Concerning the lactate shuttle:
Here is some interesting info, scroll down to the graph which shows that even when lactate is accumulating, in the muscle, there is a gradual increase in lactate oxidation, shown by the blue numbers below zero underneath the red line towards the bottom of the graph.
"It is recommended that the term "O2 debt" be used to describe a set of phenomena during recovery from exercise."
So we've corrected "oxygen debt" with "O2 debt"?
This does not seem like a remarkable step forward!
wellnow wrote:
So 100m races are mostly anaerobic because aerobic respiration cannot provide energy fast enough, but it does supply most of the energy after the race is over.
This statement just makes my head hurt . . .
wellnow wrote:
Concerning the lactate shuttle:
Here is some interesting info, scroll down to the graph which shows that even when lactate is accumulating, in the muscle, there is a gradual increase in lactate oxidation, shown by the blue numbers below zero underneath the red line towards the bottom of the graph.
http://www.lactate.com/lactate_cycling.html#VLamaxchart
I'm confused by this. First to be clear, I'm looking at the first graph from the top of the article.
I believe you are saying that the net negative slope of the blue line, net lactate production, is indicative of an increase in lactate oxidation. If that's your interpretation, how do your reconcile this with the fact that the reduction in net lactate production seems to be remarkably well correlated with net power?
The interesting part of this graph to me, and the point I've been trying to make, is illustrated by the slope of the red line, lactate concentration. For the first 10 minutes it is sharply rising indicating that anaerobic metabolisms are producing lactate faster than it is being consumed by aerobic metabolisms. I think you would agree with this. From 10 to 27 minutes the slope is slightly positive indicating near equilibrium between aerobic and anaerobic metabolisms, but still slightly anaerobic in the sense of lactate concentration is increasing. Note that in this state of near equilibrium, something in excess of 90% of power is produced via aerobic metabolisms. From 27 minutes to about 45 the lactate is essentially at equilibrium or slightly negative slope indicating the cyclist is at or slightly below lactate threshold or, in the classical sense, aerobic. In the last 3 minutes our cyclist in a "kick to the finish" is again producing lactate through anaerobic metabolisms much faster than it is consumed by aerobic metabolisms and, in the classical sense, has "gone anaerobic". Note again, that this sense of "going anaerobic" doesn't deny that the overwhelming majority of the cyclist's power is derived from aerobic metabolisms.
I believe my discussion above pretty much consistent with common usage of "aerobic" and "anaerobic" as applied training. While there has been changes in the understanding of the mechanisms and synergy of aerobic and anaerobic metabolisms, I don't see were there's anything wrong with the above usage.
Exactly right.
If we go back to the origin of all this:
There is much confusion over the definition of the words aerobic and anaerobic.
According to the popular definition, most people think that when they get out of breath towards the end of a 5000m race that they are "going into oxygen debt" or "going anaerobic"
We've now have nominations to improve our wording to "going into O2 debt" and "increased reliance on anaerobic metabolism."
I'll stick with "oxygen debt" and "going anaerobic" thank you.
Oooops.
Should read
We've now seen nominations ...
Sure would be nice to have the capacity to edit posts!
B0ulderite wrote:
"It is recommended that the term "O2 debt" be used to describe a set of phenomena during recovery from exercise."
So we've corrected "oxygen debt" with "O2 debt"?
This does not seem like a remarkable step forward!
What Gaesser and Brooks are saying is that when you call it 02 debt or oxygen debt, bear in mind that the orignal scientific explanation by Hill i.e. the supposed phenomenon of "going anaerobic" is no longer applicable:
As no complete explanation of the post-exercise metabolism exists, it is recommended that the term "O2 debt" be used to describe a set of phenomena during recovery from exercise. The terms "alactacid debt" and "lactacid debt," which suggest a mechanism, are inappropriate. Use of alternative terms, e.g., "excess post-exercise oxygen consumption" (EPOC) and "recovery O2," will avoid implication of causality in describing the elevation in metabolic rate above resting levels after exercise.
Their term EPOC has been adopted by physiologists, but the term oxygen debt will remain in the public's perception, just as they new it would 24 years ago.
Citizen Runner wrote:
wellnow wrote:Concerning the lactate shuttle:
Here is some interesting info, scroll down to the graph which shows that even when lactate is accumulating, in the muscle, there is a gradual increase in lactate oxidation, shown by the blue numbers below zero underneath the red line towards the bottom of the graph.
http://www.lactate.com/lactate_cycling.html#VLamaxchartI'm confused by this. First to be clear, I'm looking at the first graph from the top of the article.
I believe you are saying that the net negative slope of the blue line, net lactate production, is indicative of an increase in lactate oxidation. If that's your interpretation, how do your reconcile this with the fact that the reduction in net lactate production seems to be remarkably well correlated with net power?
The interesting part of this graph to me, and the point I've been trying to make, is illustrated by the slope of the red line, lactate concentration. For the first 10 minutes it is sharply rising indicating that anaerobic metabolisms are producing lactate faster than it is being consumed by aerobic metabolisms. I think you would agree with this. From 10 to 27 minutes the slope is slightly positive indicating near equilibrium between aerobic and anaerobic metabolisms, but still slightly anaerobic in the sense of lactate concentration is increasing. Note that in this state of near equilibrium, something in excess of 90% of power is produced via aerobic metabolisms. From 27 minutes to about 45 the lactate is essentially at equilibrium or slightly negative slope indicating the cyclist is at or slightly below lactate threshold or, in the classical sense, aerobic. In the last 3 minutes our cyclist in a "kick to the finish" is again producing lactate through anaerobic metabolisms much faster than it is consumed by aerobic metabolisms and, in the classical sense, has "gone anaerobic". Note again, that this sense of "going anaerobic" doesn't deny that the overwhelming majority of the cyclist's power is derived from aerobic metabolisms.
I believe my discussion above pretty much consistent with common usage of "aerobic" and "anaerobic" as applied training. While there has been changes in the understanding of the mechanisms and synergy of aerobic and anaerobic metabolisms, I don't see were there's anything wrong with the above usage.
***********************************************************
I'll tell you why it is wrong to use the term "going anaerobic"
Because, as the graph shows, both aerobic and anaerobic metabolism are used all the time. The reason why the cyclists power dips slightly after halfway should be obvious; that is how most people race. It is rare to maintain an almost constant power output in any race, especially in a cycling time trial.
Also, as you race you can become more economical as the race progresses, so that you can maintain a pace with slightly less power output.
Even though the cyclist's power drops slightly for a few minutes, lactate is still showing a general accumulation from start to finish and a general increase in lactate oxidation from start to finish.
B0ulderite wrote:
Exactly right.
If we go back to the origin of all this:
There is much confusion over the definition of the words aerobic and anaerobic.
According to the popular definition, most people think that when they get out of breath towards the end of a 5000m race that they are "going into oxygen debt" or "going anaerobic"
We've now have nominations to improve our wording to "going into O2 debt" and "increased reliance on anaerobic metabolism."
I'll stick with "oxygen debt" and "going anaerobic" thank you.
But there isn't an increased reliance on anaerobic metabolism, as the race progresses, but the opposite.
Neither are you "going into oxygen debt" when you breathe harder.
You are defending the old school misinterpretations, which is understandable, but I wish to point out the errors in these interpretations, because they conflict with what physiologists are saying.
These misinterpretations are mostly 85 or more years out of date so;
Let's get up to date here.
Citizen Runner wrote:
wellnow wrote:So 100m races are mostly anaerobic because aerobic respiration cannot provide energy fast enough, but it does supply most of the energy after the race is over.
This statement just makes my head hurt . . .
Why does the statement make your head hurt?
The text in the link from lactate.com talks about lactate as being produced by "The anerobic system" but this I feel is not only incorrect, it is dumbing down the science to a degree that will only confuse the layman even more.
Lactate is NOT produced by "The anerobic system" it is produced by the lactate dehydrogenase reaction or LDH reaction and this reaction supplies fuel for both anerobic and aerobic metabolism.
Before it was generally known that lactate was readily oxidisable (used as an aerobic fuel) the terms Anerobic Respiration and Anaerobic Glycolysis were used to describe the LDH reaction. These terms are innacurate and thus George Brooks has proposed the terms Fast and Slow Glycolyis to desribe glycolysis more accurately.
I agree with Brooks. The American researchers are trying to reduce the confusion for the layman.
The European researchers on whose work lactate.com is based are making things more confusing and thereby more profitably for them if you subscribe to their methods of coaching.
wellnow wrote:
Citizen Runner wrote:This statement just makes my head hurt . . .
Why does the statement make your head hurt?
". . . it does supply most of the energy after the race is over." That statement doesn't bother you? If our athlete were running 100 m strides, I'd be ok with something like "aerobic processes during the recovery intervals consume excess lactate produced during the hard effort, reducing the net lactate concentration, and producing ATP, which contributes in part to the next stride repeat". But in a race, energy produced after the fact doesn't do much for the race effort, don't you think?
Yes ok, but what is the problem? Does every explanation have to be longwinded?
So you want more information about lactate shuttling?
Howzabout this:
Role of mitochondrial lactate dehydrogenase and lactate oxidation in the intracellular lactate shuttle
February 1999
George A. Brooks*, Hervé Dubouchaud, Marcia Brown, James P. Sicurello, and C. Eric Butz
Exercise Physiology Laboratory, Department of Integrative Biology, University of California, Berkeley, CA 94720-3140
INTRODUCTION
Arterial lactate concentration is low and stable in resting humans (1, 2) and other mammals, such as rats (3) and dogs (4), giving no indication of relatively high flux rates that range from 0.5 to 1.0 mg/kg per min in resting men (1, 2). In resting mammals oxidation accounts for approximately half lactate disposal and gluconeogenesis approximately 20% (1-5). During sustained submaximal exercise, blood lactate rate of appearance increases as a direct function of metabolic rate (1-3); however, arterial lactate concentration increases little during sustained moderate intensity exercise because disposal through oxidation (80%) and gluconeogenesis (20%) matches appearance (1, 2, 6). During both rest and exercise, skeletal muscle is a major site of lactate oxidation as well as production (1, 2). Differences in circulating lactate concentration between individuals with similar rates of appearance are attributable to variations in clearance rate (3, 5). At exercise onset, net lactate release from working muscle contributes to the elevation of circulating lactate concentration, but as exercise continues, working muscle consumes and oxidizes lactate on a net basis as production continues (1, 7). Studies on mammalian muscles in situ demonstrate that in working muscle lactate uptake and oxidation are concentration dependent (8, 9), and similar data are available on human skeletal muscle (1, 2, 7, 10) and heart (11).
The cytosol of heart, skeletal muscle, and other cells is abundant in lactate dehydrogenase (LDH) (12). The equilibrium constant for LDH is 3.6 × 104 M1, and muscle LDH isoforms demonstrate characteristics of low Km and high Vmax, resulting in lactate production regardless of the state of oxygenation (13, 14). That working skeletal muscle tissue can simultaneously produce, consume, and oxidize lactate has been explained by the lactate shuttle mechanism (15), a model that assumes fiber heterogeneity with lactate production occurring in fast-glycolytic (type IIB) fibers and oxidation in slow-oxidative (type I) fibers. However, the model of a cell-cell lactate shuttle is less adequate for predicting lactate metabolism in resting muscle tissue, which appears fully oxygenated (14), but which releases lactate on a net basis (1, 7).
To evaluate the role of mitochondria in balancing lactate production and oxidation as part of an intracellular lactate shuttle (16), we respired isolated rat cardiac, skeletal muscle, and liver mitochondria with lactate and pyruvate in the presence or absence of known inhibitors of metabolism. As well, we probed for the presence of LDH isoforms in mitochondria by electrophoresis and electron microscopy. Results support the conclusion of a mitochondrial role in cellular lactate oxidation (16) and provide an explanation of the high correlation between lactate clearance during exercise (3) and muscle mitochondrial respiratory capacity (17).
Later in the discussion:
The lactate shuttle hypothesis (15) posited a role of muscle fiber type heterogeneity in lactate exchange among tissues. This supposition was based on the known lactate concentration and mitochondrial density differences between types I and IIB muscle fibers (29, 37). Subsequently, studies on isolated sarcolemmal vesicles (38) showed that sarcolemmal transporters facilitate lactate flux according to concentration and pH gradients. More recently, candidates for seven putative cell membrane monocarboxylate transporters have been cloned and sequenced (39, 40). Based on current evidence, we believe that this scenario of lactate flux between glycolytic and oxidative fibers holds, even if no recruitment occurs. Given similar glycolytic rates in glycolytic and oxidative muscle fibers, glycolytic fibers will tend to accumulate and release lactate because of lesser mitochondrial density. In contrast, highly oxidative fibers will act as lactate sinks because of greater mitochondrial content.
Although the model of an intracellular lactate shuttle (16) is a unique proposal for mammalian liver and striated muscle metabolism, the paradigm is apparently not unique in nature. Mitochondrial matrix LDH is well characterized in sperm of boar (41), mouse, rat, and rabbit (42), and pyruvate-lactate shuttles have been proposed for these systems. Additionally, LDH has a predominant mitochondrial localization in placental trophoblast cells (43). Thus, parallel models of mitochondrial lactate oxidation involving mitochondrial LDH exist in cells of the same and related phylogenies. Further, in Saccharomyces cerevisiae Flavocytochrome b2 is a soluble L-lactate cytochrome c oxidoreductase found in the mitochondrial intermembrane space (44) that couples lactate dehydrogenation to reduction of cytochrome c (45). Hence, S. cerevisiae readily consume and oxidize lactate by a mechanism analogous to that which we propose for mammalian striated muscle and liver mitochondria.
In conclusion, results confirm the presence of mitochondrial LDH (30-32) and support a role for mitochondrial LDH in tissue lactate clearance and oxidation. By virtue of this role, long-standing problems of understanding why fully oxygenated cells readily form lactate are obviated. Glycolysis inevitably results in cytosolic lactate production because the equilibrium constant for LDH is far in the direction of product and the free energy change (G°' = 6 kcal/mol) is large. However, mitochondrial lactate oxidation can balance cytosolic production, with resultant being zero cellular net lactate release. Glycogenolysis and glycolysis in excess of the corresponding rate of mitochondrial PDH activity results in muscle lactate accumulation and net release regardless of absolute flux rates or state of tissue oxygenation (1, 7). For example, epinephrine stimulation of glycogenolysis in resting muscle results in lactate release during constant or elevated oxygen consumption (46). Moreover, in a respiratory steady state, elevation of arterial lactate concentration results in a switch from muscle lactate net release to uptake as well as suppression of glucose uptake because exogenous lactate substitutes for endogenous (8, 10). Further, under conditions of low glycolytic flux, resting mixed skeletal muscle will release lactate on a net basis (1, 2, 7), whereas working myocardium with a high glycolytic flux rate will consume and oxidize lactate on a net basis (11). Results are consistent with the presence of an intracellular lactate shuttle.
Now, look again at the graph for the cyclist riding the 50 minute Time Trial. This kind of race is about the equivalent of a 5000m race.
http://www.lactate.com/lactate_cycling.html#VLamaxchart
From 28-36 minutes, ther is a more or less steady state of effort, but look at the muscle lactate level, it is over 16 mmols. This equates to a blood plasma lactate concentration of about 11 mmols. This is WAY above the commonly accepted "Lactate Threshold" of 4mmols and is in line with what Renato Canova was talking about when he first started posting here in 2003.
Renato wanted to talk about the lactate shuttle, but he didn't get much discussion from the letsrun coaches and physiologists.
Lactate shuttle is the new Lactate Threshold, which is really just the old Anaerobic Threshold concept with a different name. Let's get up to date here.
How can all of this information help runners to improve their performance? that is the big question.
Well, an awareness of the fact that even though we are accumulating a lot of lactate but we can still increase the oxidation of that accumulated lactate is very important for athletes and coaches to know. This shows that our ability to improve oxidative capacity of muscle fibers is much higher than many people realize.
So very hard endurance sessions at very fast paces should be seen as aerobic training, not anaerobic training.
The best athletes are not superhumans with rare physical gifts. They are largely unburdened by negative thinking about the training they do. I think of expressions such as "going anaerobic" as implanting negative thoughts in the minds of talented runners who will inevitably underachieve as a result.
Wellnow wrote:
"So very hard endurance sessions at very fast paces should be seen as aerobic training, not anaerobic training."
So what would YOU consider a VERY HARD WORKOUT for the 800/1600 runner that would be challenge the aerobic energy system?
i.e. distance; pace; sets/reps: and recovery
An example of a very hard workout that would challenge the aerobic energy system for an 800/1600 runner would be
4x600m @ 800m target pace. The recovery would be long, several minutes.
Also 10x 400 @ 1600 target pace, 60 seconds recovery.
Obviously you have to build up to these sessions, over a period of months. Also, during the peak racing period, you wouldn't want to train this hard. This type of work should be complete before the most important races.
wellnow wrote: 4x600m @ 800m target pace. The recovery would be long, several minutes.
Also 10x 400 @ 1600 target pace, 60 seconds recovery.
These two sessions are apples and oranges - or more like apples and car engines - light years apart. The second one would be demanding, but doable. The first one is just insane. INSANE I tell you. In fact, I doubt it can be done, long recovery be damned.
The 400s would be "mostly aerobic" (in the commonly accepted meaning of this term) while the 600s would NOT be. Not remotely.
The 600's would be much more aerobic than anaerobic.
That is the purpose of this thread, to point out the difference.
The first few seconds at 800 pace are mostly anaerobic, then gradually the oxidation of lactate increases, i.e. aerobic respiration increases gradually until in the last 50 metres of the race when the pace slows.
During that last 50m however, most of the energy is aerobically derived.
Yes I know this is contrary to what you have been taught, that's why I wanted to set things straight. What you have been taught is wrong, you are not "going anaerobic" in an 800m race, the opposite is true.
wellnow wrote:What you have been taught is wrong, you are not "going anaerobic" in an 800m race, the opposite is true.
Perhaps so, but like many other posters, I don't much care for the semantics, and am not particularly fussed about the strict accuracy of the common usage of terminology.
Have you ever witnessed someone completing 4 x 600 at legitimate 800 race pace in one session? I have serious doubts, but hey I could be wrong.
wellnow,
I'm finding you very irritating and tiresome. Maybe it's just the clumsiness of your writing. But you fail to see what people are telling you, that although "going anaerobic" may not exist in a technical sense (aerobic metabolism continues), the concept as understood is not all that inaccurate as it applies to training and racing.
But, hey, thanks for setting us straight. And for giving us that ridiculous 4x600m workout.