In contrast to the inhibitory effects of endurance exercise on reproductive function in women athletes, voluntary running induces estrous cyclicity in anestrous female hamsters maintained in the nonstimulatory short-day photoperiod. Increased concentrations of circulating prolactin (Prl) seen in these animals are not responsible for the reversal of photoperiodic anestrus as demonstrated by experimental manipulations of prolactin secretion. Voluntary running also facilitates growth hormone (GH) release and somatic growth in hamsters independently of the photoperiod. Thus, it appears that endurance exercise can have facilitatory as well as inhibitory effects on the reproductive function in female mammals.
Female golden hamsters exposed to short photoperiods become anestrous and exhibit daily surges of gonadotropins and progesterone. Since little is known about the transition between the cycling and anovulatory states, the following experiments were done to determine whether there are hormonal changes that precede cessation of estrous cyclicity. Females killed on the morning of estrus, up to the tenth estrous cycle in short days, showed no hormonal or ovarian morphologic evidence of changes in reproductive function. When assessed on the afternoon of estrus, however, serum levels of luteinizing hormone and progesterone increased significantly before vaginal and ovarian cyclicity ceased. Females sampled in both the morning and afternoon at increasing durations since their last vaginal estrus revealed that maximal daily surges of both gonadotropins and progesterone were not consistently manifested until the vaginal cycle had been absent for 2 weeks. By then, estrogen levels and uterine weights were low and ovaries showed hypertrophied interstitia and arrested follicular growth. We have demonstrated that there are hormonal changes in females before the loss of the vaginal cycle and onset of major daily hormonal surges. Our results suggest that alterations in feedback relationships between steroid hormones and gonadotropins may precede photoperiod-induced anestrus.
The purpose of these experiments was to determine whether daily gonadotropin surges that occur in intact or ovariectomized hamsters kept in short days (less than 12 h of light/day) are manifest because of extremely low levels of steroids. Hamsters were ovariectomized and placed in l6L:8D or lOL:l4D. After 10–13 weeks, animals in each photoperiod were divided among four treatment groups: (1) estradiol implant plus progesterone injection 5 days later; (2) estradiol implant plus water injection; (3) empty implant plus progesterone injection; (4) empty implant plus water injection. Blood samples were taken from animals in the morning and afternoon before and after various treatments. In animals not receiving estradiol, all short-day and some long-day females showed low morning values of LH and surge values in the afternoon. Estrogen suppressed morning and enhanced afternoon values of LH in long-day animals, intensifying the surge. However, in the presence of estrogen, these LH surges eventually diminished in both photoperiods. Progesterone hastened the loss of the LH surge. Hamsters did not consistently demonstrate FSH surges until treated with estrogen. Serum FSH in untreated hamsters was much higher in long-day than in short-day animals. Treatment with both steroids maximally suppressed morning and afternoon FSH levels in all hamsters. Thus, in the absence of estrogen, circadian expression of LH surges always occurs in short days; FSH surges sometimes occur. In all animals showing spontaneous or estrogen-induced surges, estrogen eventually leads to inhibition of gonadotropin secretion, particularly in the presence of progesterone. The data suggest that during anestrus caused by short days, the very low levels of estrogen in intact hamsters is permissive for circadian LH secretion which may be involved in the etiology of anestrus.
Anestrous hamsters exhibit daily afternoon gonadotropin and progesterone surges, but little estrogen secretion. In the first experiment, short day anestrous females were transferred to long days to detect hormonal changes associated with recovery of cyclicity. Morning and afternoon blood samples were taken at increasing durations in long days. Females autopsied at their first vaginal estrus after transfer to long days differed from long day estrous controls only in their lower uterine weights. Some females at all durations exhibited signs of recovery, though they had not yet shown estrus. They did not display afternoon gonadotropin surges and had low circulating progesterone but high estradiol levels, stimulated uteri, and enhanced follicular development. Results of the second and third experiments provided evidence that the daily gonadotropin surges are not the cause per se of anestrus, and that changes in estrogen secretion are essential for the transition to and from anestrus. Phenobarbital blockade of the daily surges in anestrous females did not result in increased follicular growth and estrogen secretion. Furthermore, daily afternoon injections of gonadotropins it appears that the daily surges in anestrous hamsters simply reflect low estradiol levels. It is still not known what signal promotes rapid follicular maturation during the recovery from anestrus. Once initiated, however, this recovery appears to occur within a few days, with a rapid cascade of events. First, follicular development and estrogen secretion resume, and the daily LH surges cease. Then, progesterone levels decline, and an ovulatory surge of gonadotropins is triggered.
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