Lactating Mythers – Massage and the Lactic Acid Myth (Keith Grant, HTML)

Lactating Mythers

(Massage and the Lactic Acid Myth)

Keith Eric 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:

  1. Lactic acid persists in the cellular environment long after exercise,
  2. That this byproduct of anaerobic glycolysis causes prolonged muscle
    soreness, and that
  3. 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.

Glycolysis produces energy plus pyruvic acid. Pyruvic acid then funnels
into the Krebs cycle, which produces over 90 percent of the energy needed
for distance running. There’s a problem, however. If the pyruvic acid is
not being removed as fast as it is being produced, it will build up bringing
glycolysis to a halt. To prevent this, lactic dehydrogenase converts the
pyruvic acid to lactic acid. This step both removes the pyruvate and removes
half of the free H+ produced in the formation of
pyruvate. The lactate can easily diffuse quickly into surrounding tissues
and the blood. Since lactate can later be reconverted into pyruvate, it
can act as a fuel source to tissues not working as hard.

At some point of exercise intensity between 55 and 90 percent VO2
max, the lactate threshold is passed. Up to this point, lactate is being
used aerobically at the same rate it is being produced. Now, due to shortage
of oxygen, enzymes, or cell-mitochondria, the use of lactate no longer keeps
up with production and blood lactate levels climb rapidly. This build up
acidifies the blood (lowers pH), overwhelming the natural pH buffers in
the blood and eventually blocking the rate of glycolysis. The good news
for athletes is that this lactate threshold can be dramatically increased
with the right kinds of training. Basically, training increases the body’s
ability to use the lactate quickly as an energy source by developing more
capillaries and mitochondria and storing more enzymes. Training is the main
reason that lactate thresholds range up to 90 percent of VO2
max.

Following exercise, blood lactate decreases over the next 30-60 minutes.
Faster recovery occurs with continued moderate aerobic exercise of about
35 percent VO2 max than with passive rest (Powers and Howley,
1990; p. 63). The time framework is basically a measure of the body’s ability
to start using the extra lactate for energy or for glycogen production with
exercise helping it’s distribution. Following about 60 minutes, there is
just not a significant amount of extra lactate around. The body has returned
to its homeostatic balance of production and use.

Because the lactate and H+ (i.e. lactic acid) don’t
persist, they can’t cause prolonged muscle soreness and can’t be flushed
out by massage
. Soreness occurring 24-72 hours after exercise is Delayed
Onset Muscle Soreness (DOMS). The exact mechanisms involved in DOMS are
still uncertain, but are thought by researchers to involve micro-trauma
to individual muscle fibers resulting in Ca++ (calcium
ion) leakage and a subsequent cycle of inflammation response.

One of the goals of exercise capacity training is raising one’s lactate
threshold – the rate at which the body can process lactate and H+
and stay ahead of it’s production during anaerobic exercise. This is essentially
done via pace workouts. In running, lactate threshold is highly correlated
with racing performance.

In contrast, hill running and other exercises involving eccentric muscle
contractions are used to progressively condition the body against DOMS.
Most DOMS is experienced following suddenly increased workouts; particularly
those resulting in eccentric contractions (muscles being lengthened while
resisting against the lengthening, as in walking down stairs or running
downhill).

The “lactic acid myth” is one of those cautionary notes in massage
knowledge in that something that many people “know to be true” turns out
to be totally incorrect. It does, however, raise the question that if lactic
acid is not the culprit it was once thought to be, then how does massage
result in the clinical benefits it is observed to have?

My own belief is that the answer will not be found in mechanistic studies
looking at simple effects like flushing toxins or increasing large-scale
circulation. Instead, I believe that the results stem from the interactions
of normalizing residual hypertonicity in fatigued muscles and in the systemic
effects of input to the nervous system.

Normalizing hypertonicity implies that the metabolic rate of the muscle
decreases, resulting in reduced fuel usage and reduced metabolic waste production.
As muscles relax and are stretched, pressure on the immediately surrounding
tissue is decreased, improving local circulation and lymphatic drainage.
The additional neurological effects of massage likely act to reduce hypersensitivity
of nerve endings, alleviating pain-spasm-pain reflexes, and to cause the
release of myriad chemical messengers associated with parasympathetic responses
(see Rossi, 1993). In synergy, these effects allow the body to more effectively
perform the recovery miracle it was designed to do. In short, what is being
affected by massage post-exercise is not a static state of chemical dysfunction
but the dynamic metabolic and neurochemical balance.

Acknowledgments

During late March and early April 1998, Donald
Schiff
, a massage therapist in New Mexico, and I engaged in a prolonged
series of email discussions regarding the lactic acid myth. We
ventured from initial summaries deep into the sequence of chemical steps
involved in the process of glycolysis which I have given in the Appendices
below. I wish to explicitly acknowledge the role Don’s comments and prodding
played in contributing to the development of this material. Don was particularly
persistent in pointing out that the last step of glycolysis, the conversion
of pyruvate to lactate, halves the acidification that glycolysis would otherwise
produce. He also pointed out that lactic acid does not exist as such, but
as lactate and H+ ions and that the lactate is
a further source of energy, not a waste product – in other words, lactate
has been given a bad rap. In contrast, I have used lactic acid as a term
of convenience for the net (temporary) chemical production of the glycolysis
cycle and focus on the entire glycolysis process cycle resulting in bloodstream
acidification during intense anaerobic exercise. In either case, increases
in bloodstream lactate and lowering of pH (acidification) are short lived.

References

Bruce Abernethy, Vaughan Kippers, Laurel T. MacKinnon, Robert J. Neal, and
Stephanie Hanrahan, The
Biophysical Foundations of Human Movement
, Human Kinetics, 1997,
ISBN: 088011732X.

Owen Anderson, Things your mom forgot to tell you about blood lactate,
Running Research News, 13(10),
Dec 1997.

William D. McArdle, Frank I. Katch, and Victor L. Katch, Exercise
Physiology — Energy, Nutrition, and Human Performance
, 3rd
Ed., Lea & Febiger, 1991, 0-683-05731-6 (link and ISBN are for 4th ed.,
1996).

Scott K. Powers and Edward T. Howley, 1990: Exercise
Physiology – Theory and Application to Fitness and Performance
,
Wm C. Brown Publishers, ISBN 007-235551-4 (Link and ISBN are for 4th ed.,
2000).

Ernest Lawrence Rossi, 1993: The
Psychobiology of Mind-Body Healing
, W.W. Norton, Inc., ISBN
0-393-70168-9

Online Links

Various links on exercise, training, and lactate production and threshold:

For those prone to details, these are some nice resources made available
to us by Jon Maber in the UK. They don’t contain the rigorous total stoichiometry
of Appendix B below, but they are a great aid in visualizing the entire
process).

Appendix A: Exercise, Lactic Acid Production Rates, and Blood pH Effects

To delve deeper into the information I have on blood pH, I quote from from
Abernathy et al., 1967: “The Biophysical Foundations of Human Movement”.
From p. 190-191:

Lactic acid is produced as a by product of anaerobic glycolysis [i.e.
the glycolysis process itself is an anaerobic process – KEG]. During
exercise lactic acid concentration may increase within muscle from 2
mmol/l at rest up to 30 mmol/l during maximal exercise. Excess lactic
acid [in the form of lactate ion–see below] is transported across the
muscle cell membrane into the blood and circulated throughout the body.
Blood lactate concentrations may increase from 1-2 mmol/l at rest up
to 15 mmol/l during maximal exercise.

Excess lactic acid produced during exercise is associated with muscular
fatigue. Lactic acid produced during exercise rapidly dissociates into
a lactate anion and free hydrogen ion (H+). An increase
in H+ concentration increases the acidity (lowers the
pH) of muscle and blood. Although tissues and blood contain substances
that partially buffer the increased acidity, the pH of muscle may decrease
from 7.4 to as low as 6.7 during intense exercise — nearly a 10 fold
increase in acidity. The anaerobic glycolytic system is sensitive to
changes in acidity, and the decrease in pH inhibits or slows the anaerobic
pathway. Thus, excess lactic acid accumulation resulting from anaerobic
glycolysis inhibits further ATP production. Although the excess lactic
acid causes fatigue during intense exercise, this inhibitory effect is
a protective response, since excess acidity can lead to cell death.

During and after exercise excess lactate is removed from the working
skeletal muscles and circulated to tissues such as the heart, liver,
kidney and other skeletal muscles. Lactate is not inert, rather it can
be converted back to pyruvate and degraded via oxidative metabolism to
produce ATP in these tissues. Thus excess lactate produced via anaerobic
glycolysis can become a fuel for further ATP production in skeletal muscle.

After exercise ends, excess lactate is also reconverted back to glucose
in the liver; this newly made glucose can then be used to resynthesize
glycogen depleted during exercise. It takes approximately 20-60 min to
fully remove lactic acid (lactate and H+) produced
during maximal exercise. The rate of lactic acid removal is faster during
active compared with passive recovery.

From Powers and Howley (1991), I quote from p. 244:

Under normal resting conditions, both of these acids [lactic
acid and acetoacetic acid] are further metabolized to CO2
and therefore do not greatly influence the pH of body fluids. However,
an exception to this rule is during heavy exercise (i.e., work above
the lactate threshold). During periods of intense physical efforts, contracting
skeletal muscles can produce large amounts of lactic acid, resulting
in acidosis. In general, it appears that production of lactic acid during
heavy exercise presents the greater challenge to maintaining the pH homeostasis
during exercise.

At this point, the authors present a figure showing multiple sources
of H+ and go on to discuss buffer systems, including the
biscarbonate buffer.

McArdle et al (1991) comment on p. 288:

The regulation of pH becomes progressively more difficult in strenuous
exercise where H+ in increased from both carbon dioxide and
lactic acid formation. This occurs in the case of maximal, intermittent
exercise of short duration, when blood lactate values can reach 30 mmol/l
or more.

A negative linear relationship exists at rest and bin various levels
of intermittent exercise between blood lactate concentrations and blood
pH.

Results indicate that humans are temporarily able to tolerate pronounced
disturbances in the acid-base balance, at least as low as a blood pH
of about 6.8 (one of the lowest reported for a human subject). The degree
of acidosis at pH levels below 7.00 is not without consequences, man
subjects experienced nausea, headache, and dizziness, as well as pain
in the muscle groups involved in exercise.

So, while lactic acid is produced, it immediately dissociates into lactate
and H+. In terms of how the lactate escapes into
the blood [Owen Andersons phrasing. McArdle used diffuses, Scott & Powers
transported], the mechanism is not particularly pertinent to the effect
? into the blood and on to other tissues it goes. So, effectively, the lactic
acid is transported into the blood and the pH problem is not a local muscle
problem from keeping “lactic acid” in the muscle, but a much more global
body problem during strenuous exercise.

Owen Anderson states that 90 percent of the energy from distance running
comes from aerobic metabolism. During normal homeostasis, the pyruvic acid
produce by the glycolysis cycle is fed directly into to Krebs (aka TCA –
tricarboxcylic acid) cycle without conversion to lactic acid (aka lactate
+ H+). Some sources discuss the lactate
– pyruvic acid balance as possibly depending on a difference in the lactate
dehydrogenase between slow twitch and fast twitch muscles. Also, since lactate
threshold can increase substantially without an increase in VO2 max, oxygen
availability is not necessarily the controlling factor in pyruvic acid or
lactate production.

Appendix B: The Gory Details of Glycolysis

Most of you will want to stop reading about here – the point
where this discussion turns to chemistry and the requirement that we neither
create or destroy atoms or charge (basically electrons) in chemical reactions.
If you just want to proceed to the conclusion, look for the *** below.

Hydrogen ion, H+, is not produced from
the conversion of pyruvate to lactate – it is however a product of
the glycolysis mechanism. We now look at this via the stoichiometry (i.e.
the atom-charge balance of the total glycolysis process. We start from glucose,
or C6H12O6 (6 carbon atoms,
12 hydrogen atoms, 6 oxygen atoms). There are 11 steps in the glycolysis,
but many are just molecular rearrangements, not affecting the stoichiometry.
Lets go step by step.

1. Glucose + ATP –> Glucose 6-phosphate + ADP

One phosphate, Pi gained from ATP, one H+
disconnected from the site to which the Pi binds, leaving C6H11O6Pi

2. Glucose 6-phosphate –> Fructose 6-phosphate

A rearrangement

3. Fructos 6-phospate ATP –> Fructose 1,6-bisphospate + ADP

A second phosphate gained from ATP; a second H+
disconnected, leaving C6H10O6Pi2

4. Fructose 1,6 bisphosphate –> Dihydroxyacetone phospate + Glyceraldehyde
3-phosphate

5. Dihydroxyacetone phosphate –> Glyceraldehyde 3-phosphate

A split and rearrangement giving two molecules of Glyceraldehyde 3-phosphate.
So now we have 2[C3H5O3Pi],
the same balance as before.

6. Glyceraldehyde 3-phosphate + NAD+ + H2O +
Pi –> 1,3-Bisphosphoglycerate + NADH + 2H+

This is the crucial step of glycolysis where, for the two molecules,
a phosphate is added to each by use of NAD+
as an oxidizing agent. Lets look at the balance: 2[C3H5O3Pi]
–> 2[C3H4O4Pi2]
:

For each molecule we have added an oxygen and a phosphate and removed
a hydrogen. The oxygen had to come from somewhere, so we
split it from H2O. The NAD+
also picks up an H+, but gains an electron from
the molecule being processed, so we have 2H+x2
added to the 2H+ we already produced to the
cell environment – a total of 6H+ for the cell.

7. 1,3-Bisphosphoglycerate + ADP –> 3-Phosphoglycerate
+ ATP

The balance is now 2[C3H4O4Pi2]–> 2[C3H5O4Pi] for the
molecules. Note that of the H5, one may be dissociated
as H+, giving the molecules a negative charge.
I’m including it with the molecule to maintain a neutral charge balance.
Basically what occurred was one phosphate was detached, leaving a binding
site open to take on one H+. With two molecules
the cell environment balance now reduces to plus 4H+
. This step also paid back the two ATP used in steps 1 and 3.

8. 3-Phosphoglycerate –> 2-Phosphoglycerate

(A rearrangement with no balance change for the molecules or cell environment)

9. 2-Phosphoglycerate –> Phosphoenolpyruvate + H2O

This is a process of dehydration – we just gave back the H2O
we borrowed in step 6. The molecular balance is now 2[C3H3O3Pi].
There was no change to the cell environment net H+
production; that still stands at 4H+ .

10. Phosphoenolpyruvate + ADP –> Pyruvate (Pyruvic acid)
+ ATP

The molecule balance is 2[C3H3O2Pi]
–> 2[C3H4O2]
. In loosing
the phosphate to ATP, we open a a binding site to accept
an H+ (x2) from the cell environment. With two
molecules, we have 2H+ net production.

11. Pyruvate (Pyruvic Acid) + NADH + H+ –> Lactate
(Lactic Acid).

The pyruvate takes on 2H+ plus one electron, regenerating
the NAD+ used in step 6. The molecule balance is
2[C3H4O3] –> 2[C3H6O3].
Note that each molecule gets one H+ from the cell
environment and one H+ from the NADH.
This leaves lactic acid 2 x C3H6O3 and no additional net H+
left in the cell environment.

Bottom Line

Balance wise, ignoring changes in oxidation state and arrangement, in the
whole glycolysis chain we have simply gone from 2 x C6H12O6
to 2 x C3H6O3. However the
lactic acid is born dissociated into C3H5O3
(lactate) and H+. And this last step is why glycolysis
ends up decreasing the cell and finally the blood pH. The conversion from
pyruvate to lactate does not produce H+ but absorbs
it. But since lactic acid is produced in terms of stoichiometry and since
lactic acid is a strong acid that dissociates almost completely, we end
up with two lactate ions and two H+. We normally
get sloppy and say that glycolysis creates lactic acid.

So as lactic acid is produced and dissociated into its ions at rates faster
than the body can equilibrate with, lactate levels rise and pH levels drop.
When the body stops exercising, both lactate and pH return rapidly to their
normal levels.

Appendix C: Lactic Acid Dissociation as an Equilibrium Process

In the body, lactate and pyruvate are dissociated. After the glycolysis
step in which inorganic phosphate is added in conjunction with oxidation,
the molecules dissociate into an H+ and an anion
for the remaining steps. I did not bookkeep it this way in Appendix B,
since that would have added to the complexity of an already complex series
of steps. By keeping the H+ with the anion, I avoided
having to keep a charge balance. I did add a comment to that effect in discussing
that step.

Although the lactate and H+ are dissociated, I
often refer just to lactic acid because such dissociation is true of all
strong acids and bases. Quoting from J.N. Butler, 1964: “Solubility and
pH Calculations”, Addison-Wesley:

“For purposes of mathematical classification, we shall divide acids and
bases into two classes; *strong*, or completely dissociated, and *weak*,
or partly dissociated. There is, of course, a continuous gradation from
completely dissociated acids like HCl [hydrochloric acid] down
to almost completely undissociated acids like HCN [hydrocyanic
acid]. A given acid (HIO3, for example) may be a weak
acid in concentrated solutions, but a strong acid in dilute solutions.”

Thus, a chemist will refer to a 1 molar (i.e. 1 moles/l) solution of HCl
or H2SO4 (sulfuric acid) with the understanding
that these are solutions in which the H+ are nearly
completely dissociated from the anions (Cl or
SO42-). It certainly does not seem to defer Butler
from referring to a solution of a “strong acid” as an acid. If, in fact,
lactic acid was weak enough not to dissociate, it would not have the effect
it does on blood pH. It’s also useful to remember that dissociation is a
dynamic process; i.e. H(lactate) <-- –>
H+ + lactate is occurring continually
in both directions, but that the equilibrium is heavily weighted to the
dissociated (right) side. The implication is that how lactic acid is created
does not matter, it will arrive at it’s own almost instantaneous equilibrium
with the environmental pH.

In counterpoint to the strong lactic acid, carbonate is a particularly interesting
case biologically of a weak acid. In can occur as H2CO3
(carbonic acid) in acidic solutions, NaHCO3 (sodium
biscarbonate) in neutral solutions and as Na2CO3
(sodium carbonate) in basic solutions. That the biscarbonate will take on
an H+ as it’s environment becomes more acidic,
thus counteracting the environment, or give up its last H+
as the solution becomes more basic (again counteracting), is the reason
biscarbonate is an important biological buffer. What ever the environmental
tendency is, biscarbonate acts to counteract it. This is one of the mechanisms
the body uses to keep its pH within operating limits. It is only when H+
is produced too rapidly for this to balance, that blood pH begins to drop.

Keith Eric Grant — The RamblemuseSM,
July 2000. All rights reserved.