Dubbed cell powerhouses because they transform nutrients into energy, mitochondria are tiny organelles that reside inside the cell and are essential to metabolic health. New research offers fresh insights into how they function and what makes them safe.
Research on Mitochondria
Due to the importance of mitochondria in metabolic and general health, previous research has suggested that dysfunction in these organelles may have consequences for conditions such as obesity and diabetes.
Other conditions that include mitochondrial dysfunction include age-related neurodegenerative disorders such as Parkinson’s, Alzheimer’s, and Huntington’s.
In addition, mitochondrial dysfunction can be at the root of the aging process in general. Although it is also disputed, the so-called mitochondrial-free radical aging theory is popular, and more than one study has suggested that boosting mitochondrial health can prevent cells from aging.
What Keeps Mitochondria
But what exactly keeps mitochondria in tip-top form or makes them “unhealthy” remains unknown.
Previously, researchers thought that one of the molecular pathways they called autophagy could provide valuable clues as to what keeps mitochondria healthy or makes it dysfunctional.
Autophagy — a word derived from ancient Greek to mean “self-eating“— is a” cellular-survival pathway that recycles intracellular components to compensate for nutrient depletion and ensures proper degradation of organelles. “Therefore, it is key to the health of mitochondria, and previous studies have shown that exercise stimulates autophagy, but a high fat diet impairs the process.
Recent research looked at this mechanism in mice and looked at how exercise and high-fat diets affect it, as well as how these changes affect mitochondrial health.
Sarah Ehrlicher, PhD candidate at the College of Public Health and Human Sciences at Oregon State University in Corvallis, is the first author of the paper to be published in the FASEB Journal.
Mitochondria remain healthy despite stress
Ehrlicher and colleagues “stressed” the mitochondria of transgenic mice by putting the animals on a treadmill. Genetic alterations have compromised their workout-induced autophagy pathway.
The rodents were euthanized 36 hours after their last exercise and 4 hours after their last meal, and the researchers studied mitochondria in the muscle cells of the rodents.
The researchers found that despite the genetic modification and the added stress of exercise, the mitochondrial structure of the mice’s muscles remained intact.
As a next move, Ehrlicher and his colleagues fed a high-fat diet to the mice in addition to the exercise regimen to make mitochondria even more stressful.
Again, the mitochondria of the mice showed signs of intact health and adaptation, even with the autophagy pathway blocked. This, explains the lead author of the study, suggests that mitochondria have alternative ways of stimulating recycling and limiting damage.
The findings are recorded by Matt Robinson, a researcher in the same department as Ehrlicher and the last and corresponding author of the study.
He states,”[ When] these animals were given a high fat diet, they got better off consuming the fats. If only exercise was offered, they might create more mitochondria, which is good from an exercise point of view. And these adaptations seem to be very precise.” The authors add that the results shed more light on how mitochondria function and what keeps them safe.
The research “helps lay the future groundwork on how we can improve (muscle and mitochondrial) health in order to support their health with diseases such as obesity, diabetes, and some of the effects of aging— conditions that we know have impaired mitochondria,” says Robinson.
Exercise can be one such way of improving mitochondrial and metabolic safety. “Even without weight changes, exercise has this incredible ability to improve metabolic health,” Ehrlicher says.
Obese mice do not seem to have a strong pathway malfunction in their mitochondria, and the muscles seem to respond well and adapt well to new stress, whether it is exercise or high fat diet.
This suggests that people with obesity can potentially benefit from exercise in the same way. In the future, scientists are aiming to use human volunteers to test their results.