Mitochondria, Aging and Exercise

Mice are useful scientific research tools. In world of basic scientific research, mice are easy to handle cost effective to maintain as a colony, they share many of the same biochemical pathways as humans and are readily manipulated in the lab. Sure, some of the research is difficult to stomach, and mice are not perfect analogs to humans, but for understanding the basic science in human life, mice provide the one of the best, most relevant models of mammalian biology available to basic life sciences researchers.

Most people learned in high school biology class that mitochondria are the powerhouse of the cell. Mitochondria the bulk of the energy that our cells use to maintain their normal functions, whether that be repairing themselves, communicating, responding to communications, growing, dying or other essential functions. In order for energy to produced, the mitochondria rely on a small piece of DNA known as the mitochondrial DNA (mtDNA.) This DNA encodes genes that make proteins that are parts of the protein complexes that help make energy in the mitochondria.

Just like the any DNA, the mitochondrial DNA is subjected to stress which can impair the intergrity of the information contained by the mtDNA. In many cases, DNA damage can be repaired, but if not repaired, the DNA can be mutated. Mutations can change the information in either a small way or by wholesale deletion of the information. Over the course of a lifetime, mutations in the mtDNA can accumulate and have been associated with aging and disease. Whether mutations in mtDNA cause or are caused by aging has been an open question.

A couple years ago, two groups independently developed transgenic mice strains that had a tendency to accumulate mutations in the mtDNA. These mice showed an extremely accelerated aging phenotype. Over the course of two years, these mice had all the hallmarks of a 3-4 year old mice (normal lifespan.) The theory was that the mutation of the mtDNA caused the mice to age in an accelerated fashion. In subsequent years, research has shown that the aging phenotype was due to the wholesale deletions of the DNA rather than the point mutations.

Today, some new research was brought to my attention. A group took one of these mice strains that mutate their mtDNA and subjected them to repetitive endurance exercise. The mice showed decreased symptoms of age-related phenotypes.

Why is this important? If mutations in mtDNA can cause aging in humans just like it can in mice, which plenty of circumstantial evidence suggests that it may, the importance of lifestyle factors may be more critical than previously considered. Sure, smoking can cause cancer, but the importance of other factors, like diet, exercise, sleep patterns and micronutrient intake may be involved in maintaining proper cellular metabolism, endocrine functions, maintaining a healthy population of mitochondria and limiting the accumulation of mitochondrial DNA mutations. Given the average American lifestyle, largely sedentary at home and at work, high glycemic, nutrient bereft diet and a pharmaceutical industry more interested in treating conditions than preserving health and longevity. If by making some compromises in our lifestyle, we can life longer, healthier lives maybe we should consider those compromises. Moreover, if the FDA, American Heart Association and American Diabetes Association recommended diets are not working, as Americans continue to get fatter and suffer more chronic health issues, maybe we should consider some outside the box compromises.