Pogačar Is Drinking Lactate. Here's What That Actually Means for You.
Lactate was never the enemy, and the gels may not be the story
The gel is called ExoLactate. It was developed by the Spanish physiologist Aitor Viribay, who spent seven years trying to solve a problem most of the sports nutrition world had given up on. When the first production run was ready, a single WorldTour team bought all of it, every sachet, and signed a confidentiality agreement to keep their name out of it. Viribay can talk about the product. He cannot tell you who is using it.
Meanwhile, at the front of the race, Tadej Pogačar has been taking a prototype from Enervit, UAE Team Emirates-XRG's nutrition partner, that does something similar. Ninety grams of carbohydrate, ten grams of lactate, in a mix his team has been quietly trialling since 2024.
Riders are reporting up to twenty grams of lactate an hour with no stomach trouble. Lower perceived effort. Better legs in the final hour.
Lactate. The substance you have been told, since the first time anyone explained training to you, is the thing that burns your legs, ruins your last rep, and leaves you hobbling down stairs two days later.
The professionals are now paying around €3.50 a sachet to drink it on purpose.
There are two stories here. One is about whether you should buy the gel. The other is about a hundred-year-old mistake that is still shaping how you think about every hard interval you have ever done.
The second story is far more valuable, so let's start there.
Part One: The wrong verdict
In 1922, A.V. Hill and Otto Meyerhof shared the Nobel Prize in Physiology or Medicine. Part of the work behind it involved isolated frog muscle, stimulated to fatigue in a dish, with lactic acid accumulating as it stopped producing force.
The conclusion drawn was intuitive and, for the next eighty years, essentially unchallenged: muscle runs short of oxygen, lactic acid accumulates, and the accumulation causes fatigue. Lactate became the metabolic receipt for working too hard. Waste. Exhaust. The thing you flush out.
The problem with the frog muscle is not that the measurements were wrong. It is that the preparation had no circulation. No heart, no liver, no brain, no neighbouring muscle. Nowhere for the lactate to go.
In an intact human being, lactate produced in one place travels through the bloodstream to somewhere else and gets burned for energy. A dish containing only muscle could never have shown that. The experiment was sound; the extrapolation was not. And because it arrived with a Nobel Prize attached, it went into the textbooks and stayed there for three generations.
Here is what we actually know now.
"Lactic acid" barely exists in you. At the pH of human blood and muscle, lactic acid is almost entirely dissociated. What is genuinely present is lactate, the conjugate base. When someone talks about lactic acid building up in their legs, they are describing a molecule that is not meaningfully there.
Lactate is not what makes you acidic. This is the one that surprises people. The reaction that produces lactate actually consumes a proton. The protons that acidify a working muscle come mostly from the rapid breakdown of ATP outrunning your capacity to resynthesise it aerobically. Lactate production doesn't cause that acidosis. It slows it down. Lactate is a marker that travels alongside the problem, not the problem itself.
The most useful way to think about it: an observer who only ever saw ambulances at crash sites might reasonably conclude that ambulances cause crashes. Lactate turns up wherever hard work is happening, so it got the blame for hard work.
Acidosis may not even be the main event. This is where it gets genuinely interesting. At real body temperature, as opposed to the cold single-fibre preparations that generated much of the classic data, acidosis has surprisingly little direct effect on force production. The leading candidates for peripheral fatigue today are inorganic phosphate, which accumulates during intense work and interferes with both force generation and calcium release, and potassium accumulating outside the muscle fibre, which degrades the electrical signal telling the muscle to contract. There is even reasonable evidence that mild acidosis is protective, helping action potentials keep propagating in fatiguing fibres.
And the burn? The burning sensation comes from group III and IV sensory nerve endings in the muscle responding to the local metabolic environment: protons, ATP, and other by-products binding to receptors that report back to your brain. Lactate correlates with the burn because it is produced at the same time as the actual stimuli. It is not the burn.
Nor is it your soreness. Blood lactate returns to baseline within roughly an hour of finishing. It is not sitting in your quads on Tuesday morning. Delayed onset muscle soreness is mechanical damage and the inflammatory response to it, which is why eccentric work and downhill running wreck you and steady-state cycling does not, regardless of how much lactate each produced.
So where does it actually go?
In the 1980s, the physiologist George Brooks proposed what is now textbook: the lactate shuttle.
You produce lactate constantly. At rest. Fully aerobic. Sitting reading this. Lactate production does not require oxygen shortage. That framing was the original error, and Brooks has spent forty years correcting it.
Your fast-twitch, glycolytic fibres export lactate through one family of transporters. Your heart, your slow-twitch oxidative fibres, your liver and your brain import it through another family and use it. Producers and consumers can be adjacent fibres in the same muscle, or organs at opposite ends of your body.
During exercise, your whole-body turnover of lactate can exceed your turnover of glucose. A 2017 paper in Nature went further, showing that in most tissues it is circulating lactate, not glucose directly, that serves as the primary carbon source feeding the citric acid cycle. Your brain takes up lactate in proportion to how much is in your blood, meaning the harder you go, the more of your thinking is being powered by the very molecule you were told was poisoning you.
Lactate is not exhaust. It is one of the busiest fuels in your body, and a substantial part of what makes a well-trained aerobic system well-trained is the capacity to produce it fast and clear it faster.
That is worth sitting with for a moment. Not because it changes what you should buy. Because it changes what you should feel when the burn arrives in the fourth interval. That sensation is not damage accumulating. It is a system working.
Part Two: So should you eat it?
Here is where the honest answer diverges sharply from the marketing.
The theory behind the gels is elegant. Your gut can only absorb carbohydrate so fast. Glucose and fructose each move through their own transporter, and saturating both is where modern professional cycling's ceiling of roughly 90 to 120 grams an hour comes from. Lactate uses an entirely separate transport route. So in principle you bolt lactate on top of a maxed-out carbohydrate strategy, raise your total incoming fuel, spare some muscle glycogen, and fade less in the final hour.
Physiologically plausible. Now look at the evidence.
The entire human literature on ingesting lactate amounts to roughly eight studies, most with fewer than fifteen subjects. And there is a pattern in them that anyone reading sports science should learn to recognise.
The positive results cluster in the small, older, industry-adjacent studies, often using time-to-exhaustion tests that are notoriously unreliable. The best of them, an eleven-subject study from 2011, found a 17% improvement in time to exhaustion after calcium lactate, alongside a genuine rise in blood bicarbonate.
The negative results cluster in the newer, larger, independently funded, better-controlled work. The best-designed trial in the field, published in 2024, gave fourteen well-trained cyclists the same dose as that 2011 study, in a double-blind crossover with controlled diet, across a two-hour protocol built to mimic actual road racing. Performance outcome: null. No difference. It did find lower perceived exertion, which is interesting. It also found significantly more flatulence, cramping, stomach ache and bowel urgency.
An effect that shrinks as the methods improve is usually not an effect.
But the real problem is more fundamental than any performance result, and it comes from a 2024 study that deserves more attention than it got. The researchers tried to raise blood lactate by mouth using sodium lactate. They tried it fifteen separate ways: different doses, different fluid volumes, fed and fasted, different formulations. Blood lactate barely moved. Subjects vomited repeatedly.
That 2024 cycling trial found the same thing in passing: after 120 mg per kilogram of calcium lactate, blood lactate was not significantly different from placebo.
If you eat lactate and your circulating lactate does not rise, the entire extra-fuel argument has nothing to stand on.
Then there is the arithmetic
Even granting the mechanism, run the numbers, because nobody selling this does.
Lactate carries about 3.6 calories per gram. Twenty grams an hour, the top of the range being discussed, is 72 calories. Against the roughly 480 calories an hour you get from 120 grams of carbohydrate, and against the total cost of a hard hour's riding, that is a rounding error. It is the caloric equivalent of about eighteen grams of carbohydrate.
Worse, look at how you would actually get it. ExoLactate contains 5 grams of lactate per gel. Viribay's own stated target is 10 to 25 grams an hour. Reaching 20 grams means four gels an hour, which also means 160 grams of carbohydrate an hour. That is well beyond what almost anyone tolerates, and it comprehensively defeats the premise, which was to find fuel that gets around the carbohydrate ceiling. At around €3.50 a gel, that is also roughly €14 an hour.
And there is a final point, made sharply by the sports nutrition researcher Asker Jeukendrup, that ought to end the conversation. If your goal is to raise blood lactate via your gut, fructose already does it. Fructose is substantially converted to lactate in the gut and liver, and it produces a measurable rise in blood lactate, which the oral lactate salts studied so far demonstrably do not. That transport channel everyone is excited about is already open. You have been using it every time you drank a decent drink mix.
This has happened before
In 1991, a product called polylactate arrived with the same theory, the same excitement, and the same promise of a novel fuel channel. George Brooks himself co-authored the first commercialisation study.
By 1994, an independent trial had concluded that adding polylactate to a glucose polymer solution does not improve endurance. It proved expensive to manufacture, it got sprinkled into a few sports drinks, and the story quietly died.
We are watching attempt number two. It may well go better. The new gels are a genuine formulation advance, and solving palatability and tolerance is not nothing. But nobody has published a single performance trial on any lactate gel. Not one. Everything you have read about how well they work traces back to rider testimonials relayed through press, and to the man who invented them.
Which brings up something worth knowing: Viribay is a co-author on the research that helped establish those 120 grams-per-hour carbohydrate intakes in the first place. He helped define the ceiling. He now sells the product designed to get around it. That is not misconduct, and it is not unusual in this industry. But you deserve to know that the person framing the problem is selling the solution.
Part Three: The hybrid athlete's version
Now the part nobody writing about the Tour is going to tell you, because they are writing for cyclists.
Look again at the two lactate studies that disagreed. The 2011 study that found a 17% benefit used repeated severe-intensity intervals to exhaustion, a protocol built to generate maximum acidosis. The 2024 study that found nothing used a road-race simulation. The 2024 authors explained the discrepancy themselves: their protocol produced roughly half the acid-base disturbance of the earlier one. Less acidosis to buffer, no benefit to find.
Follow that logic and something odd falls out.
If oral lactate does anything at all, it is probably working as a buffer, not as a fuel. And the athlete whose sport generates that kind of acidosis is not the Grand Tour rider spending five hours below threshold. It is the athlete doing sled pushes into burpee broad jumps into wall balls with incomplete recovery. It is the HYROX athlete. It is the person doing a brutal metcon, or a set of 400s, or the back half of a threshold session on tired legs.
The product is being marketed to Tour de France riders on a fuel argument that does not hold, while the buffering argument that might hold points squarely at us.
Before you get excited: if buffering is your limiter, there is already a better answer, and it costs almost nothing.
Calcium lactate at the doses studied raised blood bicarbonate by about 4%, with no performance benefit. Sodium bicarbonate, better known as baking soda, at 0.3 grams per kilogram raises it by roughly 20%, with a large, replicated body of evidence behind it. The historical objection was that it destroyed your stomach; modern enteric-coated and hydrogel formulations have largely solved that. It is one of the genuinely well-supported ergogenic aids available, and it is one of the cheapest.
Judged as a buffer, lactate is a weaker, more expensive, more GI-risky bicarbonate.
And on the strength side of hybrid training, the evidence is not thin. It is negative. Researchers raised plasma lactate by intravenous infusion, which is a far more effective delivery method than any gel will ever be, and measured what happened to resistance-exercise signalling and muscle protein synthesis in humans. Nothing. No effect. If anyone tells you lactate supplementation supports the strength half of your programme, the experiment has been run and it came back null.
Part Four: The filter
There will be another one of these. There was beetroot. There was ketones, which arrived with a genuinely compelling theory and delivered performance gains far smaller than anyone hoped. There was cherry juice. There will be something new in 2027, and it will arrive the same way: through the peloton, into the cycling press, into your feed, into your shopping basket.
So rather than review each one forever, here is the filter. Five questions.
1. Was it tested on people like me, doing what I do?
Trained cyclists are not HYROX athletes are not recreational runners. A benefit in a two-hour road race simulation tells you very little about a 60-minute race with a sled in it. And as we just saw, sometimes it tells you the opposite.
2. Who paid for it?
Not as an accusation. As a weighting. Notice how consistently the independently funded trials in this field came back null, and how consistently the industry-adjacent ones did not.
3. Does the dose in the product match the dose in the research?
This one catches an enormous amount. A 2024 study on a commercial lactate supplement used roughly one-sixth of the dose from the buffering literature, about 1.4 grams for a 75kg athlete, and reported a performance improvement with no accompanying change in any physiological marker that could explain it. That is not a finding. That is noise wearing a lab coat.
4. How big is the effect against how big are my gaps?
Seventy-two calories an hour is real. It is also meaningless if you are averaging six hours of sleep, under-fuelling your long sessions, and skipping the strength work that would keep you healthy enough to train consistently. Marginal gains are called marginal because they are what remains once everything else is handled.
5. Am I solving my limiter, or someone else's?
A Tour rider's limiter after five hours in the Pyrenees is glycogen availability. Yours, most likely, is not.
Running cherry juice through it
Worth doing, because the filter is not just a sophisticated way of saying no.
Tart cherry has a real evidence base. Systematic reviews find it helps recovery of muscle function and reduces soreness after strenuous exercise, with measurable effects on inflammatory markers. The certainty of that evidence is rated low-to-moderate and the findings are heterogeneous, but it is there. Performance effects are much weaker. One meta-analysis found a pooled improvement in endurance performance, but eight of ten studies showed no individual benefit, and no dose-response relationship has been established.
So: modest, real, mostly about recovery rather than performance. Passes the filter better than lactate gels do.
But there is a catch that turns this into a training question rather than a shopping question. High-dose antioxidant supplementation can blunt training adaptations. Your body adapts partly in response to the oxidative stress of hard work, and mopping it all up can interfere with that. Tart cherry's main active compound appears to work by modulating inflammatory signalling rather than directly scavenging free radicals, so it probably carries less of that risk than high-dose vitamin C and E. Probably.
The sensible conclusion is not "yes" or "no". It is when.
Use it when recovery is the goal and adaptation is not: race week, a congested competition block, a stage race, a period of two-a-days, the back end of a taper. Don't take it every day through a build phase, when the whole point of the block is to let the stress land and force an adaptation.
That is a periodisation answer to a supplement question. Which is how nearly every supplement question should be answered, and almost never is.
The point
We will tell you when something is worth your money. That is part of what this is for.
Right now, lactate gels are not there. The physiology behind them is real and genuinely exciting. The product built on top of it is running well ahead of its evidence, cannot reliably deliver the thing it claims to deliver, and would cost you around €14 an hour to find out.
But do not walk away from this thinking the story was a disappointment, because the story was never the gel.
The story is that the most feared molecule in endurance sport spent a century wrongly convicted on evidence from a frog in a dish, and that the thing you were taught to fear is, in fact, fuel. Your heart runs on it. Your brain runs on it. Your slow-twitch fibres are burning it right now. And the burn you feel in the fourth interval is not damage arriving. It is a system doing precisely what a trained system is supposed to do.
That is not a marginal gain. That is a different relationship with hard work.
Which is the whole idea. Training is a system, not a collection of purchases. Strength supports endurance. Endurance improves recovery. Consistency compounds. Everything sits on top of that base, and nothing you can buy in a sachet moves the base.
Get the base right, and one day the marginal gains will actually be worth having.
