My August article on the benefits of exercise for aging muscle, states that ‘although your genetics may have an effect, this may be the least important factor in most instances over’ a life time, in part because you cannot change your genetics. But, even if your genes aren’t the best, your genes don’t necessarily fully determine the person you actually become. That’s because your diet and exercise regime, can have huge positive influences even for people with poor genetics.

Let’s take a look at mice that have what we might consider to be ‘really bad’ genes. Scientists call these animals ‘mtDNA-mutator’ mice. They have a genotype that causes them to produce a defective mitochondrial DNA repair enzyme called ‘DNA polymerase gamma’. Their specific genetic mutation leads them to accumulate an abnormally large amount of DNA mutations in their mitochondria.

Whereas normal mice can efficiently repair damage that may occur to mitochondrial DNA throughout life, ‘mtDNA-mutator’ mice are unable to do this. Their mitochondria quickly accumulate damage, in the order of 3-5 times as many mitochondrial DNA mutations as wild type mice. This leads to:

• mitochondrial dysfunction (in biogenesis & fission),
• excessive free radical production
• oxidative stress & damage to cells
• accelerated body cell death rates
• loss of cell reserve (aging).

It is this loss of cell reserve (reduced number of properly working body cells) that leads these mice to suffer from ‘progeria’, a disorder associated with profound premature aging and early death. Like many old people these mice have reduced fertility, muscle loss (sarcopenia) and subcutaneous fat loss, hair loss, curved spines, osteoporosis, anaemia, heart enlargement, but they get all these things very early in life.

The key point here is that the mitochondrial dysfunctional changes listed above that happen first, well before the appearance of the actual signs of aging. So, can anything delay the onset of mitochondrial changes and thus delay aging?

Experiments by Safdar etal in 2011 using mtDNA-mutator’ mice, demonstrated how regular endurance exercise can help even these genetically challenged mice. They showed ‘that 5 months of endurance exercise induced systemic mitochondrial biogenesis, prevented mtDNA depletion and mutations, increased mitochondrial oxidative capacity and respiratory chain assembly, restored mitochondrial morphology, and blunted pathological levels of’ cell death ‘in multiple tissues of mtDNA mutator mice.

These adaptations conferred complete phenotypic protection, reduced multisystem pathology, and prevented premature mortality in these mice’. In short, the regular endurance exercise was able to overcome the severe genetic defects that these mice had. The authors concluded that, ‘the systemic mitochondrial rejuvenation through endurance exercise promises to be an effective therapeutic approach to mitigating mitochondrial dysfunction in aging and related comorbidities’ (i.e. diseases). Most of us will not have to overcome such a severe genetic defect.

For many of us, our lack of exercise will be the key contributor to the mitochondrial dysfunction that occurs in our tissues well before we see our outer signs of aging, including muscle loss. While, appropriate regular endurance exercise may be a key preventer of our age-related decline.