# The Lactate Shuttle: How Your Body Actually Uses Lactate During Exercise

Deep Dive | Training Physiology

If you haven’t read the Foundation article, What Is Lactate (And Why It’s Not the Enemy) , start there. It covers the basics. Lactate is fuel, not waste, the burn comes from hydrogen ions, not lactate, "lactate threshold" is a curve, not a switch. This piece assumes you’re comfortable with all of that and want the full molecular picture.

Foundational research on the mechanism

In 1985, George Brooks at UC Berkeley published a paper that should have ended the "lactic acid is bad" narrative immediately. His central argument was that lactate serves as a mobile fuel, continuously produced and consumed by various tissues in a coordinated exchange he called the "cell-to-cell lactate shuttle" and he had good evidence to prove it (Brooks, 1985).

At the time, this was borderline heretical. The prevailing view treated lactate as a dead-end waste product, and Brooks was saying no, it’s one of the body’s primary energy currencies. He was right, and the evidence has accumulated substantially since then, but I want to note that the field took its time coming around. That’s relevant because it illustrates something I think about a lot. Bad models survive in exercise science, even after the data has moved on. (More on that in the Research Literacy section of this library, eventually, when I finish it.)

The shuttle concept has expanded quite a bit since 1985. We now know there’s not just cell-to-cell transfer but also an intracellular shuttle. Lactate moves between the cytoplasm and the mitochondria within the same cell. This was initially controversial (some researchers questioned whether the relevant transporters were even present on mitochondrial membranes), but the evidence for it has gotten quite strong (Brooks, 2009; Hashimoto et al., 2006).

How the lactate shuttle works

During exercise, your fast-twitch muscle fibers (which are more glycolytic, meaning they rely more heavily on glucose breakdown) produce lactate at higher rates than they can consume it. This lactate gets exported out of the cell into the blood via a protein called MCT4.

Once in circulation, the lactate gets picked up by tissues that can oxidize it. These are slow-twitch muscle fibers, the heart, and the liver. These receiving tissues import lactate via a different transporter, MCT1, convert it to pyruvate through a reaction catalyzed by lactate dehydrogenase, and feed it into the mitochondrial citric acid cycle for aerobic energy production.

Fast-twitch fibers export, slow-twitch fibers and the heart import, the liver recycles. It’s elegant, smooth, and wonderfully designed (/evolved. You know what I mean).

The heart deserves special attention here because the numbers are striking. During hard exercise, lactate can supply more than 60% of the heart’s fuel (Gertz et al., 1988). The heart isn’t just tolerating lactate, it’s preferentially selecting it over fatty acids as exercise intensity climbs. I find this deeply satisfying as a piece of physiology. The molecule that athletes have been trained to fear is literally keeping their hearts running during the hardest efforts.

The liver plays a different but equally important role. Through the Cori cycle (a name you might remember from biochemistry, or might be happy to have forgotten), hepatocytes (liver cells) convert circulating lactate back into glucose via gluconeogenesis, then export that glucose back into the blood for exercising muscles to use. This recycling pathway becomes increasingly important as glycogen stores deplete during prolonged exercise. Your body is running its own internal economy, and lactate is one of the currencies.

So instead of being a waste product, lactate is used as fuel by your heart and turned back into sugar by your liver while you’re exercising. It’s key to everything. The body doesn’t waste. Except poop. Poop is waste.

MCT transporters and how to make them better

I mentioned MCT1 and MCT4 above. These are monocarboxylate transporters (hence MCT). They’re membrane proteins that move lactate (and other monocarboxylates like pyruvate and ketone bodies) across cell membranes. They’re the physical infrastructure that makes the shuttle possible, and they’re worth understanding because they’re trainable.

MCT1 is the importer. It’s highly expressed in oxidative tissues. These are slow-twitch muscle fibers, cardiac muscle, and the liver. It has a high affinity for lactate, meaning it works efficiently even when lactate concentrations are low. MCT4 is the exporter. It’s predominantly expressed in glycolytic tissues, your fast-twitch fibers. It has a lower affinity but higher capacity. It’s built for dumping lactate out of the cell when intracellular concentrations spike during hard efforts.

Like I said, it’s all trainable. Endurance training increases MCT1 density in oxidative fibers (Pilegaard et al., 1999; Thomas et al., 2005) and high-intensity interval training upregulates both MCT1 and MCT4 (Juel, 2006). This is one of the molecular mechanisms behind the rightward shift of the lactate curve that coaches observe when athletes get fitter. You’re not producing less lactate at a given intensity (a common misconception). You’re getting better at using it.

The MCT4 upregulation from intervals might seem counterintuitive. Why would you want to export more lactate? Remember, lactate is used by the rest of your body. Not only that, it can slow down glycolsis in muscles that have too much of it. Too much lactate and your muscles can’t break down sugar. Faster export from glycolytic fibers prevents intracellular hydrogen ion accumulation from shutting down glycolysis. It keeps the fast-twitch fibers functional. The exported lactate then becomes available fuel for oxidative fibers and the heart. The whole system gets faster. I think of it like improving traffic flow: you’re not reducing the number of cars, you’re widening the on-ramps and off-ramps. (This is in a scenario where you want more cars. Widening roads at the expense of public transportation actually creates induced demand, creating a vicious cycle that makes traffic worse again. But in your body, it’s all good. Just don’t do it in the real world.)

Lactate as a signaling molecule

Beyond its role as fuel, lactate functions as a signaling molecule. This is the part of the research that’s still actively developing.

Lactate stimulates mitochondrial biogenesis through upregulation of PGC-1α, the master regulator of mitochondrial development (Hashimoto et al., 2007). Read that again, because the circularity of it is beautiful. Hard efforts produce lactate. That lactate signals your body to build more mitochondria. More mitochondria improve your capacity to oxidize lactate. The stimulus contains the instructions for its own resolution.

Lactate also influences angiogenesis (new blood vessel formation) through effects on HIF-1α and VEGF pathways (Hunt et al., 2007). Better capillary networks mean better oxygen delivery and substrate exchange, which feed back into improved endurance performance. There’s even emerging evidence that lactate crosses the blood-brain barrier and serves as fuel for neurons during exercise, and that it modulates the immune response to training (Brooks, 2020).

The signaling story is far from complete, but the direction is clear. Lactate isn’t metabolic noise or a waste product. It’s an active participant in the adaptation to training. When you produce a bunch of it during a hard interval session, your body doesn’t just burn it and move on. It reads it as information and learns from the experience.

The "threshold" problem

The concept of "lactate threshold" is practically useful but physiologically imprecise, and the terminology around it is a genuine mess. I’ll try to untangle it, but I want to acknowledge upfront that reasonable people disagree about some of these definitions and you should go with whichever one yo like best.

LT1 (first lactate turning point): The intensity at which blood lactate begins to rise above resting levels, typically around 2 mmol/L. This roughly corresponds to the upper boundary of what most coaches call "Zone 2." Below LT1, production and clearance are well matched. Your shuttle is handling things comfortably. Above LT1, lactate is rising above resting levels.

LT2 / MLSS (maximal lactate steady state): The highest intensity at which blood lactate stabilizes rather than continuing to rise. Typically around 4 mmol/L, though this varies considerably between individuals (I’ll come back to that). This is the intensity most coaches mean when they say "threshold." At MLSS, the entire shuttle system is running at capacity. Production, transport, and clearance are in a tenuous equilibrium that will tip over if you push even slightly harder. If you go too hard, you get burn and have to back off. It’s right on the edge.

OBLA (onset of blood lactate accumulation): Defined as the intensity corresponding to a fixed 4 mmol/L blood lactate concentration. This is a convenience definition, not a physiological event. Some athletes reach their actual steady-state limit at 3.0 mmol/L, others at 5.5. Using 4 mmol/L as a universal threshold is like using a single shoe size for everyone. It works often enough to be useful, but it’s wrong often enough to matter, especially if you’re using it to set training zones.

Critical Power / Critical Speed: A mathematically derived intensity representing the boundary between sustainable and unsustainable metabolic states. Not identical to MLSS but correlated with it, and it has the advantage of not requiring you to draw blood (Jones et al., 2019). This one has been gaining traction in the research literature and I think we’ll see it used more in applied coaching settings over the next few years.

The practical upshot of all this definitional complexity is that "train at threshold" is a less precise instruction than it sounds. What you’re actually training is the shuttle. You’re building MCT density, mitochondrial volume, and capillary networks. Whether you’re doing that at exactly 4.0 mmol/L or 3.4 mmol/L matters less than whether you’re consistently working in the range that stresses these systems. This is all why top level coaches usually recommend lactate testing to define your training zones. Your training is largely determined by lactate production and clearing balances. Knowing the paces and powers that bring these on in your own body will help you set those zones.

Why polarized training makes sense through this lens

The lactate shuttle framework provides a nice mechanistic explanation for why polarized training models (lots of easy work below LT1, some hard work above LT2, relatively little in between) have shown strong results in both research and elite practice (Stöggl & Sperlich, 2014; Seiler, 2010; professional atheltes, often).

Low-intensity work below LT1 builds the oxidative infrastructure: mitochondrial density, capillary networks, MCT1 expression, fat oxidation capacity. This is the slow, structural work. You’re pouring the foundation for a more efficient shuttle. It rewards consistency and volume over intensity. If your easy runs feel "moderate," you’re probably compromising this process, which is one of the most common training errors I see in the athletes I work with. Low intensity work is too hard to cause these changes to take place.

High-intensity work above LT2 produces large amounts of lactate, which stimulates MCT upregulation, triggers mitochondrial biogenesis via PGC-1α, and drives angiogenesis. This is the stimulus that pressurizes the system.

Time in the middle, between LT1 and LT2, is metabolically stressful enough to accumulate fatigue but may not provide a sufficiently distinct adaptive stimulus compared to the other two zones. This doesn’t mean threshold work is useless. It means a program built primarily around threshold sessions may generate more fatigue per unit of adaptation than one that distributes intensity more deliberately. The research here is still evolving and individual responses vary quite a bit, but the lactate physiology gives you a framework for understanding why the polarized approach keeps showing up in the literature as competitive with (and sometimes superior to) more threshold-heavy approaches. And all of this is why Zone 2 training is so popular these days.

A clarification about acidosis

I want to be careful not to overcorrect here. Dismissing the old "lactic acid" narrative doesn’t mean that metabolic acidosis during hard exercise isn’t real. It is. Hydrogen ion accumulation during high-rate glycolysis contributes to the burning sensation and interferes with muscle contraction. That’s happening.

What’s changed is our understanding of the causal chain. Lactate production and acidosis are correlated because they share an upstream cause (high glycolytic flux). But the lactate dehydrogenase reaction, the one that produces lactate, actually consumes a hydrogen ion. This means that lactate formation technically buffers against acidosis rather than contributes to it (Robergs et al., 2004). This is still debated in some corners of the physiology literature, but the current weight of evidence supports the view that blaming lactate for the burn is mechanistically backwards.

This matters practically because interventions designed to "clear lactate" (easy spinning, massage, etc.) aren’t actually addressing the source of muscular fatigue or acidosis. They may have other benefits, and I think they do, but through different mechanisms. Parasympathetic activation, blood flow, psychological recovery. The lactate framing is wrong.

What we still don’t know

We have a few open questions, because I think intellectual honesty about gaps in the evidence is part of what makes this kind of resource worth reading. We don’t know everything and it’s important for you to know where that gap is.

The intracellular shuttle (lactate moving into mitochondria within the same cell) is still debated. Some researchers question whether MCTs are truly present on mitochondrial membranes or whether the observed transport happens through other mechanisms (Gladden, 2008). The signaling roles of lactate, particularly its effects on gene expression and immune regulation, are still being mapped. The optimal training strategies for improving shuttle efficiency in specific populations (recreational athletes, masters athletes, people coming back from injury, AKA – probably you) are not well studied. Most of what we have comes from trained or elite populations.

The interaction between lactate metabolism and nutritional state is another open area. Training in a glycogen-depleted state ("train low") upregulates some of the same pathways that lactate signaling activates. Whether these stimuli are additive, redundant, or occasionally counterproductive isn’t clear yet.

Then there’s individual variability, which is probably the biggest practical gap. MCT expression, fiber type distribution, and mitochondrial density vary substantially between individuals. Two athletes on the same training plan will experience meaningfully different lactate dynamics at the same relative intensity. This is one reason rigid zone prescriptions based on population averages are always approximations. (It’s also one of the strongest arguments for working with someone who understands this physiology, if I’m allowed a brief moment of self-promotion.)

What this means for your training

If you’ve read this far, you probably want to know what to do differently. The honest answer is that understanding the shuttle doesn’t require you to overhaul your training. But it should inform how you think about a few things.

Your easy aerobic work is building the machinery that makes the shuttle efficient. That adaptation is slow and cumulative (we’re talking months and years), which is why consistency matters more than any single session. Your hard interval work is producing the metabolic stress that signals your body to adapt. The lactate you generate isn’t damage. It’s a stimulus, and the signaling it triggers is part of how your body knows to build more mitochondria, grow new capillaries, and express more MCT transporters. Recovery between hard sessions exists to allow these structural changes to happen. Rushing back to the next hard workout before the response is complete is one path to overreaching, which is its own topic but worth flagging here.

And when someone tells you to flush the lactic acid after a race? Just smile and spin easy. The spinning is fine. The explanation is wrong.

References

Brooks, G. A. (1985). Lactate: glycolytic product and oxidative substrate during sustained exercise in mammals. Comparative Biochemistry and Physiology Part B, 83(2), 227-231.

Brooks, G. A. (2009). Cell-cell and intracellular lactate shuttles. Journal of Physiology, 587(23), 5591-5600.

Brooks, G. A. (2020). Lactate as a fulcrum of metabolism. Redox Biology, 35, 101454.

Gertz, E. W., Wisneski, J. A., Stanley, W. C., & Neese, R. A. (1988). Myocardial substrate utilization during exercise in humans. Journal of Clinical Investigation, 82(6), 2017-2025.

Gladden, L. B. (2008). A "lactatic" perspective on metabolism. Medicine and Science in Sports and Exercise, 40(3), 477-485.

Hashimoto, T., Hussien, R., & Brooks, G. A. (2006). Colocalization of MCT1, CD147, and LDH in mitochondrial inner membrane of L6 muscle cells. American Journal of Physiology, 290(6), E1237-E1244.

Hashimoto, T., Hussien, R., Oommen, S., Gohil, K., & Brooks, G. A. (2007). Lactate sensitive transcription factor network in L6 cells. FASEB Journal, 21(10), 2602-2612.

Hunt, T. K., Aslam, R. S., Beckert, S., et al. (2007). Aerobically derived lactate stimulates revascularization and tissue repair via redox mechanisms. Antioxidants and Redox Signaling, 9(8), 1115-1124.

Jones, A. M., Burnley, M., Black, M. I., Poole, D. C., & Vanhatalo, A. (2019). The maximal metabolic steady state: redefining the ‘gold standard.’ Physiological Reports, 7(10), e14098.

Juel, C. (2006). Training-induced changes in membrane transport proteins of human skeletal muscle. European Journal of Applied Physiology, 96(6), 627-635.

Pilegaard, H., Terzis, G., Halestrap, A., & Juel, C. (1999). Distribution of the lactate/H+ transporter isoforms MCT1 and MCT4 in human skeletal muscle. American Journal of Physiology, 276(5), E843-E848.

Robergs, R. A., Ghiasvand, F., & Parker, D. (2004). Biochemistry of exercise-induced metabolic acidosis. American Journal of Physiology, 287(3), R502-R516.

Seiler, S. (2010). What is best practice for training intensity and duration distribution in endurance athletes? International Journal of Sports Physiology and Performance, 5(3), 276-291.

Stöggl, T., & Sperlich, B. (2014). Polarized training has greater impact on key endurance variables than threshold, high-intensity, or high-volume training. Frontiers in Physiology, 5, 33.

Thomas, C., Perrey, S., Lambert, K., et al. (2005). Monocarboxylate transporters, blood lactate removal after supramaximal exercise, and fatigue indexes in humans. Journal of Applied Physiology, 98(3), 804-809.

New to this topic? Start with the Foundation: What Is Lactate (And Why It’s Not the Enemy) →

Dealing with a training plateau or trying to make sense of your zone training? I work with endurance athletes in Richmond, VA and remotely. Book a consultation with RVA Endurance PT.