Mitochondria: The Powerhouse of Longevity

By Shannon Kasun, Neuroscience Specialist

As the years since secondary school pass, much of the knowledge we learned as middle and high schoolers fades—buried beneath newer, more relevant information and lost to time.

However, one fact seems to stick with us: mitochondria are the “powerhouse of the cell.”

Sound familiar? Bravo—your high school biology teacher would be proud!

Doesn’t ring a bell? Don’t worry—we are about to dive into the fascinating science of bioenergetics, focusing on the crucial role of mitochondria in aging.

The word mitochondria comes from the Greek mitos, meaning “thread,” and chondros, meaning “granule,” reflecting their thread-like, bean-shaped appearance under a microscope. Through cellular respiration, mitochondria extract usable energy from food by breaking down glucose to produce adenosine triphosphate (ATP)—the molecule that powers nearly every function in the body. (Hence, they earned their title as the “powerhouse of the cell.”)

Like every other system in the body, mitochondria are not spared from the effects of aging—they gradually decline in structure and function over time. Aging brings widespread physiological changes that disrupt mitochondrial integrity and efficiency.

One key factor is the accumulation of mutations in mitochondrial DNA (mtDNA)—the genetic material inside each mitochondrion. These mutations interfere with the machinery that generates energy, making mitochondria less efficient. In fact, studies show that ATP production drops by about 8% every decade (Short et al., 2005).

As mitochondria lose efficiency, they begin to produce more reactive oxygen species (ROS)—unstable molecules that can damage nearby proteins, lipids, and DNA, including mtDNA itself. Normally, the body’s antioxidant defenses keep ROS in check, but with age, this balance shifts. The result is oxidative stress, a state where there is more oxidation than protection. Oxidative stress damages cells and also triggers inflammation, which further harms mitochondria and surrounding tissues.

Adding to the problem, the body’s ability to clear out damaged mitochondria (a process called mitophagy) declines with age. Meanwhile, mitochondrial biogenesis—the creation of new mitochondria—also slows down. Over time, this leads to a buildup of dysfunctional, ROS-generating mitochondria and a reduction in total mitochondrial mass. Together, these processes create a vicious cycle: dysfunctional mitochondria produce more oxidative stress and inflammation, which in turn causes even more mitochondrial damage.

The consequences are far-reaching. Impaired mitochondrial function contributes to many age-related conditions, from fatigue and metabolic slowdown to neurodegenerative diseases like Alzheimer’s, cardiovascular disorders, and sarcopenia (muscle wasting). In fact, mitochondrial dysfunction is recognized as one of the twelve hallmarks of aging—a fundamental process underlying physiological decline.

This suggests that mitochondrial dysfunction is not merely a byproduct of aging—it actively drives it.

It’s a disastrous feedback loop:

Aging causes mitochondrial dysfunction.

Mitochondrial dysfunction accelerates aging.

While aging itself is inevitable, how we age is not predetermined. We cannot halt the passage of time, but we can support the systems that determine how gracefully we age—starting with our mitochondria. Through strategic lifestyle and nutritional interventions, it is possible to maintain mitochondrial health and resilience across the lifespan.

A diet rich in polyphenols (found in berries, green tea, and olive oil), omega-3 fatty acids, and antioxidants helps neutralize ROS, protect mitochondrial DNA, and stimulate mitochondrial biogenesis. Fasting and caloric restriction may also enhance mitochondrial function; in one study, caloric restriction increased mitochondrial DNA content—a marker of mitochondrial biogenesis—by 35% in young adults (Civitarese et al., 2007).

Exercise is arguably the most powerful non-pharmacologic activator of mitochondrial renewal. Both endurance and resistance training boost mitochondrial density, activate key regulators of mitochondrial biogenesis, lower ROS production, and improve overall energy efficiency.

On the other hand, smoking and excessive alcohol consumption actively damage mitochondria. Cigarette smoke contains free radicals that attack mitochondrial membranes and mtDNA, while alcohol disrupts mitochondrial biogenesis and promotes ROS generation. Avoiding these habits is essential for preserving cellular energy systems as we age.

Mitochondria are the powerhouse of the cell—and perhaps the powerhouse of vitality and longevity. By nourishing our mitochondria through targeted nutrition, consistent exercise, metabolic balance, and the avoidance of toxins, we can protect one of the most fundamental engines of life. Supporting your mitochondria is, quite literally, supporting your longevity from the inside out.

References

Short, Kevin R et al. “Decline in skeletal muscle mitochondrial function with aging in humans.” Proceedings of the National Academy of Sciences of the United States of America vol. 102,15 (2005): 5618-23. doi:10.1073/pnas.0501559102

Civitarese, Anthony E et al. “Calorie restriction increases muscle mitochondrial biogenesis in healthy humans.” PLoS medicine vol. 4,3 (2007): e76. doi:10.1371/journal.pmed.0040076