Lactic Acid

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***Members may find the following information helpful:

http://www.time-to-run.com/theabc/lactic.htm

Lactic acid and running: myths, legends and reality - the ABC

Most runners still believe that lactic acid is released during hard

or unaccustomed exercise and that this is what limits running

performance, as well as being the cause of stiffness. Neither is

correct. But not even is the terminology of " lactic acid " .

Lactic acid does not exist as an acid in the body: it exists in

another form called " lactate " , and it is this that is actually

measured in the blood when " lactic acid " concentration is determined,

as is done from time to time. This distinction is important not only

for the sake of correctness, but more importantly, because lactate

and lactic acid would have different physiological effects.

The greatest myth is that lactic acid is the cause of the stiffness

felt after an event such as a marathon. Stiffness is due mostly to

damage to the muscle, and not an accumulation of lactic acid or

lactic acid crystals in the muscle.

Another misconception is that lactate is responsible for acidifying

the blood, thereby causing fatigue. To the contrary, lactate is

actually an important fuel that is used by the muscles during

prolonged exercise. Lactate released from the muscle is converted in

the liver to glucose, which is then used as an energy source. So

rather than cause fatigue, it actually helps to delay a possible

lowering of blood glucose concentration, a condition called

hypoglycemia, and which will cause a runner to feel weak and fatigued

if it occurs.

A more recent addition to the muddled thinking is that of the

anaerobic threshold. Pictures are seen of athletes having a blood

sample taken with an accompanying caption indicating that the workout

is being monitored by measuring " lactic acid " . The supposed rationale

is that as running speed is increased, a point is reached at which

there is insufficient oxygen available to the muscle and energy

sources that do not require oxygen contribute to the energy that is

needed. This results in a disproportionate increase in the blood

lactate concentration, a point identified as the anaerobic threshold.

This is also known as the lactate threshold or lactate 'turnpoint'.

There are two problems with this. Firstly, the muscle never becomes

anaerobic: there are other reasons for the supposed disproportionate

increase that is measured in blood lactate concentration. Secondly,

the so-called disproportionate increase causing a 'turnpoint' is not

correct, in that the increase is actually smooth and incremental.

This led to another way of using blood lactate concentration to

monitor running performance.

If blood lactate concentration is measured at different, increasing

running speeds, it is possible to eventually draw a curve depicting

the continued increase in concentration as the running speed gets

faster. The position of this curve changes as fitness level changes.

Particularly, the fitter a runner gets, the more the curve shifts to

the right, meaning that at any given lactate concentration the

running speed is higher than before. Often, the running speed at a

lactate concentration of 4 mmol/l is used as a standard for

comparison. This can also be used as a guide for training speed i.e.

a runner could do some runs each week at the speed corresponding to

the 4 mmol/l lactate concentration, some runs above this speed, and

recovery runs at a slower speed. Of course, as fitness changes and

the curve shifts, these speeds will change, and so a new curve will

have to be determined. This is all very well, but the problem is to

know how much running should be done below, at, and above the 4

mmol/l concentration. Remember, 4 mmol/l is a fairly arbitrarily

chosen amount. Thus the real value in determining a " lactate curve "

is to monitor how it shifts with training. The desirable shift is one

in which a faster running speed is achieved at a given lactate

concentration than before. This regular testing can be done in the

laboratory with the athlete running on a treadmill or on a track in

which running speed can be carefully controlled, such as by means of

pace lights. Both types of testing are done at the Sports Science

Institute, usually for research purposes.

While useful information can be gained from regular testing to

determine a runners' lactate curve, it is important to keep in mind

what is fact and what is fiction.

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Biochemistry of exercise-induced metabolic acidosis.

Am J Physiol Regul Integr Comp Physiol. 2004 Sep;287(3):R502-16.

Robergs RA, Ghiasvand F, D.

The development of acidosis during intense exercise has traditionally been

explained by the increased production of lactic acid, causing the release of a

proton and the formation of the acid salt sodium lactate. On the basis of this

explanation, if the rate of lactate production is high enough, the cellular

proton buffering capacity can be exceeded, resulting in a decrease in cellular

pH. These biochemical events have been termed lactic acidosis. The lactic

acidosis of exercise has been a classic explanation of the biochemistry of

acidosis for more than 80 years. This belief has led to the interpretation that

lactate production causes acidosis and, in turn, that increased lactate

production is one of the several causes of muscle fatigue during intense

exercise.

This review presents clear evidence that there is no biochemical support for

lactate production causing acidosis. Lactate production retards, not causes,

acidosis. Similarly, 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.

Thus increased lactate production coincides with cellular acidosis and remains a

good indirect marker for cell metabolic conditions that induce metabolic

acidosis. 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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Lactating Mythers

(Massage and the Lactic Acid Myth)

http://www.mckinnonmassage.com/articles/lactating_mythers.html

Grant, Ph.D.

General Concepts of Lactic Acid Physiology

Lactic acid is a continual product of carbohydrate metabolism. It holds a

position as a temporary product at the end of glycolysis and at the head of the

aerobic Krebs cycle. The very persistent “lactic acid myth” is the incorrect

concept that:

*Lactic acid persists in the cellular environment long after exercise,

*That this byproduct of anaerobic glycolysis causes prolonged muscle soreness,

and that

*Massage relieves such soreness by flushing out the lactic acid.

In truth, lactic acid is only present substantially during and immediately

following high intensity anaerobic exercise, being metabolized within 30-60

minutes after such exercise ceases. The lactate is converted back to pyruvate

and aerobically processed in the Krebs cycle to produce further energy. The H+

is quickly buffered to return the bloodstream pH to homeostasis.

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Lactate metabolism: a new paradigm for the third millennium.

J Physiol. 2004 Jul 1;558(Pt 1):5-30. Epub 2004 May 6.

Gladden LB.

For much of the 20th century, lactate was largely considered a dead-end waste

product of glycolysis due to hypoxia, the primary cause of the O2 debt following

exercise, a major cause of muscle fatigue, and a key factor in acidosis-induced

tissue damage. Since the 1970s, a 'lactate revolution' has occurred. At present,

we are in the midst of a lactate shuttle era; the lactate paradigm has shifted.

It now appears that increased lactate production and concentration as a result

of anoxia or dysoxia are often the exception rather than the rule. Lactic

acidosis is being re-evaluated as a factor in muscle fatigue. Lactate is an

important intermediate in the process of wound repair and regeneration. The

origin of elevated [lactate] in injury and sepsis is being re-investigated.

There is essentially unanimous experimental support for a cell-to-cell lactate

shuttle, along with mounting evidence for astrocyte-neuron, lactate-alanine,

peroxisomal and spermatogenic lactate shuttles.

The bulk of the evidence suggests that lactate is an important intermediary in

numerous metabolic processes, a particularly mobile fuel for aerobic metabolism,

and perhaps a mediator of redox state among various compartments both within and

between cells. Lactate can no longer be considered the usual suspect for

metabolic 'crimes', but is instead a central player in cellular, regional and

whole body metabolism. Overall, the cell-to-cell lactate shuttle has expanded

far beyond its initial conception as an explanation for lactate metabolism

during muscle contractions and exercise to now subsume all of the other shuttles

as a grand description of the role(s) of lactate in numerous metabolic processes

and pathways.

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Owen (taken from www.pponline.co.uk)

Bad stuff?

....As an athlete, you're probably no stranger to the idea that lactic acid forms

rather readily in your muscle cells, especially when you are exerting yourself

quite strenuously. In fact, you probably believe that the 'burn' you feel in

your leg muscles when you're running, cycling, or swimming very fast is caused

by lactic acid - and that the soreness you experience the day after an

especially tough workout is produced by the same 'troublesome' compound. You may

also cling to the idea that lactic acid is a 'waste product' formed in your

muscles during strenuous exercise, and that lactic acid appears in your muscles

when you 'run out' of oxygen, or because you've gone into 'oxygen debt'. In

short, you probably believe that lactic acid is really bad stuff!

Well, it isn't! All of the above statements are untrue: lactic acid doesn't

produce burning sensations, it does not induce soreness, and it's not a form of

metabolic 'rubbish' which must be eliminated from your cells as quickly as

possible. In addition, oxygen shortfalls are not required in order to make

lactic acid appear in your muscles and blood: The truth is that lactic acid is

produced in your body all the time, around the clock, even when you're at rest,

and its concentrations rise whenever you take in a carbohydrate-containing meal.

Fortunately, we're not telling you all this to improve your chances of gaining a

PhD in cell physiology: We're giving you the straight scoop because an

understanding of how lactic acid actually functions in your body can improve

your performances tremendously!

You see, instead of being a dangerous compound which wreaks havoc inside muscle

cells, lactic acid (or more accurately, lactate) is actually the key chemical

your body uses to 'dispose of' dietary carbohydrate; without it, it would be

very difficult to maintain normal blood-sugar levels or keep your liver and

muscles stockpiled with carbohydrate.....

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Chad Touchberry wrote:

I did not see the original question, but muscle fatigue was a very

strong interest of mine a few years ago. Some things you may found

helpful or interesting.

Lactate is not fatigue producing.

GA proposed a lactate shuttle system (Using Malatate-

Aspertate system) that basically states that lacate can be oxidized

by type I fibers and cardiac muscle. Thus lactate is nothing more

than a temporary storage area for energy.

There is also the Glycerol Phosphate Shuttle system to handle the H+

build up in skeletal muscle.

Robergs et al suggest that lactate does not cause fatigue and there

are other mechanisms responsible for acidosis (Robergs 2001).

Essentially the H+ are currently accepting blame.

I think in the future you are going to see that it is the role of

extracellular K+ that has the greatest impact on muscle fatigue.

There is some interesting research by Green and Nielson looking at

the role of K+ and Na+/K+ pumps, and Na+/K+ ATPase.

I would strongly urge you if you are interested in this area to

start with an article:

, G. A., Lactate doesn't necessarily cause fatigue: why are

we surprised? J. Phsiol. 536: 1. 2001.

Work from there.

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I agree with the lactate comments made for further

information on fatigue and lactate read the works of

, GA....or Nielson, OB.

See the following links for a brief introduction.....

http://www.jphysiol.org/cgi/content/full/536/1/1

http://www.jphysiol.org/cgi/content/full/536/1/161?

ijkey=fbab24b30f88f9c571a5af1\

073c1cd9c1c4caee1

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Craig Goodman:

Try looking on PubMed for papers dealing with McArdle's disease,

characterised by a deficiency in muscle phosphorylase, which results

in an inability to break down glycogen and therefore almost no

lactate is produced (glycolysis still operates at a very reduced rate

using blood glucose as a substrate). If people still experience the

sensation of pain during exercise with this condition, then its

unlikely to be caused by lactate.

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Dr Mel Siff:

Lactic acid is not a toxin which hinders performance, as some people

believe; as lactate, it is part of the normal complex group of

metabolic processes involved with life and exercise. In fact, some

researchers suggest that lactate may stimulate adaptation to

strenuous exercise.... Forget the old belief about " lactic acid "

causing the discomfort - this has far more to do with neural changes

associated with local muscle ischaemia or problems with calcium

flux. Positively charged hydrogen ions. Lactate even serves as a

useful energy substrate, not something that mystically poisons or

hinders our bodies from functioning properly. It is produced at rest

like many other biochemicals because it plays a useful role in energy

production and helping us to STAY ALIVE, not because it is some sort

of mistake of nature!

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Running (Versioning): Biomechanics and Exercise Physiology in

Practice Klomp, Frans Bosch

Proof that there is no anaerobic threshold that can possibly be

detected on the basis of ventilatory parameters was provided by a

group of patients suffering from McArdle's disease. These patients

are not able to break glycogen down into lactate because they do not

have the phosphorylase enzyme. However, as exercise intensity

increases, at a certain point ventilation will show an exponential

increase similar to the pattern found in individual s who do have

this enzyme. Furthermore, various studies have demonstrated that the

ventilatory threshold frequently does not coincide with an

exponential increase in the concentration oflactate in the blood

(Gaesser et al 1984, Gaesser & Poole 1986). For that matter, an

exponential increase in the blood lactate concentration is not

clearly seen when exercise intensity is increased in discrete steps

(Myers 1996), and thus an anaerobic threshold becomes difficult to

determine. Moreover, the sudden rise in the concentration of lactate

appears to be highly dependent on the experimental protocol employed,

the surrounding temperature, and the individual's nutritional state

( et al 1996).

Furthermore, it can be stated that the concentration of lactate in

the blood does not correctly reflect what is happening within the

muscle.......

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Ken Jakalski:

A few years back Owen wrote a wonderful little book entitled

Lactate Lift-off. The book provides excellent insights on fitness

and performance training, and Owen devotes considerable time to

explaining LT (lactate threshold). He even has an entire chapter

called " The Truth About Lactic Acid. "

Owen notes that, contary to popular belief, lactic acid isn't the

cause of that " burning sensation " we feel in muscles during strenuous

work, it doesn't induce soreness, and it isn't a form of " metabolic

garbage " that we must elminate from our cells as quickly as

possible...

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Hope those help

Carruthers

Wakefield, UK