Rethinking Blood Lactate: From Misunderstood Byproduct to Metabolic Signal

Rethinking Blood Lactate: From Misunderstood Byproduct to Metabolic Signal

An evidence-informed perspective on lactate physiology, mitochondrial function, and endurance performance, inspired by the work of Iñigo San Millán, PhD.

Introduction

Why Lactate Deserves a Rethink

Few topics are as persistently misunderstood in exercise physiology as blood lactate. For decades, lactate has been blamed for muscle burn, fatigue, and poor performance—often lumped together with the phrase "lactic acid buildup." Yet, as researchers like Dr. Iñigo San Millán have helped clarify, this framing is not only outdated, it actively obscures one of the most elegant regulatory systems in human metabolism.

Lactate is not metabolic waste. It is not poison. It is not the cause of muscle soreness.

Lactate is a fuel, a signal, and a window into mitochondrial health, glycogen status, and training readiness.

This article reframes lactate through the lens used by San Millán in his work with elite endurance athletes—from WorldTour cyclists to Olympic-level runners—and integrates foundational biochemistry and applied physiology to show how lactate data can be used to guide training prescription, nutritional strategy, and recovery monitoring.

1. The Misnomer of “Lactic Acid” in Human Physiology

The first and most important clarification is biochemical: lactic acid does not meaningfully exist in human physiology under normal conditions.

At physiological pH (~7.4), lactic acid dissociates almost instantly into lactate and a hydrogen ion (H⁺). What we measure in blood is lactate, not lactic acid.

Physiological Implications

For years, fatigue was attributed to "acid buildup." But modern biochemistry shows:

• Lactate itself is not acidic

• The burning sensation during hard exercise is related to hydrogen ion accumulation, not lactate

• Lactate production actually buffers acidity by consuming protons during its formation

In other words, lactate is protective, not harmful.

San Millán emphasizes this point because attributing fatigue to lactate obscures the true limiting factor in endurance performance: mitochondrial oxidative capacity relative to ATP demand. When mitochondria cannot keep up with ATP demand, glycolysis accelerates and lactate production rises—not because something is wrong, but because the system is adapting in real time.

2. Lactate as a Primary Oxidative Substrate

One of San Millán’s most frequently misunderstood—but well-supported—assertions is the following:

“Lactate is the preferred fuel of the mitochondria.”

The Lactate Shuttle Concept

Proposed by George Brooks and central to San Millán’s framework, the lactate shuttle describes how lactate is constantly produced, transported, and oxidized:

• Fast-twitch fibers produce lactate

• Lactate is transported via MCT transporters

• Slow-twitch fibers, heart muscle, and brain oxidize lactate directly

This happens all the time, even at rest.

Why Lactate Beats Glucose

Compared to glucose, lactate:

• Enters mitochondria more rapidly

• Requires fewer enzymatic steps

• Provides faster ATP availability

• Is heavily used by the heart and brain

During exercise, especially at moderate to high intensities, lactate becomes a primary oxidative substrate—not a backup.

This reframes endurance performance fundamentally: elite athletes are not those who avoid lactate production, but those who demonstrate a high capacity to produce, transport, and oxidize lactate concurrently.

3. Blood Lactate as a Proxy for Mitochondrial Function

San Millán consistently returns to a central interpretive principle:

“Lactate tells us how well the mitochondria are working.”

Low Lactate at Higher Power = Healthy Mitochondria

When mitochondria are dense, efficient, and well-trained:

• Pyruvate is rapidly oxidized

• Less lactate accumulates in blood

• Fat oxidation remains high

• Glycogen is spared

Conversely, elevated lactate at relatively low workloads suggests:

• Poor mitochondrial density

• Impaired fat oxidation

• Overreliance on glycolysis

This is why San Millán places such emphasis on Zone 2 training—not as easy mileage, but as targeted mitochondrial conditioning.

4. Lactate Dynamics and Glycogen Availability

One of the most practical applications of lactate assessment lies in its relationship to muscle glycogen availability and carbohydrate flux.

The Glycogen–Lactate Relationship

As muscle glycogen declines:

• Glycolytic flux becomes less efficient

• Lactate production can paradoxically rise at the same workload

• Fat oxidation may drop if mitochondrial function is compromised

In long sessions, a rising lactate at constant power or pace can indicate:

• Approaching glycogen depletion

• Inadequate carbohydrate availability

• Poor metabolic flexibility

For endurance athletes, this provides real-time feedback that heart rate alone cannot.

5. Lactate as an Indicator of Training Readiness and Systemic Stress

Resting and low-intensity lactate values can reveal more about readiness than most subjective tools.

Resting Lactate

In well-recovered, aerobically fit athletes:

• Resting lactate is typically ~0.6–1.0 mmol/L

Chronically elevated resting lactate may reflect:

• Sympathetic overactivation

• Poor sleep or under-recovery

• Illness or systemic stress

• Mitochondrial dysfunction

San Millán uses this information to adjust training before performance declines.

Warm-Up Lactate Drift

Another powerful insight comes from measuring lactate during a standardized warm-up:

• Higher-than-normal lactate at easy intensities suggests incomplete recovery

• Stable or reduced lactate suggests readiness to absorb intensity

This turns lactate into a daily decision-making tool, not just a lab metric.

6. Limitations of Conventional Lactate Threshold Models

San Millán has been notably critical of rigid threshold constructs (e.g., LT1, LT2) when applied without metabolic context.

Instead, he focuses on:

• Absolute lactate values at known workloads

• How quickly lactate rises with small power increases

• Individual metabolic fingerprints

Two athletes can have the same lactate threshold yet vastly different endurance capacities based on mitochondrial efficiency and fat oxidation.

7. Lactate Suppression, Fat Oxidation, and Zone 2 Training

Perhaps San Millán’s greatest contribution is linking lactate suppression directly to fat oxidation.

True Zone 2 training is characterized by:

• Lactate ~1.3–2.0 mmol/L

• High fat oxidation

• Minimal glycolytic stress

• Sustainable mitochondrial signaling

When lactate creeps too high, fat oxidation drops—even if heart rate still appears “aerobic.”

This explains why many athletes accumulate volume but fail to improve metabolic efficiency.

8. Applied Implications for Coaches and Endurance Practitioners

Lactate testing doesn’t require a lab or elite status to be useful.

Key Applications

• Set true aerobic intensity

• Monitor recovery and readiness

• Detect glycogen depletion early

• Track mitochondrial adaptations over time

• Individualize fueling strategies

Used correctly, lactate becomes less about thresholds and more about metabolic truth.

Conclusion

San Millán often summarizes performance with a simple statement:

“The athlete who can go the fastest while producing the least lactate wins.”

Not because lactate is bad—but because it reflects extraordinary mitochondrial capacity, metabolic flexibility, and fuel efficiency.

When we stop fearing lactate and start listening to it, training becomes clearer, simpler, and more precise.

Lactate is not the enemy of endurance performance.

It’s the message.