Lactate Vindication

Life begins and ends at the cellular level.

Endurance coaches, athletes, trainers, and sports medicine professionals mistakenly use “lactic acid” when they mean “lactate.”

Lactate and lactic acid are used interchangeably. It is incorrect to state that lactic acid accumulation is responsible for fatigue, muscle soreness, pain, and a variety of adverse effects from exertion.

Lactate is produced during anaerobic and aerobic exercise and serves as a vital fuel source for muscles. Lactic acid is similar in structure to lactate, with an additional hydrogen atom [H+] being the exception. This distinction is crucial because lactic acid is not present in any cell or physiological system.

Endurance training triggers heated debate about the metabolic pathways that fuel performance. The premise for decades held that pyruvate – a product of glycolysis – is the primary pathway through which carbohydrates [CHO] enter the mitochondria for oxidation. 

Ceaseless research and a landmark paper have fundamentally challenged this premise. The evidence now points to lactate, not pyruvate, as the primary substrate for mitochondrial CHO oxidation. Enter the mitochondrial lactate oxidation complex [mLOC].

This revelation has profound implications for endurance-sport training strategies aimed at optimizing performance, because lactate has long received a bad rap in sports science as a “waste product” of anaerobic metabolism, blamed for muscle fatigue and poor performance.

But science has steadily disproved the story of lactate. Dr. George Brooks’ work on the “lactate shuttle” concept demonstrated that lactate is not a dead-end byproduct but a critical energy substrate. It’s produced in one cell or tissue and utilized as fuel in other cells.

The paper on the mLOC highlights that lactate is not just an intermediate player but the star of the show in CHO oxidation.

The key: pyruvate is a known intermediate of glycolysis, but lactate, transported into the mitochondria by monocarboxylate transporters [MCTs], primarily drives mitochondrial oxidation.

Lactate is converted back to pyruvate by mitochondrial lactate dehydrogenase (mLDH), which then feeds into the tricarboxylic acid cycle [TCA] for ATP production. This pathway is efficient, robust, and is the foundation of endurance performance.

The Mitochondrial Lactate Oxidation Complex

The mLOC is a specialized mitochondrial system that facilitates lactate oxidation.
Find its components below:

→ Mitochondrial Lactate Dehydrogenase [mLDH]: Converts lactate to pyruvate in the mitochondria;
→ Monocarboxylate Transporters [MCT1 and MCT4]: Transports lactate across mitochondrial membranes;
→ Basigin [CD147]: A MCT protein stabilizer;
→ Mitochondrial Pyruvate Carriers [mPC1 and mPC2]: Regulate pyruvate in the mitochondrial matrix.

This system highlights mitochondria’s ability to directly oxidize lactate, bypassing the need for cytosolic conversion to pyruvate. It underscores the body’s reliance on lactate as a primary fuel source during prolonged exercise.

Our tissue pH is strictly regulated; therefore, the addition of a powerful acid such as lactic acid would disrupt the pH balance by dissociating in water, releasing hydrogen ions, and severely impact cellular activity and endurance sports performance:

→ Exercise-induced fatigue;
→ Enzyme inhibition;
→ Cellular stress;
→ Buffering system mayhem;
→ Lactate shuttle;
→ Energy production;
→ Metabolic flexibility;
→ Signaling

Lactate production increases when energy demands exceed supply. Lactate turnover within cells is ceaseless. It is produced by glycolysis and removed primarily via oxidation. Steady-state aerobic exercise converts pyruvate to lactate, which is converted to glycogen.

Lactate is a primary CHO fuel despite its villainous reputation. Lactate produced by glycolysis in the muscle fiber cytoplasm is used by mitochondria and oxidized in Type I fibers.

“The burn” results from a buildup of acidity in muscle cells. Acidity is caused by the release of hydrogen ions during the fast turnover of adenosine triphosphate [ATP]. The release of hydrogen ions within muscle cells interferes with the muscle fibers’ ability to contract properly.

Unless the intensity of the exercise decreases, the high level of burn [acidosis] will eventually cause exercise cessation. The role of lactate is to help buffer and neutralize hydrogen ions, thereby delaying the burn.

Lactate produced in muscle fibers can be utilized elsewhere via the “lactate shuttle” process described by Brooks. The lactate shuttle allows glycolysis in one cell to provide fuel for another cell via diffusion and monocarboxylate [MCT] proteins. Lactate as an exertion fuel source accounts for approximately 75% of lactate removal.

The clearance of lactate is the body’s ability to use or convert it, primarily in the liver [gluconeogenesis] or other tissues for fuel [oxidation], preventing excessive accumulation and facilitating recovery after intense exercise, with active recovery often improving clearance rates. 

Lactate produced in the muscle is transported by the blood to the liver. It is converted to pyruvate and glucose [gluconeogenesis], and then shuttled to the muscle. This is termed the Cori cycle.

If the recycling process falters, prolonged exertion is severely compromised. Lactate is transported to and oxidized by the brain based on metabolic fuel nutrients implemented during exertion.

It is unlikely that one would consider skeletal muscle an endocrine organ. The integration of bodily functions with muscle contractions triggers the release of cytokines and signaling molecules [myokines].

Lactate was classified as a myokine by Dr. Brooks because it is produced by glycolysis and shuttled to other tissues. Myokines propel catabolic adaptations during skeletal muscle fiber exertion and several related functions.

Some myokine functions include:

→ Inhibit lipolysis;
→ Limits fatty acid oxidation uptake;
→ Monitors mitochondrial biogenesis;
→ Ignites vascular endothelial propagation;
→ Enhances cardiac output and respiration;
→ Provides a source of brain metabolism

Bottom line:

The accumulation of hydrogen ions (H+) causes the burning sensation in muscles during intense exercise by lowering pH and creating an acidic environment that interferes with muscle function and ATP production.

Lactate buffers hydrogen ions, allowing the body to reuse them for energy rather than fueling a burn. Vindication for lactate.

Impact of Hydrogen Ions:

→ Energy Production: The breakdown of adenosine triphosphate (ATP) for energy releases hydrogen ions;
→ Acidic Buildup: When ions accumulate faster than their clearance pH level in the muscle tank;
→ Impaired Function: Increased acidity sabotages efficient muscle contractions and energy production

Lactate’s Misunderstood Role 

→ Lactate is formed when pyruvate [a product of glucose breakdown] binds with a hydrogen ion, but lactate is not the instigator of the “burn;”
→ Lactate acts as a crucial buffer by mitigating problematic hydrogen ions and is recycled as a valuable energy source for muscles, heart, and brain. 

The “burn” is a sign of metabolic acidosis from excess hydrogen ions, while lactate helps buffer the acidity and provides fuel.

Lactate is a crucial energy source and performance enhancer for endurance athletes, acting as a fast fuel, delaying fatigue by being recycled into energy, improving metabolic efficiency, and VO2 max.

It bolsters signaling beneficial physiological adaptations, such as enhanced mitochondrial capacity and increased blood flow, allowing athletes to sustain faster paces for longer. 

Training at the lactate threshold teaches the body to use it more effectively as fuel, improving both endurance and speed. 

Key Physiological Adaptations for Endurance Performance:

→ Fuel source;
→ Energy shuttle;
→ Hormonal signaling;
→ Energy production;
→ Improved clearance;
→ Energy byproduct;
→ Acidosis buffer;
→ Training zones;
→ Fuel usage;
→ Higher threshold;
→ Delayed fatigue;
→ Improved VO2 max;
→ Enhanced metabolic efficiency;
→ Mitochondrial biogenesis;
→ Cardiovascular health;
→ Faster recovery;
→ Brain and hormone health [BNDF];
→ Performance marker

Lactate During Exercise

→ Lactate dominates the lactate-to-pyruvate (L/P) ratio in the blood – a pivotal role as an energy substrate;
→ Lactate represents a steady supply of fuel for the muscles – especially during prolonged exertion.
→ Lactate’s ability to shuttle between glycolytic and oxidative tissues optimizes energy transfer;
→ This “lactate shuttle” allows glycolytic fibers to clear excess lactate to oxidative fibers or muscles as fuel;
→ The conversion of pyruvate to lactate in glycolysis regenerates NAD+ for sustained glycolytic activity;
→ The mLOC helps maintain cellular redox balance by transporting lactate to the mitochondria for oxidation;
→ Lactate transport and oxidation systems modulate the increased metabolic endurance demands ;
→ The limited pyruvate transport and handling systems make lactate a practical and efficient substrate;
→ The pyruvate transitions from glycolysis to the Krebs cycle is recycled into ATP

The Role of Glycogen

Muscle glycogen is the primary CHO source during prolonged exercise. Glycogen breakdown produces lactate, ensuring a steady supply of substrate for the mLOC. Depleted glycogen stores impair lactate production and energy supply. The avoidance of chronic glycogen depletion cannot be overstated.

The foremost nutritional limiter to endurance sports performance is depleted glycogen stores. Reliance by many athletes on CHO as their primary fuel source remains pervasive and indefensible because it sabotages one’s health and potential.

Enter Metabolic Efficiency [ME].

The Issue

The body shifts its primary fuel source from fat to CHO as intensity levels increase. This shift is an ineffective route to optimal health and sports performance.

The typical diet induces nutritional stress. Ingest commercial sports drinks composed of simple sugars [sucrose or fructose] or maltodextrin, and you get both quick energy and an unhealthy cycle of blood sugar spikes and crashes.

Insulin-stimulating CHO represents an insidious path to the podium of self-destruction.

The Solution

Preservation of glycogen until it is needed ought to be the maxim. Insulin sensitivity is paramount to this process, and it is attainable only via ME. Fat adaptation is paramount.

ME is the catalyst for optimal health and performance. Its profound impact on mitigating health markers while maximizing sports performance is unparalleled. It is an inside-out approach to disease prevention and sports performance.

The Benefits

→ Enhanced concentration and focus;
→ Increased sustained energy;
→ Lower caloric needs during exertion;
→ Reduced cravings;
→ Satiety;
→ Enhanced moods;
→ Better fasting blood sugar levels;
→ Improved sleep quality;
→ Accelerated body fat loss;
→ Enhanced HbA1c levels;
→ Decreased risk of chronic and degenerative diseases

The Key

ME manifests sports performance excellence because of your diet and exercise regimens — not in spite of them. A by-product of ME is its numerous benefits for health markers.

Recovery and Adaptation

Post-exercise recovery relies heavily on lactate oxidation. After intense sessions, lactate serves as a key fuel for mitochondrial ATP regeneration. Training that enhances mLOC function accelerates recovery by optimizing lactate clearance and utilization. Again, this means that, as we have always advocated, post-training CHO intake is critical.

Monitoring Lactate Dynamics

Measuring blood lactate levels during exercise can provide valuable insights into an athlete’s ME and mLOC function. LT testing remains one of the best tools for setting training zones and monitoring progress.

The revelation that lactate is the primary form in which CHO enters the mitochondria for oxidation is more than a scientific discovery. It offers revolutionary insights with important implications for how endurance athletes train, fuel, and recover.

By embracing lactate’s central role, we can refine our methods in the spirit of transcending health, performance, and longevity in life and sport.

Lactate Threshold

Lactate threshold [LT] refers to the point during intense exercise at which lactate begins to accumulate in the bloodstream. It is a critical indicator of endurance capacity and performance.

LT is measured via incremental exercise tests, during which blood samples are drawn at various intensities.
The point at which lactate levels sharply increase is labeled the LT.

The MCT1 gene plays a vital role in lactate transport in and out of muscle cells. Gene variations can affect how efficiently an athlete manages lactate. This has a profound effect on endurance and performance.

Athletes can enhance their LT through specific training regimens, such as interval training and steady-state aerobic exercise. Implementing these strategies fosters precise lactate clearance, thereby delaying fatigue.

Understanding and maximizing LT is critical for endurance athletes optimizing their sports performance. A higher LT allows athletes to perform at higher intensity levels for prolonged periods without fatigue.

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