Tag: aging

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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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In many ways (particularly around dessert time), having a rapid metabolism is a blessing. But is there a downside? No one really believes that we have a “set number of heartbeats,” and we die when we use them up. On the other hand, it seems reasonable to view aging as the consequence of a series of cellular events, and “metabolism” as basically a measure of how fast those (and other) cellular events are proceeding in your body. That would certainly fit with all the research about caloric restriction extending lifespan. But frankly, it would kind of suck to think that boosting your metabolism was going to rob you of a few of your twilight years.

A new study in the Journal of Clinical Endocrinology & Metabolism looks into this question; the study will be published in June, and unfortunately I don’t have access to the advance online version, so the only details I have come from this press release. The researchers looked at 652 healthy Pima Indian volunteers between 1982 and 2006, measuring their resting metabolic rate and/or 24-hour energy expenditure (using a metabolic chamber). During the study, 27 of the participants died, and higher metabolism was one of the risk factors:

“We found that higher endogenous metabolic rate, that is how much energy the body uses for normal body functions, is a risk factor for earlier mortality,” said Reiner Jumpertz, MD, of the National Institute of Diabetes and Digestive and Kidney Diseases in Phoenix, Ariz., and lead author of the study. “This increased metabolic rate may lead to earlier organ damage (in effect accelerated aging) possibly by accumulation of toxic substances produced with the increase in energy turnover.”

“It is important to note that these data do not apply to exercise-related energy expenditure,” added Jumpertz. “This activity clearly has beneficial effects on human health.”

So that last part is reassuring, though I’m not sure on what basis he makes the claim. (Isn’t it possible that exercise-related energy expenditure produces the same negative effects as “endogenous” energy expenditure, but the downsides are more than compensated for by other benefits provided by exercise?) And he only seems to be referring to energy burned during exercise. But what about changes in basal metabolism induced by regular exercise? I’m under the impression (though I’m just assuming here, and happy to be corrected) that regular exercise does boost your metabolism throughout the rest of the day. Is that a problem?

Anyway, nothing to get too worked up about here: it’s clear from epidemiological data that the net effect of exercise is to increase rather than decrease lifespan. Still, I’ll be curious to see the full study when it’s published, to get a fuller sense of the research in this area than the press release provides.

[As an aside, I’m now back in Toronto after a week of travelling from Sydney to San Francisco to Vancouver, so the blog should get back to full throttle after last week’s lull! Many thanks to all those who dropped by Forerunners and the Vancouver Marathon expo to say hello and pick up advance copies of the book — and sorry I ran out so quickly!]

UPDATE May 2: A friend sent me a pdf of the full paper (thanks, Joe!), so I now have a fuller sense of the argument. The authors are interpreting their results in terms of the “free radical theory of aging” (though they acknowledge that some recent experiments have cast doubt on this theory). In this theory, it’s clear that a chronic elevation of free radicals due to excess food consumption (i.e. a faster basal metabolism) is bad, while a transient spike in free radicals due to exercise (which in turn spurs the body to adapt by developing a more powerful antioxidant response) is good rather than bad. One other point: the average BMI of the volunteers was ~34, and many of the deaths were linked to alcohol. So overall, I’m not necessarily confident that the primary result (faster metabolism = earlier death) is really generalizable to, say, a group of committed runners.

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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While I’m clearing out my mailbag… I got a question from a 800-metre runner in his mid 30s asking about how quickly he should expect his (and his competitors’) times to decline. It’s an interesting question that can be approached in a number of different ways — age-group records, which obviously depend on outliers; population-level cross-sectional studies; individual longitudinal studies — and all give different answers.

I cover this in a fair amount of detail in my book, but a couple brief points: numerous studies over the past three decades have found that cross-sectional declines tend to be steeper than longitudinal declines. That makes sense: the cross-sectional data gets weaker and weaker as you get to higher ages because there are more injuries and fewer people interested. (The latter factor is interesting in its own right: there’s evidence, albeit in mice, that the “impulse to exercise” declines with age. So it’s not just that people get busy or bored with competition, they may also have less intrinsic drive to compete.) Anyway, the point is: if you remain healthy and continue training at the same relative intensity (big “ifs” in both cases), you should expect to be able to beat the “average” decline represented by data like age-graded tables.

Speaking of which, here’s some data. The WMA age-graded table expect that you don’t start slowing down at all until you hit 35. At that point, the decline until your 40 appears to be linear. For comparison, I’ve plotted the times put up by the inimitable Johnny “Twilight Zone” Gray:

Gray was obviously a one-of-a-kind performer in many respects. The question is: was he a freak because he was still capable of running 1:45 as a 39-year-old? Or was he a freak because he was still interesting and willing to train at the level required to run 1:45 when he was 39? How many other 1:42 guys could have done the same if they’d tried? We don’t really know the answer to these questions, but the general feeling among researchers that I’ve spoken with is that the fundamental physical decline is much less steep than we previously believed. It’s more about training and motivation (and, of course, injuries).

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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Scientists don’t know exactly why or how we get old, but they have a few theories. One of them is that mutations in mitochondrial DNA gradually accumulate until body systems stop working properly — a theory supported by the premature aging observed in mice genetically engineered to rapidly accumulate mutations in mitochondrial DNA. Yesterday, McMaster University researcher Mark Tarnopolsky‘s group published a paper in the Proceedings of the National Academy of Sciences in which these fast-aging mice ran on a treadmill — with extremely encouraging results:

[T]hose who had endurance exercise training three times a week looked as young as healthy mice while their sedentary siblings were balding, greying, physically inactive, socially isolated and less fertile. [press release here]

Sounds pretty good… and the changes weren’t just on the outside. In the exercising mice, their brains didn’t shrink, their muscles didn’t waste, their hearts didn’t weaken, they didn’t die prematurely, and so on and so on. Of course, mutations in mitochondrial DNA were still accumulating — but the basic cellular response to endurance training is that you increase the amount of mitochondria in your cells, so the researchers suspect that having lots of healthy mitochondria made the mice less susceptible to problems stemming from the mutations.

This isn’t the only theory about aging. Telomere length is another idea that has received a lot of attention recently, for example — but that too seems to respond dramatically to endurance exercise. Of course, conflicts of interest should be reported in studies like this: Tarnopolsky is a highly accomplished ultra-runner! 🙂