Isegoria

One in five competitive athletes suffers from exercise-induced bronchoconstriction, or EIB:

The numbers are even higher in endurance and winter sports. Puzzlingly, studies have found that athletes with EIB who somehow make it to the Olympics are more likely to medal. What’s so great about wheezing, chest tightness, and breathlessness?

The answer isn’t what you’re thinking. Sure, it’s possible that some athletes get a boost because an EIB diagnosis allows them to use otherwise-banned asthma medications. But there’s a simpler explanation: breathing high volumes of cold or polluted air dries out the airways, leading to an overzealous immune response and potential long-term damage. “It’s well established that high training loads and ventilatory work increase the degree of airway hyper-responsiveness and hence development of asthma and EIB,” explains Morten Hostrup, a sports scientist at the University of Copenhagen and lead author of a new review on EIB in the Scandinavian Journal of Medicine and Science in Sports. In other words, the athletes who train hard enough to podium are more likely to develop EIB as a result.

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Activities with the highest risk involve sustained efforts of at least five minutes, particularly if they take place in cold or polluted air. Cold air doesn’t hold much moisture, so it dries the airways. This affects skiers, runners, and triathletes, among others. Indoor environments like pools and ice rinks are also a problem, because of the chloramines produced by pool water and exhaust from Zambonis.

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Before the 1998 Winter Games, U.S. Olympic Committee physiologists examined Nagano-bound athletes to see whose airways showed abnormal constriction in response to arduous exercise. Almost a quarter of the athletes tested positive, including half the cross-country ski team.

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If you do get an EIB diagnosis, your doctor can prescribe asthma medication, including inhaled corticosteroids like fluticasone and airway dilators like salbutamol. If you’re an elite athlete subject to drug testing, you’ll need to tread carefully, since some of those medications are either banned or restricted to a maximum dosage. Hostrup and his colleagues note that there’s also evidence that fish oils high in omega-3 fatty acids, vitamin C, and even caffeine might help reduce EIB symptoms. And on the non-pharmaceutical side, you can minimize the chance of an attack by doing a thorough warm-up of 20 to 30 minutes, including six to eight 30-second sprints. This can temporarily deplete the inflammatory cells that would otherwise trigger an airway-narrowing attack

Plyometric training can make you a more efficient runner, Alex Hutchinson notes, but there’s still plenty of debate about how it works:

As a result, studies like this one in Sports Biomechanics, published last month by a group led by Aurélien Patoz of the University of Lausanne, don’t garner much attention. They found a 3.9 percent improvement in running economy after eight weeks of either plyometric or dynamic strength training, roughly comparable to what Nike’s original Vaporfly 4% shoe produced. (They also found no evidence that either form of training altered running stride in any significant way, for what it’s worth.)

Why no excitement about a free four-percent boost? As someone who has experimented on and off with various forms of plyometric training over several decades, let me venture a hypothesis: it’s perceived as too complicated, and possibly risky, for most of us.

Does it need to be that complicated?

That’s the question tackled by another recent study, this one led by Tobias Engeroff of Goethe University Frankfurt and published in Scientific Reports. They stripped plyometric training down to its bare bones, tested it on a group of amateur runners—and still found a significant improvement in running economy after just six weeks. The exact size of the improvement depends on how you measure it and at what speed, but was between 2 and 4 percent.

Engeroff’s plyometric program involved nothing but hopping on the spot. Specifically, “participants were instructed to start with both feet no wider than hip width apart and to hop as high as possible with both legs, keeping the knees extended and aiming to minimize ground contact time.” They started by hopping for 10 seconds, resting for 50 seconds, and repeating five times for a total of five minutes. They did this five-minute program daily, decreasing the rest and increasing the number of sets each week: the second week was 6 sets of 10 seconds of hopping with 40 seconds of rest; the sixth and final week was 15 sets of 10 seconds hopping with 10 seconds of rest, still totaling five minutes.

This program was based on the idea that it’s tendon stiffness that boosts running economy. In particular, the stretch and recoil of the Achilles tendon provides between half and three-quarters of the positive work required for running, by some estimates. Engeroff’s short daily program draws on recent research by Keith Baar and others suggesting that connective tissue such as tendons responds best to brief, frequent stimulus rather than longer and harder workouts. Notably, this approach didn’t injure any of the runners.

European explorers found that indigenous peoples ate rotten meat:

From arctic tundra to tropical rainforests, native populations consumed rotten remains, either raw, fermented or cooked just enough to singe off fur and create a more chewable texture. Many groups treated maggots as a meaty bonus.

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Some Indigenous communities feasted on huge decomposing beasts, including hippos that had been trapped in dug-out pits in Africa and beached whales on Australia’s coast. Hunters in those groups typically smeared themselves with the fat of the animal before gorging on greasy innards. After slicing open animals’ midsections, both adults and children climbed into massive, rotting body cavities to remove meat and fat.

Or consider that Native Americans in Missouri in the late 1800s made a prized soup from the greenish, decaying flesh of dead bison. Animal bodies were buried whole in winter and unearthed in spring after ripening enough to achieve peak tastiness.

But such accounts provide a valuable window into a way of life that existed long before Western industrialization and the war against germs went global, says anthropological archaeologist John Speth of the University of Michigan in Ann Arbor. Intriguingly, no reports of botulism and other potentially fatal reactions to microorganisms festering in rotting meat appear in writings about Indigenous groups before the early 1900s. Instead, decayed flesh and fat represented valued and tasty parts of a healthy diet.

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Many travelers such as Landor considered such eating habits to be “disgusting.” But “a gold mine of ethnohistorical accounts makes it clear that the revulsion Westerners feel toward putrid meat and maggots is not hardwired in our genome but is instead culturally learned,” Speth says.

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Fermented fish heads, also known as “stinkhead,” are one popular munchy among northern groups. Chukchi herders in the Russian Far East, for instance, bury whole fish in the ground in early fall and let the bodies naturally ferment during periods of freezing and thawing. Fish heads the consistency of hard ice cream are then unearthed and eaten whole.

Speth has suspected for several decades that consumption of fermented and putrid meat, fish, fat and internal organs has a long and probably ancient history among northern Indigenous groups. Consulting mainly online sources such as Google Scholar and universities’ digital library catalogs, he found many ethnohistorical descriptions of such behavior going back to the 1500s. Putrid walrus, seals, caribou, reindeer, musk oxen, polar bears, moose, arctic hares and ptarmigans had all been fair game.

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“Recognizing that eating rotten meat is possible, even without fire, highlights how easy it would have been to incorporate scavenged food into the diet long before our ancestors learned to hunt or process [meat] with stone tools,” says paleoanthropologist Jessica Thompson of Yale University.

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Instead, Speth speculates, cooking’s primary value at first lay in making starchy and oily plants softer, more chewable and easily digestible. Edible plants contain carbohydrates, sugar molecules that can be converted to energy in the body. Heating over a fire converts starch in tubers and other plants to glucose, a vital energy source for the body and brain. Crushing or grinding of plants might have yielded at least some of those energy benefits to hungry hominids who lacked the ability to light fires.

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Over the last few centuries, they have favored tongue, fat deposits, brisket, ribs, fatty tissue around intestines and internal organs, and marrow. Internal organs, especially adrenal glands, have provided vitamin C — nearly absent in lean muscle — that prevented anemia and other symptoms of scurvy.

Western explorers noted that the Inuit also ate chyme, the stomach contents of reindeer and other plant-eating animals. Chyme provided at least a side course of plant carbohydrates.

The popularity of GLP-1 receptor agonists, like Ozempic and Wegovy, has skyrocketed, because they do help people lose weight:

Though a certain amount of lean loss is inevitable with significant weight reduction (usually about 25% of total weight loss), the goal is to increase the body’s overall proportion of lean mass – in other words, to improve body composition.

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However, from the information we can scrape together based on sub-cohort data, these “miracle drugs” start to look a bit less miraculous. In 2021’s STEP 1 trial — the first trial demonstrating the efficacy of semaglutide as a treatment for adult obesity — a subset of 140 patients underwent DEXA scans for body composition analysis. Among these patients, lean mass accounted for approximately 39% of total weight loss — substantially higher than ideal. In a substudy of 178 patients from the SUSTAIN 8 trial on semaglutide as a diabetes treatment, the average proportion of lean mass loss was nearly identical at 40%, despite lower doses and less total weight loss than in the STEP 1 trial.

Researchers in Finland looked at 17 pairs of identical twins who didn’t have similar exercise habits:

The first thing to note is just how unusual such twin pairs are. The twins in the study were drawn from two previous Finnish twin studies that included thousands of pairs of identical twins. The vast majority of them had similar levels of physical activity. The High Runner mouse line that’s often used in lab studies took mice that loved to run, bred them with each other, and produced mice that love to run even more. I’d like to think that human behavior (and mating patterns) are a little more complex than that, but the twin data certainly suggests that our genes influence our predilection for movement.

Still, they found these 17 pairs whose paths had diverged. There were two different subgroups: young twins in their thirties whose exercise habits had diverged for at least three years, and older twins in their fifties to seventies whose habits had diverged for at least 30 years. On average, the exercising twins got about three times as much physical activity, including active commuting, as the non-exercising ones: 6.1 MET-hours per day compared to 2.0 MET-hours per day. For context, running at a ten-minute-mile pace for half an hour consumes about 5 MET-hours.

All the twin pairs came in for physical examinations, and the results were pretty much what you’d expect. The exercising twins had higher VO2 max (38.6 vs. 33.0 ml/kg/min), smaller waist circumference (34.8 vs. 36.3 inches), lower body fat (19.7 vs. 22.6 percent), significantly less abdominal fat and liver fat, and so on.

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A 2018 case study from researchers at California State University Fullerton looked at a single identical twin pair, then aged 52. One was a marathoner and triathlete who had logged almost 40,000 miles of running between 1993 and 2015. The other was a truck driver who didn’t exercise. In this case, the exercising twin weighed 22 pounds less, and his resting heart rate was 30 percent lower. Most fascinatingly, muscle biopsies showed that the marathoner had 94 percent slow-twitch fibers while the truck-driver had just 40 percent slow-twitch. No one before or since (as far as I know) has shown such a dramatic change in muscle properties.

Alex Hutchinson explains how to hold on to your sprint speed as you age:

Many of the challenges of daily living, once you hit your 70s and 80s and beyond, are essentially tests of all-out power rather than sustained endurance (though both are important).

The problem is that sprint speed starts declining after your 20s, and most endurance athletes have no clue how to preserve it.

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Older sprinters take shorter steps and their feet spend longer in contact with the ground, presumably because they’re less able to generate explosive force with each step. That’s consistent with the finding that older sprinters have less muscle, and in particular less fast-twitch muscle, than younger sprinters.

But it’s not just a question of how much muscle you’ve got. In fact, some studies suggest that you lose strength more rapidly than you lose muscle, which means that the quality of your remaining muscle is reduced. There are a bunch of different reasons for muscle quality to decline, including the properties of the muscle fibers themselves, but the most interesting culprit is the neuromuscular system: the signals from brain to muscle get garbled.

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The authors cover their bases by recommending that your resistance training routine should include workouts that aim to build muscle size (e.g. three sets of ten reps at 70 percent of one-rep max); workouts that aim to build strength (e.g. two to four sets of four to six reps at 85 percent of max); and workouts to build power (e.g. three sets of three to ten reps at 35 to 60 percent of max).

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The authors suggest training to improve coordination through exercises that challenge balance, stability, and reflexes, such as single-leg balance drills. One advantage of this type of training: it’s not as draining as typical “reps to failure” strength workouts, so it may provide more bang for your buck if you can’t handle as many intense workouts as you used to.

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On that note, the standard advice that veteran athletes give you when you hit your 40s is that you can no longer recover as quickly. Strangely, the authors point out, the relatively sparse data on this question doesn’t find any differences in physiological markers of post-workout recovery between younger and older athletes. The main difference is that older athletes feel less recovered—and in this case, it’s probably worth assuming that those feelings represent some kind of reality, even if we don’t know how to measure it.

In The Hungry Brain, neuroscientist Stephan Guyenet references a 1965 study in which volunteers received all their food from a “feeding machine” that pumped a “liquid formula diet” through a “dispensing syringe-type pump which delivers a predetermined volume of formula through the mouthpiece.”

What happens to food intake and adiposity when researchers dramatically restrict food reward? In 1965, the Annals of the New York Academy of Sciences published a very unusual study that unintentionally addressed this question. …

The “system” in question was a machine that dispensed liquid food through a straw at the press of a button—7.4 milliliters per press, to be exact (see figure 15). Volunteers were given access to the machine and allowed to consume as much of the liquid diet as they wanted, but no other food. Since they were in a hospital setting, the researchers could be confident that the volunteers ate nothing else. The liquid food supplied adequate levels of all nutrients, yet it was bland, completely lacking in variety, and almost totally devoid of all normal food cues.

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The researchers first fed two lean people using the machine—one for sixteen days and the other for nine. Without requiring any guidance, both lean volunteers consumed their typical calorie intake and maintained a stable weight during this period.

Next, the researchers did the same experiment with two “grossly obese” volunteers weighing approximately four hundred pounds. Again, they were asked to “obtain food from the machine whenever hungry.” Over the course of the first eighteen days, the first (male) volunteer consumed a meager 275 calories per day—less than 10 percent of his usual calorie intake. The second (female) volunteer consumed a ridiculously low 144 calories per day over the course of twelve days, losing twenty-three pounds. The investigators remarked that an additional three volunteers with obesity “showed a similar inhibition of calorie intake when fed by machine.”

The first volunteer continued eating bland food from the machine for a total of seventy days, losing approximately seventy pounds. After that, he was sent home with the formula and instructed to drink 400 calories of it per day, which he did for an additional 185 days, after which he had lost two hundred pounds —precisely half his body weight. The researchers remarked that “during all this time weight was steadily lost and the patient never complained of hunger.” This is truly a starvation-level calorie intake, and to eat it continuously for 255 days without hunger suggests that something rather interesting was happening in this man’s body. Further studies from the same group and others supported the idea that a bland liquid diet leads people to eat fewer calories and lose excess fat.

This machine-feeding regimen was just about as close as one can get to a diet with zero reward value and zero variety. Although the food contained sugar, fat, and protein, it contained little odor or texture with which to associate them. In people with obesity, this diet caused an impressive spontaneous reduction of calorie intake and rapid fat loss, without hunger. Yet, strangely, lean people maintained weight on this regimen rather than becoming underweight. This suggests that people with obesity may be more sensitive to the impact of food reward on calorie intake.

Only one theory can account for all of the available evidence about the obesity epidemic: it is caused by one or more environmental contaminants:

We know that this is biologically plausible because there are many compounds that reliably cause people to gain weight, sometimes a lot of weight.

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We need a theory that can account for all of the mysteries we reviewed earlier. Another way to put this is to say that, based on the evidence, we’re looking for a factor that:

1. Changed over the last hundred years
2. With a major shift around 1980
3. And whatever it is, there is more of it every year
4. It doesn’t affect people living nonindustrialized lives, regardless of diet
5. But it does affect lab animals, wild animals, and animals living in zoos
6. It has something to do with palatable human snackfoods, unrelated to nutritional value
7. It differs in its intensity by altitude for some reason
8. And it appears to have nothing to do with our diets

Environmental contamination by artificial, human-synthesized compounds fits this picture very well, and no other account does.

There are numerous pieces of evidence indicating that moderate alcohol intake has a protective effect on metabolic diseases:

Our previous studies revealed that long-term low-dose alcohol intake resists high-fat diet (HFD) induced obesity. A process in which white adipose tissue can be stimulated and turned into heat-producing brown adipose tissue named white adipose browning is associated with energy expenditure and weight loss. In this study we aimed to investigate whether alcohol causes the browning of white adipose tissue and whether the browning of white adipose tissue is involved in the resistance to the occurrence of obesity caused by long-term low-dose alcohol intake. After eight months of alcohol feeding, the body weight of mice had no significant change, but the fat content and lipid deposition in the liver were reduced. Morphological observations revealed that the browning of white adipose tissue occurred.

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Moderate alcohol drinking mice had faster lipid metabolism and slower lipid anabolism. In addition, we found that long-term low-dose alcohol intake prevented the increase of body weight, triglycerides, inflammation and energy expenditure decrease induced by HFD. Moderate alcohol consumption increased the expression of UCP1 and glucose uptake in the adipose tissue of the HFD group. In conclusion, our results show for the first time that alcohol can trigger the browning of white adipose tissue to counteract obesity.

Regular exercise and sauna bathing have each been shown to improve cardiovascular function in clinical populations:

However, experimental data on the cardiovascular adaptations to regular exercise in conjunction with sauna bathing in the general population is lacking. Therefore, we compared the effects of exercise and sauna bathing, to regular exercise using a multi-arm randomized controlled trial. Participants(n = 47) aged 49 ± 9 years with low physical activity levels, and at least one traditional CVD risk factor were randomly assigned (1:1:1) to guideline-based regular exercise and 15-minute post-exercise sauna (EXS), guideline-based regular exercise (EXE), or control (CON), for eight weeks. The primary outcomes were blood pressure (BP) and cardiorespiratory fitness (CRF). Secondary outcomes included fat mass, total cholesterol levels, and arterial stiffness. EXE had a greater change in CRF (+6.2 ml/kg/min; 95% CI, +4.2. to +8.3 ml/kg/min) and fat mass, but no differences in BP when compared to CON. EXS displayed greater change in CRF (+2.7 ml/kg/min; 95% CI, +0.2. to +5.3 ml/kg/min), lower systolic BP (-8.0 mmHg; 95% CI, -14.6 to -1.4 mmHg) and lower total cholesterol levels compared to EXE. Regular exercise improved CRF and body composition in sedentary adults with CVD risk factors. However, when combined with exercise, sauna bathing demonstrated a substantially supplementary effect on CRF, systolic BP, and total cholesterol levels. Sauna bathing is a valuable lifestyle tool that complements exercise for improving CRF, and decreasing systolic BP. Future research should focus on the duration, and frequency of exposure to ascertain the dose-response relationship.

In much the same way that everything in your fridge both causes and prevents cancer, Alex Hutchinson notes, there’s a study out there somewhere proving that everything boosts endurance:

A new preprint (a journal article that hasn’t yet been peer-reviewed, ironically) from researchers at Queensland University of Technology in Australia explores why this seems to be the case, and what can be done about it. David Borg and his colleagues comb through thousands of articles from 18 journals that focus on sport and exercise medicine, and unearth telltale patterns about what gets published—and perhaps more importantly, what doesn’t. To make sense of the studies you see and decide whether the latest hot performance aid is worth experimenting with, you also have to consider the studies you don’t see.

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One way to illustrate these results is to plot something called the z-value, which is a statistical measure of the strength of an effect. In theory, if you plot the z-values of thousands of studies, you’d expect to see a perfect bell curve. Most of the results would be clustered around zero, and progressively fewer would have either very strongly positive or very strongly negative effects. Any z-value less than -1.96 or greater than +1.96 corresponds to a statistically significant result with p less than 0.05. A z-value between -1.96 and +1.96 indicates a null result with no statistically significant finding.

In practice, the bell curve won’t be perfect, but you’d still expect a fairly smooth curve. Instead, this is what you see if you plot the z-values from the 1,599 studies analyzed by Borg:

There’s a giant missing piece in the middle of the bell curve, where all the studies with non-significant results should be. There are probably lots of different reasons for this, both driven by decisions that researchers make and—just as importantly—decisions that journals make about what to publish and what to reject. It’s not an easy problem to solve, because no journal wants to publish (and no reader wants to read) thousands of studies that conclude, over and over, “We’re not yet sure whether this works.”

In a 72-week trial in participants with obesity, tirzepatide — a novel glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 receptor agonist — provided substantial and sustained reductions in body weight. Participants lost one-fifth of their body weight.