It is known that oocytes have an excess of mitochondria compared to somatic cells, including those of highly energy dependent cells such as cardiac myocytes and neurons. Careful work by van Blerkom and colleagues has determined that the human oocyte contains between 20,000 and 30,000 mitochondria (7). This excess number of mitochondria is required to power all the components of embryo development from completion of the first meiotic division to fertilization and all embryo cleavage stages up until the blastocyst stage, at which time mitochondrial biogenesis resumes. There is some debate about the number of mtDNA copies per mitochondrion but it appears that mtDNA copies increase from a baseline of 1-2 per mitochondria in immature oocytes (8,9) to multiple copies with oocyte maturation (10). Mutations in mtDNA are therefore unlikely to affect meiosis since there is such a redundancy of mitochondria in the oocyte. Other mechanisms must be contributing and a possible candidate is chronic exposure to ROS over many years potentially damaging the nuclear spindle or resulting in shortening of telomeres (11). The presence of mtDNA mutations may become more important, however, as subsequent cell divisions during embryo development dilutes the number of mitochondria present in each blastomere. This reduction in normally functioning mitochondria may reach a critical point when the original mitochondrial cohort is reduced to 5% of the original number or less in each cell, between day 3 of cleavage and the blastocyst stage. This time frame is exactly where one observes the most likely embryo arrest and fragmentation. Boosting mitochondrial energy production around the time of fertilization and during embryo cleavage may improve the chance of blastocyst formation and subsequent pregnancy and live birth rates. This review is aimed at potential methods to accomplish this goal.