From the P&B.....may be a bucnh of scientifical BS but what I'm hearing from folks I know still involved in the silliness that is bike racing thsi stuff pans out..in....you know... like in the real world and stuff.
........ the current thinking is that lactate per se isn't actually the cause of muscular fatigue. It is a fuel and actually may buffer changes in muscular acidosis and prevent fatigue (this is probably why high intensity warmup that actually generate some lactate seem to improve performance in the actual event, the lactate ends up buffering changes in acid levels).
However, Billat's thing is getting mired in a lot of semantic crap in my opinion. The old idea of the lactate or anaerobic thresholds (as originally defined) are likely garbage. However, this doesn't negate the existence of a threshold speed or intensity above which fatigue occurs very very rapidly. That it occurs is more important practially than what you call it or what is causing it.
The simple fact is that a runner may be able to maintain (and these values are pulled out of my butt)
10mph for essentially forever
10.5 mph for an hour but it works the hell out of them
11 mph and they fatigue in a few minutes
again, values are for example only.
clearly there is a criticial threshold point above which fatigue occurs rapidly. from a practical standpoint, that's essentially what the old ideas of LT/AT/OBLA/etc. were describing.
you can graph velocity versus time to exhaustion and see that kind of pattern. below some level, the athlete can go until they get bored or run out of muscle glycogen, around some point they are working very hard but can maintain speed for extended periods (cyclists will test 20' although an hour maximum time trial isa better indicator), above that point and fatigue hits like a hammer after a few minutes.
It's actually looking like H+ production (rather than lactate per se) is the cause of this. It's also turning out (going to ccrow's point) that the aerobic engine is a much bigger determinant of this than previously thought. Mitochondria buffer acid levels and the bigger the aerobic engine, the less acid is produced.
A common trend in a lot of endurance sports is going back to volumes of low intensity aerobic work with just a bit of higher intensity stuff thrown on to top off the system (the system adapts quickly but stops adapting equally quickly, some of hte interval studies in cyclists show that 6 workouts across 3 weeks pretty uch maximizes the benefits)).
An example, there's a paper describing the training of the german track cycling team in the 1km (or was it 4k). An event last 4 minutes which most would argue is highly anaerobic. Most of their training was easy aerobic with some stage racing and a bit of specific track training thrown in at the end.
As I recall, a typical rowing race is roughly 6 minutes and even there they are going back to volumes of low intensity work to build the aerobic engine.
There's also an old idea (Maglioscho's book gets into this) that too much high intensity training can actually degrade the aerobic engine which *might* be what the US Rowing team was experiencing: if their caoches emphasized too much work around or at LT (or high intensity intervals) and lose aerobic engine size, that could actually be detrimental.
Translation of my long-winded crap: it may be better over extended periods of training to build this engine (again going to ccrow's comment) with lower intensity aerobic work. This can be topped off with higher intensity stuff as needed.
Maybe the boxer and martial artists who did extended road work weren't so wrong after all.
Absolutely true insofar as elite rowers are concerned.
You might be interested in the recent article on their huge hearts:
Muscular acidosis is due to the hydrolysis of ATP to ATP and other substrates being used for energy in the muscles.
Basically what happens is this:
ATP + H2O → ADP(hydrated) + Pi(hydrated) + H+(hydrated) ΔG˚ = -30.54 kJ/mol (−7.3 kcal/mol)
Lactic acid is directly through the following equation (FYI pyruvate is the end result of glycolysis):
Pyruvate + NADH <-> Lac + NAD+
The reason why this doesn't actually produce a H+ ion is because pyruvate itself is already a carboxylic acid Ch3-CO-COOH which is deprotonated already at body pH. Therefore, it's already pyruvic acid (pyr- + H+ + NADH <-> Lac- + H+ + NAD+) where the H+ cancel on each side of the equation. This stoichiometric mistake was why people THOUGHT lactic acid was the cause of acidosis; however, as you can see this is not true.
Lac has a pKa of ~3.85 which means that at equilibrium in the body some of the lac will be pronated but most will have no H on the carboxylic acid. However, as the pH drops, a greater proportion of the carboxylic acid becomes pronated thus effectively buffering acidosis as described above.
Alright, here's the fun part which I was actually just discussing today with someone regarding the "lactic acid threshold." What is actually happening here is a couple of things.
Basically, what happens when intensity becomes high enough (thereby increasing demand in energy) is that the body needs to produce energy. The oxidative pathway becomes bottlenecked at pyruvate/acetyl-CoA because it cannot handle the load of NADH that is being produced. Thus, NADH accumulates.
The reason why NADH accumulating is bad is because glycolysis uses the non-hydrogenated carrying form of NADH (namely NAD+) to produce NADH. Thus, lactic acid is produced for the body to change the extra NADH back to NAD+ so that glycolysis can keep running.
Here's the brilliant illustration I thought up today. Think of the oxidative pathway as a pipe. This actual "pipe" consists of the citric acid cycle (or TCA/kreb's cycle whatever you want to call it) which consists of 10 steps, transport of electron carrying coenzymes such in the form of NADH and FADH2 (from glycolysis and CAC) from the cytoplasm into the mitochondria along with ADP, dumping of electrons into the proteins of the mitochondria wall (the electron transport chain) whereby these proteins pump H+ across the membrane to create a H+ gradient. This gradient is then harnessed by ATP synthase to produce ATP. NAD+ and ATP must be shipped out of the mitochondria into the muscles. This takes some time obviously to get "running."
Note: this also why people with large aerobic engines are also buffered well against acidosis because their mitochondria pumping H+ across the membrane provides a greater buffering effect.
In any case, glycolysis is a simple pathway which consists of about 10 steps all of which occur in the cytoplasm. This occurs very quickly because ADP is readily available because the myosin-actin is close by and need very little transport activity.
Thus, let's take into account the scenario from the original/cross post:
At 10 mph the effect of what is happening is that the glycolysis funnel (we'll just call it a funnel) dumps NADH and pyruvate into the oxidative "pipe." It can handle the capacity. Thus, it can basically run forever without getting overloaded.
What happens at 10.5 MPH when it is slightly overloaded is that there is some spill over out of the glycolytic "funnel" that the oxidative "pipe" cannot handle the total volume. Thus, what occurs is that the pyruvate is converted to lactic acid to use up the NADH converting it back to NAD+. This allows the glycolytic cycle to continue to provide energy to the muscles because there is a limited amount NAD/NADH in the body. However, since there is "little" spill over, the body can handle the pace and keep continuing.
Now we arrive at 11 MPH. What is occurring here is that there is a large spill over out of the glycolytic pipe as glycolysis consumes a lot of the muscles glycogen stores very quickly. Since there is a large spill over, the body can only convert some of the pyruvate to lac to generate NAD+. Thus, it can only keep producing a limited amount of energy as the lac keep accumulating. Eventually you will reach a point where there is too much ADP (and hence pH drops enough) that glyolysis + oxidative pathway cannot keep up to reproduce ATP. This leads to muscular failure.
Here's a nice picture I made in paint to illustrate the above (click to enlarge):
In any case, what is also interesting is the adaptations that occur because of the former scenarios.
With the 10 MPH that is sustainable, it clearly strongly work the oxidative "pipe" at max capacity for a long time. This produces a strong response on the oxidative pathway increasing mitochondria, type I fibers, and other aerobic changes which is why you NEED to do long distance work to build up a sufficient aerobic base if you ever plan on competing in elite long distance racing.
What happens here is that since there is an overflow of the glycolytic funnel, the glycolytic pathway is stressed as the glycolyticenzymes need to keep up with the rate as NAD+ is resynthesized quickly. The oxidative pathway is stressed because it is working at full capacity, but the duration is shorter than the former. What you end up with is some increases in anaerobic and aerobic qualities in the muscles.
This is the interesting concept because it shows clear "pushing" against the "lactate" threshold. So basically since there is a large overflow from the glycolytic funnel we get an extremely strong stress on the glycolytic energy pathway. This induces strong anaerobic changes in the muscles. However, since the duration is extremely short, the oxidative pathway receives little to moderate stress resulting in only poor-decent gains in aerobic fitness UNLESS this is continually pressed through for a while. For example, a HIIT session that continues after you get gassed or a metcon that keeps going a couple minutes longer after max intensity drops will help produce aerobic changes.
This is why HIIT/tabata/metcon all have the tendency to produce anywhere from mediocre to strong aerobic changes as well as strong anaerobic changes in energy pathway metabolism.
Basically, for longer duration rowers/runners/etc. this is COUNTERPRODUCTIVE because they do not need improvements in the anaerobic engines which will induce changes that will counteract their aerobic engines. This is easily observable and agrees with the OP & anecdotal evidence.
I think that's about it. Hope you learned something.
What is P&B?
I think a workout like this with active recoveries would be better for working the oxidative pathways than a HIIT workout where you continue beyond the point where you are gassed.
While lactic acid doesn't cause fatigue, lactic threshold pace and VO2max pace are still 2 of the best predictors of performance and working at these paces is one of the best ways to improve performance.
I've been wondering how this applies to CF. If someone is advanced would something like an "easy" Murph every other week be useful?
I've seen very little mention of active recoveries either here or on CF. B2B tabata squats might count. I think there was a video a while back with a woman doing a minute of easy jump ropes in between her intervals. I think some experimenting with workouts of this nature would be really interesting.
Billat Fran anyone?
6-8 rounds of 11 thrusters/11 pullups
In between rounds alternate 1 minute at an easy pace of run, jump rope, air squats, bike, etc.
P&B is powerandbulk.com.
I know that Twight used to talk about incorporating some very LSD work (very slow treadmill jogging for a couple hours, or something) with his high-intensity CF stuff in order to "blend" and be able to perform at long durations.
On the other hand I guess he eventually just went back to mostly endurance work anyway.
The interval idea has been getting passed around quite a bit lately.
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