MITOCHONDRIA QUESTION for phoenix, tinman and others

I am trying to get a paper off. We've got all the data collected so I am crunching and writing. So, this week is busy for me.

Nonetheless, as far as oxidation of lactate, Hasn't Brooks made a strong case that lactate can be oxidized directly by mitochondria?

Tinman, thanks for the responses. And "?" thank you for the clarification. I was writing the last part as I was walking out the door for practice.

I have always been someone who wants to know the reason behind different rules, and this discussion is helping me to understand some of the physiology behind periodization.

Phoenix makes a good point. Dr. George Brooks is a research genius and has shown that mitochondria due oxidise lactate. In fact, the lactate shuttle theory is Brooks' masterpiece too. Other tissue not directy involved in the motor unit contractions can deal with lactate that has been shuttle via the bloodstream and convert lactate into glycogen. The heart, liver, and other non-running cells, in particular can take up lactate and convert it into usable glycogen for aerobic metabolism later. Such shuttling is part of the lactate threshold adaptation that takes place because of proper endurance training.

Great answers . . however Brooks' "genius" is certainly debatable, and the whole idea of training non-running cells (like cardiomyocytes?!?! - these are even better lactate consumers than skeletal muscle) to convert glycogen is very theoretical - you've been looking at Chap 5 in Brooks' book haven't you. The lactate shuttle theory is actually not his original idea, at least at the mitochondrial level. Look beyond the exercise literature: groups in the late 70s first recognized mitochondrial lactate shuttling in heart and testes. This is way before the concept was ever proposed by Brooks et al. Like much exercise science, this concept was cleverly applied to exercise states and viola, a genius concept! Also, take a look at studies of labeled pyruvate vs lactate mitochondrial transport and degradation - pyruvate is the overwhelmingly predominate substrate utilized for metabolism, not lactate (look back at papers by Laughlin, Poole, or Armstrong et al in the early 90s.) Furthermore, there is absolutely no evidence that training improves the performance of the lactate shuttle system - look again at Brooks book - his own group showed prior to getting into the "shuttle research" that after an initial rise in lactate at the onset of steady-state exercise, lactate levels plateau, whether the subject/rat was trained or untrained. Only in single bouts of exercise with progressively increasing workloads, does lactate increase in the blood at greater rates in untrained subjects. Brooks himself reasons that this is due do increased mitochondrial size and capillarization - if you quantitate lactate enzymes (like LDH) per mitochondrial area, the numbers remain the same!

Gotta go back to work,

Let me know what you think of this, I can provide you with specific citations if interested.

txnnvt

Sorry,

once again a typo, please read the 2nd to last sentence as (capitals inserted):

"Brooks himself reasons that this DIFFERENCE is due do increased mitochondrial size and capillarization WHICH OCCURS WITH TRAINING - if you quantitate lactate enzymes (like LDH) per mitochondrial area, the numbers remain the same!

txnnvt

sometimes I think faster than I type

Didn't Holloszy show decades ago that skeletal muscle is capable of converting lactate to glycogen? The key distinction being that skeletal muscle is not capable of gluconeogenesis like the liver.

I want to give some information about what can happen in an athlete of top level. I'm speaking about Stefano Baldini.

We use a test (Faraggiana-Gigliotti) consisting in 6 x 2000 even pace in crescent times, covering every possibility of marathon pace. For example, for Baldini, 6:15 - 6:10 - 6:05 - 6:00 - 5:55 - 5:50, with recovery time very short (only what we need for taking blood from the ear). After the last, we use 1200m free, at max speed, for controlling the level of lactate that the athlete can reach.

Every 2000m is at even pace, using an "acustic rabbit", able to send a beep every 25m (we have cones every 25m on the track) at the programmed speed.

In this way, using always the same speeds, we can test the improvement of the athlete in his SPECIFIC MARATHON ENDURANCE, that is clear when, for the same speed, the level of lactate is lower.

As Marathon is a problem of fuel, and we have to reduce the consumption of glycogen at marathon pace in order to last longer, when the lactate is lower, the athlete is more RESISTANT AT HIS MARATHON PACE.

We use this type of test about every 4 weeks, normally 4 times during the preparation of the race (last time about 10 days before the race).

Till 5 years ago, we didn't use the last test of 1200m. We added this distance in order to investigate how much glycogen the athlete had yet in his tank. HIGHER IS THE LEVEL OF LACTATE, MORE RESERVES THERE ARE IN THE TANK.

We use this test with all the best marathon runners that we follow.

Very interesting thing is to see, in longitudinal way, what happens with an athlete that, in 5 years, is able to improve his time of 3-5 minutes.

About Baldini, for example, when he ran his first Marathon in 1995 (2:11 in Venice), he had a steady state around 2 mmol/l (where physiologists normally say that there is the Aerobic Threshold). At that time, he did 6x2000 from 6:20 to 6:00, having lactates of :

1.7 (6:20) - 1.9 (6:15) - 2.0 (6:10) - 3.2 (6:05) - 4.4 (6:00).

His average in the race was 3:06 /km, that is around 2 mmol.

In 1996, Baldini won World Half Marathon Championships, after working for about two months for improving his AnT. At that time, he was able running at 2:53 pace having 4.2 mmol (and was his HM pace).

He spent 45 days in preparing NY Marathon, but was not able to individuate to speeds very close, where having a personal steady-state. His values were :

1.7 (6:15) - 2.1 (6:10) - 2.5 (6:05) - 3.4 (6:00) - 4.3 (5:55) - 5.6 (5:50).

In the race, he dropped out after 27 km, nervously empty.

He spent all winter in preparing London Marathon '97, and his last test was very different :

1.6 (6:15) - 1.9 (6:10) - 2.0 (6:05) - 2.1 (6:00) - 3.2 (5:55) - 4.8 (5:50) - 7.3 (3:21 on 1200m)

So, it was possible to identify a special Aerobic Threshold from 3:05 to 3:00, without variations of lactate. He was able running 2:07:57.

During the last period, he became more "marathoner". His best shape was this year, in London, when he was 2nd in 2:07:56 overtaken by Abera only during last 5 meters.

He was able running about 2:06, and only the tactic of the race didn't permit to run so fast. Instead, during World Championships, his shape was not the same.

Before London, the last test had these results :

1.5 (6:15) - 2.0 (6:10) - 2.5 (6:05) - 2.4 (6:00) - 2.6 (5:55) - 4.5 (5:50) - 8.6 (3:15 on 1200m).

In this case, is possible to identify a special Aerobic Threshold from 3:02.5 to 2:57.5, but the level of lactate is no more 2 mmol, but about 2.5.

If the lactate level is higher, is because the athlete is using more glycogen at that speed. But, if his endurance for marathon is OK, and the size of his tank is the same of 4 years before, this is possible only because he is able to use a higher percentage of the lactate that he can produce running, so is clear that there is a "shuttle" effect, only after some year of specific training.

So, we can say that "fibres must learn to use their lactate for improving their aerobic capacity", like a "turbo" for an engine of a car.

I think that this attitude, naturally, is the big difference between african and white runners. The AnT in kenyans is very higher than in a European runner, and they are able to use their lactate for producing energy in a higher percentage than european runners.

Renato:

Thank you for sharing such interesting information. With such good examples of real runners I can understand better your points. Indeed, the testing you have done is of very good benefit for your athlete because they know exactly what pace to run in the marathon.

I wondering if there is a correlation between the rise in Baldini's maximum steady state lacate (you called it aerobic threshold) is both due to increased lactate shuttling and an increase in anaerobic capacity. Baldini was able to run his 1200m faster and at a higher lactate level in the test just prior to the London Marathon. His lactate rose to over 8 mmols which indicates that both he had glycogen left in his "tank" and he had improved his anaerobic capacity. Am I on-target with my evaluation of Baldini? Please respond.

tinman,

on another thread, Renato talks about 10000m runners having a maximum lactate steady state (MAX LASS) OF 8-9mmols. 8mmols doesnt necessarily indicate an improvement in anaerobic capacity, its not that high even for a marathon runner.

the 1200m test at the end of the session not only shows how much glycogen is left in the tank, but helps an athlete like Baldini to train for a fast finish in the marathon which is absolutely essential at the top level.

IF YOU DONT DO IT IN TRAINING, YOU CANT DO IT IN A RACE.

now a question from me,

tinman, Renato, and others,

given that fatigue after a race or very hard session will be shown in lactate tests by a left shift on the lactate curve, would,t it be true to say that such information would be very easy to demonstrate to almost every runner from beginner to elite?

graphs showing lactate curves are very simple and informative.

By showing a runner what happens to the lactate curve when we are fatigued and when we are recovered, we can easily help them to understand when to train easy, medium, hard and very hard.

Getting a bit off topic from the original mitochondria discussion, however...

Does Renato ever look at blood buffering capacity of his runners? I as this because I have done some work looking at bicarbonate and higher blood concentrations seem to result in greater blood lactate concentrations (presumably because of greater efflux out of the muscle cells across a pH gradient). It would seem possible to me that an increased blood buffering could have the effect of effectively increasing max steady state lactate concentration. This is in line with what Renato has said in earlier posts about the elite runners having maxlass at higher lactate levels, and about improved endurance performance being largely due to an improved ability to eliminate lactate form muscle.

Some work by Lucia et al demonstrated that elite professional & amatuer cyclists had similar aerobic parameters but that the pro's had higher potential buffering capacity. Other work has also demonstrated that sodium citrate can improve 30km cycle endurance - and also blood lactate levels are higher at all times. This could even suggest that bicarbonate / citrate could be a useful ergogenic for endurance athletes and not just the 400 / 800 types who it is usually recommended for.

Must be at least a PhD in there somewhere!

First, in response to your MLSS point about SOME 10k runners having high mmol steady states, it is even more true for middle distance runners and sprinters who typically produce far more peak lactate than distance runners. I do not agree, however that 8 mmol is not high for marathoners, as you state. On the contrary, many marathoners can not raise their peak lactate concentrations during incremental testing to 8 mmols due to both to a predominant activation/use of slow twitch red fibers that produce minimal lactate and poorly trained anaerobic capacity. I bet if you asked Jack Daniels about Al Salazar's max lactate during incremental testing he would say the guy maxed out at 5 or 6 mmols.

Some 10k runners do have high lactate steady states due to two reasons:

1) they have fairly normal ratios of slow to fast twitch fibers; not disproportionate on average like Mr. Salazar

2) they do regular anaerobic capacity intervals which raises their peak lactate max, thus a level concentration of 7-8 mmols is only roughly 50% of their maximum capacities. Around 50% of max lactate capacity a conditioned athlete can maintain a steady-state. Most 5k-10k runners at the local level max out at 8 mmols on incremental treadmill tests and thus their avaerage Maximum Lacate Steady State is around 4 mmmols. For a guy like Salazar who maxes out at around 5 mmols, a max. lactate steady state may be about 2.5 mmols (which is why his theoretical lactate threshold doesn't fit into the 4 mmol model). See the idea?

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Now, in response to your question about the utility of lactate curves for showing athletes when to ease off their training (post race, for example) or push ahead, I do agree that lactate profiles can be helpful. Indeed, many swim coaches regularly test their athletes as a means of monitoring fatigue and designing appropriate workouts. In the book "Science of Winning" by Dr. Jan Olbrecht, he mentions this often. The Belgian national swim team, which kicks butt on the world scene, uses lactate profiling all the time. The know, as you say, that a tired swimmer's curve moves to the left and a recovered, super-compensated swimmer's curve moves to the right (to higher velocities).

* One critical point about lacate testing Dr. Olbrecht makes is about the necessary balance between aeobic and anaerobic capacities. Case in point, if an athlete has a lower lactate level at a given velocity, it does not necessarily mean that they are in better shape for racing. If the athlete can not raise their peak lactate to the same quantity as on the previous test and their lactate is now lower, no matter the velocity, they are not as fit. You can test and athlete today at 6:00 pace/mile (showing 4 mmols of plasma lactate) and again test them 8 weeks from today at the same pace (showing 3.5 mmols) and they may actually not be in better shape. Why? Because, as mentioned earlier, they might have a peak lactate that is less and their peak lactate is at a lower workload. Today their peak may be 10 mmols and they can't run faster than a 56 second 400m. In 8 weeks from now, their 6:00 pace lactate value is slightly lower (by .5 mmols) and their peak lactate is quite a bit lower (say 8 mmols) too (by 2.0 mmols). Consequently their time for their 400m sprint is only 64 seconds. When is such a thing possible? When a runner does a lot of slower aerobic training and very little or no anaerobic capacity training. By running a bunch of slow miles, their ability to activate fast twitch cells and generate higher forces is diminished over time and thus the peak lactate is lower, just like every other lactate for sub-maximal speeds. So, to reiiterate, lower lactates do not necessarily mean improved phyiological capacity; only when the peak lactate is at least the same and the peak velocity is at least the same.

Renato, Can you expand on the global fiber recruitment and how it saves oxidation or aerobic enzymes?

Do you mean his mitochondria broke down?

What was his training like?

In the case of Greg Lemond, this turned out to be a false alarm and that he didn't actually have a mitochondrial wasting illness.

Thank you for the explanation, great info! Now, what about speed and power athletes, are we left out of the mitochondrial bonanza? Is there any hope for us?