Thanks to the advances in medical science, humans have been able to improve healthspan significantly. However, data have shown that maximal lifespan remains unchanged, and humans have the potential to lengthen life even further. Read this article to learn about the function of the mitochondria for longevity.
More Than Just Cellular Energy Production – the Mitochondria and Longevity
The mitochondria have recently emerged as a vital factor affecting lifespan and gained widespread attention from the healthcare community. But, what are they, and how do they affect aging?
What Is the Function of the Mitochondria?
Mitochondria are cell organelles essential for a range of biological processes. They are primarily responsible for producing cellular energy by generating ATP. Our cells require ATP as the energy currency to store and transfer the energy within the cell. To produce ATP, a set of metabolic reactions and processes requiring oxygen occurs in mitochondria. These reactions and processes are known as mitochondrial respiration.
The mitochondria can also produce reactive oxygen species (ROS) during ATP production. These ROS are the harmful byproducts of mitochondrial respiration. ROS can slowly accumulate and damage the cell’s building blocks at increased levels, including DNA, protein, and lipids, which may accelerate aging. The finding of such detrimental effects of ROS laid the groundwork for the proposal of the mitochondrial theory of aging.
The Mitochondrial Theory of Aging, Increased ROS, and Aging
The mitochondrial theory of aging proposes that mitochondria are significantly involved in aging. As an organism grows older, mitochondria suffer from cumulative damage due to ROS formation. As ROS are highly reactive and can damage the building blocks of the cell, such cumulative damage exacerbates mitochondrial dysfunction. As a result, the functioning of cells and organisms deteriorate over time, resulting in the aging process.
Consistent with this theory, evidence suggests that changes in the mitochondria may affect the rate of aging in animal models. According to a study, mice with high mutation rates in their mitochondrial DNA (mtDNA) show signs of accelerated aging. However, recent studies show that both inhibition and increase in mitochondrial function can actually slow down aging and extend lifespan, creating the framework for achieving longevity.
Inhibition of Mitochondrial Respiration, Low Metabolic Rate, and Longevity
Although the mitochondrial theory of aging has gained a widespread consensus among the scientific community due to its objectivity and rationality, several recent reports show contradictory data that is discordant with the theory. These reports claim that controlled modifications in the mitochondria can actually promote longevity. According to a review, mild inhibition of mitochondrial respiration can extend the lifespan of several species.
On the other hand, a complementary theory known as the rate of living theory suggests that metabolic rate inversely correlates with lifespan, meaning that the faster the metabolism, the faster the aging process, and the shorter the lifespan. Since mitochondria are essential for energy production, reduced mitochondrial function is thought to decrease metabolic rates. Therefore, mild inhibition of mitochondrial respiration may slow down the aging process.
Consistent with the rate of living theory, a clear inverse correlation between lifespan and metabolic rates can be seen in various species. Small animals have a short lifespan and a high metabolic rate. In contrast, large animals have a long lifespan and a low metabolic rate. This finding supports the idea that organisms with controlled reduced mitochondrial respiration may have longer lifespans due to slower biological processes.
Increased Mitochondrial Respiration, Dietary Restriction, and Longevity
Reducing overall calorie intake without affecting mitochondrial health and the organism’s survival is another possible intervention for increasing longevity. Dietary restriction (DR) boosts mitochondrial respiration through a mechanism involving increased oxygen consumption. By measuring the increase in total oxygen consumption in the mitochondria, scientists can determine an enhancement in mitochondrial respiration due to DR.
According to a review, in animal experiments in which the subjects are provided with 60 to 80 percent of the regular amount of food, reducing food at a moderate level extends lifespan most effectively. In addition to these DR studies in animals, studies on humans also imply that lowering food consumption has similar beneficial effects on health and fitness, suggesting that mitochondria may play a central role in lifespan extension.
Interestingly, decreased caloric intake does not reduce ATP production, as mitochondria may function even more effectively to compensate for lowered caloric intake by increasing oxygen consumption and generating more ATP. Indeed, a study found that total ATP levels remain unaffected in human cells under DR. Therefore, it can be inferred that increased ROS due to enhanced mitochondrial respiration under DR may actually promote longevity.
Further Research Is Required
Recent research has only begun to shed light on the processes through which mitochondrial activity may affect aging. Although it is suggestive that mitochondria play critical roles in longevity, the mechanisms that lead to such functions are more complicated than initially thought. Future research is expected to determine whether the findings of the animal trials are valid in the extension of the human lifespan.
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