5s at the high end of frequency. How many contractions does a sprinters legs suffer in a near maximal sprint?

I think this is an important point. I’m pretty sure top elite sprinters are hitting 4-5 steps per second, which in an AXE repeat of 10s would be 40-50 major contractions. Sprinting is such a thing to itself. Sprinting is sprinting, everything else is well, different. 6 powerful swings is a world away from 40+ sprinting steps, very much apples and oranges.

The easier answer to this discussion is to find someone on here who is training AXE and has a lactate meter and test themselves.

 

[John K]

@Paotle if this is a concern for you, have you considered getting a lactate meter and training A&A or AXE for a few months and assessing lactate directly rather than extrapolating from sprint studies? It doesn't seem that many people have one and done this.