Lactate

For decades lactate was one of the most misunderstood molecules in exercise physiology. It became the villain of high-intensity exercise. Coaches blamed it for fatigue. Athletes blamed it for the burning sensation in their legs. Textbooks described it as a waste product that accumulated when oxygen delivery could no longer meet demand. That narrative was outdated 30 years ago but it still persists an is still passionately pursued by many coaches today.

The potential role of lactate as a supplement

Over the last 30 to 40 years, lactate has been completely re-evaluated. Today it is recognised as a rapidly oxidised fuel, a gluconeogenic precursor, an important shuttle between tissues, and perhaps most interestingly, a signalling molecule capable of influencing adaptation. Lactate is not merely tolerated by the body during exercise. In many tissues it is actively preferred as a fuel source. The heart oxidises lactate readily. The brain uses it. Slow-twitch muscle fibres consume it continuously. What once looked like metabolic failure now looks more like an elegant transport and communication system. As often happens in sports nutrition, this shift in understanding quickly led to a practical question: if lactate itself is beneficial, could ingesting lactate improve performance? It is a fascinating idea. But like many ideas in sports nutrition, the physiology may be easier than the practical application.

Here I want to summarise the evidence. The mechanisms make sense. Some findings are promising. Yet the overall evidence remains inconsistent, and the biggest barrier may simply be getting enough lactate into the bloodstream without causing severe gastrointestinal problems. But let’s break this down.

Lactate as a “buffer”

Part of the attraction of lactate supplementation comes from its role in acid-base balance. When lactate is oxidised or converted back into glucose, hydrogen ions are effectively consumed and bicarbonate is generated. In theory, this could help buffer acidosis during high-intensity exercise in a manner somewhat analogous to sodium bicarbonate supplementation, although the mechanisms are very different. Bicarbonate directly raises extracellular bicarbonate concentration. Lactate relies on metabolism to create its alkalinising effect. It is therefore slower, smaller and much more dependent on successful absorption and oxidation.

In theory, [lactate] could help buffer acidosis during high-intensity exercise in a manner somewhat analogous to sodium bicarbonate supplementation

On paper, sodium lactate appears attractive. It provides both sodium and lactate, potentially increasing strong ion difference (It helps the body handle the acid build-up that occurs during very intense exercise) while also contributing to metabolically generated bicarbonate. But oral sodium lactate supplementation has repeatedly run into a very practical obstacle: it can cause a lot of gastro-intestinal discomfort.

Gastrointestinal issues with lactate supplementation

One of the more remarkable papers in this area came from McCarthy and colleagues in 2024 (1). The researchers attempted oral sodium lactate supplementation fifteen separate times using different doses, different fluid volumes, different feeding states and different formulations. The outcome was almost painfully consistent. Blood lactate barely increased, while gastrointestinal distress was severe enough that vomiting occurred repeatedly during the experiments. It is difficult to imagine athletes adopting a supplement strategy that regularly ends with nausea and vomiting before competition.

The discomfort is likely caused by the very high osmolality of these lactate salt solutions. Many years ago, studies investigated polylactate as an alternative, in this case the molecules were larger, the sodium load was much lower and this would likely have positive effects on gastro-intestinal comfort. However, studies were very small (two studies with 5 subjects each), the results not very convincing. The ingredient also turned out to be very expensive and difficult to bring to market, although it was sprinkled into some sports nutrition products in the 90s…. but certainly not a new delivery mechanism for larger amounts of lactate.

Novel delivery methods of lactate

Pedersen and colleagues used pharmaceutical-grade intravenous-quality sodium lactate prepared at physiological pH and delivered in a tightly controlled solution volume (2). In that setting blood lactate concentrations did rise meaningfully and gastrointestinal symptoms were far less severe. The contrast between the two studies highlights something critically important in this field: formulation matters enormously. The chemistry, pH, osmolarity and purity of the solution appear to determine whether lactate supplementation is physiologically useful or simply intolerable.

This challenge has led researchers to explore alternative delivery systems. One of the more creative attempts came in the form of polylactate. Rather than delivering lactate as individual molecules, lactate was polymerised into a larger compound with lower osmolarity. The rationale was elegant. Lower osmolarity should theoretically reduce gastrointestinal stress and allow more lactate delivery into the circulation.

The chemistry, pH, osmolarity and purity of the solution appear to determine whether lactate supplementation is physiologically useful or simply intolerable.

The early work by Fahey and colleagues in the early 1990s generated genuine excitement (3). Cyclists ingesting polylactate maintained higher bicarbonate and pH during prolonged exercise and appeared to maintain blood glucose concentrations more effectively. The concept fitted neatly with the growing understanding of the lactate shuttle developed by George Brooks. Lactate could potentially function not only as a buffer-related substrate but also as a gluconeogenic precursor supporting carbohydrate availability during prolonged exercise. The original study involved only five participants and did not include a meaningful performance outcome. More importantly, subsequent research failed to show any additional endurance benefit when polylactate was added to carbohydrate feeding. The ingredient also turned out to be very expensive and difficult to bring to market, although it was sprinkled into some sports nutrition products in the 90s…. but certainly not a new delivery mechanism for larger amounts of lactate. The enthusiasm faded quickly. Eventually the commercial product disappeared altogether.

In many ways polylactate reflects the entire lactate supplementation field: scientifically interesting, mechanistically plausible, but never quite delivering convincing real-world performance improvements. Among the various forms studied, calcium lactate has probably produced the most compelling evidence so far. Studies using relatively high doses - around 120 mg/kg - have consistently demonstrated measurable alkalinisation.

The most positive findings came from work by Morris and colleagues, who observed substantial increases in blood bicarbonate alongside improvements in high-intensity cycling capacity (4). They report a time to exhaustion improved by approximately 17 percent, but this is always difficult to interpret with such short anaerobic types of exercise. Those are remarkably large effects for any nutritional intervention.

Exercise context is key

But context matters enormously. These were exercise protocols specifically designed to maximise metabolic acidosis: repeated severe-intensity intervals followed by exhaustion. This is precisely the environment where buffering interventions tend to work best.

When researchers moved closer to real-world endurance exercise, the picture became more complicated. The most rigorous recent study by Bordoli and colleagues used a prolonged cycling protocol lasting approximately two hours with repeated time trials embedded throughout the session (5). The study confirmed that calcium lactate genuinely altered physiology. Bicarbonate increased (although the changes were rather small). Interestingly, perceived exertion was significantly lower throughout exercise. However, performance itself did not improve. At the same time gastrointestinal symptoms steadily accumulated as exercise progressed. Flatulence, stomach discomfort, cramping and bowel urgency became increasingly common.

The central theme of lactate supplementation research today. The biology is compelling. The application remains uncertain.

Commercial lactate supplements introduce yet another layer of complexity. Such products contain calcium and magnesium lactate but at doses dramatically lower than those used in alkalinisation studies: 19 mg/kg. At these doses meaningful alkalinisation should probably not occur at all. Yet one recent industry-funded study still reported a modest improvement in 20-minute cycling performance (6). Knowing what we know from a substantial body of bicarbonate literature and what level of alkalinisation is needed to produce performance effects, these findings are unlikely. Also, blood lactate did not rise. Acid-base balance was not meaningfully altered. The proposed mechanism simply does not align with the observed outcome.

Lactate and training adaptation

Perhaps the most exciting future direction is not acute performance enhancement at all, but adaptation. Lactate is increasingly viewed as a signalling molecule capable of influencing mitochondrial biogenesis and cellular adaptation pathways. Animal studies suggest oral lactate administration may augment markers of mitochondrial adaptation in oxidative muscle. But again, translation to human sport remains highly speculative. The doses used in animal studies are enormous and physiologically unrealistic in humans (the equivalent of 300 grams of lactate per day!).

For now, lactate supplementation probably sits in an interesting middle ground within sports nutrition. The mechanisms are real and biologically credible. But neither is it ready to displace established strategies such as bicarbonate supplementation.

Summary

At present the evidence suggests that lactate supplementation may have some application in short severe high-intensity exercise where acid-base balance becomes a key limiter. Outside of that context, the performance benefits become much less convincing. The irony is perhaps fitting. Lactate spent decades unfairly blamed for fatigue and poor performance. Now it risks being overpromoted as the next breakthrough ergogenic aid. The truth, as usual in sports nutrition, is probably somewhere in between.

References

1. McCarthy SF, Bornath DPD, Tucker JAL, Hazell TJ. Oral sodium lactate ingestion does not increase blood lactate concentrations and is accompanied by moderate-to-severe gastrointestinal side effects. J Appl Physiol. 2024;137(5):1279–1284.

2. Pedersen MGB, Søndergaard E, Nielsen CB, Johannsen M, Gormsen LC, Møller N, Jessen N, Rittig N. Oral lactate slows gastric emptying and suppresses appetite in young males. Clin Nutr. 2022;41(2):517–525.

3. Fahey TD, Larsen JD, Brooks GA, Colvin W, Henderson S, Lary D. The effects of ingesting polylactate or glucose polymer drinks during prolonged exercise. Int J Sport Nutr. 1991;1(3):249–256.

4. Morris DM, Shafer RS, Fairbrother KR, Woodall MW. Effects of lactate consumption on blood bicarbonate levels and performance during high-intensity exercise. Int J Sport Nutr Exerc Metab. 2011;21(4):311–317.

5. Bordoli C, Varley I, Sharpe GR, Johnson MA, Hennis PJ. Effects of Oral Lactate Supplementation on Acid–Base Balance and Prolonged High-Intensity Interval Cycling Performance. J Funct Morphol Kinesiol. 2024;9(3):139.

6. Ewell TR, Bomar MC, Brown DM, Brown RL, Kwarteng BS, Thomson DP, Bell C. The Influence of Acute Oral Lactate Supplementation on Responses to Cycle Ergometer Exercise: A Randomized, Crossover Pilot Clinical Trial. Nutrients. 2024;16(16):2624.