Over the years it has been evident that physical activity increase the amount of mitochondria in the in order to compensate for the energy expenditure during exercise. However the molecular mechanisms of this process is becoming clear only very recently. Mitochondrial biogenesis is also considered as a mjor tool that is repnsible for maintaining the mitochondrial number within the cell. And it is not only a change in number of the mitochondria but it is also responsible for maintainignthe mitochondrial size and mass. To delve into a little bit more detail into the orgins of the mitochondria, the mitochondria have a bacterial origin and hence has its own genome and can auto replicate. Since the mitochondrial genome very small and only encodes …show more content…
This targeting sequence is detected by the Translocase of inner and outer mitochondrial membrane (TIM and/or TOM), and these play a very important role in mitochondrial biogenesis. The biogenesis of mitochondria is not only involved with producing new mitochondria but is also involved in thr growth and division pf pre-existing mitochondria. This important regulation of mitochondria is the reason of the changes in activity of the mitochondria in different tissues and the number of mitochondria increase with respect to the requirement of ATP.

In the recent years studies in many model organism has made it evident that Peroxisome Proliferator activated receptor co-activator 1 gamma or PGC1 alpha is the factor responsible for the control of mitochondrial biogenesis. The discovery of PGC1 alpha hs lead to the discovery of the signaling cascade that is responsible for the same. Proving this signaling …show more content…
After this discovery there have been many studies showing how PGC1 is activated studying many upstream events that lead to this induction. One of the most prominent studies show that activation of AMPK is reposible for this induction of PGC1. AMPK is the major energy sensor for the cell and it is activated when the ATP/AMP ratio inside the cell is low. This leads to the activation of AMPK which activates PGC1 aplha and NRF1/2 leading to increased mitochondrial biogenesis. Experiments performed with mice expressing the inactive version of AMPK showed a decrease in activity of PGC1 and less mitochondria per volume of the cell. On the contrary overexpression of AMPK or expressing an consitutively active version of AMPK increase PGC1 induction and increased mitochondrial content as well. AMPK overexpression in mice also protected the observed decrease in mitochondrial content with age.

Over a last few years it has been shown that nitric oxide also increase mitochondrial content. Increase in nitric oxide within the cell increased the activity of nitric oxide synthase or NOS. This increase in NOS leads to an increase in guanylate cyclase which leads to the increase in cGMP. This leads to a nuclear signal through an unknown mechanism which increase the PGC1 induction therby increasing mitochondrial