You have to be careful when you say there's not enough oxygen in the bloodstream. It can be misleading. It's actually the oxygen available in the mitochondria that is important. I know, it's picky. But, it's an important fact to keep straight when you start talking about the steps in energy production. It's easy to get caught up in the oxygen/CO2 transport/buffering mechanisms in the blood, but, the crux of the matter of energy production occurs in the mitochondrial environment. It is intracellular/mitochondrial pH, waste removal, transport of ATP, oxygen availablity, etc., at the local level that determines what happens with energy availability.

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Quid quid latine dictum sit altum videtur
(That which is said in Latin sounds profound)

[reply]no, it doesn't restate what you're saying. You said above that lactic acid production negatively affects performance.

They're saying, it doesn't.

It's not the lactic acid that's the problem. It's the hydrogen ion.[/reply]

That is not how I read it. Lactic acid is the source of the hydrogen ion you refer to. Lactic acid production would immediately adversely affect performance if it were not for the buffering to lactate which mitigates the effect of the hydrogen ion, lessening the pH change. Because of the buffering, the detriment on performance is lessened and/or delayed. That is how I read it. Where does it say that lactic acid production does not have a detrimental affect on performance?

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Frank,
An original Ironman and the Inventor of PowerCranks

[reply]You have to be careful when you say there's not enough oxygen in the bloodstream. It can be misleading. It's actually the oxygen available in the mitochondria that is important. I know, it's picky. But, it's an important fact to keep straight when you start talking about the steps in energy production. It's easy to get caught up in the oxygen/CO2 transport/buffering mechanisms in the blood, but, the crux of the matter of energy production occurs in the mitochondrial environment. It is intracellular/mitochondrial pH, waste removal, transport of ATP, oxygen availablity, etc., at the local level that determines what happens with energy availability.[/reply]

Absolutely right. It is complicated and if all of the elements are not at peak efficiency then the end result is always adversely affected. Reduce the effectiveness of the enzymes (proteins) necessary for energy production by changing the pH and the whole ball of wax starts to fall apart.

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Frank,
An original Ironman and the Inventor of PowerCranks

It's lactate that is being produced, not lactic acid. Lactic acid results when free hydrogen ions bind to lactate, forming lactic acid. From the abstract:

Lactate production retards, not causes, acidosis.

... there is a wealth of research evidence to show that acidosis is caused by reactions other than lactate production. Every time ATP is broken down to ADP and P(i), a proton is released. When the ATP demand of muscle contraction is met by mitochondrial respiration, there is no proton accumulation in the cell, as protons are used by the mitochondria for oxidative phosphorylation and to maintain the proton gradient in the intermembranous space. It is only when the exercise intensity increases beyond steady state that there is a need for greater reliance on ATP regeneration from glycolysis and the phosphagen system. The ATP that is supplied from these nonmitochondrial sources and is eventually used to fuel muscle contraction increases proton release and causes the acidosis of intense exercise.

Lactate production increases under these cellular conditions to prevent pyruvate accumulation and supply the NAD(+) needed for phase 2 of glycolysis.

If muscle did not produce lactate, acidosis and muscle fatigue would occur more quickly and exercise performance would be severely impaired.

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Josef
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blog

If you say so.

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Frank,
An original Ironman and the Inventor of PowerCranks

"...if anybody believes that lactic acid causes muscle soreness, they failed exercise physiology ;) "



Actually, I've probably passed many people that still believe lactic acid is responsible for muscle injury. There are only so many misconceptions that can be dispelled in one course.

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Steve

http://www.PeaksCoachingGroup.com

The hydrogen ion isn't necessarily the problem either. As I stated previously, Nielsen, Brooks and others have argued for the protective effect of acidosis in working muscle.

http://www.ncbi.nlm.nih.gov/...p;list_uids=11579166



http://www.ncbi.nlm.nih.gov/...p;list_uids=15326352

The Ex Phys dogma that acidosis prevented muscle from contracting was based on experiments performed under non-physiological conditions, in particular, low temp. Raise the temp to the physiological range and the negative effect of acidosis on muscle contraction is lost.

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Steve

http://www.PeaksCoachingGroup.com

"If you say so. "

I know you weren't referring to me, but I'm still happy we got that resolved.

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Steve

http://www.PeaksCoachingGroup.com

I guess that is all well and good but the studies you referenced only looked at muscle excitability and force, not energy production. Such adaptions would be good for survivability. Lacitc acid could help a weight lifter. I see no benefit for the endurance athlete. Fatique, in my view, is energy production, at least in the endurance athlete. So, your arugment that lactic acid production does not affect performance holds no water with me, at least using those references as argument.

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Frank,
An original Ironman and the Inventor of PowerCranks

I might ask one more question. Exactly what do you believe to be the mechanism that prevents the 400m runner from running at 100m speed for the entire distance. Or the 10000 runner from running at 5000 speed? etc.

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Frank,
An original Ironman and the Inventor of PowerCranks

You'd get the argument from Brooks, Robergs, Nielsen and a bunch of others that lactic acid is not responsible for acidosis. So, whether it's weight lifters or triathletes, lactic acid is of no consequence with regard to acidosis.

Fatigue, in your view, may be simply a matter of energy production, but fatigue in the view of many others is much more than that.

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Steve

http://www.PeaksCoachingGroup.com

Exactly,... impossible to say. It will certainly depend on the energy system for one. The energy systems utilized for the 100 and 400 m are quite different. I suppose, if we had 4 x the store of PCr, that would help. With regard to 5 k pace for the 10 k, well again, fatigue is a complicated matter. The fact that one could maintain 5 k pace for 5 k demonstrates that it is likely not simply a matter of acidosis and energy generation. I guess to me, I'd look at it another way. If we take 100 elite athletes, they would be able to perform a 1 hr TT approximately at their "threshold" (I use quotes so that you can insert your own identifier). The thing is, if we measured lactate levels, steady state at that, they would likely range from 3 mmol up to 10 mmol. The level of lactic acid produced does not necessarily correlate with fatigue. On an individual basis, it certainly correlates with the rate of glycogenolysis, and this is one of the primary factors dictating performance in endurance events, triathlon being a prime example. There are numerous factors contributing to fatigue though, calcium flux pertubations (SR, actinomyosin, mitochondria), electrochemical imbalances, excitability, substrate availability, metabolite accumulation...

So, I would pose the question, what is it that keeps a triathlete from maintaining 1/2 IM pace for an IM distance? Surely not lactate accumulation, or acidosis.

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Steve

http://www.PeaksCoachingGroup.com

[reply]You'd get the argument from Brooks, Robergs, Nielsen and a bunch of others that lactic acid is not responsible for acidosis. So, whether it's weight lifters or triathletes, lactic acid is of no consequence with regard to acidosis.

Fatigue, in your view, may be simply a matter of energy production, but fatigue in the view of many others is much more than that.[/reply]
We might get that argument from them but what mechanism do they put in its place to explain acidosis in the athlete who is performing anaerobically or in the very sick patient who has inadequate oxygen deivery to cellular level? The fact that someone makes an argument one way or the other does not make them right. The theory must explain the observations, all the observations.

Like I said before, I don't believe lactic acid per se is directly responsible for the acidosis observed, at least in athletes. I believe it is the secondary effects of the accumulated high CO2 levels that occur from the buffering of the persistent excessive lactic acid production that results in acidosis, which also explain the labored breathing seen under these conditions.

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Frank,
An original Ironman and the Inventor of PowerCranks

I think of it similarly to Dr. Day, right or wrong. We use up the buffering capabilities of our various systems, and the resultant acidosis interferes with the nuts and bolts of our energy systems. I'm not saying that higher acidity is bad, per se, in fact I believe it to be facilitative in some regards (rightward shift of the oxy-hemoglobin curve for example). But, too much unbuffered acid and the mitochodrial machinery gets buggered. Even if we could increase CO2 removal to a greater rate than our ventilatory system could achieve, I'm not so sure that there wouldn't be another limiter at the local level that would put the brakes on the energy production availability. I do think, right or wrong, it must be local muscle cell factors that are responsible for our exercise limitations.

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Quid quid latine dictum sit altum videtur
(That which is said in Latin sounds profound)

[reply]So, I would pose the question, what is it that keeps a triathlete from maintaining 1/2 IM pace for an IM distance? Surely not lactate accumulation, or acidosis.[/reply]

Don't tell me what is isn't. Tell me what it is. Give us a theory and the support for that theory.

Further, measuring lactate in the venous blood may have little to do with what is going on at the cellular level, especially in the limiting muscle(s). Those who have better muscle balance, working all the muscles equally may fail at higher venous lactate levels than those who are less balanced because they have greater muscle mass turning out low levels of lactate before the first muscle reaches a failure threshold (it only takes one). My colleague Andrew was at the Mapei center a couple of years ago watching D. Nardello being tested after a winter on PC's. He's riding along at 250 watts and the tester was concerned that he was "overtrained" because his HR and lactate was lower than expected. Then they thought about it and, of course, that made no sense. He was simply more efficient (lower HR and lower lactate) and better balanced (lower lactate?). If they had tested him to exhaustion and looked at lactate and he got to higher levels than he was able to achieve before then that would support my theory, but they didn't do that.

It certainly is presumptious to think that there is something substantially physiologically different about those athletes that fail at 10 mmole lactate vs those who fail at 3, or that someone can will themselves past these physiologic failure thresholds. Are some of them space aliens? The fact that these differences exist in the venous blood is not evidence that this molecule is not the culprit at the cellular level. I take that back, it is evidence, just not very good evidence.

Why on earth do you even bother measuring lactate in your athletes if you believe it is of absolutely no consequence to performance?

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Frank,
An original Ironman and the Inventor of PowerCranks

Your statement here,

"Like I said before, I don't believe lactic acid per se is directly responsible for the acidosis observed, at least in athletes. I believe it is the secondary effects of the accumulated high CO2 levels that occur from the buffering of the persistent excessive lactic acid production that results in acidosis, which also explain the labored breathing seen under these conditions."

is a far cry from your statement here,

"Lactic acid production is not good for the athlete under any circumstances as it adversely affects performance despite some of these totally theoretically possibilities. This is a crazy thread."

Athletes can exercise for a very long time with elevated lactate levels relative to rest, and, in some circumstances, this elevated lactate may contribute to the maintenance of euglycemia and cellular oxidation. This discussion has moved all over the place. Tom originally asked about the role of lactic acid duing exercise, and that it was not the evil doer everyone cracked it up to be. I have made my position known, and in an effort to wrap this up, I will say this, .. I agree that lactic acid may contribute, in some part, to the systemic acidosis that leads to hyperpnia and impaired metabolism. It is not though, solely responsible for this acidosis, nor is that acidosis solely responsible for elevated Ve, as evidenced by data from McArdle's patients. Both K+ and NH3+ have been implicated as playing a role in this process. Lactic acid accumulation is an indicator or proxy of glycogenic metabolism that cannot be sustained for a number of reasons, including disproportionately increased VCO2, as a result of disproportionately increased glycolysis. It is true that someone who is exercising while lactic acid is accumulating will fatigue. That fatigue may be due to numerous factors, not simply acidosis, cellular or systemic. We have both acknowledged that the factors playing a role in fatigue under these circumstances are complicated, so, to make a blanket statement that lactic acid production is bad under all circumstances doesn't make sense to me. Sorry, that's just the way I see it.

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Steve

http://www.PeaksCoachingGroup.com

One thing that hasn't been brought up in this discussion so far has been the role of massage therapy. Don't get me wrong, I love a good athletic massage, but one constantly hears about massage flushing the "metabolic waste" including lactate out of muscles. The problem with this idea is that, as stated above, lactate has nothing to do with post exercise muscle pain, and is actually not present in the muscle by the time one usually gets a massage. Yes, it feels good and it sure seems like it helps recovery, but they need to get the references to lactate out of there.

Deke

[reply]Your statement here,

"Like I said before, I don't believe lactic acid per se is directly responsible for the acidosis observed, at least in athletes. I believe it is the secondary effects of the accumulated high CO2 levels that occur from the buffering of the persistent excessive lactic acid production that results in acidosis, which also explain the labored breathing seen under these conditions."

is a far cry from your statement here,

"Lactic acid production is not good for the athlete under any circumstances as it adversely affects performance despite some of these totally theoretically possibilities. This is a crazy thread."

Athletes can exercise for a very long time with elevated lactate levels relative to rest, and, in some circumstances, this elevated lactate may contribute to the maintenance of euglycemia and cellular oxidation. This discussion has moved all over the place. Tom originally asked about the role of lactic acid duing exercise, and that it was not the evil doer everyone cracked it up to be. I have made my position known, and in an effort to wrap this up, I will say this, .. I agree that lactic acid may contribute, in some part, to the systemic acidosis that leads to hyperpnia and impaired metabolism. It is not though, solely responsible for this acidosis, nor is that acidosis solely responsible for elevated Ve, as evidenced by data from McArdle's patients. Both K+ and NH3+ have been implicated as playing a role in this process. Lactic acid accumulation is an indicator or proxy of glycogenic metabolism that cannot be sustained for a number of reasons, including disproportionately increased VCO2, as a result of disproportionately increased glycolysis. It is true that someone who is exercising while lactic acid is accumulating will fatigue. That fatigue may be due to numerous factors, not simply acidosis, cellular or systemic. We have both acknowledged that the factors playing a role in fatigue under these circumstances are complicated, so, to make a blanket statement that lactic acid production is bad under all circumstances doesn't make sense to me. Sorry, that's just the way I see it.[/reply]

Well, I will revise my previous statement that lactic acid production is "good" in the sense that it means the athlete is near maximum performance. How much production there is in relation to how fast the body can metabolize it determines when failure or reduced performance starts to occur. For the endurance athlete one should endeavor to minimize lactic acid production rather than encourage or maximize it. I stand by the revised statement that lactic acic production is not good for the endurance athlete under any circumstances as, when it occurs, it more or less adversely affects immediate further performance improvement and will ultimately result in "fatique" and reduced performance.

Lactic acid production probably plays a beneficial role in training in that it or the conditions associated with its production will result in training benefit for the athlete. But, again, I see it doing nothing to enhance performance at the time of its production.

Lactic acid does contribute to improved availability of oxygen and metabolism in the short term because of its immediate effects on the oxyhemoglobin dissociation curve at the cellular level but it is a stretch to say it has long-term primary performance benefits for the endurance athlete. I would love to see the research that supports that conclusion.

I say lactic acid is the bad guy here simply because I see it as the initiator of all the bad effects and results associated with "bonking", at least in the athlete exercising to maximize performance. Nothing else I have heard here or anywhere else makes any sense. There could be alternative mechanisms in for very low intensity long duration exercise fatigue (how far/long can you walk without getting tired) that doesn't involve lactic acid production but that is not what we are talking about here. What is the alternative stimulus/trigger you propose for the start of the fatigue cascade in the "max-aerobic" performance athlete? I look forward to hearing when and how lactic acid production is ever beneficial to the endurance athlete's performance.

Why don't we just ask Tom to try to maximize the production of lactic acid his next race and see how his performance compares to his previous efforts to see if there is a beneficial or adverse affect to the presence of lactic acid in the endurance athlete? Another study of one though so people will continue to believe what they want.

One other question since you mentioned it. You mention K+ as playing a possible primary role here. I personally think it probably a secondary effect and not primary but either way, don't you find it silly that fluid replacement drinks generally have K+ in them (because it is lost in sweat), which could only make the situation worse (although the amounts are so small as to probably be inconsequential)? Do you tell your clients to avoid these drinks? Is there any evidence that K+ in fluid replacement drinks taken during performance is beneficial to the endurance athlete?

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Frank,
An original Ironman and the Inventor of PowerCranks