x
A Q&A with Mike Murphy, Ph.D.
We need energy to do the work of cells—our muscle cells, brain cells, kidneys cells—everything needs energy. The energy ultimately comes from the food that we eat: carbohydrates, fat, and protein. Inside the stomach and intestines, we break food down to small molecules, and pass them to cells around our bodies. Inside our cells, these molecules pass into parts of the cell called mitochondria. The role of mitochondria is to extract energy from those molecules so that cells can use it.
The mitochondria essentially burn the molecules by reacting them with oxygen. About 95 percent of the oxygen that we breathe goes to the mitochondria, and when you burn molecules with oxygen, the energy that’s released is trapped in a currency that cells can use—for example, to contract a muscle. This energy currency is called ATP (adenosine triphosphate).
“We need energy to do the work of cells—our muscle cells, brain cells, kidneys cells—everything needs energy.”
This is why mitochondria are essential for keeping cells alive. If you deprive the brain or heart of oxygen, like in a stroke or a heart attack, a major cause of damage is that oxygen is no longer going to mitochondria. When there’s a lack of oxygen in mitochondria, they stop working, and the cells die. (Another way to think of it: The poison cyanide kills by stopping the mitochondria from working.)
If you looked at a cell, you’d see a big blob in the nucleus, where nearly all of our DNA is. Around the sides, there are a thousand or so little mitochondria scattered around the cell; they look a bit like bacteria.
One to two billion years ago, mitochondria were foreign bacteria that slowly became integrated into animal cells as the cells ate the bacteria. So mitochondria have residual DNA from their bacteria origin. The number of genes in mitochondrial DNA is very small—only 37, whereas in the nucleus of the cell, there are closer to 20,000. But while the number of genes is very small, they are critical to the way mitochondria operate and make ATP. The mitochondria wouldn’t work—and we wouldn’t survive—without this residual DNA.
Mitochondria get damaged and are recycled by cells constantly; there are many natural repair methods in the body. If the mitochondrial DNA is damaged or if the mitochondria isn’t working properly for whatever reason, it goes through a recycling process inside the cell called autophagy: The mitochondria is eaten up and some pieces of it are reused.
How often this happens is an active area of research. People are also studying whether this process changes with age and whether it’s a factor in some diseases. One hypothesis is that neurodegenerative diseases like Parkinson’s may occur when our cells are not very good at clearing the mitochondrial damage that accumulates.
A few years ago, popular theory was that mitochondrial damage was one of the main causes of aging—that this damage accumulated, that it meant the mitochondria weren’t working properly, that the cell then died, and eventually the body died. Now, it seems to be much more complicated: For some reason, the ability to remove damaged mitochondria and replace them with good mitochondria declines as we get older, but we don’t yet know if that’s a cause or a consequence of aging.
The key environmental effects we’re always looking at in terms of mitochondria are diet and exercise.
One of the best ways to improve mitochondrial health is through dietary changes; obesity is one of the most damaging conditions for mitochondria. We essentially pass what we eat to mitochondria, so they can make ATP. Having too many nutrients—too much fat, too many carbohydrates or protein coming in—causes extensive damage to the cell and its mitochondria. (We can’t say at this stage if any particular nutrients or foods are more or less damaging to mitochondria.)
You might be familiar with the idea of dietary restriction to extend lifespan. Note that this is very distinct from malnutrition—total calories consumed are reduced but it’s crucial to take in the correct amount of nutrients and vitamins. The field of dietary restriction is well-established in animal models—in studies with worms, flies, mice, monkeys, and so on, it’s been shown that animals live longer and healthier under dietary restriction. While the mechanisms by which dietary restriction works to extend lifespan are not entirely clear, it’s highly likely that mitochondrial function plays a role.
The problem with dietary restriction in humans is that it can leave you permanently hungry and cold, cause a drop in libido, and require you to spend your entire life thinking about how much and what you’re going to eat. So maybe you could live longer by this method, but what’s the point?
One of the many benefits of exercise is that it helps turn over mitochondria, use up the food you eat, and keep mitochondria working as you use ATP for your basic energy needs. If you’re consuming too many calories and not getting any exercise, your mitochondria are akin to little couch potatoes: Your food is being funneled to your mitochondria, but you’re not using all of it to make ATP. So the mitochondria is getting huge inputs and not making many outputs.
How exactly exercise benefits mitochondria is not clear at this stage, but we have some theories. If you’re training for a marathon, your muscles get bigger; and inside those muscles, the mitochondria in your muscle cells also increase. It’s likely that the mitochondria are working more efficiently and preventing buildup of lipids and sugars inside your cells. Again, this is a hypothesis—we have a lot more to learn—but it’s plausible that many benefits of exercise reside inside the cell, by increasing the number of mitochondria and using food more efficiently.
Learn More: Click Here
