Quo usque tandem — or “A few words on the tandem of lactate and anaerobic threshold”

From time to time, a relic from the past lands in your hands, and you’re struck by how much our predecessors already knew. Sports medicine is no exception. When Jiří Couf, the coach of middle-distance runner Lucie Sekanová, brought me a faded blue magazine and said, “Doctor, this article says exactly what you’ve been talking about with lactate,” I immediately knew what he meant. I remembered an article from the 1980s—one that was well ahead of its time.

Now, in 2020, we know much more than we did 33 years ago—and yet, we still battle the same dogmas. Athletes of all levels continue to undergo lactate curve testing—out of habit, ignorance, or naïveté—eagerly watching for shifts in their anaerobic thresholds as signs of progress. I have nothing against the use of lactate in testing or training. But never in the form of a simple curve (often done incorrectly, methodologically speaking), but rather as a biomarker to track the type of glucose turnover and the presence (or absence) of metabolic stability.

We’ve retyped the original article for you from its typewritten form. Even after 33 years, it still has much to offer. Sadly, Dr. Vávra has long since passed away, but I was fortunate to discuss the article and his legacy with Associate Professor Radvanský from the Department of Physical Education and Sports Medicine at Motol University Hospital, who knew the author personally. I thank him sincerely for that.

For the purists: yes, I’m aware of the nomenclature shift from “lactic acid” (LA) used at the time of writing to “lactate” (still abbreviated LA—go figure). Dear reader, as of 2020, feel free to choose your preferred interpretation of the acronym.

I wish you a pleasant summer read—and a moment to reflect on a sports physician who saw far ahead of his time and cared deeply about how the model of lactate metabolism proposed by A. Mader was being twisted into commercial simplifications for profit and personal glory.

The article itself may be quite technical for some readers. But don’t worry if you don’t catch every detail. The key ideas are there—and they are clear.

Jiří Dostal

Lactic Acid: An Overused Metabolite or an Understood Indicator?

Lactic acid has become a popular metabolite in the world of sports medicine. Its measurement has moved beyond physiological research labs and into the practical life of athletes. There’s nothing wrong with translating scientific knowledge into real-world applications—but in this case, perhaps the translation came too early.

Today, blood lactate levels (LA) are often used to draw conclusions about fitness levels, the effectiveness of various training methods, or even an athlete’s potential. Meticulous lactate tracking has become a hallmark of “scientific” training methods. Substantial (often foreign currency-based) resources are invested into obtaining the chemical reagents and equipment for its analysis.

In labs or field conditions, all sorts of exercise protocols are used—of different forms and durations—during which blood samples are repeatedly taken from athletes. The resulting lactate values are used to draw elegant curves or connection points, largely dependent on the evaluator’s training and imagination. The desired goal is typically to find the “inflection point” of the curve—what’s commonly referred to as the “anaerobic threshold.”

But What Does It Actually Mean?

Even setting aside methodological criticisms—such as the questionable legitimacy of inflection points derived from just two or four data points, or the poor reproducibility when failing to account for prior nutrition or physical exertion—we must ask:

If we accept the construction of the LA curve and its inflection point from a physiological standpoint, what does a sudden rise in blood lactate at a certain workload actually tell us?

Since the 19th century, the concepts of aerobic and anaerobic metabolism have been passed down, tracing back to early studies by Pasteur. It seemed straightforward: determine which intensity level is covered by aerobic systems, and identify the threshold beyond which energy must be produced “on credit,” through anaerobic pathways.

However, numerous researchers have pointed out the cracks in these interpretations. Only in recent decades has a mosaic of “heretical” insights begun to form a clearer—albeit still incomplete—picture.

Why Does Lactate Suddenly Rise?

The concentration of LA in the blood reflects the balance between its production in tissues (especially skeletal muscles) and its removal by organs capable of metabolizing it via oxidation or resynthesis. So the real question is: under intense effort, is lactate production increasing, is clearance decreasing—or both?

From a biochemical standpoint, pyruvic acid (PA) is the end product of glycolysis. It has two main fates:

1. Transport into mitochondria for further processing via the citric acid cycle.

2. Conversion into lactic acid by the enzyme lactate dehydrogenase (LDH) in the cytosol.

LDH is a highly active enzyme, and recent studies using isotopically labeled carbon have shown that lactate is always produced, in direct proportion to glycolytic turnover.

Sometimes, however, the issue isn’t excessive production of PA, but limited mitochondrial uptake—either due to insufficient enzyme activity in the citric acid cycle or poor hydrogen removal in the respiratory chain. This is nature’s miracle: controlled energy release by reducing oxygen with hydrogen to form water, fueling all life processes.

A lack of oxygen delivery to mitochondria—due to hypoxemia, restricted blood flow (e.g., prolonged isometric contraction), or excessive PA production—can overwhelm mitochondrial capacity. Above ~60% of VO₂ max, rising levels of adrenaline and glucagon drastically stimulate glycogenolysis and glycolysis, leading to lactate accumulation.

White muscle fibers, known for high glycolytic capacity but low mitochondrial density, are major lactate producers. These fibers are increasingly recruited as intensity rises.

The Lactate Surge: More Than Just Production

So, what happens to all this lactate? If muscle perfusion is adequate, lactate diffuses into the bloodstream. Yet, even as intensity increases and glycolysis accelerates, blood LA levels don’t rise significantly at first. This implies a balance—what enters the blood is efficiently cleared.

But where does it go?

Mainly to the liver, but also to the kidneys, heart, inactive muscles, and possibly other tissues. This clearance depends heavily on blood flow distribution. At high intensities, sympathetic activation restricts visceral and non-working muscle blood flow—especially around 60% VO₂ max—limiting lactate removal.

The result is an imbalance: increasing lactate influx, reduced clearance, and blood accumulation. This isn’t a simple matter of crossing into “anaerobic” territory. It’s a complex physiological cascade. Therefore, labeling the LA curve inflection point as “the anaerobic threshold” is fundamentally flawed.

A New Interpretation: The Stress Threshold

Instead, this inflection point marks the onset of stress—a shift into heightened neurohumoral stimulation affecting:

• Metabolic processes

• Peripheral blood distribution

• Muscle fiber recruitment (especially type II fibers)

Ventilation increases similarly, though not necessarily in response to lactate. While lactate acidosis may contribute to ventilatory compensation, it is not essential (e.g., in McArdle syndrome). The true trigger is likely central regulation of stress responses.

Abandoning Old Terms, Adopting New Ones

The term “anaerobic threshold” is outdated. So is the rigid dichotomy of aerobic vs. anaerobic metabolism. Let’s replace these with more accurate concepts:

• Glycolytic phosphorylation (energy from glycolysis)

• Oxidative phosphorylation (energy from mitochondrial respiration)

These terms reflect the actual biochemical pathways involved in ATP production.

So, What Should We Measure?

Blood lactate tells us more than just about metabolism. It reflects:

• Fiber type recruitment

• Enzymatic efficiency

• Blood redistribution

• Hormonal responses (e.g., catecholamines, cortisol, glucagon, GH, endorphins)

Other indicators of stress thresholds might include:

• Respiratory variables (ventilation rate, respiratory exchange ratio)

• Cardiovascular shifts (e.g., blood pressure spikes)

The more adapted an athlete is, the higher the intensity needed to trigger this systemic stress. But not every marker will respond at the same workload. And this is where the irreplaceable human brain must weigh context: previous exertion, nutrition, fatigue, and many other factors.

Conclusion: A Word of Caution

Lactate metabolism is a fascinating area of research—but perhaps best left to advanced physiological labs. In the world of applied sports, blood lactate testing alone won’t win medals—especially considering the financial cost.

If we are to move forward, we must shed some cherished myths:

• The anaerobic threshold

• The “oxygen debt” split into alactic and lactic phases

• The staged activation of ATP, glycolysis, and oxidation at exercise onset

Reality is more complex. Few still analyze the “components” of oxygen debt in practice. But drawing blood and plugging numbers into a training log remains tempting. Maybe it’s time we started a deeper discussion—perhaps right here, in this journal.