A runner’s guide to LT1, the first lactate threshold

LT1 is the first lactate threshold: one of two key thresholds that define your body’s pattern of physiological response to different running speeds (the other being steady-state max or “SSmax”).

Your LT1 can be intuitively understood as the boundary between paces that feel easy versus paces that feel moderate, steady, or strong.

On a physiological level, LT1 represents the point at which your aerobic system faces its first real disturbance to homeostasis.

Now, that does not mean that paces above LT1 are anaerobic—instead, your aerobic system rises to meet this challenge, and maintains an aerobic steady-state. However, the signs of this greater aerobic challenge become evident in key physiological metrics like blood lactate and oxygen consumption.

A number of my recent posts have brushed up against LT1, like my article on individual variation in heart rate zones, my transcript and commentary on Marius Bakken’s double threshold training, my article on physiological resilience for marathon runners, and of course my article linked above on SSmax, the other key physiological transition.

However, I haven’t done a full article yet dedicated to LT1, and since there’s a ton of wrongheaded information out there about exactly what LT1 represents, it’s high time we take a deep dive into the science behind LT1, the mess of various acronyms and terms related to LT1, and the practical relevance of LT1 for training.

LT1 is a key threshold that demarcates two different domains of intensity

Across the full range of running intensities, from a slow jog to an all-out sprint, there are fundamentally only three different patterns of physiological response that you’ll see from your body. These three patterns of response define the three domains of intensity.

Within each domain, different speeds produce qualitatively similar patterns of response from your body. The specifics—i.e. the exact heart rate, blood lactate level, rate of oxygen consumption, etc.—will of course change from one pace to the next, but as long as you’re in the same domain of intensity, the qualitative pattern will be the same.

The easy to moderate domain: slow jogging up to LT1

At easy to moderate speeds, your body experiences only a modest challenge to its aerobic capabilities, and the key physiological metrics that indicate your body’s internal state—oxygen consumption, blood lactate, intramuscular acidity levels, and so on—are constant. I call these speeds the easy to moderate domain; physiologists call it the “moderate” domain.

When casual runners talk about “Zone 2,” they are talking about the easy to moderate domain (whether they realize it or not is another story!).

At a constant-speed run in the easy to moderate domain, key physiological metrics show the following patterns:

• Oxygen consumption, also known as VO2, rises quickly over the first two to three minutes of the run, then plateaus.^[1]
• Blood lactate levels are not significantly different than their baseline levels after an easy jog

If you compare physiological metrics at different running speeds (again within the context of a constant-speed run), you’ll see the following trends:

• The plateau value that oxygen consumption reaches after a few minutes increases linearly with running speed, such that you can very accurately predict the VO2 plateau value of a new speed given the tread from previous speeds.
• The change in this plateau value in VO2 is proportional to speed in such a way that your running economy—measured as mL of oxygen per kilogram of body weight per kilometer of distance covered—remains essentially constant across different speeds.^[2]
• Carbon dioxide production (VCO2) rises proportional to oxygen consumption across faster and faster speeds.
• Your breathing rate and your ventilation (volume of air moved through your lungs per minute) increases as well, showing a proportional rise with faster speeds.
• Blood lactate levels remain statistically indistinguishable from baseline across different speeds.

Here's what that linear change in VO2 looks like: a very predictable trend.

(Note that the X axis ticks are annotated using minutes per mile, but the actual spacing is in meters per second, which is why the pace markers are unevenly spaced: VO2 is linear in speed, not pace.)

One metric you’ll notice that I’ve excluded here is heart rate—that’s because heart rate’s kinetics, or its evolution over time at the same intensity, are quite different from the kinetics of lactate, oxygen consumption, and carbon dioxide production. For example, heart rate can drift steadily upwards even at easy to moderate paces, and even when oxygen consumption (and therefore energetic demand) is constant.

There are some other physiological metrics that do show appreciable shifts even within the easy to moderate domain. The most notable among these is fat oxidation: as you approach the upper end of the easy to moderate domain, your reliance on carbohydrates increases, and your rate of fat oxidation (even in absolute terms) declines. This shift is related to the concept of “FatMax,” but that’s a topic I’ll leave for another day.

The high-end aerobic domain: LT1 to SSmax

Above a certain speed, the pattern of physiological response that held for easy to moderate paces no longer makes accurate predictions. Several key shifts happen all at once:^[3]

• Oxygen consumption rises swiftly for a few minutes, but instead of reaching a plateau immediately, it gradually drifts upwards for another five to ten minutes before finally stabilizing—a phenomenon called the VO2 slow component.
• The VO2 value that oxygen consumption finally plateaus at is higher than expected based on the speed/VO2 trend from slower speeds. This higher VO2 value reflects a deterioration in running economy: running is now more expensive, in terms of oxygen cost per unit distance.
• Blood lactate levels are now significantly above their baseline levels, to the tune of a 0.5 mM increase or more. However, blood lactate levels are still stable—albeit elevated—over time.
• Carbon dioxide production is noticeably higher relative to oxygen consumption. Textbooks often describe this plot (VCO2 versus VO2) as an “abrupt shift” but in reality it usually looks like a smooth, continuous curve.
• Ventilation is also noticeably higher relative to oxygen consumption. Again, many textbooks claim this is an abrupt shift, but almost always real data looks more like a smooth curve.

These changes are signs you have now crossed into the high-end aerobic domain—or what physiologists call the “heavy” domain.^[4]

Again, if you compare the pattern of response at constant-speed runs within the high-end aerobic domain, you’ll see a few additional features:

• Running economy continues to get gradually worse at faster speeds.
• Fat oxidation drops dramatically, with carbohydrate reliance quickly approaching 100% as you get faster and faster.
• Blood lactate levels stabilize at progressively higher and higher levels.

Collectively, all of these changes in physiological response have the same root cause: a progressive loss of efficiency in your muscle fibers. Data from single-muscle-fiber experiments shows that, above a given contractile intensity, force production from the same individual muscle fiber decreases over time, while energy consumption (ATP per second) remains constant.^[5]

Here's what that higher-than-expected oxygen consumption trend above LT1 looks like:

Inside your body, the consequences of this loss of efficiency in the working muscle fibers are as follows:

1. In response to the decrease in muscular force production from currently-working fibers, your body recruits additional muscle fibers to pitch in—after all, if you’re going to maintain the same running speed and the same gait mechanics, you’re going to need to keep producing the same total muscular force.
2. Some of these newly recruited muscle fibers are fast-twitch fibers. These fibers are less efficient in that they require more oxygen to produce the same amount of force^[6], and they prefer to use glycolysis for much of their energy production: they break down glycogen locally, then shuttle much of the resulting lactate out of the fiber.^[7]
3. Once lactate is shuttled out of a fast-twitch fiber, it makes its way either to adjacent fibers or the bloodstream, where it circulates until being oxidized elsewhere in the body.^[8]
4. The need for more oxygen (to power the newly-recruited muscle fibers) drives you to breathe more frequently and more deeply, which in turn drives (some) carbon dioxide out of the bloodstream.^[9]
5. The increased concentration of lactate within muscle fibers acts as a signal to inhibit fat oxidation and encourage carbohydrate oxidation, resulting in dramatic decreases in reliance on fat for energy.

So, all of the physiological shifts seen above—the gradual rise in VO2, the higher-than-expected VO2 plateau, worse running economy, increased CO2 production, increased ventilation, elevated blood lactate levels, dramatic decreases in fat oxidation—have a common cause: the increased aerobic challenge to muscle fibers that manifests as the VO2 slow component.

LT1 separates easy to moderate speeds from high-end aerobic speeds

Understood simply, LT1 represents the dividing line between these two domains: the point at which your body encounters its first real challenge to aerobic homeostasis.

As shown above, you do rise to meet this challenge: even above LT1, your body still maintains a metabolic steady-state over time. However, your body’s response to this greater challenge shows up clear as day in a wide variety of physiological metrics.

LT1 matters because the stimulus to your body above LT1 is going to be systematically different from the stimulus to your body below LT1.

That doesn’t mean that all speeds above LT1 are “the same” from a training perspective, nor does it mean that all speeds below LT1 are the same—even within a given domain of intensity, there are many different training stimuli that you can achieve—but understanding the physiological differences in paces above versus below LT1 is absolutely essential for understanding how your body will react to any given workout.

The sources of fatigue are different above versus below LT1

Another point worth mentioning regarding the high-end aerobic domain is that the main drivers of fatigue are different. Below LT1, research shows that your main sources of fatigue are muscle damage and central fatigue (rooted in the brain itself). Above LT1, you face the additional challenge of peripheral fatigue from localized glycogen depletion and (possibly) the accumulation of reactive oxygen species.^[10]

The high-end aerobic domain spans from LT1 all the way up to SSmax—and if you want to find out more about SSmax, and its relationship with the second lactate threshold (LT2) and the maximal lactate steady-state (MLSS), check out my article on steady-state max for runners.

LT1 and the mess of acronyms: VT1, GET, AT, AnT, AeT, T1, and more

Now that we’ve understood the basic physiology behind LT1, we can dig into the terminology that different sources use for it—and here’s a warning: it’s a mess!

Gas exchange threshold (GET) is a VO2 and VCO2-based estimate of LT1

Many physiology labs measure LT1 in the context of a performance test for VO2max. In this situation, you already have VO2 and VCO2 data (from the mask the athlete is wearing) and it’s very common to use these data to estimate LT1. The idea is to leverage the uptick in VCO2 relative to VO2 that occurs at (or close to) LT1.

As I noted above, the VCO2-VO2 plot is supposed to show a “clear breakpoint” but usually it looks something like this:

Various line-fitting algorithms exist for estimating LT1 from data like this, but a surprising number of labs just “eyeball it.” Because this estimate comes from data on the exchange of oxygen and carbon dioxide in the lungs, this method is termed the gas exchange threshold or GET.

GET can be noisy and requires a lot of data processing to get a nice plot like the one above. The reason physiologists often prefer GET is that it doesn’t require taking blood draws to measure lactate.

Ventilatory threshold (VT or VT1) is a breathing-based estimate of LT1

A similar technique for using metabolic testing data (again, without blood draws) from a VO2max test involves making a plot of ventilation rate against VO2. This technique leverages the uptick in ventilation that occurs near LT1.

Same caveat as above—does this really look like it shows a breakpoint?

Because it’s estimated using ventilation data, this method is termed ventilatory threshold or VT1.^[11] Again, algorithms to estimate it from data do exist, but it’s shockingly common for labs to just eyeball it.

One takeaway from the VT and GET methods is that LT1 is probably not a hard cutoff, but a smooth transition.

LT1 itself is estimated from blood lactate data

Above, I wrote that the canonical sign of crossing LT1 is when blood lactate rises to a level significantly above baseline. But what, you might ask, constitutes “significantly above”? Alas, we again find ourselves in a muddled methodological mess.

One paper, for example, notes fourteen different ways of measuring “the” lactate threshold, though these are an amalgam of methods to estimate LT1 and also LT2. The good news is that many of these methods are internally consistent: applying the same method to the same person on different days will result in similar results.

LT1 is traditionally associated with a blood lactate level of 2.0 mM, but looking at a range of different blood lactate tests, you can see that 2 mM can be far below or far above what looks to be a “typical” level where blood lactate rises above baseline.

A better standard that works pretty well both in the lab and in the real world is “LT1 = baseline + 0.5 mM.” It performs nearly as well as some of the more sophisticated curve-fitting algorithms but is totally feasible to do on your own, or during in-the-field workouts with lactate monitors.

LT1 is not the same thing as LT2—and be careful with “the” lactate threshold

LT1—the first lactate threshold—is not the same thing as LT2, the second lactate threshold. The difference gets especially confusing because runners and researchers often use the shorthand “threshold” or “lactate threshold” differently.

One of the gotchas you need to watch out for when reading physiology research—especially older papers—is that the authors will often call just call LT1 “the lactate threshold,” which is confusing because runners and coaches use the same shorthand (e.g. “doing a threshold workout”) to mean running at LT2 (or LT2 as predicted by a chart, e.g. in Daniels Running Formula). Physiologists often term LT2 the “lactate turnpoint” (LTP) or the “onset of blood lactate accumulation” (OBLA or sometimes OPLA for “plasma lactate”).

If you’ve read my SSmax article, you know that LT2 is a method of estimating SSmax, though it’s not as accurate as maximal lactate steady-state or critical speed when it comes to estimating SSmax.

First threshold (T1) is probably the best term for the biological process estimated by LT1

Some newer research is referring to the underlying biological threshold that generates LT1, GET, and VT simply as the first threshold or “T1.” This term is probably the best overall, since it de-emphasizes the importance of any one particular physiological metrics.

T1 also is a natural way to discuss the same distinction I make between SSmax—the real underlying biological phenomenon—and LT2, MLSS, and critical speed, which are different experimental techniques that aim to estimate the underlying biological phenomenon.

The analogy I like to draw is that of core temperature: there is a real biological temperature of your core organs, but in practice, we usually estimate it with a variety of different tools—oral thermometers, in-ear thermometers, or ingestible temperature pills—which vary in their reliability, accuracy, cost, and invasiveness.

So too, with T1: LT1, GET, and VT1 are all techniques to estimate T1, though unfortunately thus far none of them are true gold standards the way critical speed is the current gold standard for SSmax.^[12]

For now, though, LT1 is by far the most common term, which is why I stuck with it for this article.

Many coaches use “aerobic threshold” to refer to LT1

In much of the training literature for runners—including in my first book—LT1 is called the aerobic threshold (AeT or AT), often used in contrast with the anaerobic threshold (which is used as the coaching term for LT2).

The term “aerobic threshold” is a little unfortunate because many people believe that speeds above the aerobic threshold must be anaerobic. The confusion is compounded by blood lactate plots like this one:

This is a plot of blood lactate concentration after 3 minutes of running, across increasingly faster speeds, during a continuous exercise test. The problem with such plots is that many people subconsciously associate the X-axis with time, not speed, and believe that “blood lactate levels are rising above LT1.”

This view is not correct: blood lactate levels are stable over time above LT1, but they are stable at an elevated level.

When you look at blood lactate levels over time at a constant speed (e.g. from a maximal lactate steady-state test), the dynamics become a lot clearer:

(Note that this is from a different runner than the plot above)

So, “aerobic threshold” isn’t quite right because you’re still “fully aerobic” both above and below LT1, and blood lactate is stable, though elevated, over time above LT1.^[13]

Many physiologists use “anaerobic threshold” to refer to LT1

If the confusion caused by “aerobic threshold” wasn’t bad enough, physiologists make it worse: older papers use the term “anaerobic threshold” (AnT or AT) to refer to LT1, even though coaches use that same term to refer to LT2!

The reason the term “anaerobic threshold” is associated with LT1, and not LT2, in the physiology literature has to do with the history of the gas exchange threshold, discussed above.

The original explanation for the rise in CO2 production above what we now call LT1 was as follows—muscle fibers become starved of oxygen, use glycolysis to produce energy, and generate lactic acid, which flows into the bloodstream.

That lactic acid is neutralized by bicarbonate in the blood, producing the rise in VCO2 in the exhaled air. Therefore, a rise in CO2 production is a sign you’ve “gone anaerobic” and exceeded your body’s aerobic capabilities. Hence, the gas exchange threshold was termed the “anaerobic threshold” and was thought to represent your maximal aerobic steady-state.

We now know that this is not the correct view, but the term “anaerobic threshold” persists. Ironically, it was coaches who understood the original intent of the concept of anaerobic threshold, which is why in the training literature, “anaerobic threshold” means LT2, or more correctly, the underlying process LT2 is trying to estimate—i.e. your steady-state max (SSmax).

Practical application of LT1 in training

To apply LT1 in training, you should keep in mind that physiological thresholds are descriptive, not prescriptive.

In my article on heart rate zones, I quoted Renato Canova, who says that workouts are a proposal to your body, and your body’s answer is the training. For our purposes, this just means that running at LT1 is not necessarily the best way to improve LT1.

In fact,it’s better to run definitively above LT1 if your goal is to run in the high-end aerobic domain, and definitively below LT1 if your goal is to run in the easy to moderate domain.

Run below LT1 for easy runs and recovery runs

For example, all of your easy runs should be below LT1—otherwise, they aren’t easy! This is where I think Zone 2 advocates get it right: many people tell themselves they are running “easy,” but end up running at or above LT1: never really recovering, but never really getting a big training stimulus either. After his toughest workouts 2:06 marathoner Emile Cairess sometimes runs 8:00/mi on his recovery runs—how fast are you running the day after a hard workout?

Run above LT1 for targeted physiological adaptations

Likewise, long fast runs, fast continuous runs, and Norwegian-style sub-threshold workouts should all be done above LT1—otherwise you won’t be exposing your body to the kind of aerobic challenge that improves your high-end aerobic capabilities.

The same applies to workouts targeting physiological resilience: since the causes of fatigue above LT1 are different than the causes of fatigue below LT1, if your goal is to resist fatigue late in the marathon, you cannot expect to improve from long easy runs—they don't induce the same kind of fatigue that you’ll be facing in the marathon. Instead, you need to run long and fast to improve resilience—probably within ten percent of marathon pace.

Likewise, if your goal is to stimulate the aerobic capabilities of your fast-twitch muscle fibers, you must run above LT1: these fibers largely do not come online until the VO2 slow component starts eating into the efficiency of your already-working slow-twitch fibers.

Ditto for burning through carbohydrates. If you want to significantly tax your carbohydrate reserves, you need to run above LT1. Below LT1, fat oxidation is high enough that you are not going to severely tax your carbohydrate reserves unless you run for a very long time.^[14]

Remember that LT1 is the “floor” of the high-end aerobic domain, but there’s a ceiling too: steady-state max (SSmax). When doing aerobically-oriented workouts, you also need to keep an eye on this ceiling to avoid going too fast and dipping into the metabolically unsustainable domain.^[15]

Lastly, there’s nothing wrong with mixing domains of intensity as long as you’re being honest with yourself about what you’re doing. One of my all-time favorite workouts is the Kenyan-style progression run, which spans all three domains of intensity (though most of it does take place in the high-end aerobic domain).

How do you predict your LT1 pace?

What is your LT1 pace? Unfortunately, LT1 does not occur at a constant percentage of HRmax or even VO2max, both across runners of different fitness levels and among runners with the same fitness level.

There's an interesting pattern in LT1 across people with different VO2max values. First, here's what it looks like in absolute terms:

It looks like LT1 hovers around 15-25 mL/kg/min among normal sedentary types, but increases more than you'd expect once you get into the range of VO2max values that are typically only seen in healthy and very active people, or in trained athletes (> 45 mL/kg/min or so).

The dynamics become a little more clear when you express LT1 as a percentage of VO2max:

From this plot, two things become clear.

First, LT1 is high in a relative sense for very unfit people because their "ceiling" (i.e. their VO2max) is very low. Then it drops, down to about 50% of VO2max for a typical active person, before climbing again in endurance-trained athletes, whose training pushes up LT1 relative to their VO2max.

Second, even among runners with the same VO2max, there is quite a lot of variation in LT1!

You can use heart rate to estimate the lower bound of LT1

The good news about this individual variability is that you can estimate the lower bound of LT1, a sort of "safe boundary" for easy to moderate paces, using heart rate.

If you just want to make sure you’re doing your easy runs below LT1, you can use <70% HRmax or <65% HRreserve as good guidelines: 95% of runners will be below LT1 at these heart rate intensities. 

Finding out what intensities are above LT1 (but also below SSmax) is trickier. For a well-trained runner, LT1 is typically a bit slower than marathon pace (circa 10% or so)—at least on paper.

An RPE of 4 or 5/10 is a pretty reasonable estimate of LT1

Interestingly, a number of scientific studies support the premise that LT1 corresponds pretty closely with what people perceive as a subjectively “moderate” intensity—a “13/20” on the classical Borg rating of perceived effort (RPE) scale, which lines up (approximately) with 4 or 5/10 on a 0–10 point RPE scale.

That said, I do not think RPE alone is enough to accurately determine LT1, especially in less-experienced runners, since “RPE-only” schemes do not produce very reliable  physiological responses during real-world running.

I do not trust any of the various “field tests” for LT1 (none have been scientifically validated), nor would I trust an estimate that gets spit out by your GPS watch with no additional context (for the same reason).

For an accurate determination of LT1, you basically have three options: (1) shell out for lactate threshold testing in a lab, (2) buy your own lactate meter, or (3) wait for me to finish my LT1 predictor app (which is ~60% complete). Join my email list if you want to find out when that app is done!

Recap

The first lactate threshold, or LT1, is the boundary that separates paces that are easy from paces that are aerobically challenging.

Speeds below LT1 present only a modest challenge to your aerobic system: you can maintain a metabolic steady-state with ease.

Above LT1, two key physiological parameters change: blood lactate levels are stable but noticeably higher than baseline values, and oxygen consumption shows a slow but steady increase over the first 15 minutes or so of a run.

These two changes are signs you have entered the high-end aerobic domain: a range of speeds that still produce a metabolic steady-state, but represent a significant challenge to your aerobic system’s homeostasis.

The physiological changes above LT1 are the result of a progressive loss of efficiency in your muscle fibers, which causes increased recruitment of fast-twitch muscle fibers, and an increased reliance on carbohydrate for fuel.

LT1 is not a magic pace with special properties—it’s a tool for predicting how your body will react to different training stimuli, so you can better understand the distinct physiological effects of different workouts and the adaptations from your body that they trigger.

Learn more about the science of running

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Footnotes

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^[1] VO2 is sometimes written as , with the dot indicating a derivative with respect to time, i.e. volume of oxygen per unit time, hence the units mL/kg/min or L/min.

^[2] Running economy can vary by ~5% across the easy to moderate domain but compared with walking economy—which shows a remarkably steep U-shaped curve across different walking speeds—running economy is very nearly constant.

^[3] Or at least in theory these shifts happen all at once. In reality, the rise in VCO2 relative to VO2 often occurs at a slightly lower speed than the rise in blood lactate levels, and ditto for the rise in ventilation.

^[4] I don’t like the term “heavy” at all—a well-executed threshold workout should feel anything but “heavy!”

^[5] In fact this “mirror image slow component” shows exactly the same time dynamics as the whole-body VO2 slow component, which provides strong evidence for a causal connection.

^[6] Technically fast-twitch fibers require more ATP to produce the same amount of force for a given amount of time. Fundamentally, the reason they require more ATP is simply that the molecular “machines” inside the fibers cycle through their “attach, pull, release” cycle much faster than a slow-twitch fiber. So, each cycle still requires the same amount of energy, but producing force for, say, 500 milliseconds requires more of these attach-pull-release cycles and hence more ATP consumed in that 500 ms window. If we’re talking about speeds below SSmax, that ATP is ultimately getting regenerated via aerobic energy production, at least in aggregate, so this difference at the molecular level translates to a difference in whole-body oxygen-to-forward-motion efficiency in the form of worse running economy.

^[7] Again, technically the product of glycolysis is pyruvate, but pyruvate is very rapidly converted into lactate; the intracellular equilibrium of lactate:pyruvate during exercise is something like 100:1. Lactate is still being produced below LT1 but because more of it is being produced in aerobically strong slow-twitch muscle fibers, more of that lactate is oxidized in-situ, decreasing the lactate influx into the bloodstream.

^[8] Circulating blood lactate can also be stored as glycogen in the liver or kidneys. One major muscle that oxidizes a lot of lactate is actually the heart: it has a massive oxygen supply and ready access to all lactate in the blood.

^[9] An increase in H+ levels in the blood, and resulting bicarbonate buffering, also contribute to increased carbon dioxide production above LT1.

^[10] The causes of fatigue in the high-end aerobic domain are a major unsolved problem in exercise physiology. Is it solely due to glycogen depletion? Or do compounds like reactive oxygen species, ammonia, or other metabolic byproducts also play a role?

^[11] There is also, allegedly, a VT2 that occurs near LT2, though it is noisier and less reliable than VT1.

^[12] This is another unsolved problem in exercise physiology: is there a gold standard for T1 that’s more repeatable, and more reliable, across different exercise protocols VT1, LT1, and GET? You might imagine a MLSS-like test that attempts to pinpoint when the slow component of oxygen consumption begins, but I haven’t seen any research attempting this sort of technique.

^[13] Because “anaerobic” glycolysis is the first step in “aerobic” oxidation of carbohydrates, it’s not obvious what “fully aerobic” should mean, exactly. As we saw earlier in the article, one thing your body does above LT1 (and below it, though to a lesser extent) is allow individual muscle fibers to operate at an intensity that’s “locally” unsustainable, while letting other muscle fibers pitch in to take up the slack by oxidizing the lactate and neutralizing the excess acidity kicked off by localized glycolytic energy production. The result is that there’s no net accumulation of metabolic byproducts, and no depletion of your finite “anaerobic” energy reserves, but arguably still some “anaerobic” energy contribution. There’s an analogous situation with metabolically unsustainable aerobic energy production above SSmax, a topic which will have its own article in the coming weeks.

^[14] At an easy pace, the typical runner can go 30 miles or more without running out of glycogen even with no external fuel. At marathon pace, that number is more like 18–22 miles!

^[15] I suspect a major reason why so many runners have success with Norwegian-style sub-threshold workouts is simply that they are doing their classical threshold work too fast: indeed, as I show in my writeup for my threshold, CV, and VO2max pace calculator, you actually don’t want to run right at your predicted (second lactate) threshold: there’s a 50% chance you’ll be in metabolically unsustainable territory! Instead, you want a pace with a >90% chance of being metabolically stable, i.e. below SSmax and within the high-end aerobic domain.

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