Characterizing the Effects of Acute and Chronic Heat Stress on Porcine Ovarian Function

Heat stress (HS) negatively impacts many aspects of animal health and productivity but is especially detrimental to reproductive parameters. HS-induced seasonal infertility is phenotypically observed as increased spontaneous abortions, longer wean-to-estrus interval, decreased first service conception rate, reduced litter size, and fewer total number born. These physiological consequences have economic implications for the U.S. swine industry, amounting to approximately $450 million annually. Study objectives were to characterize the impacts of acute and chronic HS on porcine ovarian function. We hypothesized that alterations in ovarian physiology due to HS are contributory to infertility. In the acute study, twelve post-pubertal gilts (126.0 ± 21.6 kg) were synchronized for 14 d by orally administering Matrix® to ensure that gilts received treatment during the follicular phase of the estrous cycle. Immediately after Matrix® withdrawal, gilts were split in two groups (n = 6) and exposed to HS or thermal neutral (TN) conditions for 5 d. Gilts were exposed to either constant TN conditions (20.3˚C ± 0.5˚C; 33 ± 13% humidity) or cyclical HS (25.4 – 31.9°C; 24 ± 6% humidity). In the chronic study, six pre-pubertal gilts (35 ± 4 kg) were split into two groups (n = 3) and exposed to either TN (20˚C; 35-50% humidity) conditions or constant HS (35˚C; 20-35% humidity) for 35 d. From both studies, gilts were euthanized, ovaries were collected, and protein extracted for Western blotting. Superoxide dismutase 1 (SOD1), a marker of oxidative stress, and 5-methyl cytosine, an indicator of DNA damage, were used to assess cellular stress caused by HS. SOD1 and 5-methyl cytosine abundance were unchanged in ovaries after acute HS, though there was a tendency for SOD1 to be increased via chronic HS (P < 0.1). Insulin receptor substrate 1 (IRS-1) protein abundance was not affected by either acute or chronic HS. Steroid acute regulatory protein (STAR), the enzyme catalyzing the first step in ovarian steroidogenesis, was increased by chronic HS (P < 0.05) whereas CYP19A1 protein, the enzyme which converts testosterone to estradiol, was not affected. Phosphorylated nuclear factor kappa B (pNFκB) and the ratio of phosphorylated AKT to total AKT were increased (P < 0.05) by chronic HS. This data suggests that different HS loads have differing effects on ovarian physiology and cellular response. This work was supported by Iowa Pork Producers Association and a Land O’Lakes fellowship to MJD.