Back in 1969, naval researchers took blood samples from the crew of a Polaris nuclear submarine over the course of an eight-week patrol. Three-quarters of the sailors were smokers, so carbon monoxide levels were chronically elevated in the sealed confines of the sub. After a few weeks in this toxic miasma, the crew’s levels of hemoglobin, the crucial protein in red blood cells that ferries oxygen from the lungs to the muscles, had shot up by an average of 4.4 percent. Secondhand smoke had somehow turned the submariners into aerobic superstars.

This finding, along with others like it, was filed away for decades. After all, smoking destroys your lungs, so any performance benefits are outweighed by the harms. But then, last year, the idea exploded. Scientists published fresh data showing that huffing carbon monoxide could boost endurance. Other scientists responded with editorials warning against fooling around with a gas whose nickname is “the silent killer.” And headlines around the world trumpeted the news that —confirmation, seemingly, of the cliché that elite athletes will accept any risk in exchange for victory. The full story, though, is a bit more complicated.

The quest for endurance is, in part, about hemoglobin. More hemoglobin means more oxygen delivered to your muscles, which means you can run or ride or swim faster, for longer. Starve your muscles of oxygen in training and your body responds by secreting EPO, a hormone that stimulates the production of hemoglobin-carrying red blood cells. That’s how altitude training works: There’s less oxygen available, so your body produces more EPO to compensate. (It’s also why synthetic EPO is the banned drug of choice among endurance athletes.)

Virtually all performance-enhancing drugs are associated with health risks, and that hasn’t harmed their popularity.

When you inhale carbon monoxide, some of your red blood cells ferry molecules of it (instead of oxygen) around your body. Carbon monoxide attaches to hemoglobin and ��DZ����’t let go, making those red blood cells unavailable to carry oxygen for many hours. It’s like altitude training in a bottle: Your body will sense the oxygen shortage and respond by producing EPO. But inhale too much and you won’t deliver sufficient oxygen to your heart and brain—and once your hemoglobin is clogged with carbon monoxide, it’s not easy to reverse. Around 1,200 people die every year in the United States from deliberate or accidental carbon monoxide poisoning.

So carbon monoxide as a performance booster has been understood but mostly unspoken. It wasn’t until 2018 that the idea got more concrete. An initial study confirmed that deliberately breathing carbon monoxide boosted EPO. The next year, researchers in China, tasked with preparing their country’s athletes for the 2022 Beijing Winter Olympics, reported that college soccer players who inhaled the gas five times a week increased their hemoglobin levels. A , in which subjects inhaled the gas five times a day, reached similar conclusions. Most recently, a by researchers in Norway combined altitude training with twice-daily carbon monoxide inhalation for a synergistic effect.

But there hasn’t been a single verified report of an athlete actually using this technique. I reached out off-the-record to contacts in several elite endurance sports, as well as researchers in the field, and none of them had heard even rumors of real-life usage. The risk, so far, is theoretical. The headlines during the Tour de France referred to the use of small doses of carbon monoxide to measure hemoglobin levels. This technique has long been used in elite sport to check how athletes are responding to altitude training, but the doses are too low to boost performance. There is a gray area here: Once you’ve got the carbon monoxide device in the team van, there’s a temptation to use it. But would elite athletes, these paragons of super-fitness, really take such a dumb risk?

Whether rational or not, we all accept nonzero risks in pursuit of goals.

It’s a fair question. In the 1980s and ’90s, Chicago doctor Robert Goldman circulated a now-infamous series of questionnaires among elite athletes, asking if they would take an undetectable drug that would make them unbeatable for five years—and then die of the side effects. Roughly half the athletes accepted the bargain, he reported. Goldman’s Dilemma, as it’s now known, is often cited as evidence of the modern athlete’s off-the-charts focus on winning, regardless of the costs. And indeed, virtually all performance-enhancing drugs are associated with health risks, and that hasn’t harmed their popularity. “You have guys who will go to the funeral of a friend who died from this stuff, come home, and inject it again,” an anonymous Olympic runner told Sports Illustrated in a 1997 article about Goldman’s Dilemma.

But it’s not clear whether Goldman’s respondents were taking the question seriously, or whether attitudes have changed. Recent attempts to replicate Goldman’s results raise doubts. A 2018 study from Duke University estimated the “maximum acceptable mortality risk” that nearly 3,000 athletes would accept in exchange for the guarantee of Olympic gold. No one took the deal if it meant certain death. Depending on the sport and the level of competition, athletes were, on average, willing to accept somewhere between 7 and 14 percent risk of a fatal heart attack.

That’s still a big risk. But it’s comparable, the researchers point out, to the risks people say they’re willing to accept in exchange for other life-changing outcomes, like relief from their rheumatoid arthritis. And it’s not fundamentally different from the types of risk you might encounter on mountain expeditions, in extreme sports, or in the backcountry. Whether rational or not, we all accept some risks in pursuit of our goals. So it seems unlikely that the theoretical possibility of a fatal mishap will be enough, on its own, to dissuade athletes from trying to get a boost from carbon monoxide.

In February, the UCI, cycling’s international governing body, to boost performance, while the use of single doses to measure hemoglobin will still be allowed. This may seem like one of those wishy-washy compromises that’s almost impossible to enforce: the substance itself is permitted, but you have to promise you’re using it for the right reasons. But I think it’s the right call. Anti-doping agencies should, of course, be trying to catch unrepentant cheaters. But they also have a crucial role to play in setting broader norms about what risks we should or shouldn’t be willing to accept in pursuit of gold. Motivated athletes will do whatever the rules permit—so let’s not ask them to suck on a tailpipe five times a day, any more than we would lock them in a nuclear sub with a crew of chain-smokers.

This piece first appeared in the summer 2025 print issue of �����ԹϺ��� Magazine. Subscribe now for early access to our most captivating storytelling, stunning photography, and deeply reported features on the biggest issues facing the outdoor world.

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You’d have a hard time finding any serious endurance athlete in 2025 who thinks protein ��DZ����’t matter. Gone are the carb-centric days of pasta and Gatorade and nothing else. But figuring out how much protein runners, cyclists, and other endurance junkies actually need—and when they need it—remains a work in progress.

I’ve grappled with these questions a few times recently—in a piece busting some common protein myths, and in another discussing the idea of maximum protein intake. But now a in Sports Medicine, from a research team led by Oliver Witard of King’s College London, offers a comprehensive overview of the current state of knowledge. Witard and his colleagues focus on two key questions. First, how much protein do endurance athletes need on a daily basis to stay healthy and optimize long-term training adaptations? And second, what role can the tactical use of protein play in speeding up short-term recovery and boosting performance?

Protein for the Long Term

Government guidelines currently recommend getting at least 0.8 grams of protein per kilogram of body weight (g/kg) each day. For someone who weighs 150 pounds, that works out to 55 grams of protein. For reference, a standard 5-ounce can of tuna has about 20 grams of protein.

There are two main problems with this guideline, however. First, it’s intended to be the minimum required to stay healthy, not the optimal amount to maximize performance. Second, it was formulated using a measurement technique that involves tracking the amount of nitrogen being consumed and excreted from the body, which some scientists believe underestimates protein needs. A newer approach called the “,” which involves labeling one specific type of amino acid with a carbon isotope to see how quickly it’s burned, gives higher numbers and is also more practical for testing specific populations like athletes.

The usual argument for getting lots of protein is that it provides the building blocks—amino acids—for building new muscle. That’s important for strength training, but endurance athletes need it for other reasons. One is that these building blocks are used to repair the muscle damage incurred by hard training: the longer and harder you run, the more damage you incur, and more protein you presumably need for repairs.

During prolonged exercise, your body also starts burning amino acids for fuel. The amounts are generally small, and how much you burn depends on the nature of the exercise and what else you’re eating, but in some cases 5 to 10 percent of the fuel you need for a given workout is provided by protein. If you’re training hard, you’ll need to eat extra protein to replace those losses.

There are some more subtle possibilities, too. Muscle isn’t the only part of the body that’s built from protein. One of the key adaptations athletes gain from endurance training is an increase in the amount of protein in the mitochondria, where cellular energy is generated. The more protein in the mitochondria, the more efficiently it creates energy. A few studies have sought to  figure out whether eating more protein boosts the mitochondrial response to exercise. The results so far haven’t been convincing, but it’s still an open question.

Witard and his colleagues pooled data from various indicator amino acid studies to assess protein needs for endurance athletes under various conditions. Here are some of the key numbers:

The indicator amino acid data suggests that even untrained people need about 1.2 g/kg of protein per day, 50 percent more than the FDA’s recommended daily intake of 0.8 g/kg. And endurance athletes need another 50 percent more than untrained people, with a level of 1.8 g/k/g ensuring that 95 percent of people are getting all the protein their bodies can use. In comparison, using the same indicator amino acid method find that resistance-trained athletes need somewhere between 1.5 and 2.0 g/kg per day, raising the possibility that endurance athletes might actually need more protein than lifters.

There’s an important point to bear in mind, though: endurance athletes also tend to eat a lot more than the average person, which means they automatically get more protein. among American adults averages 1.25 g/kg for men and 1.09 g/kg for women, pretty close to the overall target of 1.2 g/kg for untrained people. In comparison, found that endurance athletes average 1.4 to 1.5 g/kg—not quite at the 1.8 g/kg level, but not that far away.

There are some other nuances in that graph. Data on male-female differences is very sparse, but there are some hints that women might require more than men relative to their body weight. That might be particularly true during the luteal phase of the menstrual cycle, since progesterone can affect protein burning. Witard and his colleagues make a blanket recommendation that both male and female endurance athletes should aim for 1.8 g/kg, but they throw in the speculative possibility that females “may consider” upping it to 1.9 g/kg during the luteal phase of their cycle.

Short-Term Protein Tactics

The big surprise in the data above is that endurance athletes seem to use more protein on their rest days than on training days. This finding has popped up in , and it’s definitely not what the scientists were expecting. It’s possible that there’s some quirk of metabolism that’s skewing the measurements used to assess protein needs when you try to compare exercise and non-exercise days.

But it’s also possible that the effect is real—that when you give your body a break, its repair and adaptation mechanisms kick into overdrive and thus use more protein than usual. If this is true, it’s an argument for upping your protein intake on rest days: Witard and co. suggest aiming for 2.0 g/kg. And on a more fundamental level, it’s an argument for including true rest days in your training program periodically, since they seem to trigger recovery processes that don’t happen on normal training days. At this point, I’d say the jury is still out on whether the effect is real.

Either way, the researchers suggest aiming for 0.5 g/kg of protein following exercise to help repair any muscle damage incurred during the workout. For a 150-pound person, that’s 34 grams of protein, which is what you’d get in a substantial meal with a good protein source. How soon is “after exercise”? I don’t think there’s any convincing data that says it has to be immediately after. Your next meal is fine—unless your workout was after dinner and you’re planning to head to bed, in which case you should make a special effort to get some protein in.

The data also suggests that athletes use more protein when they’re training in a carbohydrate-depleted state. In this case, we’re not talking about a consistently low-carb diet, but rather doing certain training sessions in a low-carb state to help the body adapt to burning fat more efficiently. There’s decent evidence that protein can help power these workouts, and Witard suggests taking in 10 to 20 grams of protein before and/or during this type of session.

This idea of using protein to compensate for low carbs also connects to one of the most hotly debated ideas about protein for endurance athletes. There have been various research-backed claims over the years that adding protein to a sports drink that you consume during a race or training session will enhance your performance, and that taking in some protein in the immediate post-workout window will speed up the rate at which you refill the carbohydrate stores in your muscles.

All these claims, Witard and his colleagues argue, are the result of studies where the subjects didn’t get enough carbohydrates. If you’re meeting your carb needs, adding protein to a sports drink will neither boost your performance nor accelerate your muscle refueling. There may be exceptions for ultra-endurance events, which haven’t been well-studied and have somewhat different metabolic challenges compared to a marathon. But the researchers’ final conclusion is a reminder that for endurance athletes, despite protein’s current popularity, carbohydrate is still king.

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Failure is a big topic in the weight lifting world these days. When you’re doing an exercise, do you need to push each set to the point that you literally can’t complete one more rep? Old-school practical wisdom says yes. More recent scientific studies have suggested that training to failure isn’t necessary, and might actually be counterproductive because it takes such a big toll on both your muscles and your mind.

The truth is probably somewhere in the middle, according to a in Medicine & Science in Sports & Exercise—but the results lean toward the idea that failure isn’t necessary for most of us. The study finds that getting close to failure produces strength gains that are similar to going all the way. That said, training to failure does build a little more muscle mass at some locations. The results of the study also offer some useful clues for those of us seeking the biggest muscle gains from the least amount of time and effort in the gym—not because we’re lazy, I hasten to add, but because we want to spend that time and effort in other ways.

Brad Schoenfeld and his colleagues at City University of New York (CUNY) Lehman College put 42 participants—34 men and 8 women—through an eight-week full-body training program. One group was assigned to complete all their sets to failure while the other was instructed to always stop short of failure. The volunteers were all experienced lifters who had been hitting the gym at least three times a week for more than a year, which means there were no easy gains to be had. And the experimental lifting protocol called for just two workouts a week, with each workout consisting of just one set of nine different exercises. In total, each workout took about half an hour.

This idea of short, single-set workouts isn’t radical or new. Back in the 1970s, Arthur Jones, the inventor of Nautilus exercise machines, an approach that relied exclusively on single sets to failure. The problem is that pushing to true failure is no joke. It takes a lot of mental focus, and it also takes more time to recover. If your primary interest is another sport like running, you don’t necessarily want your legs to feel like lead the day after a strength workout. So it would be nice if it were possible to get most of the benefits of a hard workout while stopping short of true failure.

To test that theory, the approach Schoenfeld and his colleagues used is called “repetitions in reserve.” The subjects in the non-failure group were instructed to continue each set until they felt they had two repetitions in reserve, meaning that they would be able to squeeze out two more complete reps before failing on the subsequent one. It seems like a much more humane way to train—and it also turned out to be fairly effective.

The most surprising result of the study is that both groups got measurably bigger and stronger even though they were working out less often than they were before the study period. That fits with a bunch of previous research on the “minimum effective dose” for strength training. It ��DZ����’t mean that half an hour, twice a week is sufficient to maximize your gains. But it does mean that those of us for whom strength training is mostly a means to some other end (like staying healthy, avoiding injury, or being able to carry a heavy pack) can make progress with a relatively modest investment of time.

As far as the efficacy of training to failure goes, there were a whole bunch of different outcomes in the study. The simplest were one-rep max in the bench press and squat, as measures of upper and lower body strength. To test explosive power, the researchers used a countermovement jump (CMJ), which simply involves squatting down then leaping as high as possible in a single motion. To test muscular endurance, they had the subjects complete as many reps as possible (AMRAP) on a leg-extension machine lifting 60 percent of their body weight.

The four tests of strength (bench press, squat, CMJ, and AMRAP) are at the bottom. The solid vertical line at 0.0 corresponds to no change after eight weeks of training. Both bench press and squat increased, with no significant difference between groups. For example, max squat increased by 13.2 percent on average in the failure group and 12.4 percent in the reps-in-reserve group. Same with muscular endurance (AMRAP). Power (CMJ), on the other hand, increased more in the group that trained to failure.

The picture was different for muscle size, which is shown in the upper part of the graph above. Researchers used ultrasound to measure various points along the mid and lateral quadriceps (MQ and LQ on the graph) as well as the biceps and triceps. In most (but not all) cases, training to failure produced bigger gains in mass—which might be ideal if you’re working out for aesthetic reasons, but not necessarily if you’re training for a weight-to-strength ratio sport like cycling or climbing.

There’s a key caveat here, which is that estimating reps in reserve is an inexact art. To check how inexact it was, the researchers sometimes asked their subjects to keep going after they’d estimated they had two reps left. The estimates were fairly good and got better over the course of the eight-week study. But these were experienced lifters who had presumably experienced true failure many times before. For newbies, , it’s probably a good idea to do at least some training to failure so that you know what it feels like. Then, once you have a good internal benchmark, switch to a reps-in-reserve approach.

In some ways, this line of research reminds me of the current debate in the endurance world about Norwegian double-threshold training. The underlying premise of the Norwegian method is that hero workouts that leave you crumpled by the side of the track are counterproductive. Better to push hard enough to stimulate adaptation but not so hard that you can’t recover for the next workout. Those who hope to win bodybuilding competitions will undoubtedly—and wisely—keep lifting to failure. On the other hand, for those who want muscle and strength but care more deeply about tomorrow’s run, keeping a rep or two in reserve sounds like a great plan.

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Like all great villains, lactic acid has been misunderstood. We’ve been blaming it for the pain we suffer during intense exercise for more than two centuries. There’s nothing worse, we say, than the “lactic burn” that locks our failing muscles into immobility. More recent tellings of the story have tried to rehabilitate lactic acid’s reputation, insisting that it’s actually trying to fuel our muscles rather than shut them down. But that version ��DZ����’t capture the full complexity, either.

Into this confusion steps , from veteran physiologists Simeon Cairns and Michael Lindinger. It’s a dense 35-page doorstop titled “Lactic Acidosis: Implications for Human Exercise Performance,” and the clearest conclusion we can draw from it is that the precise causes of muscle fatigue during intense exercise are still a topic of active research and vigorous debate among scientists. But the sudden popularity of baking soda as an acid-buffering performance aid has renewed conversations about how, exactly, lactic acid works in the body—and how we might counteract it. Here are some highlights from the latest research.

The Lactic Backstory

The first scientist to draw the connection between exercise and lactic acid was Jöns Jacob Berzelius, the Swedish chemist who devised the modern system of chemical notation (H2O and so on). Sometime around 1807, he noticed that the chopped-up muscles of dead deer contained lactic acid, a substance that had only recently been discovered in soured milk. Crucially, the muscles of stags that had been hunted to death contained higher levels of lactic acid, while deer from a slaughterhouse who had their limbs immobilized in a splint before their death had lower levels, suggesting that the acid was generated by physical exertion.

A century later, physiologists at the University of Cambridge used electric stimulation to make frogs’ legs twitch until they reached exhaustion, and high lactic acid levels. The levels were even higher if they performed the experiment in a chamber without oxygen, and lower if they provided extra oxygen. That finding helped establish the prevailing twentieth-century view: your muscles need oxygen to generate energy aerobically; if they can’t get enough oxygen, they switch to generating energy anaerobically, which produces lactic acid as a toxic byproduct that eventually shuts your muscles down.

There are two small problems—and one big one—with this picture. The first detail is that, while lactic acid can be measured in the muscles of dead deer and frogs, it ��DZ����’t actually exist in living humans. In the chemical milieu of the body, what would be lactic acid is split into two components: lactate and hydrogen ions. That’s not just being persnickety about terminology: lactate and hydrogen ions behave differently than lactic acid would. In fact, they can have separate and sometimes even opposing effects.

The second detail is that lactate (and hydrogen ions) aren’t really produced because your muscles are “running out of oxygen.” The chemical reactions that use oxygen to turn food into muscle fuel are efficient but slow, great for powering relatively easy and sustained exercise. But they can’t provide energy fast enough to supply an all-out sprint. For that, you’ll eventually need to rely on lactate-producing anaerobic reactions, even if you’re huffing pure oxygen from a can.

The big problem with the old view of lactic acid is the idea that it’s a metabolic villain. It turns out that, far from being an inert byproduct, lactate can be recycled into fuel for your muscles. In fact, one of the key superpowers that well-trained athletes develop is the ability to reuse lactate more quickly. This rehabilitation of lactate’s reputation has been going on for now (though it still has ), but athletes are still left with an unanswered question: if lactate isn’t what causes muscle fatigue, what is?

What the New Review Reveals

The first thing that Cairns and Lindinger establish is that, yes, levels of lactate and hydrogen ions increase during intense exercise. This is most obvious during intense exercise lasting between about one and twenty minutes. Longer bouts of exercise are less intense, so they can be mostly fueled by non-lactate-producing aerobic energy, and bouts of exertion shorter than one minute simply don’t have time to produce much lactate.

The evidence is now clear that lactate itself ��DZ����’t interfere in any significant way with muscle function. But lactate and hydrogen ions are produced simultaneously in exactly the same quantities during anaerobic exercise, which complicates the “lactic acid is a good guy after all” narrative. Lactate may be great, but it comes with an equivalent helping of hydrogen ions—and that may be a problem.

When you increase the concentration of hydrogen ions in a solution, you’re increasing its acidity. That’s how the pH scale is defined: it’s a measure of hydrogen ion concentration. During intense exercise, the pH in your fast-twitch muscle fibers (which seem to be particularly susceptible to hydrogen ion buildup) can drop from around 7.0 to 6.0. That change represents a ten-fold increase in the concentration of hydrogen ions—a situation that can wreak havoc on muscle contraction.

The idea that hydrogen ions are what cause muscle fatigue isn’t entirely straightforward either, though. When you start hard exercise, the concentration of hydrogen ions actually decreases for about 15 seconds while you use up another source of fast-acting muscle energy called phosphocreatine. And yet your muscles are already getting fatigued during this initial burst, losing some of their maximal force, while hydrogen ion levels are still lower than normal.

There’s also a disconnect when you stop exercising, or take a break between hard intervals. Hydrogen ion (and lactate) levels keep climbing for a few minutes, which is why the highest lactate levels are generally recorded several minutes after hard exercise. But you don’t get weaker after you stop exercising; you get stronger as you recover, despite the rising concentration of hydrogen ions. So hydrogen ions may play a role in muscle fatigue, but they can’t be the whole story.

Another possibility is that hydrogen ions may interact with other molecules to disrupt muscle contraction. The most prominent candidates are potassium and phosphate, both of which increase during exercise and are associated in some studies with muscle fatigue. What these and other candidates have in common is that there are a ton of conflicting results: they have different effects on muscle fibers depending on the level of acidity, the muscle temperature, and the test protocol. This suggests—not surprisingly—that there isn’t a single molecule that causes your muscles to lose their power. Instead, it’s the whole cocktail of things going on inside your muscles during hard exercise that matters.

What About the Burn?

Most of the research that Cairns and Lindinger describe deals with muscle properties: how quickly are your fibers losing their twitch force, and why? It’s true that, as a middle-distance runner, I’ve sometimes staggered down the finishing straight of a race with the sense that my legs were literally ceasing to function. It’s an awful feeling to experience, but satisfying to look back on: you know you left nothing out there.

Far more common, though, is a softer limit. You feel a red-hot burn and spreading numbness in your legs, and you choose to back off a bit. This feeling that we used to describe as “going lactic” is significant in its own right. In interviews with athletes who’ve begun using baking soda, a common theme is that they’re able to push harder for longer before feeling that burn in their legs, which in turn enables them to race faster.

One theory about the feeling of going lactic is that you’re literally starving your brain of oxygen. If you push hard enough, it’s not just your muscles that go more acidic; your whole bloodstream follows. Thanks to a phenomenon called the Bohr effect, rising acidity reduces the ability of your red blood cells to ferry oxygen from your lungs to the rest of your body, including your brain. In one study, all-out rowing caused oxygen saturation to drop from 97.5 to 89.0 percent, which is a big drop—big enough, perhaps, to slow you down and contribute to the out-of-body feeling at the end of hard races.

We also have nerve sensors that keep the brain informed about the metabolic status of the muscles. These group III/IV afferents, as they’re known, keep tabs on the real-time levels of molecules like lactate and hydrogen ions. If you block these nerves with spinal injections of fentanyl, exercise feels great—too great, in fact, because you’ll lose all sense of pacing, go out too hard, then hit the wall.

The most telling finding about the lactic burn, in my view, was where they injected various molecules into the thumbs of volunteers in an attempt to reproduce that familiar feeling. Injecting lactate didn’t do it. Neither did injecting hydrogen ions, or ATP, a fuel molecule whose levels are also elevated during hard exercise. Injecting them in pairs didn’t do it either. But injecting all three at the levels you’d experience during moderate exercise produced a sensation of fatigue in their thumbs, even though they weren’t moving them. And injecting higher levels turned fatigue into pain.

That’s a distinction I try to keep in mind in the late stages of hard workouts, and at the crux of races. That burning feeling is real, and it’s associated with lactate and acidity and muscular fuel levels. But it’s just a feeling. The lactate and ATP are actually helping me. The hydrogen ions, in combination with various other metabolites accumulating in my muscles, not so much. They’ll eventually stop me. But until they do, I can keep pushing.

***

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For a while, it really looked as though beet juice would beat the odds. Most hot new performance-boosting supplements, even if they claim to be backed by science, don’t hold up to scrutiny. But after making thanks to high-profile adherents like marathon star Paula Radcliffe, the first wave of high-quality studies supported the idea that beet juice really does improve endurance.

After a decade, though, the bloom had partly faded. There were concerns about its gastrointestinal effects (much as there were with baking soda, another popular endurance-booster), questions about the appropriate dosage, and rising suspicion that beet juice only worked in untrained or recreational athletes but not in serious competitors. These days I rarely hear runners talking about beet juice, and the flow of new studies has tailed off. But a new review takes a fresh look at the accumulated evidence, and concludes that we shouldn’t be too quick to dismiss the potential benefits of the juice.

Why Beet Juice Might Help

The key ingredient in beet juice, from an endurance perspective, is nitrate. Once you eat it, bacteria in your mouth convert nitrate to nitrite. Then the acidity in your stomach helps convert the nitrite to nitric oxide. Nitric oxide plays a whole bunch of roles in the body. That includes cueing your blood vessels to dilate, or widen, delivering more oxygen to the muscles, faster.

In 2007, Swedish researchers that consuming nitrate—that nitric oxide precursor—makes exercise more efficient, enabling you to burn less oxygen while sustaining a given pace. Two years later, a team led by Andrew Jones at the University of Exeter that you could get a similar effect by drinking nitrate-rich beet juice.

In subsequent years, researchers tested the effects of beet juice on various types of exercise. Crucially, Jones’s group figured out how to strip the nitrate from beet juice to create an undetectable placebo, and found that athletes improved their performance when given regular beet juice but not nitrate-free beet juice. That made the claims much more convincing. Meanwhile, a company called began selling beet juice with standardized nitrate levels, and eventually added to make the doses more palatable.

When the International Olympic Committee put together on sports supplements in 2018, they included beet juice as one of just five performance-boosting supplements with solid evidence. (The others were caffeine, creatine, baking soda, and beta-alanine.)

What the New Review Found

Over the years, scientists have made numerous attempts to sum up the evidence for and against beet juice. The latest attempt, by a group led by Eric Tsz‑Chun Poon of the Chinese University of Hong Kong, is an “umbrella review” of nitrate supplementation, mostly from beet juice. It pools the results of 20 previous reviews that themselves aggregated the data from 180 individual studies with a total of 2,672 participants.

The problem with lumping that many studies together is that they measure outcomes differently, use different dosing protocols, and have different study populations. Still, the broad conclusion is that beet juice works—at least for some outcomes. Most significantly, it improves time to exhaustion: if you’re asked to run or cycle at a given pace for as long as you can, beet juice helps you go for longer.

On the other hand, there was no statistically significant benefit for time trials, where you cover a given distance as quickly as possible. That’s the type of competition we care about in the real world, so this non-result is concerning. Time-to-exhaustion tests produce much bigger changes than time trials: a common rule of thumb is that a 15 percent change in time to exhaustion corresponds to about one percent in a time trial. So it may simply be that the studies were too small to detect subtle improvements in time trial performance.

Check out the relative effect sizes for time to exhaustion and time trial in these forest plots. Each dot represents an individual study with its error bar; the farther to the right of the vertical line it is, the greater the performance boost nitrate provided.

Taking the time trial data at face value, the results still look pretty encouraging. They’re all positive; they just need more participants so that the error bars will get smaller and no longer overlap zero. Of course, eyeballing the data like that is risky because it allows us to draw whatever conclusions we want. But I find it difficult to imagine a scenario where improving your time to exhaustion ��DZ����’t also translate into an advantage in time trials. The two tasks are different psychologically, but they both rely on the same underlying physiological toolset.

Poon and his colleagues also run some further analysis to check whether the dose makes a difference. They conclude that the effects are biggest when you take at least 6 mmoL (just under 400 milligrams) of nitrate per day, which happens to be almost exactly how much a single concentrated shot of beet juice contains. The effects are also maximized when you supplement for at least three consecutive days rather than just taking some on the day of a race.

What We Still Don’t Know

The big open question that Poon’s review ��DZ����’t address is whether beet juice works in highly trained athletes. Several studies have found that the effect is either diminished or eliminated entirely in elite subjects. This isn’t surprising. Pretty much every intervention you can think of, including training itself, will have a smaller effect on people who are already well-trained. This ceiling effect is presumably because elite athletes have already optimized their physiology so thoroughly that there’s less room to improve.

The flip side of that coin is that, for elite athletes, even minuscule improvements can be the difference between victory and defeat. The size of a worthwhile improvement at the highest level is a fraction of a percent, which is all but impossible to reliably detect in typical sports science studies. For top athletes, the decision of whether or not to use beet juice will have to remain an educated guess for now.

There are other unanswered questions, like whether beet juice is better than consuming nitrate straight. There have been several studies suggesting that this is indeed the case. The theory is that other ingredients in beet juice, like polyphenols—which function as antioxidants—might act synergistically with nitrate to produce a bigger effect. But as pointed out last year, the evidence for this claim is too shaky to draw any reliable conclusions either way.

Probably the biggest risk in the beet juice data is the preponderance of small studies, some with fewer than ten subjects. It’s easy to get a fluke result with small sample sizes, and it’s human nature to get unduly excited about positive results—which is why positive flukes often get published more often than negative flukes. So we should remain cautious about our level of certainty.

Despite that caveat, my overall impression is positive. I sent the following summary to Andy Jones, the scientist most associated with beet juice research, to see whether he would agree:

“It works. It probably works less well in elites, like most things, but there may still be an effect. Higher doses taken for at least a few days in a row probably increase your chances of a positive effect.”

Jones thought that sounded reasonable. He pointed out that there’s a  of evidence emerging that beet juice also enhances muscle strength and power in some circumstances, an effect that Poon’s review confirms. For endurance specifically, looking at the totality of evidence, Jones figures there’s a real effect. And he’s in good company. “Eliud remains a big believer,” he pointed out. That would be Eliud Kipchoge.

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The Nike Vaporfly 4% wasn’t shy about how much of a boost it claimed to give runners: the promise was right there in the name. When the shoe was released back in 2017, researchers at the University of Colorado published data showing that it improved athletes’ running economy (i.e., efficiency) by an average of 4 percent over the best marathon shoes at the time. Chaos—and a whole bunch of world records—ensued.

The key ingredients in the Vaporfly were a stiff, curved carbon-fiber plate embedded in a thick layer of soft-but-resilient midsole foam. Neither of these elements was magical on their own, but they somehow combined to make runners substantially more efficient, for reasons that scientists don’t fully understand and are still arguing about. Since then, virtually every major shoe brand has come up with multiple iterations of the so-called “supershoe,” tweaking these basic ingredients in minor and sometimes major ways.

But a key question has remained mostly unanswered: are the newest shoes significantly better than the original Vaporfly? A few researchers have run head-to-head tests of models from different brands, with generally muddled results. Some newer shoes might be a percent or two better, but there’s so much individual variation that it’s hard to be sure. Since Nike’s bold move in 2017, the shoe brands themselves have mostly steered clear of making explicit claims about how good their shoes are.

That’s about to change. Puma, a veteran shoe brand that relaunched its serious running line in 2018, has a new shoe dropping in time for this month’s Boston and London marathons. They think it’s dramatically better than anything else on the market—about 3.5 percent better, in fact. They’re so convinced that they arranged to have the shoe tested by Wouter Hoogkamer, the head of the Integrative Locomotion Laboratory at UMass Amherst and, as it happens, the man who led the external testing of Nike’s Vaporfly back in 2017. Hoogkamer released his data earlier this week, and it’s impressive.

What the New Data Shows

Hoogkamer’s study is posted as a preprint on bioRxiv, a site where scientists share their results while awaiting peer review. He and his colleagues brought in 15 volunteers, all of whom had run under 21 minutes for 5K (for women) or 19 minutes (for men). To test their running economy, he had them run on a treadmill for five minutes at a time while measuring their oxygen consumption. The more oxygen you consume at a given pace, the more energy you’re burning and therefore the less efficient your movements. A good shoe should maximize your efficiency—and therefore minimize your oxygen needs—at a given pace.

Each runner had their economy tested eight times: twice each in four different shoes. The comparison shoes were the Nike Alphafly 3 (which Kelvin Kiptum used to set the men’s marathon world record and Ruth Chepngetich used to set the women’s record); the Adidas Adios Pro Evo 1 (which Tigst Assefa used to set the previous women’s marathon world record in 2023); and Puma’s top-of-the-line . The newest Puma supershoe is an update of this latter model. It’s been dubbed the Fast-R Nitro Elite 3 (original, I know).

Without further ado, here’s the running economy data for the four shoes. Metabolic rate, in watts per kilogram, tells us how much energy the runners were burning at a prescribed pace that was assigned based on their 5K PR, ranging between 6:00 and 7:30 per mile. The thick line shows the average results, the thin lines show the individual ones.

It’s clear that the Fast-R3 resulted in the lowest metabolic rate across the board—which means it’s the most efficient shoe. The runners burned 3.6 percent less energy wearing the Fast-R3 than they did in the Nike shoe, and 3.5 percent less than in the Adidas. (Some free marketing advice: they should have called the new shoe the Fast-R3.5.) It also burned 3.2 percent less energy than the Fast-R2—making the new model pretty significant update from its own previous edition. What’s even more remarkable, given the wide range of individual results seen in previous supershoe studies, is that every single one of the 15 runners was most efficient in the Fast-R3.

Puma has also run its own internal testing on more than 50 runners, according to Laura Healey, who heads the brand’s footwear innovation team. In their data, the shoe is 3.3 to 3.5 percent better than its rivals. Running economy ��DZ����’t translate directly to race time, but a boost of 3.2 percent (the margin between the Fast-R2 and the Fast-R3) is expected to reduce race times by about 2.0 percent for a 2:00 marathoner, 2.6 percent for a 3:00 marathoner, and 3.3 percent for a 4:00 marathoner.

What’s the Magic Ingredient?

With the Vaporfly, it was easy to understand—at least superficially—why the shoe was different from its peers at the time: it had that thick foam and carbon plate. It’s harder to get a handle on what makes the Fast-R3 special, because the basic architecture is the same. The differences between the Fast-R2 and Fast-R3 are subtle, but the running economy data shows that they’re significant.

Puma’s team started with the Fast-R2 and created a virtual model of the shoe using biomechanical data collected from ten runners wearing pressure-sensing insoles while running on a force-sensing treadmill. The model showed exactly what was happening inside the shoe at each instant during a running stride: where the forces and strains were highest and lowest, how the shoe was bending and compressing, and so on.

Then they went through a process of iterative computational design and optimization. For example, if the virtual model showed that a particular area in the midsole wasn’t experiencing much strain, they would remove some of the foam in that location. Or if it showed that a region of the carbon plate was excessively strained, they would reinforce it with a rib of extra carbon. All this was done digitally within the virtual model, so they could see if the changes made the situation better or worse without going through the hassle and expense of building a new prototype.

By the time they finished this virtual optimization process, they’d snipped away enough superfluous foam and carbon to reduce the weight of the shoe by more than 30 percent, from 249 grams to 167 grams. There’s a rule of thumb that adding 100 grams to a shoe worsens running economy by about 1 percent, so this 82-gram reduction accounts for about 0.8 percent of the Fast-R3’s advantage. As for the rest, there’s no single obvious change that explains it. Instead, the iterative process of making sure every bit of foam and carbon fiber is contributing seems to have created a more efficient shoe.

There are some other subtle differences. The Fast-R3 is a little less stiff than its competitors when you try to bend it along its length, and a little less stiff when you compress the midsole—but it returns slightly more energy when it springs back. The foam in traditional running shoes returns about 65 to 75 percent of the energy you spend compressing it. Superfoams such as PEBA in the Vaporfly and other supershoes return about 85 percent. Puma’s Nitro Elite foam, an “aliphatic thermoplastic polyurethane” (A-TPU), returns over 90 percent. In Hoogkamer’s testing, compressing the whole shoe (not just the midsole foam) returned 89.9 percent of the energy, compared to 85.0 percent in the Nike shoe and 85.7 percent in the Adidas.

What Happens Next?

There are a lot of reasons to be skeptical of any shoe company’s claims about its newest model. Hoogkamer ��DZ����’t work for Puma, but his study was funded by them, just as his Vaporfly study was funded by Nike. Both studies were small. Subsequent events showed that the Vaporfly’s 4-percent boost was real and spectacular. Over the coming weeks, we’ll get a sense of whether the Fast-R3’s 3.5-percent boost also passes the real-world test.

One problem is that Puma’s roster of elite road runners isn’t as impressive as Nike’s or Adidas’s. At first glance, they don’t have anyone who’s likely to set an attention-grabbing world record. Still, we’ll start seeing the new shoe in action at the Boston Marathon on April 21 and the London Marathon on April 27.

One of the athletes who will be wearing it in Boston is Rory Linkletter, a 2:08 marathoner from Canada. He’s been training in the shoe, so I asked whether he could tell that it was different. He said the first thing you notice is how light it is, and the second is the springiness: “It’s softer than previous supershoes, and that softness is met with some pretty remarkable bounce.” He ��DZ����’t have enough experience with it to know whether it’s faster, but he’d just done an 8-mile tempo run along Lake Mary Road in Flagstaff that was a minute faster than he’d ever previously done.

If Linkletter sets a big PR in Boston, it will be impossible to know how much credit, if any, should go to the shoe. But over the months to come, we might start seeing some patterns—and seeing whether other shoe companies adopt similar computational approaches, if they haven’t already. The “many small tweaks” approach of the Fast-R3 means there’s no single gimmick to copy. It also means that further refinements might be possible. Five years ago, I wondered whether supershoes were like klapskates in speedskating (one big innovation followed by a plateau) or tech suits in swimming (a series of innovations that kept making swimmers faster and faster). It’s starting to look like option B.

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Inflammation is a major buzzword these days—and not just in the context of sprained ankles or itchy insect bites. Much of the discussion instead surrounds the chronic low-grade inflammation that tends to increase throughout your body as you age. This phenomenon is thought to contribute to a wide range of ills, like heart disease, cancer, and chronic pain. It even has a catchy name: “inflammaging.” Whether exercise helps or hinders this process has long been a topic of debate.

It’s clear that exercise causes a short-term surge of inflammation. One of the earliest in sports science, in 1901, tested blood samples from four competitors in the Boston Marathon. The results showed a spectacular surge of inflammatory markers after the race, which was, at the time, interpreted as worrisome evidence that “the exercise had gone far beyond physiological limits.”

In the years since then, we’ve come to a more nuanced view of the links between exercise and inflammation. Yes, exercise triggers acute inflammation. But the body responds by deploying its own anti-inflammatory molecules. One theory is that the body’s defenses against inflammation then get stronger over time, so regular exercise actually protects you from inflammaging. Evidence for this claim is mixed, though, so researchers in Spain recently pooled the available data to investigate the effect of decades of serious athletic training on inflammation.

What’s the Problem with Inflammation?

Inflammation is a double-edged sword. It’s part of the body’s emergency response to stressors like an infection or a twisted ankle, a biochemical cascade that often results in swelling or soreness, but also calls in key molecules that initiate the defense and repair process. That’s why sports doctors use anti-inflammatory drugs more sparingly than they used to, because shutting down inflammation might delay recovery. In this context, inflammation is good—as long as it turns off again once the danger is past.

Inflammation becomes a problem when it’s chronic (meaning that it ��DZ����’t shut off once a threat has been successfully dealt with) and systemic (meaning that it’s everywhere in the body rather than just at the site of an injury). Chronic inflammation is a characteristic——of heart disease, cancer, diabetes, and various other conditions. To put it bluntly, if you have high levels of various inflammatory markers when you’re at rest, you’re likely to than someone with lower levels.

There are various reasons that you might have chronic inflammation: a lingering infection, high levels of psychological or emotional stress, and so on. Your diet can contribute, although there’s plenty of debate about which foods help or hinder (fiber, fruit, and vegetables are ; sugar and trans fats, not so much).

The big factor, though, is aging. As you get older, baseline levels of various inflammatory markers creep inexorably upward. It’s not entirely clear why it happens. is that dead or damaged cells accumulate and keep triggering the immune system at a low level; is that it’s caused by gradual changes in your gut microbiome. Whatever the cause, it’s bad news.

How Being an Athlete Affects Inflammaging

The new study, , comes from a joint research team led by Iñigo Pérez‑Castillo of Abbott Nutrition in Spain, along with medical staff from the Real Madrid soccer club and the Real Madrid Graduate School, a sports-focused unit of the European University of Madrid. (Yes, that’s a real thing. .)

Previous research has shown that if you train for a few months, your baseline levels of inflammation will go down—but then if you stop training, the levels go back up. What Pérez‑Castillo wanted to know was whether, if you train at a reasonable level and simply never stop, you can avoid inflammaging altogether. To find out, he and his colleagues pooled the results of 17 studies with 649 participants in total, comparing lifelong masters athletes—people over the age of 35 who train and compete regularly in a sport—with healthy but untrained people both young and old.

One challenge with studying inflammation is that there’s no simple measure of it. Instead, there’s a whole collection of molecules that respond to various types of stimulus in various ways that increase or decrease inflammation. Some do both. Interleukin-6, for example, surges sharply and temporarily after exercise in a way that fights inflammation, but at higher levels during rest can promote inflammation.

This means you have to look holistically at a bunch of markers to get a sense of overall inflammation levels. When you do this, a fairly convincing pattern emerges in the data. If you compare masters athletes with age-matched peers who don’t train, the athletes have consistently lower levels of baseline inflammation. But if you compare them to young people in their 20s who don’t train, the young people have even lower levels. Youth trumps training, in this case.

The data isn’t totally uniform. The strongest results show up in comparisons of C-reactive protein, which is associated with inflammation, and interleukin-10, which fights inflammation. Older athletes have less of the former and more of the latter. Training didn’t seem to make any difference for tumor necrosis factor alpha, another inflammatory molecule.

For interleukin-6, the results were mixed. Training didn’t lower baseline levels by a statistically significant margin. But when you break out the data by sport, endurance training did have a significant benefit while resistance training didn’t. That might be because endurance training has unique powers, or it might simply be that there haven’t been enough resistance training studies to see an effect. At this point, there’s no way of knowing.

If you were hoping for proof that running is the fountain of youth, you might see these results as a let-down. (I’ll admit, I was hoping for better news.) It’s possible that we might eventually stop inflammaging entirely by pulling more levers: maybe it’s lifelong endurance training and eating some yet-to-be-determined mix of vegetables and fish and never raising your voice in anger. The more likely scenario, I suspect, is that nothing can halt the flow of time entirely. If that’s the case, then I’ll take these results as a win.

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As headlines go, “Social Media is Bad” ��DZ����’t raise many eyebrows these days. TikTok and its ilk are said to be harming mental health, stifling creativity, eroding privacy, fueling disinformation, undermining national security, and so on. These are all big issues worthy of careful debate. But there’s a narrower and more tangible risk that Sweat Science readers might be concerned about. What if social media is making us slower?

A , from Carlos Freitas-Junior of the Federal University of Paraiba in Brazil and his colleagues, presents data on what happens when athletes scroll on their phones before training sessions. Surprisingly, it ��DZ����’t just mess with that specific workout. Instead, over time, the athletes make smaller gains in performance. The findings tell us something about social media—and they also suggest that the benefits of a workout may depend in part on the state of mind you’re in while doing it.

The Problem(s) With Social Media

Several studies over the years have examined social media use in athletes. Most famously, back in 2019 found an association between late-night tweeting (as it was then called) and next-day game performance in NBA players. If the players were tweeting after 11:00 P.M., the players tended to score fewer points, grab fewer rebounds, and shoot less accurately the next day.

You might argue—correctly—that the problem here is sleep deprivation rather than social media. But have found direct links between the usage of apps such as TikTok and sleep patterns in young athletes, suggesting that the root of the problem is the apps. Researchers have also linked social media use to mental well-being and even eating disorders in athletes, both of which impact performance.

These indirect impacts aren’t always straightforward: the TikTok-hurts-sleep study also found that Instagram usage was associated with greater calmness, for example. But there’s also a more immediate concern, which is that social media apps leave you mentally fatigued, which in turn directly compromises your endurance and decision-making abilities.

The Mental Fatigue Debate

The study that kicked off the modern conversation about mental fatigue in sport was a 2009 experiment from a researcher named Samuele Marcora. He showed that 90 minutes of doing a cognitively challenging computer task by about 15 percent compared to spending 90 minutes watching a documentary.

More studies followed, each investigating different types of mental fatigue and their effects on different types of athletic performance. Many of them echoed Marcora’s original results, but . One of the big unresolved questions is the extent to which the findings apply in real life. If you have to write an exam or do your taxes right before you run a marathon, that’s probably bad news. But what about the normal activities we engage in on a daily basis—like scrolling through the social media apps on your phones? Do they induce sufficient mental fatigue to affect performance?

Back in 2021, found that 30 minutes of social media use hurt athletes’ times in 100- and 200-meter freestyle trials, but not in the 50 meters. found that boxers made worse decisions after using social media, but that their jumping performance was unaffected. found no effect of social media use on strength training performance. These results are consistent with the general pattern of research on mental fatigue and related stressors like sleep deprivation: with sufficient motivation, you can still exert maximal force, but your decision-making and endurance may be compromised.

What the New Data Shows

Freitas-Junior’s new study looks at volleyball players, testing their jumping performance and their “attack efficiency,” a measure of how hard and how accurately they can hit the ball in a sequence of attacks. What’s different about the study is that it looked at long-term rather than immediate effects. Fourteen athletes spent half an hour before practice either using Facebook, WhatsApp, and Instagram on their phones, or watching documentaries about the history of the Olympics. After three weeks, their performance was assessed and then they switched groups and repeated the process for another three weeks.

At the end of the three-week period, jumping performance wasn’t affected under either condition, but athletes’ attack efficiency was worse following the three weeks of social media use. The difference was statistically significant, but to be honest the data isn’t very convincing.

For starters, take a look at the mental fatigue data. This shows how much, on average, mental fatigue (on the vertical axis) increased after watching the documentary (DOC) or using social media (SMA):

This is nice clean data. Watching the documentary increased the subjective perception of mental fatigue in almost every individual. Using social media increased it even more, again with uniform results in all the individuals. We can say with confidence that social media use increases mental fatigue compared to chilling with a doc.

Now take a look at the attack efficiency data, measured in arbitrary units where a higher number is better:

This time the individual data is all over the map. The statistical analysis tells us that, on average, the social media group got worse while the documentary group got better. This average effect may or may not be real—only more and larger studies can confirm if it is. Based on the body of previous research, I’d guess that it’s probably real. But the pattern is so inconsistent on an individual level that I’d hesitate to use it as a basis for advice to athletes. Some athletes got better after social media use. That might be a fluke, or it might indicate that they have a healthier relationship with their apps such that a little phone time before practice gets them in a better headspace.

In the end, then, the narrative isn’t as tidy as we might like. It’s not that social media is uniformly bad, will leave you mentally fatigued, and will automatically rob you of training gains. There’s still a valuable message here, though. The things we do—social media, yes, but also real-world socializing, reading a book, listening to music, working, commuting, daydreaming, and so on—affect our mental state and readiness to perform. We all respond to these things differently, so there’s no universal list of dos and don’ts. But it’s worth figuring out what gets you in the right headspace and leaves you mentally energized, so that you can replicate it when it matters.

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It’s the single most iconic vista in all of Newfoundland, all the more prized because it’s so hard to reach. By the time we clambered over the final set of boulders to get there, we’d been climbing for more than six hours, accompanied by clouds of voracious and seemingly waterproof black flies that were undeterred by the steadily falling rain. We turned to look back at the route we’d traveled: the sinuous, glacier-carved fjord 2,000 feet below us, the billion-year-old cliffs that hemmed it in, the jumble of rocks and rainforest that led steeply up to the plateau where we now stood. This view of Western Brook Pond is a staple of the island’s ; we’ve seen the pics, but on that particular day it was nothing but a blanket of mist.

We didn’t have time to linger anyway. It was nearly noon by the time the boat had dropped us off at the head of the fjord, then climbing up the gulch had taken twice as long as we’d anticipated. We were barely halfway to the alpine pond where we’d hoped to camp that night. As the mist thickened, finding landmarks was getting increasingly difficult. Muddy game trails carved by the area’s ubiquitous moose and caribou led in every direction through the boggy grass, frequently disappearing into sinkholes filled by several days of nonstop rain. No matter how often we stopped to orient ourselves, we were turned around again within minutes.

I felt panic rising in me. We were already a day behind schedule, because the waters of the fjord had been too choppy for the boat on our scheduled departure day. That had forced us to burn a day of food while camped by the dock waiting for our ride, leaving us with just four days to complete the hike instead of the planned five. And while my wife, Lauren, and I were capable of hiking as long into the night as we needed to, we couldn’t ask the same of our daughters, Ella and Natalie. They were just eight and six, respectively—and, aside from being exhausted, they were being driven bonkers by the flies, despite their full-body bug suits. But there were no exits from this hike. No roads traverse this part of Newfoundland. The boat was gone, and so was our cell signal. The only way out was onward. In that moment of maximal uncertainty, a puzzling thought nagged at me.

“You know,” I said to Lauren, “this isn’t bad planning or bad luck. It’s exactly what we asked for.”

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Back in 2021, I wrote about the case of Daniel Granberg, a 24-year-old from Colorado who died at the summit of a Bolivian mountain called Illimani of what turned out to be high-altitude pulmonary edema (HAPE). What was notable about the incident was that Illimani is only 21,122 feet above sea level, well below the notorious Death Zone, which starts around 26,000 feet and is where most climbing fatalities in the Himalaya occur. And Granberg hadn’t seemed notably distressed: the HAPE snuck up on him without obvious warning signs.

That’s a little scary for anyone venturing to these sorts of high-but-not-extreme altitudes. Ideally, you’d like to have a better sense of the risk factors and warning signs that signal the difference between run-on-the-hill acute mountain sickness and more severe forms of altitude illness like HAPE.

offers some useful clues. Emergency physicians from the University of Vermont and the medical staff at Aconcagua Provincial Park, led by Vermont’s Andrew Park, crunched the data on all climbers diagnosed with HAPE during the month of January in 2024 and compared their responses to climbers who didn’t get HAPE. Sure enough, there were some notable differences in how fast they climbed, how long they acclimatized to various stages of elevation, and what symptoms they displayed.

Aconcagua, in Argentina, is the highest mountain in Americas at 22,838 feet. It’s also the highest mountain outside Asia, and more significantly is perhaps the highest non-technical summit in the world, meaning that it’s possible to ascend without specialized climbing skills and equipment. That makes it accessible, but it also means that climbers can hurry up the mountain at a dangerous pace. found that roughly three climbers die each year out of more than 3,000 who attempt it. HAPE was the second-leading cause after trauma, accounting for a fifth of the deaths.

Park medical staff screen climbers at camps at roughly 11,000 feet and 14,000 feet. Crucially, there are no standard sleeping camps between those two elevations, which means you have to make that 3,000-foot jump in one night. Standard guidelines on altitude illness from the Wilderness Medical Society (which I wrote about in detail here) suggest increasing your sleeping elevation by no more than 1,500 feet per night once you’re above 10,000 feet. If logistics force you to make a bigger jump, you need to add rest days to keep the average rate of climbing below that threshold.

A total of 17 climbers were diagnosed with HAPE in January 2024. The key feature of HAPE is a potentially dangerous build-up of fluid in the lungs that interferes with the delivery of oxygen into the bloodstream. It’s mainly diagnosed on the basis of shortness of breath, lower than expected blood oxygen levels for a given altitude, and a crackling sound in the lungs. None of the HAPE victims died; all were quickly evacuated by helicopter to lower elevations, which is the main recommendation for treating HAPE.

Overall, the climbers diagnosed with HAPE were very similar to a group of 42 climbers surveyed during the same period who weren’t diagnosed with HAPE. But a few suggestive differences emerged. The most significant was the number of nights they spent at the 14,000-foot camp, after that 3,000-foot jump in sleeping elevation. The HAPE climbers spent an average of 3.6 nights at that camp, compared to 5.0 nights for the non-HAPE climbers, a statistically significant difference.

Interestingly, both groups had planned a total of 10.4 nights, on average, to reach the summit. The HAPE group actually spent slightly longer getting to 14,000 feet, but they spent less time adjusting to that elevation. Typically the risk of altitude illness starts ramping up beyond about 10,000 feet, so once you get to 14,000 feet you’re well into the zone where many people will be experiencing altitude-related symptoms.

On a related note, 71 percent of the HAPE patients reported that they had symptoms of acute mountain sickness (AMS) at 14,000 feet. AMS is the most common and mild form of altitude illness, typically manifesting as a headache plus other symptoms like nausea and lethargy. The typical advice for AMS is that you should stop ascending, and if symptoms don’t resolve within a few days, descend to a lower elevation. Notably, every single one of the climbers who had AMS at 14,000 feet then went on to develop HAPE (at a median elevation of 18,000 feet) reported that their AMS symptoms hadn’t resolved before they continued their ascent.

There are a few other observations that raise more questions than answers. Just under half the HAPE climbers reported taking acetazolamide, a diuretic known to climbers under the brand name Diamox that helps ward off AMS. In contrast, only a fifth of the non-HAPE climbers used it. It seems unlikely that Diamox is causing HAPE. Presumably climbers who were struggling to handle altitude were more likely to try Diamox and also more likely to eventually develop HAPE. Still, the researchers suggest that it’s an observation that’s worth following up on.

Similarly, 44 percent of the HAPE group reported having a recent upper respiratory tract infection, compared to just 29 percent of the non-HAPE group. This difference wasn’t statistically significant, but it’s plausible it might have been significant with a larger sample size. Lingering inflammation in the respiratory tract might contribute to the leaky capillaries associated with HAPE. For now, it’s another idea to check out in future research.

The strongest conclusions we can draw from the data are also the most familiar ones: ascend slowly, and if AMS strikes, pause your ascent until symptoms resolve. That’s easy advice to give, but hard to follow, especially because AMS symptoms like headache and fatigue are so vague and commonplace at high elevations. But the data here offers a stark warning: ignoring this advice heightens your risk of progressing to more serious forms of altitude illness that sometimes, with little warning, turn out to be fatal.

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