← All research articles

Brain energy, sport and research · 20 October 2026

Brain lactate: backup fuel, ageing and the sporting threshold

Why useful fuel, persistent accumulation and a sporting test result need different interpretations—and why fuelling matters more than chasing a low lactate number.

Develops the discussion in Billy Craig’s Controlling Intuitive Appetite, original Volume Two, Chapter 35: Starving Brain.

A research perspective drawing on human experiments, ageing studies in mice and the author’s book. Proposed EPK applications have not been validated as a training or dementia intervention.

The question already raised in Controlling Intuitive Appetite

A substance can help a system cope without its continued accumulation being a sign that the system is working well. That distinction shaped the discussion of brain lactate in Controlling Intuitive Appetite. Lactate may provide supplementary fuel when demands change or glucose supply is constrained; persistent accumulation raises a different question about production, transport and use.

Sport brings the same distinction into focus. A lactate measurement is useful information, but it becomes misleading when the number takes priority over the athlete’s capacity to perform, recover and remain adequately fuelled.

From the book

Billy Craig, Controlling Intuitive Appetite, original Volume Two, Chapter 35: Starving Brain.

Indeed, it is suggested by the author that lactate as a brain fuel has a neuroprotective effect in specific short-term situations.

The original chapter also considered whether longer-term accumulation might accompany impaired metabolism in ageing. The research question is how to distinguish useful compensation from a system struggling to meet demand.

Backup fuel does not mean emergency-only fuel

In a human tracer experiment, van Hall and colleagues studied six healthy people at rest and during exercise, including lactate infusion. The brain took up and oxidised circulating lactate. This establishes a physiological fuel role; it does not show that chronically raising brain lactate improves health. [1]

“Backup” or “emergency” fuel can describe particular situations, but lactate also participates in ordinary metabolism. A temporary increase in circulating lactate during exercise cannot be equated with persistent accumulation within ageing brain tissue. The compartment, time course and ability to use the substrate all matter.

What the ageing evidence actually shows

Ross and colleagues found approximately doubled brain lactate in normally ageing mice and mice with accelerated ageing associated with mitochondrial DNA mutations. Mitochondrial dysfunction and a shift in lactate dehydrogenase expression accompanied the finding. This supports investigating lactate accumulation as a sign of altered metabolism. It does not establish that lactate caused the ageing process. [2]

Human findings are not uniform. An exploratory study of 24 people with Alzheimer’s disease, 10 with Lewy body dementia and 15 controls found no significant group difference in lactate in the measured brain regions. [3] The mouse findings remain relevant, but elevated brain lactate is not established as a universal feature or diagnostic test of dementia. Neither result tells us that an athlete’s post-exercise blood lactate predicts brain degeneration.

What does keeping the pyruvate pathway clear mean?

Glycolysis converts glucose to pyruvate. The pyruvate dehydrogenase complex, PDH, links pyruvate to mitochondrial oxidation by producing acetyl-CoA. Lactate dehydrogenase interconverts pyruvate and lactate; the lactate-forming reaction also regenerates NAD+, allowing glycolysis to continue. These are connected processes rather than two completely separate energy systems.

“Keeping the pathway clear” is a useful shorthand for supporting carbohydrate oxidation, provided it is not treated as a literal blockage that a meal removes. Enzyme regulation, substrate supply, mitochondrial capacity and work rate contribute. Raising carbohydrate availability can support oxidation while also supporting more glycolytic flux and lactate production.

In a small crossover experiment in seven male cyclists, Stellingwerff and colleagues found reduced PDH activation and carbohydrate utilisation after a short high-fat adaptation period, despite subsequent carbohydrate restoration. That gives a concrete basis for discussing dietary effects on carbohydrate metabolism. It does not establish one universal fat percentage or prove that eating more carbohydrate always lowers lactate. [4]

The problem with making lactate threshold the goal

Threshold testing can help describe an athlete’s response to increasing work. The concern is treating a threshold as a prize detached from test conditions, fuelling and actual performance. A blood concentration reflects the balance between lactate entering and leaving the blood; it is not a direct measure of how much lactate the muscles or brain are using.

There is also no single interchangeable threshold measurement. In a glycogen-depletion experiment, the relationship between lactate and ventilatory thresholds changed: the lactate threshold shifted relative to ventilation without proving a new aerobic capacity. [5] A different test-day nutritional state can therefore complicate comparisons.

The useful target is greater sustainable output with appropriate recovery. A lactate result can inform that judgement, but a low reading alone cannot establish that the athlete is better fuelled or fitter.

Carbohydrate depletion changes the meaning of the lactate reading

A 2024 crossover experiment compared higher and restricted carbohydrate intake for two days after a glycogen-depleting session in eleven competitive runners. The restricted-carbohydrate condition produced a slower 1500 m run by about 4.5 seconds, roughly 2%, with lower baseline and peak blood lactate. [6]

This compared dietary recovery after depletion, not lactate in isolation. Total calorie intake also differed substantially between conditions. Faster performance cannot be attributed to higher lactate, nor slower performance to lower lactate. The finding does not establish that relying more on lactate is preferable to supporting pyruvate oxidation.

Glycogen supplies glycolysis, which produces pyruvate for both mitochondrial oxidation and lactate formation. Reduced carbohydrate availability can affect the supply feeding both routes. However, the study did not measure muscle glycogen, pyruvate or PDH activity, so it cannot establish pyruvate depletion or identify the limiting pathway.

Its relevance is narrower: interpret lactate alongside diet and workload. This dietary comparison supports attention to fuelling, not a claim about lactate’s independent effect on performance.

Comfortable breathing as a practical guide

For an easy endurance session, choosing a pace that permits comfortable conversation offers a practical way to avoid turning every outing into a hard effort. Studies comparing the talk test with physiological thresholds support its usefulness, although the relationship varies with the protocol and population. [7,8]

This is a way to regulate effort, not a home test of PDH activity. Comfortable breathing cannot confirm that no lactate is being produced, and hard breathing during demanding exercise does not by itself establish a blocked pathway or inadequate oxygen delivery. Deliberately restricting breathing is not the objective.

Easy training and appropriately planned harder work serve different purposes. The proposal here is to support sustainable aerobic work and adequate fuelling, not to require every athlete to avoid breathlessness or abolish lactate production.

An EPK approach worth testing

EPK means Energy per Kilogram. Its practical emphasis here is meeting the person’s energy needs, supplying carbohydrate appropriate to the work, and judging the result through function and recovery. Avoiding unnecessary underfuelling is a more useful aim than trying to make the body independent of lactate.

The proposed approach is to fuel the work, build sustainable capacity and use breathing comfort to help control easy-session intensity. Lactate testing can complement that approach when conditions are standardised. There is not yet evidence that this EPK approach is superior to a well-designed threshold-guided programme.

A useful study would record diet and prior exercise, compare the same absolute workloads as well as performance tests, and measure lactate alongside gas exchange, perceived effort and recovery. Lower lactate at an unchanged workload with improved function would mean something different from lower lactate because the participant could no longer produce the same power. Brain-ageing claims would require separate research.

Related EPK articles

Research and guidance

Explore more studies in the research library.

  1. van Hall G, et al. Blood lactate is an important energy source for the human brain. Journal of Cerebral Blood Flow & Metabolism. 2009. Human tracer experiment, six participants.
  2. Ross JM, et al. High brain lactate is a hallmark of aging and caused by a shift in the lactate dehydrogenase A/B ratio. PNAS. 2010. Mouse study.
  3. Musaeus CS, et al. Normal cerebral oxygen consumption and lactate levels in patients with Alzheimer’s disease and Lewy body dementia. GeroScience. Published online 2025; issue 2026. Exploratory human study.
  4. Stellingwerff T, et al. Decreased PDH activation and glycogenolysis during exercise following fat adaptation with carbohydrate restoration. American Journal of Physiology–Endocrinology and Metabolism. 2006.
  5. The effect of exercise induced glycogen depletion on the lactate, ventilatory and electromyographic thresholds. 1997. Human experimental study.
  6. Venckunas T, et al. Effect of Low vs. High Carbohydrate Intake after Glycogen-Depleting Workout on Subsequent 1500 m Run Performance in High-Level Runners. Nutrients. 2024;16:2763.
  7. Consistency of the talk test for exercise prescription. 2004. Human treadmill and cycling study, 16 volunteers.
  8. Quinn TJ, Coons BA. The Talk Test and its relationship with the ventilatory and lactate thresholds. Journal of Sports Sciences. 2011. Human study, 15 participants.

Related working papers

Read the relevant PDFs: EPK–001 to 007 are the revised version 1.2 papers; EPK–008 to 010 are version 1.0 supplements. Earlier PDFs and DOI records remain on the paper archive.