The title of the talk is "Exercise and Nutrition in Mitochondrial Disorders".
My name is Mark Tarnopolsky.
I'm a Professor of Pediatrics and Medicine at McMaster University in Hamilton, Canada.
What we'll be talking about today is an overview of mitochondrial cytopathies.
Then, we'll go into the diagnostic criteria for mitochondrial cytopathies.
We'll then talk about the consequences of mitochondrial dysfunction.
We'll move then into exercise therapy in mitochondrial disease and
finish with nutrition and nutraceutical therapies for mitochondrial disorders.
The mitochondria were thought to be
originally a purple photosynthetic bacteria which
invaded a protoeukaryotic cell about 1.5 billion years ago.
At the time, it was estimated that
approximately 1300 genes were used to encode for these bacteria.
Throughout the course of evolution,
there's been a sharing of the genetic material whereby
the original genetic material in the bacteria
is retained at something called the mitochondrial DNA.
This contains 37 genes.
Now, most of the proteins which encode for the bacteria,
now called the mitochondria,
are done so through the nuclear DNA.
In addition to the 22,000 genes that encode for other proteins,
1300 now encode for mitochondrial proteins.
The mitochondria are the main site for intermediary oxidative metabolism of fats,
proteins, and carbohydrates through the electron transport chain,
which we'll discuss in just a minute.
These are also important in apoptosis,
which is preprogrammed cell death,
the production of reactive oxygen species,
activation of the inflammasome,
and it's even been linked to aging through telomere length.