Lactic Acid Update

balance wrote:

For the record the muscles can not use lactate as fuel, only Pyruvate.

balance,

are you sure that is correct? What about the "lactate shuttle"

From what I have learned, lactate acid is produced during resting states, as well as in increasing amounts of increased exercise intensity. Brooks (4) proposed that lactate is not a useless byproduct of glycolysis but may be the most important fuel used by muscle, especially during exercise. Red blood cells are one well-known source of production as they are capable of glycolysis but have no mitochondria. Thus, pyruvate and lactate, instead of accumulating, diffuse out of the red blood cells into the plasma. Skeletal muscle can also produce and release lactate into the bloodstream. Along with this production of lactate is its’ use as a fuel. Non-exercising skeletal muscle will metabolize lactate (5), so will the liver (12), along with the kidneys and heart (14). The end-product of glycolysis is taken into the mitochondria for further metabolism in the Krebs cycle or is released into the blood stream, where the heart or skeletal muscle fibers may use it for energy production or by the liver for production of blood glucose (4). During exercise, when lactate production rises to the point where it exceeds the rate of consumption in exercising skeletal muscles, it is shuttled to other tissues for metabolism. The liver takes in lactate to produce new glucose and glycogen. The heart uses lactate as the preferred fuel source for oxidative metabolism, and the inactive muscles store lactate and lower concentrations in the blood and active muscles. Brooks labeled this phenomenon as the lactate shuttle (4).

This is a good post guys, thanks for all the info. Since we are on the topic of lactate and the use for the purpose of aid in exercise performance, what method is the most reliable? There are so many definitions.

The anaerobic threshold (AT) is also defined as lactate threshold, lactic acid threshold, gas exchange threshold, or ventilatory threshold, the predictor of the onset of metabolic acidosis caused by the increase in arterial lactate during exercise. One problem in understanding and interpreting the literature about blood lactate response to exercise is the numerous methods used to determine it. These methods include aerobic threshold which is a fixed 2.0 mmol/L value (9), lactate threshold, a point of deflection in the log (blood lactate) vs. log VO2 transformation (2), lactate threshold, workload preceding nonlinear rise in blood lactate during progressive work (8), maximal steady state, a fixed 2.2 mmol/L value (10), onset of plasma lactate accumulation, exercise intensity that elicited a blood lactate concentration 1.0 mmol/L greater than baseline (6), aerobic-anaerobic threshold (11), onset of blood lactate accumulation (OBLA) (12), 4 mmol/L threshold (7) a fixed 4 mmol/L value, anaerobic threshold, a steep part of exponential increase in lactate concentration, approximately 4 mmol/L (9), individual anaerobic threshold based on a model to define workload at maximal lactate steady state (rate of diffusion in equilibrium with rate of elimination) (11), maximal steady-state workload (MSSW), fixed 3 mmol/L value (3).

These methods of defining lactate threshold become even more complicated when researchers use the same word as another investigator, but refer to a different cause. A number of researchers have independently suggested that there are at least two apparent thresholds (1). The first threshold, lactate threshold corresponds to a sustained increase in blood lactate values above resting levels. This point is generally consistent with blood lactate concentrations of less than 2.0 mmol/L. The second threshold, anaerobic threshold is described by a very rapid rise in blood lactate indicating the upper limit of equilibrium between lactate production and clearance. The second point is associated with blood lactate concentrations between 2.5 and 5.5 mmol/L (1).

Is there a valid protocol out that works best?

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1. Antonutto, G. and P. E. Di Prampero. The concept of lactate threshold. A short review. J. Sports Med. Phys. Fitness. 35:6-12, 1995.

2. Beaver, W. L., K. Wasserman, and B. J. Whipp. Improved detection of lactate threshold during exercise using a log-log transformation. J. Appl. Physiol. 59:1936-1940, 1985.

3. Bransford, D. R. and E. T. Howley. Oxygen cost of running in trained and untrained men and women. Med. Sci. Sports. 9:41-44, 1977.

4. Brooks, G. A. Lactate production under fully aerobic conditions: the lactate shuttle during rest and exercise. Fed. Proc. 45:2924-2929, 1986.

5. Essen, B. and T. Haggmark. Lactate concentration in type I and II muscle fibres during muscular contraction in man. Acta. Physiol. Scand. 95:344-346, 1975.

6. Farrell, P. A., J. H. Wilmore, E. F. Coyle, J. E. Billing, and D. L. Costill. Plasma lactate accumulation and distance running performance. Med. Sci. Sports. 11:338-344, 1979.

7. Heck, H., A. Mader, G. Hess, S. Mucke, R. Muller, and W. Hollmann. Justification of the 4-mmol/l lactate threshold. Int. J. Sports Med. 6:117-130, 1985.

8. Ivy, J. L., R. T. Withers, P. J. Van Handel, D. H. Elger, and D. L. Costill. Muscle respiratory capacity and fiber type as determinants of the lactate threshold. J. Appl. Physiol. 48:523-527, 1980.

9. Kindermann, W., G. Simon, and J. Keul. The significance of the aerobic-anaerobic transition for the determination of work load intensities during endurance training. Eur. J. Appl. Physiol. Occup. Physiol. 42:25-34, 1979.

10. LaFontaine, T. P., B. R. Londeree, and W. K. Spath. The maximal steady state versus selected running events. Med. Sci. Sports Exerc. 13:190-193, 1981.

11. Mader, A. and H. Heck. A theory of the metabolic origin of "anaerobic threshold". Int. J. Sports Med. 7 Suppl 1:45-65, 1986.

12. Wahren, J., L. Hagenfeldt, and P. Felig. Glucose and free fatty acid utilization in exercise. Studies in normal and diabetic man. Isr. J. Med. Sci. 11:551-559, 1975

13. Weltman, A., R. L. Seip, D. Snead, J. Y. Weltman, E. M. Haskvitz, W. S. Evans, J. D. Veldhuis, and A. D. Rogol. Exercise training at and above the lactate threshold in previously untrained women. Int. J. Sports Med. 13:257-263, 1992.

14. Yudkin, J. and R. D. Cohen. The contribution of the kidney to the removal of a lactic acid load under normal and acidotic conditions in the conscious rat. Clin. Sci. Mol. Med. 48:121-131, 19

Antonio,

"Finnaly, permit me that i ask you a question. Taked for granteed that the Central Governator is a correct theory, stricktly from the prespective of the Central Governator theory - not muscular benefits - what may be the benefits from running all-out hilly workout from a flat all-out flat workout - if in both cases you work in a all-out intensity?"

Assuming I've understood your question correctly, here is my answer.

Running uphill at max effort would influence the Central Governor in terms of max power output and how long it can be maintained. The pace at which the runner runs uphill will be less than the pace achieved running on a flat surface so presumably the rate of firing for the muscle fibers would be slower, though a greater mass of muscle fibers are activated. Adaptations in the body, including the central governor, would be specific to strength & power output then, not speed.

Running on a level surface, at a max effort, would result in a faster pace and hence faster contration speed and rate of firing, so the adaptations in the Central Governor (and the rest of the body too) would be specific to maximizing muscle fiber firing rate.

I guess I would illustrate the differences between these two workouts by looking at the extremes - compare the differences in performances in sprint cyclists like Mario Sipolini (spelling?) and cyclists that climb really well like Richard Verenque (spelling?).

rivas,

In terms of "lactate threshold" did you note anywhere in the research that, instead of a threshold, blood lactate levels rise geometrically with increases in exercise intensity and hence carb usage? This is now fairly well recognized by physiologists (that no "threshold" exits, the muscle cells aren't going "anaerobic" and that instead lactate rises as a f(x) of carbo utilization). I believe that even Runners World is now on board with the latest understanding of lactate threshold as I saw an article in a recent issue on this topic.

Now what needs to happen is to come up with a new term to adequately describe the intensity associated with what used to be incorrectly known as "lactate threshold".

I really only want to talk about the Noakes' theory and the related intermittent training data, but it appears to me that BOTH Richard and Phoenix have misinterpreted/misrepresented some data, and I'll mention one case for each:(1) On Richard's website, there is discussion of RC Hickson's research on competitive running and aerobic power done at the University of Illinois at Chicago in the 1970's. As noted by Richard, the training consisted of running as far as possible for 40 minutes and training at VO2max on a cycle ergomometer on alternate days, resulting in perhaps the largest increase in VO2max ever reported for a whole training group (+44%!). What is not mentioned by Richard, however, is that this research was duplicated with trained runners by Miksell and Dudley (MSSE, Aug. 1981). They found, even with trained competitive distance runners, a very large increase in VO2max (56.1 to 65) with this training style. But they also found, that experienced runners peaked in 6 weeks on this training style and the rate of improvement reported by Hickson ended quickly. So while this research perhaps points to a way to catch up with Africans in terms of aerobic power, it is also a justification for doing base training--high intensity and just high intensity doesn't work for that long.(2) Regarding Phoenix' contention that all successful marathoners use moderately-high to very-high mileage, Noakes points out on p. 477 of "Lore of Running" that Gert Thys runs 140km per week (this is not the low mileage that Richard mentions, but it is roughly half of what certain gurus on letsrun say you "have" to run) yet the average of his 5 fastest times makes him the fastest marathoner of the 20th century. Steve Jones, another "low" mileage marathoner, was the second fastest on average times, according to Noakes. So, "Where are the low mileage marathoners?" At the top of the list.I'll preface my comments about the Central Governor with the following quote from Renato's training journal for Shaheen (this is from the end of April):

Thu 1 hr moderate 30 min easy + 2 sets of 6 x 100m (track) in 13" recovery 15" between every test, and 5 min between sets (this one is called "intermittent training", and is the best way of training for improving the threshold before some lactacid training)

If the entire theory about anaerobic threshold training was correct--and the Central Governor theory wasn't--the above quote would make no sense: 1200 meters of very fast work would not raise the threshold better than a larger volume of work at/near the threshold. But I use a similiar workout (somewhat faster but with more rest) and I know that Renato's right about this.

I am not saying (nor is Noakes) that everything is about the brain and that everything else going back to Hill goes out the window. But it seems to me that with the Central Governor, we have a situation analogous to the Theory of Relativity in that the best justfifications for the new theory are the things that we can measure which the existing theories don't explain adequately.

There are a series of research studies on intermittent training conducted at intensities that are now referred to by physiologists as "supramaximal," which is effectively sprint level intensity. MacDougall(1998) makes the point that above 140% VO2max the stimulus is intensity-based, while at lower intensities, the stimulus is volume based (which would be consistent with a Central Governor, of course). In the case of MacDougall, an average of 7 bouts of 30 seconds on a cycle ergonometer (210 seconds of training) 3X a week for 7 weeks resulted in an increase in VO2max of 7% and an increase in Citrate Synthase of 36%; Other researchers such as Izumi Tabata have results as high as a VO2max increase of 15% and CS increase of 45% for training periods no longer than 4 minutes at workloads as high as 210% VO2max. These results are largely based on humans, not rats, and the results are consistent across both untrained and trained subjects; The largest VO2max increase demonstrated thus far for intermittent training (Tabata's results) are in fact based on trained, elite subjects. Tabata has similiar results on glucose transporter activity, and, in a rat study, results showing intermittent training endurance improvement similiar to the swimming equivalent of LSD.

Antonio, I think the reason that this new stuff seems to work while (mostly) hard intervals did not work for the Portuguese runners is the intensity levels. 140% VO2max pace faster than 800 meter race pace, and distance runners, aside from 400-800 or Coe types, rarely train at this pace. Also, the sprint-based training is NOT lactate tolerance (the rest in some cases is very short, but the repeats are also short), so it does not perhaps produce the same lactate loads as 8X400 @60 second rest. Very high intensity training is not new (Astrand did research on it), but I don't think the intensity levels being used now were used decades ago.

Speed,

Great post.

I would like to address your point about misinterpret/misrepresenting data on my website. Before doing so though, we are talking about the article where I reviewed Hickson's 5 studies, yes? Did you note if I discussed either peaking or overtraining in that article?

rivas,

What do you mean what about the "lactate shuttle?" I pretty much described the lactate shuttle process, just because I didn't call it by name does not mean I did not talk about it. Please tell me you recognized it. As for "the 'lactate shuttle' as described by George Brooks and his colleagues at the University of California-Berkeley, the lactate shuttle involves the following chain of events:

1. Lactate is formed in ample amounts in tissues in which glycogen and glucose are being broken down at high rates (for example, in your leg muscles when you are running at a strenuous pace). As we indicated, pyruvate is actually formed first; as pyruvate 'piles up', it is readily converted to lactate.

2. After pyruvate is converted to lactate, the lactate can slip quickly and quietly out of cells and into surrounding tissues and the blood. This 'lactate escape' in effect prevents glycolysis (the conversion of glucose into pyruvate) from shutting down (if pyruvate built up to overly generous levels, glycolysis might 'back up', thwarting energy production). As lactate leaves hard-working muscle cells, it can be 'picked up' by other muscle cells and tissues. This departure of lactate from cells engaged in strenuous activity is sometimes called the 'spilling' of excess lactic acid into the blood.

3. The muscle cells and tissues receiving the lactate have the option of either breaking down lactate for fuel (lactate is a rich source of ATP, the key 'energy currency' within cells) - or else using lactate as a building block for the formation of glycogen. The glycogen created from lactate can simply hang around quietly in cells until energy is needed at a later time."

I got the above info from Peak performance online if you want to go and view it.

Sounds pretty much like what I stated earlier.

Nice citations on your post by the way. I am very impressed. Makes my posts look amateur. I might have to start working harder at this so I can keep up.

Richard,

I agree that a lactate threshold may not exist, but your lactate does not start steadily climbing until after a particular speed or intensity is reached. I can maintain a steady blood lactate level at a range of pace from 6:00-5:30 per mile. This is a 30 second range and shows that just because I increase pace, I do not increase my blood lactate concentration in a linear fashion. This is probably different for everyone so you can’t just suggest that blood lactate levels climb in a linear fashion, because this is not necessarily true. I am sure we could still just refer to the ventilatory threshold, since this change in breathing frequency is often observed, not always however.

balance,

I guess it would depend on the meaning of "steadily climbing" (sorry if that sounds too similiar to "depends on the meaning of 'is'"). My understanding is that lactate begins increasing as soon as exercise begins and increases with each increase in exercise intensity. Early on, at low intensities the rise in lactate is small. As intensities get inceasingly closer to max though lactate increases in increasingly larger amounts. So, lactate increases at an increasing rate from the on-set of exercise to max intensity - a geometric rise.

My preference would be to prescribe intensities with no reference to lactate at all. %HR, RPE, or pace reference (10k pace, 5k pace, etc) could reasonable used in lieu of.

On another note, it sure has been enjoyable reading your comments and discussing these things with you. I appreciate your knowledge, passion, and ability to articulate your thoughts.

Best regards,

Speed Kills wrote:

So, "Where are the low mileage marathoners?" At the top of the list.

DING-DING-DING-DING-DING! You practically broke me with this one. When Richard_ speaks of "low-mileage marathoners," he's talking about people training three or four days a week, *not* guys regularly logging 90 and 100 miles a week. Surely you can't be this stupid. (When Richard tells you that you've made a "great post," that's a sure sign you need to be more careful with your words.)

I'm trying to take a neutral position about Richard, but some people need to get their facts straight. I'm not talking about some recreational weekend runner doing marathons on light mileage, I'M TALKING ABOUT ONE OF THE BEST MARATHONERS IN THE WORLD training on "light" mileage.

Personally, I don't care about marathons at all, but the facts speak for themselves here. According to Noakes, Gert Thys has run 2:06:33, 2:07:45, 2:07:52, 2:08:30, and 2:09:31, and he runs three quality sessions on the track or road for a volume of 140 km/wk.

The contention has been made thatCANNOT run a fast marathon without high mileage (which to me means 100+ mi/wk). Well, here IS one.

Speed Kills wrote:

I'm trying to take a neutral position about Richard, but some people need to get their facts straight. I'm not talking about some recreational weekend runner doing marathons on light mileage, I'M TALKING ABOUT ONE OF THE BEST MARATHONERS IN THE WORLD training on "light" mileage.

The contention has been made thatCANNOT run a fast marathon without high mileage (which to me means 100+ mi/wk). Well, here IS one.

My point is that your comments about Thys and Jones are completely outside the scope of this horror show of a thread. To people like Richard_, 140 km/wk is MEGA-mileage. There are other threads in which pointing out that people have run 2:06 or 2:07 without the supposedly requisite 120-140 mi/wk would have smackdown value, and I understand your urge to tout the notable exceptions to the "gotta run 20 mi/day" dictum. But in the context of Wingnut Central, you might as well be discussing the price of a large Domino's thin crust vs. a regular Papa John's medium.

I used the phrase "moderately high" to include the outliers like Thys and Jones and stand by my original statement.

Speed KillsBefore to answer Richard i try my best to answer your post, because i finish to read it, and i know right quickly to point in what i guees you are wrong.First let me say that that´s very surprise that in what most claim to be a debate with a scientific goal and about ohysilogy you quotes Renato. Let clarify why i say this. I´ve seen and read lots of Reanto´s stuff in the last years. I also did share some personal e-mails with Renato. Then i think i know what i´m talking about. Renato may be a very good coach, a very generous coach, with big influence etc. but he himself says that the physilogistys may not pay attention to his definitions because since he posts as a coach he don´t use the scientific and physilogy terminology.Reanto calls endurance what´s different than the scientific meaning of endurance, Renato also calls "anaerobic thershold" may be to something diffrent than the normal use of anaerobic thershold. This is just an example. If you pay attention to Renato in one of his writes ro articles (even here in LetsRunCom)he says today one thing, tomorrow he will forget what he said and he will say differently.Haven´t you see no incorence to what he said earlier on and with the last MensRacing interview. I can quote uyou more than 50 points od his statements in that interview that he says diffrently in other articles, interviews, he simply don´t cares. If you are interest to know point by point in what i think that he says diffrently e-mail me and i will tell you later on. Besides, Renato himself needed to clarify some points of that interview - in my opinion becvause not all is perfect. This is one point - REnato dismissses himnself and isn+t accurate at all with the treminologie, and the problem that´s not about english, that´s about his temperament, because i know italian enough to see that´s the same in italian.Second point is about this.

Spped Kills. First what Renato or you calls intermittent training that´s a training that is named "ultra-short intervals" since all training that´s not in continuum that´s intrermittent. then the meaning of intermittent means all that´s not continuum. Second, may be that you and Renato you are right - that this coorespond to an anaerobic threshold - but you miss the reason. Since the pace is fast (let´s say for a 7:53 steeple/7:30 flat (?) runner like Saheenan that´s fastyer than pace race 7:30 that´´s 15sec in 100m, then 13 sec that´s not all out but that´s in an intensity that if you delay the effort that´s also anaerobic, but of course 13 secs 100m bouts that´s not enough to bring a 7:30 flat in anaerobic threshold. The reason that when he ends 20 bouts=1200mts he is anaerobic that´s not the number of reps. He could go for 10kilos without really no anaerobic lactate concentration. the reson why he goes into anaerobic threshold that´s THE SHORT INTERVAL PAUSE. This is no more than back to the 50s to Gresheler and Reidell physilogists - to create "artificially" anaerobic concentration you don´+t need to go longer or faster, you simply need to have incomplete intervals. Why? If you read the Renato´s lacatate tests about his 800m runners - you will see that right after they end each rep and each set they have less lactate acumulation than after the next minute. What i want to say is this, despite that the cardio-vascular system recovers during the standing interval pauses, the lactic acid increases. This is the basic and original principle of

interval training from the Freiburg school, they use quite incomplete intervals to produce an extra "load" of latic acid and since the reps that gioes on and on with that uncomplete pauses they move up to an hard effort. Each new rep/set that´s harder than the past one, despite that the pace avarege may be the same. This is a detail (as to say) that most of the americans and many nother they ignore and they misunderstood. That what´s named interval training is based "in the incomplete interval pause - and originally active pause as Zatopec or Gordon Pirrie or Gaston Reiff or Schade the used to do, not passive intervals but active one recover. But back to the main issue of my post, yiun are right about that this 2X6X100m/13sec rec=15sec works in the anaerobic threshold zone, but the reason that´s not because the Central Governator but because he uses a "artificial" very sophisticate to high up the lactic acid- uncomplete reps that does´t give him enough time to recover, and then the lkactic acid is going up. Try the same 2X6X100m in 13sec for that same runner but witth 1 minute interval or 3minutes interval (why not) that+s the same 1200m in 13sec poace but in the end he isn´t in the anaerobic thershold lactate. Do you see my point ?

Now about other subject. It really amazzing how people that claims from the scientific debate uses some data. Let´s see

Do you call this a scientific point of view ?

To quote some "cirurgical scalpe" examples to make us belive that he is right?

Do you know anything of statistic calcul of probabilities?

(forgive me my english). Is a universe of 5 more interesting to prove a hyphotesis than a larger universe fo hundreds or thousands?

What is the improvement from the potencial of Thys when he start training and later on whe he did that 2:07 ?

Last weekend they did Rotherdam marathon, the 2:07:12 that Lopes did in 1985, is better than what they did this weekend. But i think that Lopes trained less than they do actually. but i don´t want to fool no one with a so weak argument. I dare to say why someone like you or Noakes, that uses to have a scientific ming uses a so weak argument.

I also could argue that after that Steve Jones did that 2:07:12 he was no more able to do less than 2:30min. And about Thys, he uses to do so many bad runs - both they did/do lack of consistency due to lower mileage.

First we need to know what 140 kilos by week that means what? 140kilos in terms of a 12 specific marathon plan, of a whole season, of a whole career of what? Not Gerard Thys, neither Steve Jones they didn´t prove that they are consistent marathon runners.

I also can claim that Lopes isn´t also an high volume mileage relate to actual standards, and alkso he wasn´t consistent enough - he give up from 3 marathons in 7 attemps. Of course in one he did 2h07:12m WR - he didn´t use to do long runs, he competes a lot, and he was Olympic winner, so may be lopes is one more for the Noakes list. But he used to win over Steve Jones in all track runs - and as Ruichard says (and i agree) the faster wins if he trains. But wait...when he did start specific marathon plan why is the reason he did try to do more miles tha he used to do when he wanted to be ready for short runs ? Why? If the intensity runs that works he would have tried intenser ones but he didn´t,,he knew that despite he hates to train high volume that works.

Finally i want t comment what you said about what you say in the sentences

Excuse me Speed. I´m one of the men in the world that knows more data about the portuguese and since i´m 50 yeras old and my father he were also a runner, since young kid that i´m close to the portuguese tracks. In the past, the portuguese workout system is this one. A group of runners. they start a a workout in group. ex: 10X400m or 6X800m.

Sometimes it was short reps (200m to 400m, sometimes it was medium distance reps (600m to 800m), some are long reps,. the total distance that´s from 2000m to 4000m total - no more.

Ther´s no previous pace estimate. The coach advise them to run the faster they are able - then all-out. What you said about that not faster tha 800m makes me smile. I see you never seen that or you would say what you said. That´s simply the faster and intenser that they were able. Of course that they did each rep like a competition. The start each rep as a start line and they end like that they havewith place classifications for each rep ! Some do 58seconds - the runners of short distance events or the runners that are the best of the group. But this doesn´t mean that the fast runners in the reps (those who end the reps quickly) they try harder than the last/worst runner. the last runner tried to run all out, despite that the first did 58seconds for that 400m and the lat one did 65sec.

Then they participate in competitions and what´sthe conclusion? That the faster runner did best performances according his workouts range pace. Ex: the 8X400m 58sec did 1500m in 3:45 (a 60sec pace for 400m) but the 8X400m 65sec he did 4:20 pace (a 72sec pace). need to say that they use long intervals to able all runners to recover.

I'm pretty sure I'm in agreement with most of what Antonio says, but damn if it's not almost impossible to tell.

Calm down, speedy. I think if you read e-meter's post again you'll understand. Nobody says Thys is not a great marathoner. Most would say that he is a "low-mileage" marathoner but you should be cautioned in your response. Two thoughts you may wish to consider:

1. If your contention is that since Thys (the most consistently great marathoner of the last 10 years) runs great on 140k so the rest of us would do well to train the same then you've got a slight quandry. I've read several times (though I don't have the actual reference--Bakken's website?) that El Guerrouj routinely hits 180-200k during base training. Does this therefore mean that marathoners should train 100mi/wk? Maybe Noakes will put his in better perspective:

2. What you forgot to post was "This observation that many of the top athletes achieved world-class performances on little training emphasizes the importance of genetic ability--not everyone can achieve such performances on what others might consider to be relatively little training. It also highlights the law of diminishing returns. To improve performances even further, these athletes have to increase their training markedly, thereby risking overtraining. For example, Jim Peters had to double his training distance and maintain the same intensity to lower his marathon time by nearly 12 minutes from 2:29:28 to 2:17:39."

sorry

slomo wrote:

Does this therefore mean that marathoners should train

... 100mi/wk?

apparently you can't use brackets on this forum. my mistake. the third time's the charm, I promise:

does this therefore mean that marathoners should train less than 100 miles per week and milers train more than 100 miles per week? obviously not. go on to point #2.

Meter,

I appreciate you trying to speak for me, but would appreciate it if you could be more accurate as to what I would say or what I mean, etc.

To clarify for Speed, here is what I recommend. Training frequency should be based on recovery. Some people recover really fast. Others recover really slowly. Most fall somewhere in the middle.

Recovery rate falls on a distribution curve. I can't prove it but I believe the mean for recovery is somewhere around 2-3 days. Half will recover faster and half will recover slower. (of course workouts of different intensities and distances tax the body to different degrees and hence result in different recovery times but you get the idea.)

If you are one of those people that recovers in one day, it makes sense to train daily.

If it takes you a couple of days to recover you should run less frequently.

For people with average recovery ability I basically recommend 3 days per week of running, 1-2 days per week of cross training, and 1 day of strength training.

For runners with above average recover rates, I suggest more frequent running - say 4-5 days per week.

For those exceptional few who recover really fast, the elites of the world, they can train 6-7 days per week. Even more if their recover rate permits. (I recall a study that found one individual recovered in about 4 hours. I'd train that dude twice daily.)

I once worked with a runner that recovered so slowly that more than 1 workout per week resulted in stress fractures. How often should she train? After her third stress fracture I advised her to stop running and take up another activity.

It seems that some people see the "2-3" days per week of running and miss everything else. Perhaps their brains stop working at that point? Who knows?

Lastly, it seems to me to be a mistake to say that 100+ mpw is what all marathoners or all distance runners or all ... should strive to run. People have different abilities. I would guess there isn't a single person on this forum who would sincerely make the case that we are all exactly the same in terms of abilities. Suggesting that we should all strive to eventually run the same high weekly mileage flatly contradicts the belief that individuals are just that - individuals.

Richard,

In the research that I have done, and I have so much because my thesis incorporated lactate metabolism. According to McLlroy (16), were the first to name anaerobic threshold to define a particular workload at which blood lactate levels first begin to rise above resting levels during a test to measure exercise tolerance. An increase in expired ventilation in milliliters per minute that was greater that the rate of on going increase in O2 uptake also began to occur. The term anaerobic threshold seemed logical to suggest the notion that the anaerobic metabolic process supplemented the aerobic process to provide energy for movement. The term anaerobic refers to region of change (2,16).

The literature that I have come across has never stated that lactate causes muscle to stop contraction. Measurement of blood lactate is an easier way to measure what is happening inside the cell. (Just like we measure ferritin to get an indication of bone marrow iron storage for athletes that are anemic.)

As discussed, during intense exercise at anaerobic threshold, a build up of hydrogen ions and attache to hemoglobin, lower muscle ph inhibits enzymes that generate ATP for muscle contraction (12,13,14). If more lactate that is cleared the further use of the oxidative (aerobic) system (15). Lactate is the byproduct of glycolysis which is produced and used by the muscles. The production of lactate is a reaction catalyzed by lactate dehydrogenase which involves the reduction of pyruvate to lactate. The rate of production increases as the exercise intensity increases. The problem with increased lactate production is the association of acidosis.

As the level of exercise intensity increases, the body reaches a point at which the oxygen system can no longer be utilized. At this point, the body begins to produce more lactate. The demands for energy overstress the second phase of the oxygen system and when the systems cannot efficiently and effectively neutralize and metabolize lactate beyond it’s production, acidosis sets in. An emergency system is then activated whereas only carbohydrates are used as fuel. Within seconds or minutes, depending on the athlete’s level of training, exercise performance is drastically reduced (17).

A high lactate value is evidence that the aerobic energy system is failing causing acidosis in and around the cells. Enzymes in the muscle cell may become damaged, which decrease aerobic endurance capacity. Cell wall damage causes leakage from the muscle cell into the blood. A high intensity workout without sufficient recovery causes acidosis which in turn may then lead to injury and overtraining (8).

Lactate threshold, which is also termed anaerobic capacity is expressed as a percentage of VO2 max, is one of the best determinants of an athlete’s pace in endurance events such as distance running and cycling. It has also been thought to reflect the interaction of aerobic and anaerobic energy systems. Researchers have said that this may represent the shift toward anaerobic glycolysis (18).

As exercise intensity approaches 60% of VO2 max, lactate production also increases and correlates with muscle lactate. The intensity at the lactate threshold represents the maximal intensity at which steady state exercise can be maintained (10,18). Every individual can maintain a certain running pace for a long period of time without lactate accumulation. If the pace is increased to a level where acidosis occurs, this forces the person to stop or slow down.

Other explanations for the lactate threshold include a decreased removal of lactate from circulation, an increased recruitment of fast-twitch glycolytic motor units, an imbalance between the rate of glycolysis and mitochondrial respiration, a decreased redox potential, muscle hypoxia (a lower muscle oxygen content), and ischemia (lower blood flow to skeletal muscle) (12).

I know you don’t believe in VO2max concept because we have disagreed on that topic but this is just as an example.

Change in maximal oxygen consumption is used to indicate a change in exercise endurance. Blood lactate response to training adapts to a greater degree than VO2 max. This is especially true with highly trained individuals who may show little or no change in VO2 max, but a change in endurance performance (4).

Coyle et al. (3) compared six ischemic heart disease patients to healthy runners with similar training programs. The patients hade a significantly (P < 0.05) lower

VO2max. Despite having a lower cardiac output the trained patient were able to keep the same speed as the normal subjects. The ability to maintain the same pace was associated with high lactate threshold relative to VO2max. Much research has shown that blood lactate related thresholds can increase with training beyond the point where VO2 max fails to increase (5,6,7,10,11,17).

How can you deny the benefits of using lactate as an aid to exercise performance?

When research has proven that it may help.

Balance,

Ok, I gotcha that sentence that you wrote just through me off.

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11. Poole, D. C., S. A. Ward, and B. J. Whipp. The effects of training on the metabolic and respiratory profile of high-intensity cycle ergometer exercise. Eur. J. Appl. Physiol. Occup. Physiol. 59:421-429, 1990.

12. Robergs, R. A. and S. Roberts. Fundamental principles of exercise physiology: for fitness, performance, and health. Boston: McGraw-Hill, 2000, xvii, 287 p.

13. Sjodin, B., I. Jacobs, and J. Karlsson. Onset of blood lactate accumulation and enzyme activities in m. vastus lateralis in man. Int. J. Sports Med. 2:166-170, 1981.

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16. Wasserman, K. and M. B. McLlroy. Detecting The Threshold of anaerobic metabolism in cardiac patients during exercise. Am. J. Cardiol. 14:844-852, 1964.

17. Weltman, A., R. L. Seip, D. Snead, J. Y. Weltman, E. M. Haskvitz, W. S. Evans, J. D. Veldhuis, and A. D. Rogol. Exercise training at and above the lactate threshold in previously untrained women. Int. J. Sports Med. 13:257-263, 1992.

18. Wilmore, J. H. and D. L. Costill. Physiology of sport and exercise. 2nd ed. Champaign, IL: Human Kinetics, 1999, xvii, 710 p.