For more than 50 years, lactate profile testing has been a central tool in endurance training.

Graded exercise tests with incremental increases in speed or power, blood lactate measurements at each stage, and the resulting lactate curve are deeply embedded in the way endurance performance is assessed.

The age of this concept alone does not make it wrong. But…

Lactate Profile Curve

Newton’s theory of gravity is several centuries old and still correct. Age is not the issue. The issue is how a concept is used — and whether its interpretation has kept pace with advances in science.

For decades, lactate curves have offered something highly attractive to coaches and practitioners: a methodology that appears to provide an objective assessment of endurance performance.

A lactate profile curve provides a speed or power at anaerobic threshold — commonly used as a proxy for maximal lactate steady state — which is then used to create intensity zones for training [1,2].

Curves from the same or different athletes can be compared over time, and a shift of the curve is interpreted as a shift in endurance performance. Lactate profile curves seem to summarise endurance capacity in a straightforward and widely accepted test methodology.

Over time, an implicit belief has emerged from this practice: that the position and shape of the lactate curve reflect aerobic performance itself.

This belief is rarely stated explicitly, but it quietly underpins how lactate data are interpreted. As long as lactate remains low and stable, metabolism is assumed to be aerobic. When lactate begins to rise sharply, an “anaerobic” contribution is assumed to dominate. The power or speed at this transition — often labelled an anaerobic threshold — is therefore interpreted as a marker of aerobic endurance performance, or more precisely “the highest intensity which can be covered aerobically without the accumulation of lactate” [1].

In this logic, the curve becomes the performance. A right-shifted lactate curve is taken to indicate improved endurance and aerobic capacity, as higher speed or power can be sustained without (anaerobic) lactate accumulation. The threshold becomes a proxy for how “endurance-trained” an athlete is.

This reasoning did not emerge by accident. It is rooted in an outdated view of metabolism in which lactate was considered a by-product of anaerobic metabolism occurring when oxygen supply was insufficient [3]. If lactate appeared only under oxygen-limited conditions, its rise would naturally signal the limit of aerobic performance.

That view shaped the interpretation of lactate curves for decades — and it still strongly influences how lactate testing is used today.

If you’re more interested in watching these concepts explained step by step, Sebastian Weber goes deeper into the same ideas in this webinar. He shows why conventional lactate curve interpretation falls short — and how the very same tests can be used to extract VLamax, VO₂max, substrate utilization, and comprehensive metabolic insights, without additional testing, equipment, or time.

Continue reading below for the full explanation.

Something doesn’t add up

If lactate profile curves truly reflect aerobic endurance performance, they should behave accordingly.

However, several observations challenge this assumption.

A fundamental one is the relationship between aerobic capacity and the position of the lactate curve. Aerobic performance is commonly associated with maximal oxygen uptake (VO₂max) and the capacity of the oxidative system. If lactate curves were a direct representation of aerobic endurance, athletes with comparable aerobic capacity should show comparable lactate curve positions.

In practice, they do not.

Athletes with similar VO₂max values can exhibit markedly different lactate profile curves. In some cases, these differences are substantial and are often interpreted as large differences in “aerobic endurance performance.” Yet the underlying aerobic capacity, as quantified by VO₂max, remains essentially the same.

Conversely, significant right-shifts of the lactate curve can be observed without meaningful changes in VO₂max. If aerobic capacity has not changed, improved aerobic performance cannot be the explanation.

This inconsistency becomes even more apparent when comparing athletes from different event specialisations. Historical data from elite runners show that lactate curves of 100 m, 400 m, 800 m, 1500 m, and marathon athletes differ profoundly. While it is tempting to explain this purely by differences in aerobic endurance, this explanation quickly breaks down.

The aerobic capacity of 800 m and 1500 m runners is not dramatically lower than that of marathon runners. In some cases, VO₂max values are comparable. Yet their lactate curves can be shifted far to the left. If lactate curve position were primarily a measure of aerobic performance, such discrepancies would be difficult to justify.

These differences point toward an alternative explanation: lactate curve position is not determined by aerobic capacity alone.

Another important performance determinant that is entirely absent from lactate profile testing, yet strongly influences the results, is economy and efficiency. In running, for example, a better running economy means lower energy demand and therefore lower oxygen uptake at a given speed. 

Even if one accepts the idea that an inflection point in lactate concentration marks aerobic capacity, a closer look reveals a problem: the inflection point refers to a speed or power output on the x-axis of the lactate curve. Differences in economy mean that the oxygen uptake at this intensity can vary substantially between athletes, rendering a direct link between the inflection point and aerobic capacity questionable.

Body composition adds another frequently overlooked factor. Lactate concentration is measured in mmol·L⁻¹ — a ratio. The dilution space depends on total body water, which is influenced by muscle mass and fat mass. Changes in body composition — through diet, strength training, or seasonal adaptations — can alter measured lactate concentrations without any change in metabolic performance, thereby shifting the apparent position of the lactate curve. 

And then there is the protocol.

Lactate profile curves are highly sensitive to testing protocols. Step duration, workload increments, and sport-specific testing conditions substantially influence measured lactate concentrations. Different protocols — particularly differences in stage duration — can produce different curves in the same athlete, even when physiological capacity has not changed.

This has two important consequences. 

First, lactate curves obtained with different protocols are not directly comparable. 

Second, any threshold concept or method used to estimate MLSS must be matched to the specific protocol employed.

For example, the well-known 4 mmol·L⁻¹ threshold was validated only in treadmill running tests using five-minute stages with short recovery intervals. Deviations from these conditions alter the lactate curve and render a fixed threshold concept invalid.

Taken together, these observations reveal a core problem. Lactate curves are expected to answer a question they are not designed to answer. Even if the protocol is standardised and the threshold concept is properly matched, fundamental interpretational issues remain unresolved.

If curve position can change without changes in aerobic capacity; if large differences appear between athletes with similar aerobic performance; and if economy and body composition substantially alter the curve, then lactate profile curves may not be the robust tool they are often assumed to be for assessing endurance performance and guiding training decisions. 

Something does not add up.

Outcome is not the cause

To understand why lactate profile curves behave the way they do, it is necessary to step back from traditional sport-science interpretations and look at lactate from the perspective of modern biomedical sciences.

Much of the conceptual framework still used in lactate testing originated in the 1970s and 1980s, when lactate was widely considered a waste product of anaerobic metabolism [3].

Since then, the understanding of lactate metabolism has fundamentally changed.

Decades of research in biochemistry, physiology, and cellular metabolism have established that lactate is not a waste product. 

Lactate is continuously produced — even at rest and at low exercise intensities — and, crucially, even under optimal oxygen availability [4–6]. At the same time, lactate is continuously oxidised as a fuel, primarily within working muscle.

This concept is often referred to as the lactate shuttle [4,5]. Glycolysis produces lactate, which is transported and oxidised within mitochondria, thereby linking glycolytic and oxidative metabolism. Lactate is therefore not a sign that aerobic metabolism has failed; it is one of the substrates aerobic metabolism actively uses.

From this perspective, a crucial implication follows.

Lactate concentration does not indicate whether metabolism is aerobic or anaerobic. Instead, lactate concentration reflects the balance between two concurrent processes:

Lactate concentration = lactate production − lactate clearance [6,7]

This is not a conceptual model or theoretical assumption. It is a quantitative, physiologically established relationship.

Lactate production is driven by glycolytic flux. Lactate clearance is closely linked to oxidative metabolism and oxygen uptake. Both processes occur simultaneously across all exercise intensities. Changes in lactate concentration therefore reflect changes in the balance between production and oxidation, not the presence or absence of oxygen.

At low intensities, lactate clearance can exceed production, resulting in stable or decreasing concentrations. As intensity increases, lactate production rises disproportionately and eventually exceeds clearance, leading to increasing lactate levels.

The key point is not that lactate rises.
The key point is why it rises.

Once lactate concentration is understood as an outcome, it can no longer be treated as a primary causal variable. It does not explain what limits performance or which physiological systems are adapting. It simply reflects where the system has arrived.

Confusing a result for a cause

Using lactate concentration as a primary control variable in training is a subtle but fundamental mistake — one that is difficult to detect precisely because “everyone does it this way.”

Consider medicine. A physician does not treat fever by targeting body temperature itself. Fever is an outcome — a signal that something else is occurring. Treatment targets the underlying cause, such as infection or inflammation. Temperature is monitored for assessment, not manipulated as the cure.

The same logic applies to engineering.

An engineer tasked with improving fuel efficiency does not optimise fuel consumption directly. Fuel consumption is an outcome of engine design, drivetrain efficiency, aerodynamics, rolling resistance, and many other factors. Engineers intervene at the level of these mechanisms and then observe fuel consumption to assess the result.

Yet in endurance training, lactate concentration is often treated as both assessment and control.

If lactate concentration is the outcome of multiple physiological processes — including oxidative capacity, glycolytic flux, substrate utilisation, economy, and body composition — then targeting lactate values alone provides no information about which of these processes should be changed.

Outcomes are informative.
But outcomes do not tell us what to change.

Using lactate concentration to unlock a holistic performance assessment

At this point, one thing is clear:

Lactate concentration is not useless.
But it is not what it has often been used for.

Instead of asking what a certain lactate value means, we can ask what creates it.

Lactate concentration results from two processes with fundamentally different physiological origins and kinetics: lactate production in glycolysis and lactate clearance via oxidative metabolism. 

Across multiple workloads, the differing behaviours of these processes constrain the possible solutions, making it possible to infer how much lactate must be produced and oxidised to generate the observed concentrations.

In other words, lactate concentration can be decomposed into its components.

Glycolytic lactate production is a function of workload and maximal glycolytic flux (VLamax). Because workload is known during an incremental test, VLamax can be calculated.

The same logic applies to oxidative metabolism. Lactate clearance depends on oxygen uptake, which itself reflects workload and maximal aerobic capacity (VO₂max). As a result, lactate profile curves can be used to calculate both VLamax and VO₂max without additional testing and with gold-standard accuracy [8].

Because lactate is produced exclusively from carbohydrate metabolism, glycolytic flux is directly linked to carbohydrate utilisation. Knowing lactate production therefore provides information about carbohydrate oxidation. The remaining energy demand, not covered by carbohydrates, must be supplied by fat oxidation — allowing fat oxidation rates, FatMax, and maximal fat oxidation to be derived.

Together, this forms a coherent physiological chain described in the literature:

External performance determines energy demand.
Energy demand is met through oxidative and glycolytic metabolism.
Glycolytic flux determines lactate production.
Oxidative capacity determines lactate clearance.
The balance between both determines lactate concentration and substrate utilisation.

This structure is not speculative. It is grounded in established physiology and supported by decades of research. Interpreted this way, lactate profile testing moves from description toward understanding.

From understanding to application

Lactate testing does not need to be abandoned.
But it does need to be used differently.

When lactate concentration is embedded in a causal framework, the curve stops being the answer and becomes the starting point for asking better questions.

This shift does not change what is measured.
It changes what becomes possible.

How to go deeper

1. Learn the framework in practice (in person)

We offer intensive weekend workshops focused on applying physiology-based analysis in real performance diagnostics. 👉 https://inscyd.com/workshop/

2. Check if your testing qualifies for a 360° performance assessment

Not every lactate test provides the information required for this type of analysis.

👉 Check whether your testing qualifies to be transformed into a holistic 360° performance assessment.

Book a demo: turn testing into a scalable, client-ready performance service

See how INSCYD helps you move from raw test data to a complete physiological assessment—so you can start testing faster, deliver clearer insights, and grow a repeatable service across athletes.

Sebastian Weber - Founder Of INSCYD
Renowned sports scientist and creator of INSCYD, has significantly influenced elite sports training with his expertise in exercise physiology and metabolic profiling. Sebastian has developed the first ever test to measure glycolytic power aka VLamax back in 2003. He has used his knowledge to some of the best world tour cyclists to win 9 world championship titles, Olympic medals and Tour de France victories.
Sebastian Weber
Founder of INSCYD & World-renowned Sport Scientist

References

  1. Mader A et al. Sportarzt und Sportmedizin, 1976
  2. Jamnick NA et al. PLoS One, 2018
  3. Brooks GA. J Appl Physiol, 1986
  4. Brooks GA. Physiol Rev, 2009
  5. Brooks GA et al. J Physiol, 2022
  6. Stanley WC et al. Am J Physiol, 1985
  7. Poffé C et al. Front Sports Act Living, 2024
  8. Podlogar T et al. J Sci Cycl, 2022

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