Farrowing managers measure success by the number of live pigs produced for each pregnancy.
Confounding this measure of success is the miracle of physiology, which requires the harmonious functions of the sow, the boar, the sow's uterus, the fetal piglets' placentas and the fetal piglets themselves. Adding to the mystery, much of the process is invisible to the producer.
Knowledge of the contribution of each can improve sow performance.
The number of live piglets produced by a sow is limited by ovulation rate, the number of ova or eggs shed during each estrous cycle. From this upper limit, the number of live born piglets is progressively whittled away due to failure of sperm to fertilize the ova (5-10%) and loss of developing embryos before the 30th day of pregnancy (about 20%).
Although fertilization failure and embryo death represent losses of live pigs, both can be overcome by increased ovulation rate — through genetic selection for the trait, for example — resulting in more live embryos in the uterus on Day 30 of pregnancy.
In contrast, uterine capacity — defined as the number of piglets a sow can support during pregnancy — also limits the number of live piglets born. This limitation cannot be overcome simply by increasing ovulation rate.
So, for practical purposes, the number of piglets born alive is determined by the least limiting of two factors — ovulation rate or uterine capacity.
The sow's uterus, the fetal piglets' placentas and the fetal piglets themselves combine to influence the number of fetal piglets the sow can support during pregnancy.
The uterus provides the nutrients needed to support the fetal piglets. The placentas transport those nutrients from the sow to each developing piglet. The efficiency of each function influences the number of piglets born alive.
Improvements in any of these functions improves litter size, as long as ovulation rate is greater than uterine capacity. For maternal line sows available today, the average ovulation rate is typically greater than the average uterine capacity, even after accounting for losses due to fertilization failure and embryo death.
For the last 10 years, our research has focused on the contribution of the fetal piglet blood supply to uterine capacity. Fetal piglet red blood cells carry oxygen from the placenta to the various parts of the fetal piglet, and return carbon dioxide from those parts to the placenta, where it is transferred back to the sow for disposal.
Our results have shown that individual fetal piglets differ in their hematocrit, which is a measure of the proportion of blood made up of red blood cells. More importantly, we have shown that hematocrits are lower in small fetal piglets during pregnancy.
The size of the fetal piglet is progressively reduced as litter size increases. Therefore, fetal piglet red blood cells are fewer in small fetal piglets from large litters during pregnancy.
Since the availability of oxygen and the removal of carbon dioxide are essential to piglet survival during pregnancy, based on these results, we suggested that suppression of the fetal piglet red blood cell supply in large litters contributes to piglet losses due to limitations in uterine capacity.
We reasoned that if impaired fetal piglet blood supply contributes to decreased uterine capacity, differences in genes that increase fetal piglet blood supply would increase uterine capacity and litter size.
A hormone called erythropoietin, which interacts with a hormone receptor called the erythropoietin receptor, primarily controls blood supply to the fetal piglet, like other mammals. Together the two proteins, increase the production of red blood cells.
We explored the erythropoietin receptor gene for genetic differences that might increase its function. We found a change in the gene that we predicted would increase production of the receptor and, subsequently, lead to increased red blood cell production, greater uterine capacity and litter size.
Recently, we've shown this change in the gene is associated with increased uterine capacity and the number born alive in two different pig populations at the U.S. Meat Animal Research Center. The change in the gene was relatively rare in both populations.
The increase in uterine capacity and litter size was found to average between one and two piglets/litter, depending on the experiment and population. These results indicate that this change in the erythropoietin receptor gene could be used as a genetic marker to select for improved uterine capacity and litter size.