Original episode & show notes | Raw transcript
For decades, lactate (often mistakenly called lactic acid) has been the scapegoat for everything from muscle burn and fatigue to next-day soreness. However, as the podcast transcript details, a deeper dive into the history and biochemistry of this molecule reveals a story that is far more complex and interesting. Modern science has not only debunked these myths but has repositioned lactate as a critical player in energy metabolism—a key fuel source, not a metabolic villain.
The story of lactate begins in the late 18th century when it was first isolated from sour milk by the German chemist Carl Wilhelm Scheele. The name itself, from the Latin root lac (milk), is a direct nod to this origin.
Fermentation and the Oxygen Link: Early on, lactate was associated with fermentation—a process that occurs in the absence of oxygen. Louis Pasteur observed that bacteria produced lactate in oxygen-poor environments. This was a crucial, yet ultimately misleading, observation.
Discovery in Muscle: In 1807, lactate was found in the muscles of hunted stags that had been exhausted from a chase. Later, experiments in the early 1900s solidified the connection: when a muscle was deprived of oxygen, lactate levels rose. When oxygen was reintroduced, lactate levels fell.
The Birth of “Lactic Acidosis”: Around the same time, in 1907, it was discovered that intense exercise made muscles acidic (lowered their pH). Because this occurred simultaneously with the rise in lactate, scientists, equipped with a limited understanding of acid-base chemistry, concluded that lactate was an acid and the direct cause of the burn. This gave rise to the term lactic acidosis, a concept that has persisted for over a century despite being incorrect.
The foundational myths about lactate stem from these early, correlation-based conclusions. Modern biochemistry allows us to correct the record.
This is the most pervasive myth. The “burn” felt during intense exercise is due to an increase in acidity, but lactate is not the culprit.
The Chemistry of Acidity: Acidity is caused by the accumulation of hydrogen ions (protons, H+). The primary source of these protons during intense exercise is the breakdown of ATP (the cell’s energy currency) for muscle contraction.
Lactate is a Base, Not an Acid: Lactate is formed from a molecule called pyruvate. In this reaction, the enzyme lactate dehydrogenase (LDH) actually consumes a proton from the cell. Therefore, the production of lactate helps to buffer or reduce acidity, it does not cause it.
The Henderson-Hasselbalch Equation: As the podcast explains, at physiological pH, the vast majority of the molecule exists as lactate, not lactic acid. The chemical equilibrium is overwhelmingly shifted away from the acidic form. In fact, for every one molecule of lactic acid, there are thousands in the non-acidic lactate form.
This myth is the origin of the term “anaerobic threshold,” a concept developed by scientist Karlman Wasserman in the 1960s. He hypothesized that when you exercise hard enough, your cardiovascular system can no longer deliver enough oxygen to the muscles (a state called dysoxia), forcing them to switch to “anaerobic” metabolism, which produces lactate.
The Reality: While it’s true that a complete lack of oxygen will cause lactate to accumulate, this is not what happens during exercise. Lactate production begins to increase significantly long before the body reaches its maximum oxygen consumption (VO2 max). Elite athletes, for instance, may reach their “lactate threshold” at 80-90% of their VO2 max, meaning there is still plenty of oxygen available.
Evidence Against the Hypoxia Theory:
Experiments on tumors in the 1920s showed high lactate production despite normal oxygen levels.
Studies on contracting animal muscles showed an initial, transient spike in lactate that then declined as the muscle became a net consumer of lactate, all while oxygen delivery remained constant.
The term “anaerobic threshold” is therefore a misnomer. Anaerobic processes are happening at all intensities, even at rest. The threshold simply represents a point where lactate production begins to outpace lactate clearance.
So, if lactate isn’t a waste product, what is it? Modern physiology recognizes lactate as a crucial metabolic intermediate—a way to shuttle energy between cells. This is known as the Lactate Shuttle Theory, pioneered by Dr. George Brooks at UC Berkeley.
During high-intensity exercise, the breakdown of glucose (glycolysis) for energy speeds up dramatically. This produces pyruvate. Pyruvate has two main fates:
Enter the mitochondria to be used in aerobic metabolism.
Be converted to lactate.
The conversion to lactate becomes necessary when pyruvate is produced faster than the mitochondria can use it. This process serves two vital functions:
Regenerating NAD+: Glycolysis requires a molecule called NAD+. During the process, NAD+ is converted to NADH. If all the NAD+ were used up, glycolysis would grind to a halt, and high-power exercise would be impossible. The conversion of pyruvate to lactate regenerates NAD+, allowing glycolysis to continue at a high rate.
Buffering Acidity: As mentioned, the reaction consumes a proton, helping to temporarily reduce the acidity caused by other metabolic processes.
Lactate is not trapped in the muscle where it’s produced. It is transported out into the bloodstream via specialized proteins (MCT1 and MCT4) and used as a preferred fuel source by other tissues:
Working Muscles: Nearby slow-twitch muscle fibers, which are rich in mitochondria, readily take up lactate, convert it back to pyruvate, and use it for aerobic energy. A well-trained muscle is both a major producer and a major consumer of lactate.
The Heart: The heart is highly aerobic and loves lactate. During intense exercise, it can become the heart’s primary fuel source.
The Brain: The brain also utilizes lactate as a fuel.
The Liver: The liver can take up lactate and use it to create new glucose through a process called gluconeogenesis (the Cori Cycle).
Lactate is not a dead-end waste product to be “cleared.” It is a valuable energy source that the body meticulously recycles.
Given that lactate isn’t harmful, the concept of “lactate tolerance” workouts is misleading. You are not training your body to “tolerate” a poison.
What’s Actually Being Trained: These high-intensity interval workouts are actually improving your body’s ability to use lactate. Training stimulates an increase in the number of MCT transporter proteins, which enhances the rate at which lactate can be shuttled out of producing cells and into consuming cells. It also increases mitochondrial density, improving the capacity to use lactate as an aerobic fuel.
Trained vs. Untrained Athletes: A highly trained endurance athlete produces more lactate at a given absolute intensity than an untrained person, but they also clear it and use it much more efficiently. This results in a lower blood lactate concentration at any given submaximal power output. Their “lactate shuttle” is simply more developed.
The Michael Phelps example from the podcast is a perfect illustration of this popular misconception. His legendary performance is not due to producing less lactate, but rather to an incredibly efficient physiological engine that is exceptional at producing and utilizing energy from all available sources, including lactate.
In summary, the scientific understanding of lactate has undergone a revolution. It has been transformed from a symbol of fatigue and anaerobic failure into a central player in metabolic flexibility and energy distribution. It is a key fuel, a buffer against acidity, and a molecule whose efficient use is a hallmark of elite athletic performance.