cellular vigor that the diabetes drug metformin, which
stimulates AMPK, is now being studied for its potential as a
geroprotective, or anti-aging, agent. (Preliminary research
suggests it may improve symptoms in early Alzheimer’s
disease and help reduce one’s risk for developing it.) But
you don’t need drugs and their potential side effects to
activate AMPK, because short bursts of intense exercise do
it as effectively.
One of the most important ways that AMPK enhances
your metabolism is by stimulating the creation of more
mitochondria, a process called mitochondrial biogenesis.
Having more mitochondria is generally considered a good
thing, and we know this because chronic disuse of muscle,
sedentary behavior, and aging each independently result in
a decline in mitochondrial content and function.
By creating new mitochondria in our muscle, we
improve fitness and metabolic health—including sensitivity
to insulin. This is why stimulating AMPK with anaerobic
exercise (like weight training and sprinting) is one of the
best known means of reversing insulin resistance, along
with dietary change.* But AMPK doesn’t just spur this
dramatic increase in mitochondria in our muscle tissue. It
also does this in our fat cells, a process called browning.
Once believed to be present only in newborns, brown fat is
mitochondria-rich fat tissue whose main purpose is to burn
calories to warm us up when we get a little chilly (a process
called thermogenesis).
Mitochondrial biogenesis, spurred by exercise, was also
shown to occur in brain cells in animal research.^8 This has
obvious implications, not only with regard to fighting