Few misconceptions in endurance sport have been as persistent, or as misleading, as the idea that "lactic acid" causes fatigue. The reality is more nuanced, more interesting, and more practically useful than the simplified version most athletes were taught. Understanding what actually happens at high intensities can change how you think about training, pacing, and session preparation.
The lactic acid myth
For decades, the prevailing narrative in exercise science was straightforward: during intense exercise, the body produces lactic acid, which accumulates in the muscles and causes the burning sensation associated with fatigue. This narrative was intuitive, easy to explain, and widely repeated.
It was also wrong, or at best, incomplete.
The work of George Brooks, spanning from 1985 through to 2018, fundamentally reshaped our understanding of lactate metabolism. Brooks demonstrated that lactate is not a metabolic waste product but rather a valuable fuel substrate. His "lactate shuttle" theory showed that lactate produced in one tissue can be transported to and oxidised by other tissues — including the heart, brain, and less-active muscle fibres — as an energy source (Brooks, 2018).
In fact, at moderate exercise intensities, lactate is continuously produced and consumed in roughly equal measure. It circulates as a fuel. The "burning" you feel during hard efforts is not caused by lactate itself.
So what actually causes the burn?
The critical distinction, clarified by Robergs et al. (2004), is between lactate and hydrogen ions (H⁺). When glucose is metabolised at high rates, the reactions involved produce both lactate and H⁺ ions. It is the accumulation of H⁺ ions, not lactate, that leads to a drop in intracellular pH, a state known as metabolic acidosis.
This drop in pH interferes with muscle contraction mechanics, enzyme function, and the excitation-contraction coupling process. In practical terms: as H⁺ accumulates, your ability to sustain high-intensity effort declines. That burning sensation, the heavy legs, the moment you have to back off — those are driven by acidosis, not by lactate.
Lactate, meanwhile, is doing exactly what it should: shuttling carbon between cells, serving as fuel, and being produced at rates proportional to metabolic demand. It correlates with high intensity, but it does not cause the limitation.
Buffering: the body's defence against acidosis
The body has several mechanisms to manage H⁺ accumulation and defend intracellular pH. These buffering systems include:
- Intracellular buffers, including proteins, phosphate groups, and carnosine within the muscle cell that neutralise H⁺ directly.
- Bicarbonate buffering, the primary extracellular system, where bicarbonate (HCO₃⁻) reacts with H⁺ to produce carbon dioxide and water, which are then exhaled.
- Ventilatory compensation, meaning increased breathing rate to expel CO₂, indirectly reducing H⁺ concentration.
When these systems are overwhelmed, when H⁺ production exceeds the body's capacity to buffer and clear it, performance at high intensities is compromised. This is the physiological reality behind the "threshold" concept that coaches and athletes refer to in training.
External buffering strategies
Given that buffering capacity is a limiting factor in high-intensity performance, researchers have investigated whether it can be enhanced through external means. The most extensively studied approach is sodium bicarbonate supplementation.
Carr et al. (2011) conducted a comprehensive review of sodium bicarbonate as an ergogenic aid and found evidence suggesting that pre-exercise ingestion can increase extracellular buffering capacity, potentially allowing athletes to sustain higher intensities for longer before acidosis becomes limiting. Burke and Peeling (2018) further examined buffering agents in the context of high-intensity performance, noting that while the theoretical basis is sound, practical application is often limited by gastrointestinal side effects.
This is a critical point. Sodium bicarbonate, in the doses typically studied (0.2–0.3 g/kg body mass), frequently causes significant GI distress — bloating, cramping, nausea, and diarrhoea. For many athletes, the practical discomfort outweighs the potential performance benefit.
Beyond bicarbonate: alternative buffering approaches
Research suggests that extracellular buffering capacity can influence tolerance of high-intensity efforts, although gastrointestinal tolerance is a practical limiting factor for many athletes. This has led to interest in alternative buffering strategies that may offer a more tolerable route to the same physiological goal.
Citrate-based compounds, for example, have been studied as buffering agents with potentially lower GI burden. Sodium citrate has shown some evidence of buffering effects, though results are less consistent than bicarbonate. The broader category of alkalising agents — including various sodium and potassium salts — represents an area of ongoing research interest.
The practical question for athletes is not simply "does buffering work in a lab?" but "can I tolerate this in a real-world training or competition environment?" Stomach tolerance determines real-world usefulness. This is one reason why some athletes explore formulations designed to deliver buffering potential without the GI burden that limits conventional approaches. HYDRAX PRIMER is being developed with this practical constraint in mind.
VO₂ max, threshold training, and the bigger picture
Understanding the lactate-H⁺ distinction has practical implications for how athletes structure threshold and VO₂ max training. The intensity at which H⁺ accumulation begins to outpace buffering capacity is closely related to an athlete's lactate threshold, which itself is a key determinant of endurance performance alongside VO₂ max.
The goal of threshold and VO₂ max sessions is not to "clear lactic acid." It is to develop the metabolic and cardiovascular systems that support sustained output at intensities where H⁺ production is high. This includes improving mitochondrial density (so more pyruvate is oxidised rather than converted to lactate), enhancing lactate shuttle efficiency (so lactate is redistributed as fuel), and developing buffering capacity (both intracellular and extracellular).
For endurance athletes, this understanding connects directly to the preparation-execution-recovery framework. High-intensity sessions create a specific metabolic stress. How an athlete prepares for and recovers from that stress determines the quality of adaptation over time.
Summary
- Lactate is a fuel, not a waste product. The "lactic acid causes fatigue" narrative is outdated and misleading.
- H⁺ accumulation — not lactate — drives the drop in pH that limits high-intensity performance.
- The body's buffering systems (intracellular, bicarbonate, ventilatory) defend against acidosis but can be overwhelmed at high intensities.
- External buffering strategies exist but are often limited by gastrointestinal tolerance in real-world application.
- Training at threshold develops the metabolic systems that manage H⁺ production — the true limiter of sustained high-intensity output.
References
- Brooks GA. The Science and Translation of Lactate Shuttle Theory. Cell Metabolism. 2018;27(4):757–785.
- Robergs RA, Ghiasvand F, Parker D. Biochemistry of exercise-induced metabolic acidosis. American Journal of Physiology – Regulatory, Integrative and Comparative Physiology. 2004;287(3):R502–R516.
- Carr AJ, Hopkins WG, Gore CJ. Effects of acute alkalosis and acidosis on performance: a meta-analysis. Sports Medicine. 2011;41(10):801–814.
- Burke LM, Peeling P. Methodologies for investigating performance changes with supplement use. International Journal of Sport Nutrition and Exercise Metabolism. 2018;28(2):159–169.