American black bears, Ursus americanus, are seasonal breeders with a mating season in late spring to early summer. The objectives of this study were to determine whether there are seasonal changes in spermatogenesis and immunolocalization of testicular steroidogenic enzymes, and to correlate these changes with peripheral steroid concentrations. Three captive mature bears were maintained in open cages during the summer season and provided with chambers for denning during the winter. Testicular biopsies and blood samples were obtained from anaesthetized bears on 12 March, 15 June, 12 October and 15 January. Steroidogenic enzymes were immunolocalized using polyclonal antisera raised against bovine adrenal cholesterol side-chain cleavage cytochrome P450 (P450scc), human placental 3 beta-hydroxysteroid dehydrogenase (3 beta HSD), porcine testicular 17 alpha-hydroxylase cytochrome P450 (P450c17) and human placental aromatase cytochrome P450 (P450arom). Spermatogenesis changed seasonally: spermatogonia and degenerating spermatocytes were observed in October; spermatogonia and primary spermatocytes were present in January; spermatogonia, spermatocytes and round spermatids were present in March; and spermatogonia through spermatozoa were present in June. P450scc and P450c17 were immunolocalized in spermatids and Leydig cells in June, whereas in October these enzymes were present only in Leydig cells. 3 beta HSD was localized in Leydig cells in June and October with more intense staining in June. Localization of P450arom changed seasonally: no immunostaining in October; positive immunostaining in Sertoli cells in January; more extensive immunostaining in Sertoli cells, peritubular-myoid cells and round spermatids in March; and strong immunostaining in Sertoli cells and round and elongating spermatids in June. Serum testosterone and oestradiol concentrations changed seasonally: testosterone and oestrogen were low in October and January, slightly higher in March, and high in June. The present study demonstrates that in the black bear seasonal changes in spermatogenesis are accompanied by changes in the immunolocalization of testicular steroidogenic enzymes that are correlated with changes in serum testosterone and oestradiol concentrations. The presence of P450arom in Sertoli cells at the beginning of testicular recrudescence suggests that aromatase and oestrogen may play a role in re-initiating spermatogenesis.

The adaptation of black and polar bears to their environments is proportional to the severity of climate and food restriction. Both black and polar bears mate during the spring, despite differences in their recent metabolic state. Reproductive activity in black bears follows 4 mo of torpor, whereas reproduction in polar bears occurs prior to torpor. The goals of this study were to measure the annual changes in serum sex steroids in male and female black and polar bears, and to determine if changes in serum levels of these steroids were associated with metabolic condition or photoperiod. Serum testosterone (T) concentrations were elevated during spring in black and polar bears. Moreover, this increase in serum T in polar bears during spring was correlated with age and testis size. Serum progesterone (P4) concentrations increased in pregnant polar bears in fall coincident with the time of expected implantation. No increases in serum P4 were observed in nonpregnant black and polar bears. Serum estradiol (E2) was elevated in nonpregnant and pregnant polar bears 2 mo prior to the time of expected implantation. We found that serum sex steroids measured in black and polar bears change independent of torpor. Therefore, our results suggest that photoperiod may be a more important regulator of serum steroid levels and reproduction than metabolic condition.

Human growth hormone (hGH) levels were measured during rest, prolonged treadmill exercise at 60% maximum O2 uptake (VO2max), and immediate recovery in four groups of subjects (n = 7/group), ages 21-30 yr, classified as male runners (MR), female runners (FR), male controls (MC), and female controls (FC) to determine whether sex differences in the hGH response are related to resting 17 beta-estradiol (E2) and/or cardiorespiratory endurance (CRE). Glucose (Glc), E2, and hGH levels were determined from serial blood samples taken from an intravenous catheter. Glc did not change significantly during exercise, but different trends for the runners (increases) vs. controls (decreases) resulted in higher (P less than 0.01) postexercise levels in the runners. Resting hGH was higher (P less than 0.05) in the FRs and FCs than the MRs and MCs, respectively, and continued to be higher in the FCs (vs. MCs) during the first 30 min of exercise. The MRs achieved higher peak hGH levels and exhibited higher values than the MCs throughout exercise and recovery. There were no statistically significant training differences in the females. The strongest predictors for peak hGH were absolute work load and group (runners vs. controls), both of which combined accounted for 32-36% of the variability (P less than 0.01) in hGH response. Significant sex-related variables (sex, resting E2) accounted for 11-19% of the variability in peak or percent change in hGH, with E2 having a positive effect at rest but a negative effect during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of this study was to determine the influence of menstrual phase and menstrual status on the cortisol response during 90 minutes of treadmill running at 60% VO2max. Eight eumenhorrheic athletes were tested in the early follicular (EF) (day 3-5), late follicular (LF) (day 13-15) and mid-luteal (ML) (day 22-24) phases. Six amenorrheic athletes were tested on two separate occasions. The resting cortisol levels were similar in each menstrual phase and overall a decreasing pattern of cortisol response to exercise was observed in all menstrual phases (P greater than .05). The amenorrheic athletes had a significantly greater (P less than .01) pattern of cortisol response than was observed in eumenorrheic athletes. The net increment in cortisol levels during exercise were distinctly greater (P less than .01) in amenorrheic than eumenorrheic athletes (amenorrheic: 413.8 +/- 113.1, eumenorrheic: EF: -482.8 +/- 88.3, LF: -311.8 +/- 102.1, ML: -386.3 +/- 146.2 nmol.l-1). In conclusion the cortisol levels are independent of menstrual phase. Also a larger cortisol increment is observed in amenorrheic athletes in response to prolonged submaximal exercise. The elevated cortisol levels in amenorrheics at rest and throughout exercise provides further evidence that disturbances in the hypothalamic-pituitary-adrenal function are associated with exercise-induced amenorrhea, although the site(s) of physiological disturbance have not been identified.

No abstract