Every day, your body performs maintenance you never notice. Inside your cells, worn or damaged components are dismantled and their materials recycled. One part of this maintenance system is called mitophagy: the selective removal of damaged mitochondria.
The name may sound complicated, but the idea is straightforward. Even a power station needs maintenance—and your cells have their own maintenance crew.
What are mitochondria?
Mitochondria are structures inside most of your cells that produce much of the energy needed to function. Your muscles, heart and brain depend heavily on them.
Mitochondria can become damaged or work less efficiently. Mitophagy helps the cell remove those that are no longer functioning properly. This is one part of mitochondrial quality control; cells also repair, reshape and make new mitochondria.
How does mitophagy work?
In one well-studied pathway, the cell recognises a damaged mitochondrion and surrounds it with a membrane. This package is delivered to a lysosome, a cellular compartment containing enzymes that break down its contents. Some of the resulting materials can be reused.
You may already have heard of autophagy, the broader process of recycling cellular material. Mitophagy is a specialised form that targets mitochondria.
Researchers are interested in this process because mitochondrial maintenance can become disrupted with aging and disease. However, a promising cellular mechanism is not, by itself, proof that a treatment will extend human life.
Exercise: a practical place to start
Regular exercise is a sensible way to support mitochondrial health. Human studies have found that endurance training is associated with changes in proteins involved in mitophagy. Research comparing active and sedentary adults suggests these differences can occur in older people too.[1]
Strength exercise also appears relevant. A study using human muscle samples found evidence that a single resistance-training session could initiate mitophagy.[2]
For everyday life, this means combining activities such as walking, cycling or swimming with strength exercises appropriate to your ability, such as resistance bands, weights or chair rises. Begin at a manageable level and build gradually.
There is an important scientific qualification: many human studies measure markers associated with mitophagy, rather than observing the entire recycling process. We cannot yet prescribe an exact exercise session that produces a known amount of cellular recycling.
Does fasting help?
Fasting is often presented as a switch that turns on cellular cleaning. The evidence is more complicated, especially when discussing mitophagy specifically rather than autophagy in general.
Laboratory and animal research provides reasons to investigate fasting, but human findings remain limited and vary with the tissue and conditions studied. There is no established number of fasting hours that reliably activates mitophagy throughout the human body.
Nor is exercising on an empty stomach necessary to obtain an exercise response. One human endurance-exercise study found no activation of the measured mitophagy pathways during or soon after exercise, whether participants were fasted or fed.[3] This illustrates why simple claims about a universal “fasting switch” deserve caution.
Prolonged fasting is not a necessary recommendation for someone seeking healthier mitochondria. Older adults should be particularly careful about approaches that compromise adequate nourishment or muscle preservation.
Where does urolithin A fit in?
Urolithin A is a compound that certain gut bacteria can produce from plant substances found in foods such as pomegranates, walnuts and some berries. Production varies between people because their gut bacteria differ.[6]
It is also available as a supplement and has been studied for its effects on mitochondrial maintenance. In a four-month trial in middle-aged adults, supplementation increased some mitophagy-related proteins and improved certain measures of muscle performance, although the primary outcome of peak power output did not significantly improve.[4]
A separate trial in older adults found improvements in certain muscle-endurance tests. However, its primary outcomes—walking distance and maximal mitochondrial energy production—did not significantly improve compared with placebo.[5]
These findings are encouraging, but they do not establish that urolithin A reverses aging or extends human lifespan. Several influential trials also involved the supplement manufacturer, making independent replication particularly valuable.
Supporting healthy aging
Mitophagy helps explain part of the remarkable maintenance work happening inside us. It also offers researchers a useful target for studying age-related changes.
For now, regular movement and strength exercise are practical priorities. Urolithin A remains an interesting supplement with developing evidence, while fasting should not be treated as a guaranteed route to mitochondrial renewal.
The goal is a well-regulated maintenance system that supports everyday health and independence. Your cellular power stations need care, but they do not need you chasing a permanent “maximum recycling” setting.
This article is for general information. Before making substantial changes to your diet, fasting routine, supplements or exercise—particularly if you have a medical condition or take medication—discuss them with your healthcare practitioner.
Sources
- Regular Endurance Exercise Promotes Fission, Mitophagy, and Oxidative Phosphorylation in Human Skeletal Muscle Independently of Age (2019)
- A single bout of resistance exercise triggers mitophagy, potentially involving the ejection of mitochondria in human skeletal muscle (2024)
- Lack of Activation of Mitophagy during Endurance Exercise in Human (2017)
- Urolithin A improves muscle strength, exercise performance, and biomarkers of mitochondrial health in a randomized trial in middle-aged adults (2022)
- Effect of Urolithin A Supplementation on Muscle Endurance and Mitochondrial Health in Older Adults: A Randomized Clinical Trial (2022)
- Direct supplementation with Urolithin A overcomes limitations of dietary exposure and gut microbiome variability in healthy adults (2021)