Naturally Boosting AMPK with Exercise for Life Extension

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AMPK is said to serve as a “mitochondrial guardian.”

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Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.

How can we naturally boost the enzyme AMPK to slow aging without starving ourselves? AMPK is activated by a fuel shortage. If we don’t want to limit the amount of energy going in through our mouths, then we have to ramp up the amount of energy going out through our muscles. Put people on a bike and start taking muscle biopsies while they cycle, and you can detect a near tripling of AMPK activation within twenty minutes in both diabetics and nondiabetics. That makes sense. The muscles use up the ATP to contract, so AMP builds up and AMPK is activated. That may be one of the ways exercise leads to weight loss.

AMPK activation also leads to mitochondrial biogenesis, meaning the formation of extra mitochondria, the power plants within our cells where fat is burned and ATP is created. So, AMPK doesn’t just cause more fat to be shoveled into the furnace—it also causes more furnaces to be built. In this way, AMPK helps explain why endurance training eventually enables us to run faster and farther. So, might an AMPK activator be like the fabled exercise-in-a-pill? Indeed, AMPK activation can dramatically enhance performance. An AMPK-activator drug given to sedentary mice for a month boosted their running endurance by 44 percent. After one such drug was discovered at the famed Tour de France, AMPK activators were banned by the World Anti-Doping Agency.

So not just fasting in a pill, but an exercise mimetic too? People are often “unwilling to perform even a minimum of physical activity …” wrote a group of pharmacologists, “thus, indicating that drugs mimicking endurance exercise are highly desirable.” The “mass appeal” of such a pill may tempt “’big pharma’ to view physical inactivity as a market to be medicalized for profit.” But that vision pales in comparison to the universal market for an anti-aging remedy.

In his essay ‘‘On youth and old age,” the Greek philosopher Aristotle described death as the loss of inner heat. Indeed, the progressive loss of function of the estimated 10 million billion mitochondria spread throughout the body is considered a core tenet of the biology of aging. But mitochondrial dysfunction isn’t just a consequence of aging, but one of its causes. Dysfunctional mitochondria are thought to actively contribute to the aging process––an insight illustrated by a pioneering experiment published over 30 years ago.

If you inject mitochondria from a young animal into a human cell, nothing happens. The cell doesn’t appear to notice. Human skin cells average about 300 mitochondria each, and adding 10 to 15 extras from a young rat didn’t appear to have any effect. But add the same number of mitochondria from an old rat, and the human cells start to show signs of degeneration within just a few days. Even just having a few percent of those old mitochondria was enough to drive the human cells to an early grave. So, age-impaired mitochondria don’t just become less efficient, but may become actively harmful. So, if centenarian-equivalent rat mitochondria are so toxic, how do centenarian human cells survive? A group of Italian researchers took some centenarian skin biopsies to find out.

Skin samples taken from the forearms of young individuals were compared to those of elderly individuals. As expected, each mitochondrial mite from the older cells was comparatively defective—less efficient, leaking free radicals. But to the scientists’ surprise, the total amount of ATP the centenarian cells were pumping out was even greater than that of the younger cells. How is that possible? Because of a bulked up mitochondrial mass. It’s like if an older Mike Tyson took on a featherweight. Even if pound-for-pound, the whippersnapper’s biceps were more energy-generating, Mike’s sheer muscular mass might prevail. So how did the centenarian mitochondria get swole? AMPK.

Mitochondria can take up anywhere between 2 percent and 50 percent of the volume of a cell, and are in constant motion, merging together and splitting apart like the molten wax of a lava lamp. In times of starvation or stress, the fusing of individual mitochondria together into a large tubular network can be advantageous, in part by diluting the effects of damaged mitochondria by mixing their contents in with others. AMPK appears to accomplish this by tipping the lava lamp balance from fission to fusion by blocking one of the proteins necessary to break mitochondria back apart. This is thought to be one of the routes by which endurance exercise can rejuvenate mitochondrial function. Thanks to AMPK, working out may magnify your mitochondria as well as your muscles.

Our mitochondrial function does decline with age, in part through the impaired ability of AMPK to generate new mitochondria. But AMPK can build new cellular power plants, expand existing ones, and decommission old ones (so-called mitophagy). AMPK is said to serve as a “mitochondrial guardian,” and in that role may help guard against the ravages of age-related disease.

If an AMPK-activating drug really could help us reap the fat-burning and health-promoting benefits of fasting and exercise without the hunger and sweat, one could imagine how it would become one of the best-selling drugs on the planet. And it is. It’s called metformin, prescribed more than 90 million times a year in the U.S. alone. But should we all be taking it to prolong our lives? That’s what I’ll be covering next.

Please consider volunteering to help out on the site.

Motion graphics by Avo Media

Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.

How can we naturally boost the enzyme AMPK to slow aging without starving ourselves? AMPK is activated by a fuel shortage. If we don’t want to limit the amount of energy going in through our mouths, then we have to ramp up the amount of energy going out through our muscles. Put people on a bike and start taking muscle biopsies while they cycle, and you can detect a near tripling of AMPK activation within twenty minutes in both diabetics and nondiabetics. That makes sense. The muscles use up the ATP to contract, so AMP builds up and AMPK is activated. That may be one of the ways exercise leads to weight loss.

AMPK activation also leads to mitochondrial biogenesis, meaning the formation of extra mitochondria, the power plants within our cells where fat is burned and ATP is created. So, AMPK doesn’t just cause more fat to be shoveled into the furnace—it also causes more furnaces to be built. In this way, AMPK helps explain why endurance training eventually enables us to run faster and farther. So, might an AMPK activator be like the fabled exercise-in-a-pill? Indeed, AMPK activation can dramatically enhance performance. An AMPK-activator drug given to sedentary mice for a month boosted their running endurance by 44 percent. After one such drug was discovered at the famed Tour de France, AMPK activators were banned by the World Anti-Doping Agency.

So not just fasting in a pill, but an exercise mimetic too? People are often “unwilling to perform even a minimum of physical activity …” wrote a group of pharmacologists, “thus, indicating that drugs mimicking endurance exercise are highly desirable.” The “mass appeal” of such a pill may tempt “’big pharma’ to view physical inactivity as a market to be medicalized for profit.” But that vision pales in comparison to the universal market for an anti-aging remedy.

In his essay ‘‘On youth and old age,” the Greek philosopher Aristotle described death as the loss of inner heat. Indeed, the progressive loss of function of the estimated 10 million billion mitochondria spread throughout the body is considered a core tenet of the biology of aging. But mitochondrial dysfunction isn’t just a consequence of aging, but one of its causes. Dysfunctional mitochondria are thought to actively contribute to the aging process––an insight illustrated by a pioneering experiment published over 30 years ago.

If you inject mitochondria from a young animal into a human cell, nothing happens. The cell doesn’t appear to notice. Human skin cells average about 300 mitochondria each, and adding 10 to 15 extras from a young rat didn’t appear to have any effect. But add the same number of mitochondria from an old rat, and the human cells start to show signs of degeneration within just a few days. Even just having a few percent of those old mitochondria was enough to drive the human cells to an early grave. So, age-impaired mitochondria don’t just become less efficient, but may become actively harmful. So, if centenarian-equivalent rat mitochondria are so toxic, how do centenarian human cells survive? A group of Italian researchers took some centenarian skin biopsies to find out.

Skin samples taken from the forearms of young individuals were compared to those of elderly individuals. As expected, each mitochondrial mite from the older cells was comparatively defective—less efficient, leaking free radicals. But to the scientists’ surprise, the total amount of ATP the centenarian cells were pumping out was even greater than that of the younger cells. How is that possible? Because of a bulked up mitochondrial mass. It’s like if an older Mike Tyson took on a featherweight. Even if pound-for-pound, the whippersnapper’s biceps were more energy-generating, Mike’s sheer muscular mass might prevail. So how did the centenarian mitochondria get swole? AMPK.

Mitochondria can take up anywhere between 2 percent and 50 percent of the volume of a cell, and are in constant motion, merging together and splitting apart like the molten wax of a lava lamp. In times of starvation or stress, the fusing of individual mitochondria together into a large tubular network can be advantageous, in part by diluting the effects of damaged mitochondria by mixing their contents in with others. AMPK appears to accomplish this by tipping the lava lamp balance from fission to fusion by blocking one of the proteins necessary to break mitochondria back apart. This is thought to be one of the routes by which endurance exercise can rejuvenate mitochondrial function. Thanks to AMPK, working out may magnify your mitochondria as well as your muscles.

Our mitochondrial function does decline with age, in part through the impaired ability of AMPK to generate new mitochondria. But AMPK can build new cellular power plants, expand existing ones, and decommission old ones (so-called mitophagy). AMPK is said to serve as a “mitochondrial guardian,” and in that role may help guard against the ravages of age-related disease.

If an AMPK-activating drug really could help us reap the fat-burning and health-promoting benefits of fasting and exercise without the hunger and sweat, one could imagine how it would become one of the best-selling drugs on the planet. And it is. It’s called metformin, prescribed more than 90 million times a year in the U.S. alone. But should we all be taking it to prolong our lives? That’s what I’ll be covering next.

Please consider volunteering to help out on the site.

Motion graphics by Avo Media

Doctor's Note

This is the second video in a five-part series. If you missed the first one, see Naturally Boosting AMPK with Caloric Restriction for Life Extension. 

Stay tuned for:

AMPK is one of the anti-aging pathways I highlight in my longevity book, How Not to Age, available in print, e-book, and audio. (All proceeds I receive from the book are donated directly to charity.)

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