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Why some mitochondria ramp up aging
Lately, I’ve noticed that I don’t quite have the same energy I used to…
I’m not always up for taking the long route on my daily walk and my workout stamina is almost non-existent. Late nights? I’d like to say I could hang with the best of them, but the truth is I do well to make it past 10 p.m. before nodding off.
I do my best to eat right, so where is this energy shortage come from?
The short answer is that it’s simply part of getting older. But why?
One of the most common answers scientists have to that question lies in our mitochondria — the energy organelles that power our cells. They generate ATP, the cellular equivalent of fuel so that our cells can perform their countless functions.
As we age, our mitochondria slow down and become impaired, and the number of mitochondria declines. This can especially hurt our muscle cells, which require more energy.
Researchers have been working to gain direct evidence that can support this idea of mitochondria being connected to the aging process. One team led by Columbia University researchers appears to have found that link — and it’s not exactly what they expected….
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Do mitochondria burn out or fade away?
Scientists tended to assume mitochondrial defects impair the conversion of food sources into usable energy, forcing cells to slow their metabolic rate to conserve energy.
With that assumption in mind, the Columbia-led research team analyzed metabolic activity and energy consumption in cells from patients with rare mitochondrial diseases. To their surprise, they found cells with impaired mitochondria actually kick into high gear and double their energy expenditure in a process known as hypermetabolism.
In other words, they ramp up their efforts for energy — and crash and burn.
When re-analyzing the data from hundreds of patients with different mitochondrial diseases, the researchers saw that hypermetabolim increases the energetic cost of living across the entire body.
And though it might help the short-term survival of the mitochondria, it dramatically increases the rate at which they age.
It does this by degrading the cells’ telomeres, the caps that protect the ends of chromosomes, as well as activating stress responses and inflammation in the cells. Combined, all these effects accelerate biological aging.
Principal investigator and Columbia professor Dr. Martin Picard says that although the findings were made in cells from patients with rare mitochondrial diseases, they may also have relevance for other conditions that are impacted by mitochondria. That could include neurological and inflammatory conditions, as well as Alzheimer’s, Lou Gehrig’s Disease and diabetes which are considered secondary mitochondrial diseases.
“In addition, hypermetabolism may be a key reason why most cells deteriorate as we get older,” Picard says.
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Sustaining energy
The hypermetabolic state could be why people with mitochondrial diseases or defects experience symptoms like fatigue and exercise intolerance.
“To make up for the extra energy use in your cells, your body ‘tells’ you not to overexert yourself, to conserve energy,” Picard says. “We likely see the same dynamic as people age and their vitality diminishes.”
But more movement — or exercise — may indeed be the answer…
“That may seem counterintuitive, since if you’re more active, you’re going to expend more energy and possibly make your symptoms worse,” Sturm says. “But exercise is known to increase the efficiency of an organism. An individual who runs, for example, uses less energy to sustain basic bodily processes than someone who is not physically active.”
As far as exercise goes, any type of exercise will help protect your mitochondria. However, high-intensity interval training has been shown to increase mitochondrial capacity, which stops aging at the cellular level.
Since it seems hypermetabolism plays a key role in driving the aging process, targeting this process may be a way to improve fatigue, improve people’s quality of life or even slow biological aging.
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Sources:
Overactive Cell Metabolism Linked to Biological Aging — Columbia University Irving Medical Center
OxPhos defects cause hypermetabolism and reduce lifespan in cells and in patients with mitochondrial diseases — Communications Biology
By Carolyn Gretton
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