Isegoria

If you hope to live a long time, Alex Hutchinson (Endure) reminds us, your two best strategies are to be really healthy and really rich:

That’s the conventional wisdom and the statistics seem to back it up. But a surprising new study that links the longevity of Olympic athletes to their socioeconomic status offers a more nuanced picture of why elite athletes tend to outlive the rest of us. It’s not just about muscles and money — it’s also about the stress of competition, not only in sport, but in life.

Adriaan Kalwij, an economist at Utrecht University in the Netherlands, combed through the records of every Dutch athlete who competed in the Summer and Winter Games between 1896 and 1964, excluding more recent years because most of those athletes are still alive. Using their birth dates, death dates and stated occupation, he was able to explore how socioeconomic status (SES) influenced their longevity.

The results, published in PLOS One in December, confirmed that the 934 Olympians outlived their age-matched Dutch peers by a few years, as other studies of elite athletes have previously found. They also found that the influence of SES has steadily increased over the past century.

In the oldest cohort of athletes, born between 1852 and 1899, SES had no significant effect on longevity. In a sense, Kalwij says, this is what you might expect of Olympians: “excellent innate health could make them ‘immune’ to a SES-lifespan gradient.”

But in the next cohort of athletes, born between 1900 and 1919, a gradient emerges. Those classed as low SES, such as unskilled labourers, lived on average five years less than medium (teachers, office workers) and high (lawyers, doctors) SES athletes.

And in the most recent cohort, born between 1920 and 1947, an even wider gap emerges: High SES athletes lived five years longer than medium SES athletes, who in turn lived six years longer than low SES athletes — a stunning difference of 11 years between the top and bottom group, despite their healthy youth.

What’s most surprising about this trend is that it’s going the wrong way. You’d expect that the strengthening of social programs such as universal health care and state pensions over the past half-century would have reduced the health penalty incurred by poverty. Instead, Kalwij’s results join a large body of data across numerous countries, including Canada, suggesting that the influence of social class on lifespan has been growing since the 1950s.

While there are numerous factors that could contribute to an SES-health gradient, including access to health care and behaviours such as smoking and drinking, Kalwij believes that psychological stress may play a role.

I think we need to keep in mind that socio-economic status changed dramatically over the 20th Century, from inherited wealth and titles to inherited traits.

Running, Alex Hutchinson notes, is surprisingly complicated:

The physiologist and coach Jack Daniels once filmed a bunch of runners in stride, then showed the footage to coaches and biomechanists to see if they could eyeball who was the most efficient. “They couldn’t tell,” Daniels later recalled. “No way at all.” Famously awkward-looking runners like Paula Radcliffe and Alberto Salazar sometimes turn out to be extraordinarily efficient. Smooth-striding beauties sometimes finish at the back of the pack.

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One solution to this problem is to slow it all down. Film a runner and watch the footage in slow motion. Or better yet, attach a bunch of markers to key joints, feed the data into a computer, and create a three-dimensional model of the runner’s stride, so that you can analyze every joint angle and acceleration at your leisure. That’s what biomechanics researchers have been doing for years now, trying to link certain gait characteristics — a knee that rotates inward more than usual, say — with particular injuries like patellofemoral pain or IT band syndrome. They’ve had hints of success, but overall the results have been somewhat muddled and hard to interpret.

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They ran the data from 3D gait analysis of a bunch of runners, some injured and some healthy, through a form of artificial intelligence called unsupervised machine learning, to see if it could group the runners into categories based on their strides, and whether those categories would reflect the types of injuries the runners were subject to. The answers — yes to the first question, no to the second — are both worth thinking about.

A 2010 study from the University of Oregon found that 10 days of training in 104 degrees Fahrenheit boosted cyclists’ VO2max by 5 percent, Alex Hutchinson notes, even when the subjects were later tested in cool temperatures, and a new study out of Swansea University supports this finding:

The study involved 22 cyclists (all male, alas), all of whom were serious amateur cyclists training an average of 14 hours a week and competing regularly. The adaptation protocol was 10 consecutive days of cycling in the lab for 60 minutes at an intensity equal to 50 percent of their VO2max, with half of them in the heat group at a room temperature of 100.4 F (38 degrees Celsius) and the other half in a control group at 68 F (20 C). They also continued with their normal training outside the lab, subtracting their lab rides to maintain roughly the same training volume as usual. The outcome measure on the test days was VO2max, a marker of aerobic fitness that has a reasonably good correlation with race performance, tested at 68 F (20 C).

If you looked at the data right after the heat adaptation period, or even a couple of days later, you’d conclude that it makes you worse. The VO2max readings were lower. But three days after the heat adaptation, VO2max readings started to climb, and four days afterwards, they peaked at 4.9 percent higher than baseline, strikingly similar to the 2010 Oregon study. The control group, meanwhile, hardly saw any change.

Rapamycin is an immunosuppressant for transplant patients, but it’s also been found to increase lifespan in lab animals. Dr. Alan Green, who prescribes rapamycin for anti-aging purposes, recommends Blagosklonny’s paper, Disease or not, aging is easily treatable:

Is aging a disease? It does not matter because aging is already treated using a combination of several clinically-available drugs, including rapamycin. Whether aging is a disease depends on arbitrary definitions of both disease and aging. For treatment purposes, aging is a deadly disease (or more generally, pre-disease), despite being a normal continuation of normal organismal growth. It must and, importantly, can be successfully treated, thereby delaying classic age-related diseases such as cancer, cardiovascular and metabolic diseases, and neurodegeneration.

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As the simplest example, calorie restriction (CR) slows aging in diverse organisms, including primates [43-50]. Similarly, intermittent fasting (IF) and ketogenic diet (severe carbohydrate restriction) extend life span in mammals [48, 51-54]. CR (as well as carbohydrate restriction and IF fasting) improves health in humans [45, 48, 53, 55-62]. However, CR is unpleasant to most humans and its life-extending capacity is limited. Nutrients activate the mTOR (molecular Target of Rapamycin) nutrient-sensing pathway [63-65] and, as we will discuss mTOR drives aging, inhabitable by rapamycin. Rapamycin-based anti-aging therapies have been recently implemented by Dr. Alan Green (https://rapamycintherapy.com).

There’s a bit of circularity there.

Lifting to failure is generally better, but not always:

Amid the confusing torrent of advice about the best ways to build strength, I’ve taken comfort from a series of reassuringly simple studies from McMaster University over the past decade. Researcher Stuart Phillips and his colleagues have repeatedly demonstrated that if you do a series of lifts to failure — that is, until you can’t do another rep — then it doesn’t much matter how heavy the weight is or how many reps you do. As long as you’re maxing out, you’ll gain similar amounts of strength with light or heavy weights.

But there’s an interesting caveat to this advice, according to a new study from a team at East Tennessee State University led by Kevin Carroll, published in Sports: just because you can lift to failure doesn’t mean you always should.

Researchers have previously pointed out that it takes longer to recover from a strength training session when you go to failure than when you stop a few reps short, with negative neuromuscular effects lasting 24 to 48 hours. You also recover more quickly even if you do the exact same number of reps but take a little extra rest halfway so that you don’t quite hit failure. On the surface, this is a trivially obvious point: of course it takes longer to recover if you work harder! The question, though, is whether there’s something particularly damaging or exhausting about going all the way to failure that outweighs the positive training effect you get from working harder.

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So, in summary, two groups doing almost the same training, except one group was hitting failure on the last set of each exercise in every workout. The initial results from this study were published last year, showing that the relative intensity group had greater improvements in maximum strength and vertical jump. The new paper adds a bunch of information based on muscle biopsies and ultrasound, showing a greater increase for the relative intensity group in overall muscle size, the size of individual muscle fibers, and the presence of several key molecular signals of muscle growth.

Before we conclude that failure is bad, there’s one other detail of the training program that’s worth mentioning. While the failure group was hammering away three times a week, the relative intensity group was doing two harder (though not to failure) workouts and one easier workout each week. For example, a max strength workout of three sets of five reps might start at 85 percent for the two hard workouts, but then drop to 70 percent for the easier one.

This seems like a whole different variable thrown into the mix, and it reminds me of a study from Marcas Bamman’s group at the University of Alabama at Birmingham a couple of years ago. In a big study of older adults, he found that doing two harder workouts and one easier workout each week produced better strength gains that just two hard workouts or just three hard workouts a week. He suggested that lingering inflammation in the muscles made the subjects unable to fully benefit from three hard workouts a week. Instead, doing a third easier workout added some fitness gains compared to just two weekly workouts, but still allowed the muscles to recover.

So to me, the message from the new study isn’t necessarily that lifting to failure is bad. It’s that lifting to failure all the time might be counterproductive (and especially so as you get older, Bamman’s results suggest). The point Phillips has been trying to make is that, for the vast majority of us, all the variables that make your head spin — sets, reps, one-rep max percentages, and so on — are utterly minor details compared to the main goal of simply doing the work, and sometimes pushing pretty hard.

You have your parents’ tendons:

A study from Ritsumeikan University, home to one of the top collegiate running programs in Japan, looked at injury risk in 24 elite long-distance runners. The researchers weren’t concerned with mileage levels, shoe type, stretching routines, or any of the usual factors we associate with running injuries. Instead, they were focused on spit.

Over the past decade or so, a series of studies have suggested that certain gene variants can affect the structure of your collagen fibrils, the basic building blocks of tendons and ligaments. Some versions of these genes make you less likely to develop problems like Achilles tendinopathy; others make you more likely. Researchers have found, for example, that rugby players who make it to the elite level are more likely to have the tendon-protective gene variants, presumably because those who don’t are more likely to have their careers derailed by injury.

In the new Japanese study, the athletes were asked about their history of tendon and ligaments inflammations and injuries during their university career, then gave a spit sample for DNA analysis. The injury data was compared to five specific variants in four different genes that have previously been associated with tendon and ligament structure. For three of the five variants, those with the “bad” version were indeed significantly more likely to have suffered tendon and ligament injuries. (The fourth variant didn’t have any predictive value in this group, and the fifth didn’t yield any information because all the runners in the study had the same version of the gene.)

Given previous research, these results aren’t particular surprising. The question is what you do with this information. There are companies that offer personal genetic testing that includes some of these gene variants (COL5A1 was the best predictor in this study), so you can find out your status and…do what, exactly?

In a review of the field a few years ago, some of the leading researchers suggested  that, rather than getting a DNA test, you should simply be aware of whether you have a personal or family history of tendon and ligament injuries. Either way, it’s worth thinking about what you would change in your training if you suddenly discovered that your tendons were, say, 10 or 20 percent more likely to get inflamed compared to the average person. If you think you would start doing more stretching or strengthening or icing or “listening to your body” or whatever, then my question is simple: why aren’t you doing that already?

Do ice baths suppress muscle gains?

Fuchs and his colleagues had 12 volunteers do a strength-training session, then hop into an ice tub—or actually, half an ice tub. One leg was submerged in cold water at 46 degrees Fahrenheit (8 Celsius), while the other leg was submersed in tepid water at 86 degrees Fahrenheit (30 Celsius), for 20 minutes. Then they chugged a recovery shake with 45 grams of carbohydrate and 20 grams of protein, the latter of which contained a tracer that allowed the researchers to determine how much of the protein was incorporated into new muscle. Over the following two weeks, the researchers took frequent blood samples and muscle biopsies to track their progress.

Sure enough, the rate of muscle protein synthesis was significantly lower in the cooled leg than in the leg that got the lukewarm bath, with a difference over the course of two weeks of about 13 percent. Now, lab measures like muscle protein synthesis are still not the same as measuring actual differences in strength over a longer period of time. It’s awfully suggestive, though, and bolsters the case that ice baths—and, presumably, other recovery enhancers—may come with a hidden cost to fitness gains.

Muscle soreness is in you head — at least partly:

The usual explanation of delayed-onset muscle soreness (DOMS) is something like this: when you do exercise that’s unfamiliar or harder than usual, you inflict microscopic tears in your muscle fibers. Over the next 24 to 48 hours, a cycle of inflammation and repair leads to soreness that can persist for several days. But it has long been clear that this explanation doesn’t tell the whole story. For example, if you exercise your right leg only, your left leg will be less likely to get sore after future workouts, which suggests that the perception of soreness isn’t just about what’s happening in your muscle fibers.

In this spirit, an ACSM presentation from a team led by Einat Kodesh of the University of Haifa in Israel explores the potential role of mental traits in post-exercise soreness. They had 32 volunteers complete a series of psychological questionnaires and pain tests, then perform an exercise designed to induce DOMS. A day later, another questionnaire found that 17 of the subjects had developed DOMS, while 15 hadn’t.

Sure enough, there were some notable psychological differences between those who did and didn’t get sore. The DOMS sufferers had reported higher levels of anxiety, depression and stress before any exercise took place. The higher a subject’s anxiety, the more intense their subsequent muscle soreness was likely to be. Less surprisingly, the pre-exercise pain tests, which basically involved poking the subjects with a blunt needle to see how much pressure it took to make them hurt, also successfully predicted who was likely to develop DOMS.

The message here isn’t that pain and soreness are all in your head, or that admitting you feel sore is a sign of weakness. But it is a reminder that recovery is a murkier and less objective concept that we like to think. When we try to understand athletes’ obsession with things like ice baths, if we focus only on what’s happening in the muscle fibers, then we’re not necessarily seeing the whole picture.

A recent study put 20 men through an eight-week training program involving single-leg presses and extensions, with the catch that they did a different workout routine with each leg:

With one leg, they did a plain-vanilla progressive training program involving four sets of each exercise with a two-minute rest, with the load chosen to reach failure between 9 and 12 repetitions. With the other leg, they did a variable routine that systematically switched up some of the parameters. Some workouts had a lighter load enabling 25 to 30 repetitions before failure; some involved six sets of each exercise rather than four; some involved eccentric contractions only; and some had four minutes of rest between sets rather than two.

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So the main result of the study is that following a complicated variable weight-training routine rather than a simple unvarying one doesn’t seem to make any significant difference to how much muscle you accrue.

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But there’s a further analysis that the single-leg design enables: you can look at the variation in results from two legs in the same person following different training plans, and see how that compares to the variation between two legs in different people following the same training plan. That analysis is pretty eyebrow-raising: there’s 40 times more variability between people than there is between training plans. The people who gain lots of muscle do so regardless of the exact workout routine they follow; and it’s the same for the people who don’t.