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Biology of Reproduction 61, 614-620 (1999)
©Copyright 1999 Society for the Study of Reproduction, Inc.

Articles

Sustained but Not Repeated Acute Elevation of Cortisol Impaired the Luteinizing Hormone Surge, Estrus, and Ovulation in Gilts1

A.I. Turnera, P.H. Hemsworthb, B.J. Cannya, and A.J. Tilbrook2,a

a Department of Physiology, Monash University, Clayton, 3168, Victoria, Australia b Animal Welfare Centre, Victorian Institute of Animal Science, Werribee, 3030, Victoria, Australia


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
We tested the hypothesis that sustained and repeated acute elevation of cortisol would impair the LH surge, estrus, and ovulation in gilts. Cortisol was injected intramuscularly, to achieve a sustained elevation of plasma concentrations of cortisol, or intravenously, to achieve an acute elevation of plasma concentrations of cortisol. Control gilts received i.m. injections of oil and i.v. injections of saline. These treatments were administered to gilts (n = 6 per treatment) at 12-h intervals from Days 7 to 11 of the estrous cycle until after estrus ceased or until Day 27 or 28 of the estrous cycle, whichever came first. The repeated acute elevation of cortisol had no effect on the LH surge, estrus, or ovulation. In contrast, when the elevation of cortisol was sustained, the LH surge, estrus, and ovulation were inhibited. We conclude that cortisol is capable of direct actions to impair reproductive processes in female pigs but that plasma concentrations of cortisol need to be elevated for a substantial period for this to occur.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
It has been proposed that acute stress at a critical time of the estrous cycle will disrupt reproduction [1], and this proposal has been supported by studies in sheep [2], cows [3], and rhesus macaques [4]. In contrast, studies that we have conducted in pigs do not provide support for this proposal [5, 6]. We have shown that the twice-daily [5] or once-daily [6] imposition of stressors during the period prior to and during estrus resulted in transient acute elevations of cortisol but did not impair reproductive performance. If acute stress is capable of impairing reproduction in female pigs, it is likely that the stressor would need to occur immediately prior to and/or during the endocrine events of the estrous cycle that culminate in the LH surge. Presumably, if an acute stress occurred repeatedly, it would be more likely to disrupt the mechanisms that control the onset and timing of the LH surge; but this proposal has not been systematically tested in female pigs.

A common response to stress is activation of the hypothalamo-pituitary adrenal axis with a consequent increase in the secretion of cortisol. While twice-daily i.m. injection of cortisol blocked the LH surge and ovulation in gilts [7], this treatment resulted in a sustained elevation of plasma concentrations of cortisol. The impacts of repeated acute elevation of cortisol on the LH surge and reproduction are unknown. Although we have addressed this issue using stressors to repeatedly elevate plasma concentrations of cortisol during the period prior to and during estrus [5, 6], there was no impairment of ovulation in these experiments, indicating that the LH surge was not inhibited. Nevertheless, in these experiments, cortisol may not have been elevated to an extent and/or with a frequency sufficient to disrupt the LH surge. Therefore, in the current experiment, we administered cortisol by i.v. injection to gilts twice daily, commencing about 10 days prior to estrus, to achieve substantial acute elevation of plasma concentrations of cortisol; we investigated the effects of this treatment on the secretion of LH and on reproduction. We also assessed the effects of sustained elevation of plasma concentrations of cortisol on the secretion of LH and reproduction in gilts. Thus, in this experiment, we tested the hypothesis that repeated acute and sustained elevation of cortisol will disrupt the LH surge, estrus, and ovulation in gilts.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Animals

Puberty was induced in 18 gilts (Large White x Landrace) by frequent exposure to mature boars commencing at 168–182 days of age, and estrous cycles were subsequently synchronized by the oral administration of a synthetic progestogen (Altrenogest, Regumate for Pigs, donated by Tony Fahy of Hoechst Roussel Vet, Melbourne, Australia) for at least 18 days [8]. Venous catheters were inserted [9], and gilts were weighed before the experiment commenced.

The care and experimental use of the animals in this experiment conformed with the requirements of the Australian Prevention of Cruelty to Animals Act 1986 and the NHMRC "Australian code of practice for the care and use of animals for scientific purposes."

Experimental Procedure

Gilts (n = 6 per treatment) were allocated randomly to three treatments. Treatment consisted of i.v. and i.m. injections (2 ml) of cortisol or the appropriate vehicle for cortisol at 0900 h and 2100 h each day commencing on Days 7–11 of the estrous cycle (Day 0 being the first day on which estrus was detected) and continuing until the day after estrus or until checks for estrus were discontinued (see below). Gilts in the "control" treatment received i.v. injections of saline via their indwelling catheter and i.m. injections of corn oil. Gilts in the "repeated acute" elevation of cortisol treatment received i.v. injections of 10 mg cortisol (hydrocortisone sodium succinate, Solu-Cortef sterile powder; Upjohn Pty Ltd, Rydalmere, Australia) in saline and i.m. injections of corn oil. The decision to use this dose was based on a study by Dalin et al. [10] in which an i.v. injection of 5 mg of cortisol in gilts was shown to result in a transient elevation of cortisol (mean peak = 96 ng/ml) similar to that reported to follow severe acute stressors such as 6 min of electrical stimulation (mean peak = 70 ng/ml), 60 min of confinement in a box (mean peak = 94 ng/ml), [11] and 5 min of constraint using a snout rope (mean peak = 108 ng/ml) [12]. Gilts in the "sustained" elevation of cortisol treatment received i.v. injections of saline and i.m. injections of 250 mg cortisol (hydrocortisone 21-acetate; Sigma Chemical Co., St. Louis, MO) in corn oil. This treatment has previously been shown to impair the LH surge and ovulation in gilts [7]. On the third day of treatment, samples of blood (10 ml) were collected at 60, 50, 40, 30, 20, 10, and 0 min before and 2, 5, 10, 15, 20, 30, 45, 60, 75, 90, 105, and 120 min after the 0900-h treatment. Plasma concentrations of cortisol were measured in plasma harvested from these blood samples. Checks for estrus were conducted twice daily commencing on Days 12–16 of the estrous cycle. To check for estrus, the experimenter applied pressure to the back of each gilt during fence-line exposure to boars. Gilts that responded with a characteristic immobile stance [13] lasting for at least 10 sec were recorded as estrous. If gilts did not display estrus when expected, checks for estrus were continued until Day 27 or Day 28 of the estrous cycle and then discontinued. By this time, the length of their estrous cycles exceeded the mean length of the estrous cycle of control gilts by more than five standard deviations of the mean. It was recorded that such gilts did not display estrus.

To characterize the LH surge, blood samples were collected every hour commencing on Days 13–17 of the estrous cycle and continuing until 36 h after the onset of estrus or, if estrus was not displayed, until Day 27 or Day 28 of the estrous cycle. Plasma concentrations of LH were measured in these blood samples. This blood-sampling protocol was based on those used in previous studies that measured the LH surge in pigs [7, 14–16]. In addition, a mean daytime plasma concentration of cortisol was estimated in each gilt by measuring the concentration of cortisol in a pool of plasma that consisted of 200 µl of plasma from blood samples collected at 3, 4, 5, 6, 7, 8, and 9 h after the 0900-h treatment. This was done for each gilt on each day from 3 days before to 1 day after the onset of estrus (or expected estrus). The number of corpora lutea, follicles, and cystic follicles, as well as the weight of the ovaries and the paired weight of the uterine horns, was assessed for each gilt at slaughter. Gilts that displayed estrus during the experimental estrous cycle were slaughtered on Days 5–12 of the subsequent estrous cycle, and those that did not display estrus were slaughtered on Day 29 or 30 of the experimental estrous cycle. All gilts were weighed prior to slaughter.

Cortisol RIA

Total plasma concentrations of cortisol were measured, after extraction of plasma using dichloromethane, by an RIA that was developed for fetal sheep plasma [17] using hydrocortisone (H-4001; Sigma) as standard and that has since been validated for analysis of pig plasma [5]. The mean (± SEM) recovery of [3H]cortisol from gilt plasma using this extraction procedure was 96 ± 2%. Seven assays were conducted that had a mean (± SEM) assay sensitivity of 0.4 ± 0.1 ng/ml. Samples that fell below assay sensitivity were assayed again using a larger volume of sample. The intraassay coefficient of variation was 7% at 25 ng/ml and 8% at 49 ng/ml, and the interassay coefficient of variation was 13% at 28 ng/ml and 9% at 52 ng/ml.

LH RIA

Plasma concentrations of LH were measured using a double-antibody RIA developed for analysis of porcine LH by Niswender et al. [18] and modified by Peacock [19] and Klupiec [20]. Primary antibody (#566 anti-porcine LH serum; Dr. G.D. Niswender, Colorado State University, Fort Collins, CO) was raised in rabbits according to the procedure described by Niswender et al. [18]. Porcine LH (LER-1786–3; Dr. L.E. Reichert Jr., Albany Medical College, Albany, NY), for use in standards and tracer, was purified according to the procedure described by Reichert [21]. A commercial second antibody (Sac-Cel, solid-phase second antibody-coated cellulose suspension, anti-rabbit IgG; Immuno Diagnostics, Tyne & Wear, England) was used. Purified porcine LH was labeled with radioactive iodine (125I; NEN Life Science Products, Boston, MA) using the iodogen (1,3,4,6-tetrachloro-3{alpha},6{alpha}-di-phenylglycouril; Sigma) protocol described by Salacinski et al. [22]. Nine assays were conducted with a mean (± SEM) assay sensitivity of 0.17 ± 0.04 ng/ml. Samples that fell below assay sensitivity were assayed again using a larger volume of sample. The intraassay coefficient of variation was 8% at 0.8 ng/ml and 7% at 1.7 ng/ml. The interassay coefficient of variation was 7% at 0.8 ng/ml and 9% at 1.6 ng/ml.

Statistical Analyses

Plasma concentrations of cortisol, both around the time of treatment and around estrus, as well as the live weights of gilts, were compared between treatments by repeated-measures ANOVA. Post hoc multiple comparisons for these and subsequent analyses of variance were made, where appropriate, using least-significant differences. An LH surge was defined, according to the procedure described by Barb et al. [7], as values that were 50% greater than the overall mean for >= 8 h in succession. The proportions of gilts in each treatment that displayed an LH surge and estrus and that ovulated were compared by chi-square analysis. One-way ANOVA was used to compare between treatments for the amplitude of the LH surge, area under the LH surge, duration of the LH surge, mean LH for the sampling period, pre-LH surge baseline, length of estrous cycle, duration of estrus, timing of estrus relative to the LH surge, number of corpora lutea, weight of ovaries, and weight of paired uterine horns. Gilts that did not exhibit an LH surge or estrus or that did not ovulate were assigned the value "0" for the purposes of presenting and analyzing the amplitude of the LH surge, the area under the LH surge, the duration of the LH surge, the duration of estrus, and the number of corpora lutea. The pre-LH surge baseline was calculated as the mean of values from 72 h before to 48 h before the onset of estrus or, if estrus was not displayed, from 72 h before to 48 h before the time when the onset of estrus was expected. For the presentation and analysis of the length of the estrous cycle, gilts that did not display estrus were assigned the number of days from the onset of the previous estrus to the day when daily checks for estrus were discontinued (i.e., 27 or 28 days). The only gilt in the sustained elevation of cortisol treatment that exhibited an LH surge (gilt 16) was the sole representative of that treatment in the presentation and analysis of the timing of estrus relative to the LH surge.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Plasma Concentrations of Cortisol

Around 0900-h treatment on the third day of treatment Plasma concentrations of cortisol in gilts in the repeated acute elevation of cortisol treatment were significantly (p < 0.05) higher than those in control gilts 2 min after treatment (Fig. 1). These concentrations had returned to control levels by 60 min after treatment. Plasma concentrations of cortisol in gilts in the sustained elevation of cortisol treatment were significantly (p < 0.05) higher than those in control gilts 45 min after treatment and for the remainder of the sampling period (120 min after treatment, except at 90 and 105 min after injections, where p = 0.11 and p = 0.07, respectively). Pretreatment plasma concentrations of cortisol were generally not significantly different between treatments except at 10 min before treatment, at which time plasma concentrations of cortisol were significantly (p < 0.05) lower in control gilts than in gilts in the sustained elevation of cortisol treatment.



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  		FIG. 1. Plasma concentrations of cortisol in gilts in the control, repeated acute, and sustained elevation of cortisol treatments for 60 min before to 120 min after treatment. This treatment occurred at 0900 h (time = 0 min) on the third day of treatment. Significant differences are described in the text.

Daytime mean, before and during estrus For 3 days before the start of estrus (or expected estrus) until 1 day after the start of estrus (or expected estrus), mean daytime plasma concentrations of cortisol were significantly (p < 0.05) higher in gilts in the sustained elevation of cortisol treatment than in control gilts and in gilts in the repeated acute elevation of cortisol treatment (Fig. 2). Mean daytime plasma concentrations of cortisol did not differ significantly between control gilts and gilts in the repeated acute elevation of cortisol treatment.



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  		FIG. 2. Daytime plasma concentrations of cortisol in gilts in the control, repeated acute, and sustained elevation of cortisol treatments for 3 days before to 1 day after the first day on which estrus was detected or expected (Day 0). Daytime plasma concentrations of cortisol in gilts in the sustained elevation of cortisol treatment were significantly (p < 0.05) higher than those in gilts in the other two treatments throughout this period.

Reproductive Performance

Reproductive measures, including plasma concentrations of LH, the timing of estrus, and the number of corpora lutea at slaughter, are shown for individual gilts in the control, repeated acute, and sustained elevation of cortisol treatments in Figures 3, 4, and 5, respectively. The catheter of gilt 2 (Fig. 5) became blocked, and therefore a complete set of LH data was not available. Nevertheless, the administration of cortisol did not require a catheter in this gilt, and therefore treatment continued and measurements were made of estrus and ovulation. These data were included in the analyses of these parameters.



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  		FIG. 3. Plasma concentrations of LH are plotted against day of the estrous cycle for individual gilts in the control treatment. An asterisk denotes a surge of LH; the timing of estrus is indicated by the horizontal bar, and CLs refer to the number of corpora lutea at slaughter. The times when i.v. and i.m. injections of vehicle were administered are indicated by the arrowheads.



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  		FIG. 5. Plasma concentrations of LH are plotted against day of the estrous cycle for individual gilts in the sustained elevation of cortisol treatment. A complete set of LH data was not available for gilt 2. The asterisk denotes a surge of LH; the timing of estrus is indicated by the horizontal bar, and CLs refer to the number of corpora lutea at slaughter. The times when i.v. injections of vehicle and i.m. injections of 250 mg cortisol were administered are indicated by the arrowheads.

Plasma concentrations of LH Whereas all gilts in the control and repeated acute elevation of cortisol treatments exhibited an LH surge, significantly (p < 0.05) fewer gilts in the sustained elevation of cortisol treatment exhibited an LH surge (Table 1). There were no significant differences between control gilts and gilts in the repeated acute elevation of cortisol treatment in any parameters of LH secretion (Table 1). In contrast, in gilts in the sustained elevation of cortisol treatment, the mean (± SEM) amplitude of the LH surge, area under the LH surge, and duration of the LH surge were significantly (p < 0.05) lower than in control gilts and gilts in the repeated acute elevation of cortisol treatment (Table 1). The mean (± SEM) plasma concentrations of LH across the entire sampling period, and baseline plasma concentrations of LH prior to the LH surge (or prior to when the LH surge was expected), did not differ significantly between treatments.


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  		TABLE 1. Characteristics of reproduction in gilts in the control, repeated acute, and sustained elevation of cortisol treatments.

Estrus In contrast to gilts in the control and repeated acute elevation of cortisol treatments, which all displayed estrus, significantly (p < 0.05) fewer gilts in the sustained elevation of cortisol treatment displayed estrus (Table 1). There were no significant differences between control gilts and gilts in the repeated acute elevation of cortisol treatment in any measures of estrous behavior (Table 1). In gilts in the sustained elevation of cortisol treatment, however, the length of the estrous cycle was significantly (p < 0.05) greater and the duration of estrus significantly (p < 0.05) shorter than in control gilts and gilts in the repeated acute elevation of cortisol treatment (Table 1). The time from the peak of the LH surge to the onset of estrus did not differ significantly between treatments.

Ovulation and reproductive tract Ovulation occurred in significantly (p < 0.05) fewer gilts in the sustained elevation of cortisol treatment than in the control and repeated acute elevation of cortisol treatments, under which all gilts ovulated (Table 1). There were no significant differences between control gilts and gilts in the repeated acute elevation of cortisol treatment in any measure of ovulation or the reproductive tract (Table 1), but gilts in the sustained elevation of cortisol treatment had significantly (p < 0.05) fewer corpora lutea than gilts in the other two treatments. The weight of paired uterine horns in gilts in the sustained elevation of cortisol treatment was significantly less than that of control gilts, but not significantly different from that of gilts in the repeated acute treatment (Table 1). The weight of ovaries did not differ significantly between gilts in any treatment.

Changes in Live Weight

While there was significant (p < 0.05) weight gain (mean ± SEM change in live weight from after estrus synchronization to before slaughter; 34 days) in control gilts (3.8 ± 1.9 kg) and gilts in the repeated acute elevation of cortisol treatment (5.1 ± 1.3 kg), gilts in the sustained elevation of cortisol treatment lost weight (-2.6 ± 1.3 kg) during the treatment period, but this loss was not statistically significant. The change in weight of gilts in the sustained elevation of cortisol treatment was significantly (p < 0.05) different from that of gilts in the other two treatments, but there was no significant difference in weight change between control gilts and gilts in the repeated acute elevation of cortisol treatment.

Gilt 16

Gilt 16 was in the sustained elevation of cortisol treatment (confirmed by her mean daytime plasma concentrations of cortisol; data not shown), but, whereas the other five gilts in the sustained elevation of cortisol treatment lost weight during the treatment period (range = -1.5 to -5.5 kg), gilt 16 gained weight (+3.5 kg). This made her a significant outlier in this group. Furthermore, she was the only gilt in this treatment that had a surge of LH (Fig. 5). Indeed, for all of the parameters for which gilts in the sustained elevation of cortisol treatment were significantly different from control gilts, gilt 16 was within one (weight change, area under the LH surge, duration of LH surge, length of estrous cycle, number of corpora lutea, and weight of paired uterine horns), two (duration of estrus), or three (amplitude of LH surge) standard deviations of the mean of control gilts.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The repeated acute elevation of cortisol during the period leading up to estrus and ovulation did not impair the LH surge, estrus, or ovulation in gilts, indicating that this series of events in the estrous cycle of the gilt is not sensitive to such treatment. Therefore, the release of cortisol that would result from severe acute stress is not likely to disrupt reproduction in gilts, even if it occurs repeatedly during the period prior to and during the LH surge. These results confer the findings of our previous experiments in female pigs showing that the repeated application of an acute stressor did not inhibit reproduction [5, 6]. The repeated acute treatment with cortisol substantially elevated plasma concentrations of cortisol for 1 h every 12 h from Days 7 to 11 of the estrous cycle until after estrus had ceased. The peak of these elevations was in excess of the peak that has been previously reported to follow a severe acute stressor [11, 12]. In contrast to the lack of an effect of repeated acute elevation of cortisol, sustained elevation of cortisol that commenced around 10 days prior to estrus impaired reproduction, confirming previous findings that this treatment can disrupt reproductive parameters such as the LH surge and ovulation [7]. Thus, while it is clear that cortisol can have direct actions to impair reproductive performance in female pigs, it appears that its secretion needs to be elevated for a substantial period in order to have this effect.

Despite the impairment of the LH surge, estrus, and ovulation by the sustained elevation of cortisol, this treatment was not effective in totally inhibiting reproduction. These parameters were blocked or delayed in some gilts, but not in others (Fig. 5). Although the treatment rendered at least three of the six gilts infertile (gilts 2, 17, and 20), it is not clear whether the other three gilts would have been capable of a fertile mating. These remaining three gilts (gilts 7, 14, and 16) displayed estrus and ovulated, even though only one of the three (gilt 16) had a "statistically significant" surge of LH. Nevertheless, the disruption of reproductive events in these three gilts may have been sufficient to prevent successful fertilization. These results confirm that the administration of cortisol can disrupt reproduction in female pigs [7, 23–26]; but they are not entirely consistent with the findings of Barb et al. [7], who administered this same treatment to five gilts and found that the LH surge and ovulation were blocked in all gilts. In the present experiment these reproductive events were exhibited by some gilts. Furthermore, in the study of Barb et al. [7], estrus was blocked in only one gilt whereas in the present experiment, estrus was blocked, delayed, and/or shortened in all gilts. The reasons for the differences between these studies in the effect of treatment with cortisol on reproduction are not apparent. The treatment regimens for cortisol were similar in the two studies, although in the present experiment, treatment started earlier during the estrous cycle (Days 7–11 vs. Day 14) and sampling continued later in the estrous cycle (Days 27–28 vs. Day 22). The longer period of treatment in the present experiment may have contributed to the discrepancies between studies, but it is not likely that the longer period of sampling could explain the different findings. It is possible that the discrepancies were due to differences in the sexual maturity and/or sexual experience of the gilts used in the two studies or to genetic differences between the herds/breeds of pig used. The breed of pig used by Barb et al. [7] was not specified.

In addition to the effects on reproduction, the sustained elevation of cortisol clearly inhibited growth. This is consistent with previous findings that prolonged stress that elevated plasma concentrations of cortisol decreased growth rates [27]. In contrast, but consistent with its lack of effects on reproduction, the repeated acute elevation of cortisol did not affect changes in weight. Collectively, the results of this study suggest that repeated exposure of female pigs to acute stress is unlikely to influence a number of physiological processes, whereas prolonged activation of the adrenal glands can clearly be detrimental. An exception was gilt 16, which, despite having a sustained elevation of cortisol, exhibited no impairment of growth or reproduction. This suggests that gilt 16 was less susceptible to the effects of sustained elevation of cortisol than the other gilts in this treatment, and it highlights the variation between individuals in the impact of cortisol on physiological processes. Individual variation was also demonstrated in female pigs in the response of cortisol to injection of a standard dose of adrenocorticotropic hormone [28]. This response varied considerably between individuals but was consistent over time within individuals [28].

In summary, repeated acute elevation of cortisol did not disrupt the LH surge, estrus, or ovulation in gilts, suggesting that the elevation of cortisol that would result from a severe acute stress would not impair reproduction even if this were to occur repeatedly during the period prior to and during the LH surge. In contrast, the sustained elevation of cortisol impaired the LH surge, estrus, ovulation, and growth, confirming that this treatment has detrimental effects on a range of physiological processes. Finally, our results show that, for cortisol to impair reproduction in gilts, its secretion must continue for a prolonged period.



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  		FIG. 4. Plasma concentrations of LH are plotted against day of the estrous cycle for individual gilts in the repeated acute elevation of cortisol treatment. An asterisk denotes a surge of LH; the timing of estrus is indicated by the horizontal bar, and CLs refer to the number of corpora lutea at slaughter. The times when i.v. injections of 10 mg of cortisol and i.m. injections of vehicle were administered are indicated by the arrowheads.


   ACKNOWLEDGMENTS
 
We thank Sam Turner, Helen Knowles, Michelle Serapiglia, Bruce Schirmer, Tina Ambrose, Ashleigh Michael, Samantha Borg, and Ellen Jongman for technical assistance. We also thank Tony Fahy of Hoescht Roussel Vet for donating Regumate; the late Ron Parr, Richard Fry, and Graham Jenkin for comments on the protocol; and Paul Hughes for his comments on this manuscript.


   FOOTNOTES
 
1 This research was funded by the Pig Research and Development Corporation of Australia. Back

2 Correspondence. FAX: 61 3 9905 2547; alan.tilbrook{at}med.monash.edu.au Back

Accepted: April 13, 1999.

Received: January 22, 1999.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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