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Posts Tagged ‘aging’

Does a rapid metabolism make you die earlier?

May 1st, 2011

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.

Athletes have superior street-crossing abilities

March 21st, 2011

How’s this for a compelling reason to take up sports, from the conclusions of a newly published University of Illinois study:

Compared to non-athletes, collegiate Division I athletes showed higher street crossing success rates, as reflected by fewer collisions with moving vehicles.

It’s actually an interesting study, though it’s hard not to snicker while reading it. Researchers assembled 18 D1 athletes from a variety of sports (baseball, XC, gymnastics, soccer, swimming, tennis, track, wrestling) and 18 non-athlete controls matched for age, gender, height, weight, GPA and video-game experience, then had them all try to successfully cross a busy street in a 3-D virtual environment, while walking on a manual self-paced treadmill. The results: athletes made it to the other side without getting splatted 72.05% of the time, while non-athletes only made it 55.04% of the time.

The purpose of the study was to find out whether sports training improves multitasking ability:

An ability to efficiently process information is said to improve multitasking performance. That is, if information passes through the bottleneck efficiently and quickly, more information can be processed in a shorter time frame and performance can be maximized.

The athletes also outperformed the non-athletes in a simple test of reaction time — that difference alone is enough to account for the difference in street-crossing success. Of course, there’s a glaring cause-and-effect question here, which the researchers acknowledge:

We speculate that athletes are faster multitaskers than non-athletes, but it is also possible that successful virtual reality street crossers with fast processing speed are more likely to excel at sports.

It’s by no means obvious to me which direction the arrow of causality runs here. I suspect it’s a bit of both. Interestingly, these researchers are also part of the group that has been publishing some very encouraging findings about the effects of aerobic exercise on the brain. Just last month, they published a Proceedings of the National Academy of Sciences paper showing that aerobic exercise increases the size of the hippocampus by 2% in older people, reversing the effects of 1-2 years of age-related decline. In this case, cause and effect were clear.

Bottom line: sports skills may help you cross the street successfully, but if you want to remember how to get home again, make sure you’re doing some aerobic exercise.

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How much will I slow down in my late 30s?

February 26th, 2011

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).

Running halts mitochondrial aging (and hair loss!) in mice

February 23rd, 2011

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! 🙂

Average age of elite male and female marathoners

October 18th, 2010
Comments Off on Average age of elite male and female marathoners

One of the stats that aroused interest at the 2008 Olympics was the age of the two marathon champs: Sammy Wanjiru was a young lion of 21, while Constantina Tomescu-Dita, at 38, was more of a cougar. Philip Hersh wrote an interesting article a few weeks ago in the Chicago Tribune about why top marathoners are getting younger — on the men’s side, at least. Is it really a trend? And if so, does it apply to both men and women?

Researchers at Marquette University tackled that question in a paper available online ahead of print in Medicine & Science in Sports & Exercise. They analyzed the ages of the top five men and women from the last decade or so of the World Marathon Majors — Chicago, London, New York, Berlin and Boston — plus the Olympics and World Championships. They found:

  • The women were 29.8 on average, while the men were 28.9 — a difference, but almost certainly not a physiological difference. (All of the difference came from Chicago and London, which had some unusually old female winners and young male winners.)
  • The difference didn’t change over the years, which puts another nail in the coffin of the now-discarded theory that women would one day out perform men over long distances because of greater ability to burn fat as fuel. On the contrary, it suggests that women’s marathoning is now a “mature” sport, since they’re no longer closing the gap to men’s performances.
  • The difference between men and women was smallest for first place and largest for fifth place, suggesting that there’s less depth in elite women’s marathoning ranks — something that’s fairly obvious to see.

So that’s the scoop. Nothing too earth-shattering here, but a reminder that one pair of unusual events (an old winner in the women’s race and a young winner in the men’s race) does not a trend make!

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Sarcopenia redux: running preserves “motor units”

September 9th, 2010

I posted a few thoughts last week about an article on sarcopenia — the gradual loss of muscle with age — and new attempts to find drugs that will slow it down. I’d be remiss if I didn’t point out some of the research on the obvious drug-free ways to avoid withering away to nothingness. For instance, I just noticed an article in the current issue of Medicine & Science in Sports & Exercise that compares the number of “motor units” in the muscles of masters runners (average age 65) with age-matched controls, and with a younger group (average age 25). The news is good.

First off, a motor unit is “a single alpha-motor neuron and all of the corresponding muscle fibers it innervates.” Losing motor units is one of the several mechanisms that combine to produce the muscle loss grouped as sarcopenia. In this case, it’s not the muscle fibres themselves that die; rather, it’s the motor neurons that control them. When you’re young, the orphaned neurons often sprout new axons that connect them to other motor neurons — so the number of motor units decreases, but the amount of muscle you can use stays the same. This can hide the problem until your 60s or 70s, at which point you’re no longer able to reinnervate orphaned fibres as well, and motor unit loss becomes a serious issue.

Anyway, the study itself was quite simple. Testing the tibialis anterior (shin) muscle, they found that the masters runners had 140 motor units on average, compared with 150 for the young group but just 91 for the old non-runner group. So there it is: consistent training preserves muscle — not the muscle fibres, in this case, but the motor neurons that control them. As the researchers put it:

The significance of the (…) findings centers on providing an improved understanding of the neuromuscular system through ‘‘elite aging’’ and provides support into the favorable value of long-term physical activity and exercise for protecting neural function.

Sarcopenia: muscle loss is the new bone loss?

August 31st, 2010

For an article I’m working on, I’ve been digging through the literature on sarcopenia, the age-related loss of muscle mass that most of us face starting in our 30s. I’ve found several conflicting estimates of how much muscle you can expect to lose, with a high end of 1-2% per year starting in your fourth decade (from this paper). That’s a lot more aggressive than I’d expected. I get the sense that it’s one of those problems whose implications we’re just now beginning to grasp — so I was interested to see this article by Andrew Pollack in the New York Times, which offers a good introduction to the topic:

Bears emerge from months of hibernation with their muscles largely intact. Not so for people, who, if bedridden that long, would lose so much muscle they would have trouble standing.

(Nice lede!)

Why muscles wither with age is captivating a growing number of scientists, drug and food companies, let alone aging baby boomers who, despite having spent years sweating in the gym, are confronting the body’s natural loss of muscle tone over time.

Comparisons between age groups underline the muscle disparity: An 80-year-old might have 30 percent less muscle mass than a 20-year-old. And strength declines even more than mass…

Much of the article focuses on attempts to agree on a clinical definition of the condition — which would then make it possible for drugmakers to win approval from regulators for drugs to treat it. But the key point for me is:

Researchers involved in the effort say doctors and patients need to be more aware that muscle deterioration is a major reason the elderly lose mobility and cannot live independently.

In other words, I need to start doing my push-ups again. Soon.

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Exercise vs. calorie restriction for brain aging

August 8th, 2010

One of the clearest signs that you’re getting older, microscopically speaking, is that your synapses start to degenerate. This means that signals from your brain have a harder time getting through to your muscles (for neuromuscular synapses) and to other parts of the brain (for brain synapses). Harvard researchers decided to investigate how exercise and calorie restriction — “among the most effective anti-aging treatments known” — affect the age-related changes in mouse neuromuscular synapses (PNAS abstract here, press release here). The results:

“With calorie restriction, we saw reversal of all aspects of the synapse disassembly. With exercise, we saw a reversal of most, but not all,” [lead researcher Joshua] Sanes says.

Score one for calorie restriction? Not so fast…

Because of the study’s structure — mice were on calorie-restricted diets for their whole lives, while those that exercised did so for just a month late in life — Sanes cautions against drawing conclusions about the effectiveness of exercise versus calorie restriction. He notes that longer periods of exercise might have more profound effects, a possibility he and [Jeff] Lichtman are now testing.

That makes me hope that, with longer and more consistent exercise, we might one day discover that all the benefits of calorie restriction are in fact available from consistent and vigorous exercise. (That being said, a month in a mouse’s life does correspond to a considerably longer period in human terms. The “old” mice were about two years old.)

On a somewhat related note, another just-published study found a correlation between how much blood your heart can pump and how quickly your brain ages. The study didn’t include anyone with heart disease, so it applies to people with normally functioning hearts: the more blood you can pump, the more blood gets to your brain, and the less the brain shrinks. The study can only measure correlation, not causation — but it sounds like more confirmation that aerobic exercise is the best “brain training” around.

How calorie restriction extends lifespan

July 21st, 2010

British researchers are presenting some new research on how calorie restriction works at a conference on aging research this week. In a mouse experiment, they found that it reduces cell senescence (the point at which a cell can no longer replicate) and helps protect telomeres (which exercise does too, researchers have recently found). Interestingly, the effects seems to be significant even if if it’s only started later in life and maintained for a relatively short period of time.

As I blogged about recently, I’m a little ambivalent about this whole calorie restriction thing. I just can’t see a happy ending — if it works, you feel guilty about eating for the rest of your life, and if it doesn’t, you die! Ultimately, I respect that we want to know how the body works, and this line of research is part of that. But I was happy to see some of this ambivalence reflected in the quotes from the press release describing the research:

Professor Thomas von Zglinicki, who oversaw the research, said: “It’s particularly exciting that our experiments found this effect on age-related senescent cells and loss of telomeres, even when food restriction was applied to animals in later life. We don’t yet know if food restriction delays ageing in humans, and maybe we wouldn’t want it. But at least we now know that interventions can work if started later.

And a recognition that extra years aren’t the only thing that counts:

Prof Douglas Kell, BBSRC Chief Executive and keynote speaker at the BSRA Conference, said: “As lifespan continues to extend in the developed world we face the challenge of increasing our ‘healthspan‘, that is the years of our lives when we can expect to be healthy and free from serious or chronic illness.

Caloric restriction extends your life, but may make you stupider

May 23rd, 2010

Okay, that’s not really a fair headline or a good summary of the research I’m describing (which is a neat study by researchers at Princeton, explained in an excellent and detailed press release). But I have to admit, I’m not always perfectly neutral — like everyone, I prefer to see some results more than others. And research into caloric restriction is a good example: there’s been plenty of evidence over the past few years of the age-defying benefits of starving yourself:

To date, caloric restriction has been observed to extend lifespan in every organism tested, including worms, mice and monkeys, [Princeton prof Coleen] Murphy said. While the reasons for this are still under investigation, scientists generally believe that the benefits of caloric restriction go well beyond preventing diseases associated with obesity, such as heart disease and diabetes, Murphy added. It appears that limiting food intake actually slows the aging process.

In general, I’m used to leafing through studies and press releases that give me a nice pat on the back. Aerobic exercise is good? Super, I do tons of it! Eating lots of fruits and vegetables is good? Fantastic, I do pretty well on that front. But caloric restriction? That’s the antithesis of everything I stand for, which is doing ridiculous amounts of exercise and consequently being able to eat more or less until I get bored with no ill effects — or at least, no ill effects that I knew of until the emergence of this idea that eating less slows down aging.

So you should read the press release for yourself, and judge its merits in an unbiased manner… but here’s what I took from it:

Young worms whose calories were restricted had normal short-term memories, but their long-term memories were severely impaired; the memories faded within 24 hours, as opposed to 40 hours in normal worms.

(40 hours in worm time corresponds to about 15 people years.)

Now, the study has a lot more to say. While caloric restriction impaired long-term memory, the (impaired) memory abilities didn’t decline as much with old age as they normally do. The study also investigates how insulin-signalling pathways affect longevity and cognitive function (this appears to operate independently of the calorie-restriction effects). So there’s a lot of on-the-one-hand-this, on-the-other-hand-that going on. But it’s the first sign I’ve seen that caloric restriction, even if it extends life, may have some significant downsides:

“The assumption in the field of longevity research has been that organisms able to live longer will function longer as well,” said [Murphy]. “It seems we need to revisit that.”

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