Mitochondria are the power plants of the cell, working in herds to produce the energy stores that power other cellular processes. They are the evolved descendants of symbiotic bacteria and as such the blueprints for some of their protein machinery are encoded in their own DNA, separate from the DNA in the cell nucleus. This mitochondrial DNA is inherited wholesale from the mother, and numerous common variants known as haplogroups are distributed among the world's cultures and population.
Mitochondrial damage and function appears to be very important in the aging process and many common age-related diseases. In recent years evidence has accumulated to suggest that some variants of mitochondrial DNA are just plain better than others, but linking these genetic variations to damage and function remains a work in progress. Still, the genetic lottery we all participate in very definitely applies to the mitochondria we inherit, and not just our nuclear DNA. So far the widespread variant known as haplogroup H looks like a winner:
Before 1920 there is no significant difference between the longevity of individuals in haplogroup H and U. During the caloric restriction of the Great Depression, 1920-1940, haplogroup H shows significant increase in longevity compared to haplogroup U [with a] mean difference [of] 2.6 years.
Participants from haplogroup T had a statistically significant increased risk of developing dementia and haplogroup J participants experienced a statistically significant 8-year [cognitive decline], both compared with common haplogroup H.
Here is another paper demonstrating a possible facet of the superiority of haplogroup H mitochondrial DNA:
It has been suggested that human mitochondrial variants influence maximal oxygen uptake (VO2max). Whether mitochondrial respiratory capacity per mitochondrion (intrinsic activity) in human skeletal muscle is affected by differences in mitochondrial variants is not known. We recruited 54 males and determined their mitochondrial haplogroup. Haplogroup H showed a 30% higher intrinsic mitochondrial function compared with the other haplogroup U. There was no relationship between haplogroups and VO2max.
Interestingly, we are moving into an era in which wholesale replacement of mitochondrial DNA throughout the body is a practical possibility. This was accomplished in mice via protofection eight years ago, and since then numerous research groups have achieved mitochondrial DNA replacement in cell cultures via other mechanisms. In the future you will have optimal mitochondrial DNA, periodically replaced to clear out any damage that might have occurred.
But it is of course that damage that is the important factor here, not the details of your mitochondrial haplogroup. We age in part because our mitochondrial DNA becomes damaged, that being the start of a long chain of cause and effect that leads to dysfunctional cells, floods of harmful reactive compounds, and eventually fatal manifestations such as atherosclerosis. So work on mitochondrial DNA replacement is important because it will lead to a way to mitigate and reverse one facet of degenerative aging, not because you will be able to have an athlete's mitochondria as the result of a simple clinical procedure.