Isegoria

Infrared saunas have become incredibly popular, even though they aren’t really saunas:

To the untrained eye, they basically look the same as what you’d expect a sauna to look like—wood paneling, benches, some guy who just had to bring his phone inside—and both actually share a bunch of the same health benefits.

[…]

Infrared saunas give off way less heat, thus making the surrounding area a much more habitable place for those who’d prefer not to partake.

[…]

A true traditional sauna, also called a Finnish sauna, uses a wood fire to heat stones, which in turn heat the air inside the sauna. Nowadays, you can also find electric saunas (these tend to get filed under “traditional”), which also use stones, but the stones are heated by electricity rather than fire. Traditional saunas can maintain temperatures between 150-220 degrees Fahrenheit.

[…]

Unlike traditional saunas, Infrared saunas do not have a central heat source. Instead, they utilize ceramic or metallic panels to emit far-infrared light. “An infrared sauna uses infrared light to directly heat your body, rather than heating the air around you like a traditional sauna,” Dr. Setareh says. Hence, infrared saunas are able to operate at much lower temperatures—between 100–165 degrees—while still giving you a similar, albeit decidedly less intense, sensation to sitting in a traditional sauna.

According to Dr. Setareh, “both types of saunas share common benefits—like improving circulation, promoting relaxation, and encouraging recovery,” and studies have also found both to have positive effects on lowering blood pressure.

[…]

Research, including a landmark 2015 Finnish study that surveyed 2,315 men over the course of two decades, has long associated sauna use with heart health and a decreased risk of cardiovascular disease and all-cause mortality. But it wasn’t until a recent study, published earlier this year in the American Journal of Physiology, that researchers have formally begun weighing the benefits of traditional saunas against their infrared counterparts. (This latest study also compared both types of sauna to a hot tub, which surprisingly emerged as the most beneficial of the three when it came to promoting heart health.)

The hot tub has other benefits:

In addition to a greater increase in heart rate, the researchers also observed higher production of interleukin-6—a critical protein involved in the body’s immune and inflammatory responses—from hot tub exposure compared with sauna use. In fact, the hot tub even appeared to spur production of T cells, helper T cells, and natural killer cells, all of which play an essential role in the body’s immune system—something the study authors saw none of during participants’ stints in the saunas. “If you can acutely raise your inflammatory responses and then drop them back down again,” he says, “it’s a challenge to the system—it activates it and then shuts it back down again—and that’s aligned with better health.”

Dietary fiber is extremely heterogeneous, so a recent study analyzed the impact of different plant-based fibers (pectin, ?-glucan, wheat dextrin, resistant starch, and cellulose as a control) on the gut microbiota in high-fat diet (HFD)-fed mice:

Only ?-glucan supplementation during HFD-feeding decreased adiposity and body weight gain and improved glucose tolerance compared with HFD-cellulose, whereas all other fibers had no effect. This was associated with increased energy expenditure and locomotor activity in mice compared with HFD-cellulose. All fibers supplemented into an HFD uniquely shifted the intestinal microbiota and cecal short-chain fatty acids; however, only ?-glucan supplementation increased cecal butyrate concentrations. Lastly, all fibers altered the small-intestinal microbiota and portal bile acid composition.

Beta-glucan is found in a number of foods:

• Oats: Whole oats, oat bran, and oatmeal are among the best sources, with about 1-2 grams of beta-glucan per 100 grams.
• Barley: Whole barley and barley products like barley flour contain 2-8 grams per 100 grams.
• Mushrooms: Certain varieties, such as shiitake, maitake, reishi, and oyster mushrooms, are rich in beta-glucans, particularly in their cell walls.
• Yeast: Nutritional yeast and baker’s yeast contain beta-glucans, often used in supplements or fortified foods.
• Seaweed: Some types, like laminarin-containing brown seaweed, provide beta-glucans.
• Rye and Wheat: Whole grain rye and wheat contain smaller amounts of beta-glucan compared to oats and barley.

Or you can buy it as a supplement.

Adam Strandberg works on metabolism and has run into the claim that chess grandmasters burn 6000 calories per day during tournaments:

I assumed when I dug into it that I would find a specific methodological error. But while methods enter the story, the real problem is that the number was completely made up.

As far as I can tell, the “patient zero” that caused this claim to become so widespread is this 2019 ESPN article:

Robert Sapolsky, who studies stress in primates at Stanford University, says a chess player can burn up to 6,000 calories a day while playing in a tournament, three times what an average person consumes in a day. Based on breathing rates (which triple during competition), blood pressure (which elevates) and muscle contractions before, during and after major tournaments, Sapolsky suggests that grandmasters’ stress responses to chess are on par with what elite athletes experience.

This story was then picked up by many outlets, such as CNBC, Men’s Health, Inc, GQ, Marginal Revolution, and Joe Rogan.

So the claim came from Robert Sapolsky. However, a Google Scholar search turned up no primary literature from him on the topic. Fortunately, someone on Reddit was also curious and shared an email from Professor Sapolsky explaining the number. He first references a footnote from his 1994 book Why Zebras Don’t Get Ulcers:

The definitive study on chess players was carried out by the physiologist Leroy DuBeck and his graduate student Charlotte Leedy. They wired up chess players in order to measure their breathing rates, blood pressure, muscle contractions, and so on, and monitored the players before, during, and after major tournaments. They found tripling of breathing rates, muscle contractions, systolic blood pressures that soared to over 200—exactly the sort of thing seen in athletes during physical competition. See the original report, Leedy’s thesis, “The effects of tournament chess playing on selected physiological responses in players of varying aspirations and abilities” (Temple University, 1975) or their brief report (Leedy, C., and DuBeck, L. 1971. Physiological changes during tournament chess. Chess Life and Review, 708). In a telephone conversation, DuBeck also tells the story of the international match in the early 1970s between grand masters Bent Larson and Bobby Fischer, in which the former had to be given antihypertensive medication in the middle of his losing match; his blood pressure remained elevated for days afterward. And for that special chess fan out there who just can’t get enough of this subject, may I suggest as the perfect gift a copy of Glezerov, V., and Sobol, E. 1987. Hygienic evaluation of the changes in work capacity of young chess players during training. Gigiena i Sanitariia 24, in the original Russian.

This doesn’t say anything about calories, though the “tripling of breathing rates” matches part of the ESPN quote. He goes on:

The figure of 6K calories/day is an extrapolation that DuBeck generated, based on those measures and the typical duration of tournaments. Obviously, it’s a pretty soft, squishy number. I’d asked the ESPN people to mention that the 6K was an indirectly derived measure, the number of calories shouldn’t be presented as gospel, so if they were going to cite the 6K, they should cite these caveats as well. But I guess the caveats didn’t make the editing process…

Hope that helps.

Robert Sapolsky

[…]

To summarize: a grad student took physiological measurements of 11 ordinary chess players (not grandmasters). They reported in a summary in a chess magazine that the maximum chest movement rate they measured in a 10 second period was almost three times that of an average measurement from a different study. Robert Sapolsky then cited this thesis in his popular book, dropping the distinction between maximum and average to give a 3X breathing rate. He later took the 3X number and multiplied that by 2000 calories per day to get the number 6000, adding the “grandmaster” rhetorical fluorish along the way. He spread this fact through his own talks at Stanford and through interviews with journalists, who accurately repeated him. When questioned about the source of the number, he then claimed on multiple occasions that the number actually came from someone else, and that journalists had distorted his argument.

A new study published in the International Journal of Sports Physiology and Performance compares seven different ways of calculating training load:

Four of them are variations on a concept known as TRIMP, which is short for “training impulse” and is based on heart rate measurements, using equations that account for lactate levels, breathing thresholds, and other details. A fifth uses heart-rate variability, and a sixth uses a subjective rating of effort. (Most fitness wearables, by the way, likely use a combination of the above methods, though their exact algorithms are typically proprietary.) The seventh method is the NASA questionnaire, which we’ll come back to.

The gold standard against which all these methods were compared is the “acute performance decrement,” or APD. Basically, you do an all-out time trial, then you do your workout, then you do another all-out time trial. Your APD is how much slower the second time-trial is compared to the first one, as a measure of how much the workout took out of you.

[…]

The performance test was running at VO2 max pace until exhaustion. When they were fresh, the runners lasted just under six minutes on average. After the one-hour easy run, their APD was 20.7 percent, meaning they gave up 20.7 percent earlier in the post-workout VO2 max run. After the medium-intensity run, the APD was 30.6 percent; after the long intervals, it was 35.9 percent; after the short intervals, it was 29.8 percent.

So how well were each of the seven training load calculations able to predict this APD? The short answer is: not very well.

[…]

The NASA questionnaire, on the other hand, bears a striking resemblance to the APD data, and the statistical analysis confirms that it’s a good predictor. In other words, it’s the only one of the seven calculations tested that, according to this study, accurately reflects how exhausted you are after a workout.

It’s called the NASA Task Load Index, or NASA-TLX, and was developed in the 1980s. It’s simply a set of six questions that ask you to rate the mental demand, physical demand, temporal demand (how rushed were you?), performance (how well did you do?), effort, and frustration of a task. You answer each of these questions on a scale of 1 to 100, then the six scores are averaged—and presto, you have a better measure of how hard your workout was than your watch or heart-rate monitor can provide.

New research from Brigham Young University suggests that where your sugar comes from matters just as much as how much you consume:

In the most extensive analysis of its kind, researchers from BYU and institutions in Germany examined data from over 500,000 people across multiple continents. Their discovery? Sugars from drinks like soda and even fruit juice were consistently linked to a higher risk of developing type 2 diabetes (T2D). Surprisingly, sugars from other sources did not show this same risk. In fact, some were even linked to a lower risk.

[…]

With each additional 12-oz serving of sugar-sweetened beverages (i.e., soft drinks, energy drinks, and sports drinks) per day, the risk for developing T2D increased by 25%. This strong relationship showed that the increased risk began from the very first daily serving with no minimum threshold below which intake appeared to be safe.

With each additional 8-oz serving of fruit juice per day (i.e., 100% fruit juice, nectars and juice drinks), the risk for developing T2D increased by 5%.

The above risks are relative not absolute. For example, if the average person’s baseline risk of developing T2D is about 10%, four sodas a day could raise that to roughly 20%, not 100%.

Comparatively, 20 g/day intakes of total sucrose (table sugar) and total sugar (the sum of all naturally occurring and added sugars in the diet) showed an inverse association with T2D, hinting at a surprising protective association.

[…]

Sugar-sweetened beverages and fruit juice supply isolated sugars, leading to a greater glycemic impact that would overwhelm and disrupt liver metabolism, thereby increasing liver fat and insulin resistance.

On the other hand, dietary sugars consumed in or added to nutrient-dense foods, such as whole fruits, dairy products, or whole grains, do not cause metabolic overload in the liver. These embedded sugars elicit slower blood glucose responses due to accompanying fiber, fats, proteins, and other beneficial nutrients.

The first scientist to draw the connection between exercise and lactic acid was Jöns Jacob Berzelius, Alex Hutchinson explains, the Swedish chemist who devised the modern system of chemical notation (H2O, etc.):

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 observed 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.

Athletes going lactic feel the burn and typically back off a bit:

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 a 2013 study 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 deregulation of the immune system with age eventually leads to chronic inflammation, or inflammaging, but blood sharing between young and old mice has shown rapid and robust pro-geronic and rejuvenative influences:

Interestingly, the procedure of small animal plasma exchange to dilute the circulating factors in plasma effectively reset the age-elevated systemic proteome and restored youthful healthy maintenance and repair of muscle, liver, and brain, without any added young blood, young plasma, or young factors.

For people, plasma dilution is known as plasmapheresis or therapeutic plasma exchange (TPE); it replaces a patient’s plasma with saline and purified albumin. The blood cells are returned to the patient so that while the cell profile does not change, the circulating blood proteins are diluted, including cytokines, autoreactive antibodies or toxins, and such pathogenic determinants of specific disorders.

Although its full therapeutic benefits are still being discovered, TPE is one of the treatments for autoimmune and neurological diseases such as myasthenia gravis, Alzheimer’s disease, and Guillain–Barre syndrome.

Moreover, TPE has the capacity to relieve the symptoms of long-haul COVID-19, including prevention of pneumonia, reduction of “brain fog,” and attenuation of the cytokine storm and hyper-inflammation.

This came up when eccentric life-extension fanatic Bryan Johnson (“Don’t die!”) shared the news — accompanied by a delightful photo — that he;s no longer injecting his son’s blood:

I am no longer injecting my son’s blood.

I’ve upgraded to something else: total plasma exchange.

Steps:
1. Take out all blood from body
2. Separate plasma from blood
3. Replace plasma with 5% albumin & IVIG

Here’s my bag of plasma. Who wants it?
???? pic.twitter.com/rUScTIDea6

— Bryan Johnson /dd (@bryan_johnson) January 28, 2025

Pilot studies of TPE involving mice and three human patients look promising:

The results demonstrate significant and lasting rejuvenation of both humoral and cellular blood compartments in people who underwent repeated plasmapheresis. The rejuvenative changes are not limited to a reduction of inflammaging but encompass diminished circulatory protein markers of neurodegeneration and cancer, as well as reduced senescence, lower DNA damage, and improved myeloid/lymphoid homeostasis. Mechanistically, these and previously reported positive effects of TPE become better understood through longitudinal comparative proteomics of the blood plasma, demonstrating a youthful recalibration of the canonical signaling pathways, broadly regulating tissue health, and interacting through the node of TPR-4. Lastly, a novel application of Levene’s test to profile the noise of the systemic proteome uncovered several proteins: new biomarkers that collectively quantify a person’s biological age, removing a need for predictions.

Sports scientists have been obsessed with the benefits of heat training, Alex Hutchinson notes:

The extra stress of heat triggers various adaptations that help you handle hot conditions, like more sweating. Some of these adaptations, like increased blood volume, may even give you a boost when competing in cooler conditions. As a result, many top athletes now incorporate elaborate heat protocols into their training.

Dominique Gagnon‘s research suggests that cold training has its own advantages:

Back in 2013, for example, he published data showing that cold-weather exercise relies on a different fuel mix than warmer conditions, burning more fat and less carbohydrate.

[…]

Human metabolism is only about 25 percent efficient — comparable to the internal combustion engine in your car — so three-quarters of the energy in your food is released as heat in the muscles. That means that the temperature inside your muscles can be high even when the rest of you is cool. The advantage of exercising in the cold, then, is that it prevents your muscle cells from overheating and enables them to keep burning more fat for aerobic energy, which relies on the mitochondria in your muscles. In the long run, that should boost mitochondria levels and train your body to become more efficient aerobically.

[…]

In Gagnon’s new study, 34 volunteers trained three times a week for seven weeks, doing interval workouts on an exercise bike. Before and after the training period, they had muscle biopsies, which involve removing a small chunk of muscle from the leg, in order to analyse how much mitochondria was present. Sure enough, the group that trained in 32-degree air [versus 77 degrees Fahrenheit] had a significantly greater increase in several different markers of mitochondrial content.

[…]

Stephen Cheung and his colleagues at Brock University in Canada showed that getting superficially cold, with no drop in core temperature, reduced time to exhaustion in a cycling test by about 30 percent. That involved sitting in a 32-degree room with a light breeze for half an hour before the subjects even started cycling. Staying in the room for longer, so that their core temperature actually dropped by a degree, reduced endurance by another 30 to 40 percent. This is not what Gagnon is aiming for.

The Guardian reviews Gary Taubes‘ Rethinking Diabetes: What Science Reveals About Diet, Insulin, and Successful Treatments

Gary Taubes is probably the most single-minded person I have ever met. In 2002, when he was a little-known science journalist and author of two books on scientific controversies, an article of his was published in the New York Times, headlined: What If It’s All Been a Big Fat Lie? In it, he argued that the low-fat dietary advice of the previous couple of decades wasn’t only incorrect, but actively dangerous and the reason for, as he put it, the “rampaging epidemic of obesity in America”. For Taubes, dietary fat wasn’t a problem at all. Instead, the real danger was carbohydrate, he asserted, sparking a backlash, and fuelling the ongoing conversation about what constitutes a “healthy diet”. He wasn’t the first to assert that carbs were bad (Robert Atkins got there before him), but perhaps because of his serious and scientific background — he has a physics degree from Harvard and studied aerospace engineering at Stanford — he has been a polarising figure, with as many ardent followers as detractors.

[…]

Before the discovery of insulin in the 1920s, diet was the only way to manage diabetes and although various options were tried by early practitioners, low-carb was, says Taubes, among the most popular (with medics, at least). Insulin was a gamechanger. Not only did it almost magically save the lives of children with type 1 diabetes, who would often arrive at hospital comatose and die swiftly afterwards, but it also meant that people with diabetes of both types could eat a more or less normal diet.

[…]

What Taubes would like to see is low-carb diets being offered alongside or instead of diabetes medications. “When insulin therapy started in the 1920s, they had no idea what the long-term side-effects were or what the long-term consequences of living with diabetes were [because most people with type 1 died],” he says. “Then doctors find out that it’s just easier to let patients eat whatever they want and give them drugs to cover them. Then it’s another five, 10 or 20 years before they start seeing the long-term complications, which they think of as long-term complications of the disease.” What he wishes scientists at the time had concluded was: “The reason we’re keeping them alive is insulin therapy. So what we’re seeing is the long-term complications of the disease as controlled by insulin therapy, and the insulin therapy might be causing the complications as much as the disease is.

“By the late 1930s, you have this tidal wave of diabetic complications: the heart disease, the atherosclerosis, the neuropathy, the kidney failure, the blindness, amputations. And nobody ties it back.” By then, the low-carb diet had fallen far from favour. “Nobody wants to eat a diet. So nobody’s being told: ‘Look, if I give you insulin, I’m going to keep you alive until you’re 30, especially if I give you a lot of insulin and you do eat your carbs. But if I tell you not to eat the carbs and we minimise the insulin use — which for type 2 could be no insulin — I might keep you alive as long as anyone else in your family.’”

In the book, which is laden with references, studies and dense historical detail, Taubes mentions case records from the 1700s in which patients on low-sugar diets beg for a medical solution, suggesting that the preference for medication over a highly prescriptive diet has been with us for a long time. “If you’re told, a pill or a diet, we all want the pill. But if you’re told a pill or a diet and the diet will keep you healthy and the pill will give you a chronic degenerative disorder where you’re still going to have these horrible complications, they are just going to be 20 to 30 years later… the pill is going to be easier, because it always is. But if you change the diet, it’s not a hypothetical change: you can put your diabetes into remission, you can stop taking these medications.”

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.

[…]

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.

[…]

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.

[…]

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.