Original episode & show notes | Raw transcript
To understand endurance performance, we must first understand the engine that powers it: our cellular metabolism. At its core, exercise is a question of energy—specifically, how quickly and efficiently our muscles can produce Adenosine Triphosphate (ATP), the body’s universal energy currency. Our two primary fuel sources for this process are carbohydrates and fats. This lesson, drawing from the podcast’s detailed discussion, will explore the intricate mechanisms that govern which fuel your body chooses to use, and when. We will then apply this deep understanding to critically evaluate the concept of VLA-Max (Maximum Lactate Production Rate) and its relevance to training.
Before diving into the regulation, let’s quickly review the basic metabolic pathway.
Carbohydrate Breakdown (Glycolysis): Glucose (from stored glycogen or blood sugar) is broken down in the main body of the cell (the cytosol) into pyruvate and lactate. This is a very fast process.
Transport into the Mitochondria: This pyruvate and lactate, along with fatty acids, are then transported into the mitochondria—the cell’s “power plants.”
The Common Intermediate (Acetyl-CoA): Inside the mitochondria, both the products of glycolysis and the fatty acids are converted into a common molecule: Acetyl-Coenzyme A (Acetyl-CoA).
The Krebs Cycle & ATP Production: Acetyl-CoA enters the Krebs Cycle (also known as the Citric Acid Cycle). This cycle generates electron carriers that are then used by the Electron Transport Chain to produce vast amounts of ATP aerobically (with oxygen).
A key takeaway is that once a fuel source becomes Acetyl-CoA, the subsequent steps of aerobic energy production are largely the same. Therefore, the critical point of regulation—the decision to burn fat or carbs—happens before this stage.
Unlike the smaller molecules from glucose, long-chain fatty acids are too large to simply diffuse into the mitochondria. They require a dedicated transport system, often called the carnitine shuttle.
The Transporter: An enzyme on the outer mitochondrial membrane, CPT1 (Carnitine Palmitoyltransferase 1), acts as the gatekeeper. It attaches the fatty acid to a carrier molecule called carnitine.
The Shuttle: This fatty acid-carnitine complex can now move inside the mitochondria.
The Release: Once inside, another enzyme, CPT2, splits the carnitine from the fat. The fat is now trapped inside, ready for oxidation, and the carnitine is shuttled back out to be reused.
The amount of CPT1 is a primary limiting factor for fat oxidation, especially at lower intensities. A major adaptation to endurance training is an increase in the number of these CPT1 “gates,” which enhances your ability to use fat as a fuel source.
The body has two distinct and brilliant mechanisms to regulate fuel choice, one for rest and one that activates during exercise.
When you are at rest, especially after a high-carbohydrate meal, your body needs a way to prioritize burning the abundant glucose and stop tapping into its precious fat stores.
A large influx of glucose into the muscles leads to a high rate of glycolysis and an “overload” of Acetyl-CoA inside the mitochondria.
This excess Acetyl-CoA is transported out of the mitochondria.
In the cytosol, this Acetyl-CoA is used to create a molecule called Malonyl-CoA.
Malonyl-CoA is a powerful inhibitor of CPT1. It effectively locks the gate for fat transport into the mitochondria.
This is a simple and effective feedback loop: when carbohydrate fuel is abundant, the body turns off the fat-burning machinery to deal with the immediate supply of sugar.
The Malonyl-CoA system is too slow and counterproductive for the dynamic demands of exercise. During exercise, it is shut down by the enzyme AMPK (which signals high energy demand). A different, more elegant mechanism takes over.
The Problem: As exercise intensity rises, the demand for ATP becomes immense. The body relies on the rapid breakdown of carbohydrates to produce Acetyl-CoA. This process can become so fast that it threatens to overwhelm the Krebs Cycle. This would cause all the free Coenzyme A (CoA) in the mitochondria to be locked up as Acetyl-CoA. Without free CoA, key enzymatic reactions, including the one that converts pyruvate to Acetyl-CoA, would grind to a halt. This would be catastrophic, shutting down aerobic metabolism almost instantly.
The Solution: The body uses carnitine—the same molecule used for fat transport—for a second, higher-priority job. It acts as an acetyl group buffer.
An enzyme called Carnitine Acetyltransferase takes the “excess” acetyl groups from Acetyl-CoA and attaches them to carnitine.
This forms acetylcarnitine, which can be shuttled out of the mitochondria.
This action frees up Coenzyme A, allowing aerobic metabolism to continue functioning even under immense glycolytic pressure.
The Consequence: This is the brilliant part. The carnitine that is now busy buffering acetyl groups is no longer available to transport fats into the mitochondria.
This is the primary mechanism by which increasing exercise intensity inhibits fat oxidation. It’s not a direct “inhibition” in the classic sense, but rather a competition for a limited resource (carnitine). As intensity rises, carnitine’s priority shifts from fat transport to ensuring the survival of the mitochondrial system, and as a result, fat burning necessarily decreases.
With a firm grasp of these metabolic principles, we can now analyze the concept of VLA-Max.
The Theory: VLA-Max is purported to be the maximum rate of lactate production, reflecting the “strength” of your glycolytic system. The theory posits that:
Your FTP occurs at the intensity where lactate production exceeds lactate clearance.
A high VLA-Max (a “strong” glycolytic system) means you produce lactate readily, causing your FTP to occur at a lower percentage of your VO2 max. Conversely, a low VLA-Max allows for a higher FTP relative to VO2 max.
A core assumption is that at this threshold (FTP), fuel use is 100% carbohydrates because the system is overwhelmed by glycolysis.
The Critique (Based on Metabolic Reality):
Fuel Use at FTP is Not 100% Carbohydrate: As the podcast highlights, empirical data shows that athletes can utilize a significant amount of fat at FTP—sometimes as much as 40-50%. This directly contradicts the foundational premise of the VLA-Max theory.
The “Cart Before the Horse” Problem: The VLA-Max test requires a maximal, all-out sprint. This recruits a huge number of muscle fibers, including powerful, highly glycolytic Type II fibers that are not heavily relied upon during a sub-maximal FTP effort. The test result is therefore driven by your maximal power output (sprint ability), which is determined by neural drive and muscle strength. Glycolysis is demand-driven; it reacts to the ATP demand created by the muscle contraction. A stronger sprint creates more demand, which results in a higher measured lactate value. The theory incorrectly frames this as the “strength” of glycolysis causing a certain performance profile.
Decoupling of Sprint and Endurance Performance: An athlete can significantly increase their sprint power (and thus their measured VLA-Max) through strength and sprint training without seeing a corresponding drop in their FTP, provided they maintain their aerobic training. The two systems are not as tightly and inversely coupled as the theory suggests.
Confounding Role of Lactate Clearance: The final number produced by a VLA-Max test is a net result of lactate production and lactate clearance. An athlete with a highly developed aerobic system (more mitochondria, better lactate shuttling) will clear lactate extremely rapidly. This can result in a lower measured VLA-Max value, even if their sprint power and gross lactate production are identical to another athlete’s. The test can’t distinguish between low production and high clearance.
Understanding the body’s elegant and complex fuel regulation systems reveals that human performance cannot be boiled down to a single, simple metric. The competition for coenzyme A and the dual role of carnitine provide a far more robust explanation for fuel selection during exercise than older, more simplistic models.
The practical advice derived from this understanding is clear and time-tested:
To Increase Fat Utilization and FTP: Engage in a high volume of aerobic training. Progressively extending the duration of your efforts at and around your threshold is a powerful stimulus for building mitochondria and improving fat oxidation capacity.
Don’t Fear Anaerobic Work: Sprint and anaerobic capacity training are essential for most cycling disciplines. This training will not inherently lower your FTP. The key is to perform this work within a program that also maintains and develops your aerobic base.
Focus on the Engine, Not Just the Gauges: Rather than chasing a specific VLA-Max number, focus on developing the underlying physiological systems: the aerobic engine through volume and duration, and the neuromuscular system through specific high-intensity work.