It is well established that full competence of an oocyte (and thus-ovary) requires synchronous nuclear and cytoplasmic maturation. An oocyte contains numerous organelles and molecules that are required for the development. Any mitochondrial malfunction, DNA mutation, defects in maternal mRNA storage, insufficient synthesis of proteins or untimely destruction of proteins, results in ovarian insufficiency. The impaired bioenergetic capacity in oocytes correlates with the decline of quality in eggs.
Mitochondria are the most prominent cell organelles in oocytes, and they represent one of the important maternal contributions to embryogenesis. Mitochondria also replicate during oogenesis, and their number rises from about 200 per oogonia to 6,000 per oocyte in primordial follicles and reaches up to 300,000 – 400,000 in the mature human oocyte. Owing to their role in energy generation and apoptosis, the mitochondrial status has been recognized as a determinant of the oocyte’s developmental competence.
During the past decades, the adverse impacts of maternal ageing on oocyte mitochondria have been revealed. Mitochondrial swelling and cristae disruption is the common structural features of oocytes from women of advanced reproductive ages. Moreover, metabolic dysfunction of mitochondria may be responsible for aberrations in the assembly of the meiotic spindle, cell cycle regulation, and timely chromosome segregation, as shown for oocytes from aged women and mice.
To overcome these problems, clinical protocols of mitochondrial donation were developed, using the oocyte cytoplasm extracted from a young donor that was transferred into the eggs of the recipient woman. The procedure, however, had a short life because of concerns regarding the consequent mitochondrial heteroplasmy, whose result was that children generated by this protocol possessed three different sources of genetic material (three parents child), namely the biological parents and the oocyte donor, for the presence of maternally inherited DNA in mitochondria. Therefore, according to the U.S. Food and Drug Administration (FDA), this procedure was considered a genetic manipulation of human germ cells and was no longer applied.
The discovery that OSCs are present in fertile women ovaries has driven to an emerging modified version of ooplasmic transfer, called AUGMENT (autologous germline mitochondrial energy transfer) in which autologous germline-derived cytoplasmic extract or purified mitochondria can be used for the bioenergetics reinforcement of oocytes. Another potential approach to overcome the defective egg energy includes the improvement of both biological and chemical compounds bioavailability, with the purpose to enrich the mitochondrial number or the efficacy of ATP production in oocytes.
In SEGOVA protocol, a different approach was implemented. This treatment includes boosting mitochondrial energy production of ovarian cells with a specific workout regime – Sex HIIT (High-Intensity Interval Training). It is a workout in which you alternate very high-intensity intervals of predominantly anaerobic exercises, with slower intervals to recover. It causes energy conversion and biogenesis of mitochondria (part of the cell responsible for energy production).