Strength training for older endurance athletes

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My new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Also check out my new book, THE EXPLORER'S GENE: Why We Seek Big Challenges, New Flavors, and the Blank Spots on the Map, published in March 2025.

- Alex Hutchinson (@sweatscience)

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This week’s Jockology column in the Globe and Mail looks in more detail at a study suggesting that masters cyclists get more benefit from strength training than younger athletes. (I blogged very briefly about the study back in June.)

Exercise physiologists call it the “principle of specificity”: Swimmers gotta swim, cyclists gotta cycle, runners gotta run. That’s why many endurance athletes believe that other forms of training, like lifting weights, simply waste time that could be devoted to doing more of their main sport.

Of course, as with any good rule, the most interesting discussions involve figuring out when it should be broken. It turns out that the principle of specificity may apply less rigidly to older athletes than it does to their younger counterparts, according to a new study from researchers in France. The difference: The steady loss of muscle as you age means that you get an extra boost from weight training – even in endurance sports like cycling. [READ THE REST OF THE ARTICLE.]

The article is accompanied by a nice graphic from Trish McAlaster suggesting three key lower-body strengthening exercises that might benefit aging endurance athletes:

Being overweight may not extend life after all

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My new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Also check out my new book, THE EXPLORER'S GENE: Why We Seek Big Challenges, New Flavors, and the Blank Spots on the Map, published in March 2025.

- Alex Hutchinson (@sweatscience)

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Is it good to be a little bit overweight as you get older? That’s the message from a series of large, reputable studies (including one that made lots of news two years ago). The theory is that having a few extra pounds is good as you get old and frail, so that you don’t waste away to nothing if you get sick or break a hip. And the data seems to back up this theory.

But wait a sec. A new study in the Journal of the American Geriatrics Society from researchers at Loma Linda University in California (abstract here, press release here) shows the opposite:

[M]en over 75 with a body mass index (BMI) greater than 22.3 had a 3.7-year shorter life expectancy, and women over 75 with a BMI greater than 27.4 had a 2.1-year shorter life expectancy.

Why the contradiction? Actually, there are some very good reasons. The authors start by explaining some of the potential flaws with the earlier studies that seemed to show that being a bit chubby helped you live longer. The key problem is that the earlier studies measured weight just once, at the beginning of the study, and then waited to see how quickly the subjects died. But people who were skinny at the beginning of the study might have been skinny because they were already sick, possibly without having being diagnosed yet. If you’re skinny because you’re partway through a dramatic weight loss than ends with your death, that’s not quite the same as being thin with a long-term stable weight and healthy lifestyle.

The new Loma Linda study is able to address this problem, along with a few others. It relies on two large studies of Seventh-Day Adventists in California, one in 1960 and the second in 1976. Weight was measured on both occasions, and mortality was monitored until 1988. By looking only at the people whose weight stayed the same (within 5 kg) between 1960 and 1976, you get to study the effects of having extra weight, rather than the effects of gaining or losing it for whatever reason (both of which could have significant effects, but are separate questions).

Another quirk of the study is that Seventh-Day Adventists are forbidden to smoke. So to further eliminate confounders (e.g. people who were thin because they were puffing on cancer sticks), the analysis was able to completely exclude any past or present smokers, plus anyone with any history of coronary heart disease, stroke or cancer at baseline, and still have a total of 6,030 people aged 25-82. The point here is that we’re looking just at the effects of extra weight, stripped away of as many confounders as possible.

And sure enough, higher BMI corresponded to higher risk of death for 75- to 99-year-olds: above 22.3 was bad news for men, and above 27.4 was bad news for women. Obviously this study can’t tell us why there’s a difference between men and women, but the researchers suggest that women may benefit from having a bit more fat because that’s where estrogen is produced after menopause; too little estrogen may leave them susceptible to everything from hip fracture to insulin sensitivity problems. Here’s how the “hazards ratio” (basically your odds of dying relative to the healthiest group) looks as a function of BMI:

So what does this mean? Well, we’re not going to rewrite the medical textbooks based on a few Seventh-Day Adventists in California. It’s just one study, etc. etc. But given the methodological differences between this study and the previous ones, it certainly seems reasonable to wonder whether the apparent paradox of overweight people living longer is simply an artifact of the confounders this study managed to eliminate. I’m not saying you should panic if you’re overweight — I’m just saying you shouldn’t panic if you’re not.

The philosophy of ignoring health journalism

THANK YOU FOR VISITING SWEATSCIENCE.COM!

My new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Also check out my new book, THE EXPLORER'S GENE: Why We Seek Big Challenges, New Flavors, and the Blank Spots on the Map, published in March 2025.

- Alex Hutchinson (@sweatscience)

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There’s an interesting opinion piece in the New York Times by Notre Dame philosopher Gary Gutting that starts out asking some questions that I find interesting, and then answers them in a way I find ridiculous. The problem statement:

Almost every day I read about a new medical study that says I would be healthier if, for example, I ate more fish, drank red rather than white wine, took enchinacea [sic], or began practicing yoga.   Do such studies represent a significant body of knowledge that I should pay attention to?

Good question, and particularly of interest given that this blog (and a large part of my professional journalistic output) is devoted to parsing and disseminating such studies. Gutting goes on to discuss the difference between observational studies and prospective trials — correlation and causation — and laments that the media chooses to cover so many observational findings. This is a problem, he suggests, because keeping up on the details of all these studies is so time-consuming, and the results are “subject to constant reevaluation as new results come in.” So what’s the solution?

Taking a broader view, it would seem preferable to keep healthy by a method that is simple, reliable and doesn’t require constant revision and fine-tuning.  We do, after all, have such a method available: simply follow the humdrum standard advice we’ve heard all our lives about eating sensibly, exercising regularly, and having recommended medical tests and exams. Doing this and foregoing the endless calibration of our behavior to the latest research results will be far less stressful, make it more likely that we’ll stick to the method, and allow more time for fulfilling pursuits.  From this point of view, the media’s constant updates on the latest observational studies are counterproductive.

Now, I’m certainly not going to argue against “eating sensibly, exercising regularly, and having recommended medical tests and exams.” That’s great advice. But where does he think that advice comes from? Does the great body of ancestral knowledge passed down from our caveman forebears include any guidance on when to start getting prostate exams, or what the pros and cons of regular mammography are? And what is eating “sensibly” — is that eating like people did 50 years ago? 100 ? 10,000? In Europe? Asia? Africa?

The “common sense” behaviours that Gutting suggests following (as opposed to following “the media’s constant updates on the latest observational studies”) aren’t some sort of innate knowledge that we’re all born with. Those behaviours are learned, and constantly evolving as society absorbs and assesses the studies he’s counselling us to ignore. What his argument really boils down to is a recommendation that we should defer to authority — let the experts decide what constitutes “sensible” living, and just do it. Don’t worry about what the studies say, because if they’re convincing enough, the results will eventually find their way into the canonical set of public health recommendations.

This is perfectly reasonable. I know plenty of people who aren’t interested in the gory details of how their bodies work: they just want to be told what to do, and they want the advice to be simple, easy to implement, and relatively unchanging. Fair enough. But there are also many people who are interested in peeking behind the curtains of the public-health-recommendation sausage factory and evaluating the evidence for themselves. If a new study suggests that previous recommendations about, say, salt recommendations are shakier (yes, that’s a pun) than previously thought, they want to know about it and evaluate its significance themselves.

Of course, there’s plenty of terrible health reporting out there. But even good health reporting is often complex and reports on studies than seem to contradict each other. It has to be that way, because health research is complex and often contradictory. We’re complicated animals in a complicated world. If you want a simple, reassuring message that promises to answer all your questions and solve all your problems, your best bet is probably late-night infomercials.

Anyway, back to Gutting. His final message is that it’s simply not worth the hassle of worrying about all the factors that may or may not improve health and prolong life:

We are all going to die sometime, from something.  Even if I find just the right blend of exercise, diet and herbs that saves me from a heart attack at 60, I may have merely ensured that I will die of cancer at 70.

And really, there’s not much I can argue with here. If dying at 60 and dying at 70 are entirely interchangeable to him, then he’s perfectly right not to waste his time worrying about health. But if you ascribe some value to an extra decade of life (or a greater probability thereof), then you might reach a different conclusion.

Platelet-rich plasma for tennis elbow

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My new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Also check out my new book, THE EXPLORER'S GENE: Why We Seek Big Challenges, New Flavors, and the Blank Spots on the Map, published in March 2025.

- Alex Hutchinson (@sweatscience)

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Platelet-rich plasma therapy was a super-hot topic a couple of years ago (see earlier blog posts about it), in part because of reports that top athletes like Tiger Woods were using it to speed their recovery from injuries. These days, the fuss has died down a bit. The novelty is gone, subsequent studies haven’t produced the “miracle” results promised by initial case reports, and maybe no one wants to emulate Tiger Woods anymore.

Anyway, studies of PRP continue to trickle in, but the picture isn’t necessarily getting much clearer. Two new studies have just been posted online at the American Journal of Sports Medicine, one of which is a randomized trial of PRP for tennis elbow by researchers in Greece. The design seems pretty good in theory: 28 patients were split into two groups; one group received an injection of PRP (their own blood, spun to produce plasma with elevated levels of healing-enhancing platelets), while the other group received an identical injection of their own unenriched blood. This should eliminate the problem of placebo effects (which are very big in invasive procedures that involve lots of needles), and test only whether the platelets themselves make any difference.

But there’s a problem:

This is a single-blind study. Patients were aware of the treatment because it was practically difficult to mask the process.

I don’t understand this. Maybe there’s something I’m missing — if you know why it would be “practically difficult” to mask the process, please let me know. It seems to me that all you have to do is put the blood-spinning machine in the room next door, and you’re in business with a double-blind study. But that’s not what they did — and to me, that’s an enormous problem, given how much publicity PRP has received over the past few years.

Anyway, the results: they measured subjective pain and perceived elbow function at various points over the next six months. There was only one case where the two groups showed statistically significant differences: pain was lower in the PRP group after six weeks, though the difference was no longer significant at the next measurement (3 months). On the other hand, if you ignore “statistical significance,” the trend was that the PRP patients did better in every measurement.

So how do you interpret these results? It’s pretty clear that the authors of the paper are big boosters of the technique:

[T]here is enough proof to support the superiority of PRP treatment over autologous blood, regarding pain, in the short term…

More studies on this topic could further enlighten aspects of this promising treatment…

In conclusion, we showed that PRP led to pain relief earlier than autologous whole blood, and we believe its application will be increasingly widened in the near future…

Really, I don’t think they showed any such thing. They found results that were statistically insignificant in five of their six outcomes, using two measurements that are largely subjective, in an experimental design that does nothing to eliminate placebo effect for one of the most heavily hyped sports medicine treatments of the past decade. To justify the cost and extra effort required for PRP therapy, they’re going to need more definitive results than that.

What it takes to live to 95

THANK YOU FOR VISITING SWEATSCIENCE.COM!

My new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Also check out my new book, THE EXPLORER'S GENE: Why We Seek Big Challenges, New Flavors, and the Blank Spots on the Map, published in March 2025.

- Alex Hutchinson (@sweatscience)

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I’m a big fan of studies (like this one from a few months ago) that paint exercise as a fountain of youth that will stave off aging. I’m less fond of studies like the one just published in the Journal of the American Geriatrics Society, from the Albert Einstein College of Medicine, that suggest that longevity is in your genes, and nothing you do makes much difference (abstract here, press release here). But what you can you do? Data is what is (or “are what they are,” if you prefer — Audrey!).

The study: researchers interviewed 477 people between the ages of 95 and 112 to find out about their lifestyles way back when they were 70 (which was considered loosely representative of their adult habits): weight, alcohol consumption, smoking, exercise, whether they ate a low-calorie, low-fat or low-salt diet, etc. This data was compared to similar data collected back in the 1970s from several thousand people born around the same time, representing the general population. The punchline:

Overall, people with exceptional longevity did not have healthier habits than the comparison group in terms of BMI, smoking, physical activity, or diet.

Doh! On the other hand, the same research group has found distinct genetic patterns among people who live to be 100, such as one that gives them abnormally high levels of “good” cholesterol. So does this mean our longevity is written in our DNA and we might as well not worry about silly things like exercise and nutrition?

Well, there was one statistically significant difference between the super-agers and the general population: obesity. Being overweight (BMI 25-30) didn’t seem to make a difference, but fewer of the old folks were obese (BMI over 30): 4.5% versus 12.1% in the men, and 9.6% versus 16.% in the women. Still that’s a relatively minor difference.

The more important thing to remember is that this is a study of extreme outliers. So, if the results hold up and are confirmed by other studies, it may tell us that all the broccoli and chin-ups in the world won’t make you live to 100. You need the genes to make it that far. But if you don’t have the genes, then you do need the lifestyle factors to make it as far as possible — after all, there’s no question that factors like exercise and not smoking are linked to longer lifespans. They may not get you to 100, but there’s still a big difference between, say, 65 and 85!