Lactating Mythers

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:

• Jay T. Kearney, Training the Olympic Athlete, Scientific American
• Patti and Warren Finke, Is Lactic Acid a Four Letter Word?, Team Oregon
• Owen Anderson, 5 Keys to Improvement, Runner's World
• Owen Anderson, On the Threshold, Runner's World
• Owen Anderson, Five Easy Pieces, Runner's World
• Owen Anderson, Lactate Liftoff, Running Research News, 140 pages $21.95 — Dr. Anderson covers the facts and myths of lactic acid and provides information and a work-out schedule to cure a sickly lactate threshold(LT) or make a good LT sensational.
• Pete Pfitzinger, New Look At An Old Foe: Lactic Acid, American Running Association.
• Capt. Micael Ross, 1999: Delayed-Onset Muscle Soreness —Work Out Now, Pay Later?, The Physician and Sportsmedicine (http://www.physsportsmed.com/issues/1999/01_99/muscle.htm)
• Stephen Seiler, The Lactate Threshold
• SportsMedWeb, Anerobic Theshold, Rice University (also see the main index for this site).

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). These links are current as of July 2007.

• Introduction to Glycolysis
• Step by Step Glycolysis
• Design It Yourself Glycolysis

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⁺ x 2 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 SO4^2-). 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 Ramblemuse^SM, 2000, 2007. All rights reserved.