Growth hormone pulsatility profile characteristics following acute heavy resistance exercise.

This investigation examined the hypothesis that acute heavy resistance exercise (AHRE) would increase overnight concentrations of circulating human growth hormone (hGH). Ten men (22 +/- 1 yr, 177 +/- 2 cm, 79 +/- 3 kg, 11 +/- 1% body fat) underwent two overnight blood draws sampled every 10 min from 1700 to 0600: a control and an AHRE condition. The AHRE was conducted from 1500 to 1700 and was a high-volume, multiset exercise bout. Three different immunoassays measured hGH concentrations: the Nichols immunoradiometric assay (Nichols IRMA), National Institute of Diabetes and Digestive and Kidney Diseases radioimmunoassay (NIDDK RIA), and the Diagnostic Systems Laboratory immunofunctional assay (DSL IFA). The Pulsar peak detection system was used to evaluate the pulsatility profile characteristics of hGH. Maximum hGH was lower in the exercise (10.7 microg/l) vs. the control (15.4 microg/l) condition. Mean pulse amplitude was lower in the exercise vs. control condition when measured by the Nichols IRMA and the DSL IFA. A differential pattern of release was also observed after exercise in which hGH was lower in the first half of sleep but higher in the second half. We conclude that AHRE does influence the temporal pattern of overnight hGH pulsatility. Additionally, because of the unique molecular basis of the DSL IFA, this influence does have biological relevance because functionally intact molecules are affected.     

Overnight responses of the circulating IGF-I system after acute, heavy-resistance exercise.

This study evaluated the individual components of the insulin-like growth factor I (IGF-I) system [i.e., total and free IGF-I, insulin-like growth factor binding protein (IGFBP)-2 and -3, and the acid-labile subunit (ALS)] in 10 young, healthy men (age: 22 +/- 1 yr, height: 177 +/- 2 cm, weight: 79 +/- 3 kg, body fat: 11 +/- 1%) overnight for 13 h after two conditions: a resting control (Con) and an acute, heavy-resistance exercise protocol (Ex). The Ex was a high-volume, multiset exercise protocol that alternated between 10- and 5-repetition maximum sets with 90-s rest periods between sets. The Ex was performed from 1500 to 1700; blood was obtained immediately postexercise and sampled throughout the night (every 10 min for the first hour and every hour thereafter) until 0600 the next morning. For the first hour, significant differences (P < or = 0.05) were only observed for IGFBP-3 (Ex: 3,801 > Con: 3,531 ng/ml). For the overnight responses, no differences were observed for total or free IGF-I or IGFBP-3, whereas IGFBP-2 increased (Ex: 561 > Con: 500 ng/ml) and ALS decreased (Ex: 35 < Con: 39 microg/ml) after exercise. The results from this study suggest that the impact that resistance exercise exerts on the circulating IGF-I system is not in the alteration of the amount of IGF-I but rather of the manner in which IGF-I is partitioned among its family of binding proteins. Thus acute, heavy-resistance exercise can lead to alterations in the IGF-I system that can be detected in the systemic circulation.     

Age diminishes the testicular steroidogenic response to repeated intravenous pulses of recombinant human LH during acute GnRH-receptor blockade in healthy men

Testosterone (Te) concentrations fall gradually in healthy aging men. Postulated mechanisms include relative failure of gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH), and/or gonadal Te secretion. Available methods to test Leydig cell Te production include pharmacological stimulation with human chorionic gonadotropin (hCG). We reasoned that physiological lutropic signaling could be mimicked by pulsatile infusion of recombinant human (rh) LH during acute suppression of LH secretion. To this end, we studied eight young (ages 19-30 yr) and seven older (ages 61-73 yr) men in an experimental paradigm comprising 1) inhibition of overnight LH secretion with a potent selective GnRH-receptor antagonist (ganirelix, 2 mg sc), 2) intravenous infusion of consecutive pulses of rh LH (50 IU every 2 h), and 3) chemiluminometric assay of LH and Te concentrations sampled every 10 min for 26 h. Statistical analyses revealed that 1) ganirelix suppressed LH and Te equally (> 75% median inhibition) in young and older men, 2) infused LH pulse profiles did not differ by age, and 3) successive intravenous pulses of rh LH increased concentrations of free Te (ng/dl) to 4.6 +/- 0.38 (young) and 2.1 +/- 0.14 (older; P < 0.001) and bioavailable Te (ng/dl) to 337 +/- 20 (young) and 209 +/- 16 (older; P = 0.002). Thus controlled pulsatile rh LH drive that emulates physiological LH pulses unmasks significant impairment of short-term Leydig cell steroidogenesis in aging men. Whether more prolonged pulsatile LH stimulation would normalize this inferred defect is unknown.     

Serum thyrotropin response to thyrotropin-releasing hormone and free thyroid hormone indices in patients with familial thyroxine-binding globulin deficiency.

The response in serum thyrotropin (TSH) to synthetic thyrotropin-releasing hormone (TRH) as well as serum free thyroxine index (FT4I) and free triiodothyronine index (FT3I) was investigated in six patients with familial thyroxine-binding-globulin (TBG) deficiency. The total serum thyroxine (T4) and triiodothyronine (T3) concentrations were significantly decreased, compared with those of normal subjects (3.4 +/- 0.9 microgram/dl, mean +/- SD. vs. 9.0 +/- 1.5 microgram/dl, p less than 0.01 and 87 +/- 27 ng/dl vs. 153 +/- 37 ng/dl, p less than 0.01, respectively). FT4I was lower than the normal range in all but one (5.3 +/- 1.5 vs. 8.9 +/- 1.6, p less than 0.01), whereas FT3I was all in the normal range and of no significant difference from the normal control (132 +/- 22 vs. 148 +/- 25). Serum TSH concentrations in TBG deficiency were all in the normal range (1.0-4.2 muU/ml) and the maximum TSH increments following TRH 500 microgram iv were 8.9 +/- 2.0 muU/ml and of no significant difference from the normal control (10.2 +/- 4.5 muU/ml). These results indicate that the euthyroid state in familial TBG deficiency is more clearly defined by TRH-test and the normal response to TRH in familial TBG deficiency is presumably under the control of the serum free T3 level rather than the serum free T4 level.     

Relationship between serum luteinizing hormone and estradiol in prepubertal boars

Effects of estradiol on serum luteinizing hormone (LH) were studied in prepubertal boars. In Exp. 1, 15-wk-old boars were given (iv) 50 mug estradiol, 1 mg testosterone or 1.5 ml ethanol. Estradiol (P<0.05) decreased LH over a 2.5-hr period, but testosterone did not. In Exp. 2, an estradiol implant reduced LH sample variance (P<0.01) while LH (547 +/- 96 vs 655 +/- 43 pg/ml) and estradiol (14.2 +/- 3.3 vs 18.4 +/- 1.0 pg/ml; control vs implant) were unchanged in 12-wk-old boars. Pulsatile LH releases (4.3 +/- 1.1 vs 3.0 +/- 0.4 pulses/pig/8 hr; control vs treated) and pulse amplitude (272 +/- 34 vs 305 +/- 40 pg/ml) were not affected. The implant tended to decrease serum testosterone (4.86 +/- 0.75 vs 7.66 +/- 1.51 ng/ml; P<0.10). In Exp. 3, LH was higher after zero implants than after four implants (279 +/- 7 vs 227 +/- 9 pg/ml; P<0.01), and LH after two implants was also higher than after four implants (263 +/- 7 pg/ml; P<0.01) in 14-wk-old boars in a Latin square design. Peak LH after 40 mug gonadotropin releasing hormone (GnRH) was less after two and four implants (1,100 +/- 126 and 960 +/- 167 pg/ml, respectively; P<0.01) than after zero implants (1,742 +/- 126 pg/ml). Slope of the first 20 min of LH response to GnRH was greater after zero implants (45.3 pg/min; P<0.05) than after either two or four implants (20.6 and 16.9 pg/min, respectively). Implant treatment decreased serum testosterone (P<0.025) but increased estradiol (P<0.10). Small changes in serum estradiol resulted in changes in LH. These changes in sample variance and mean LH were recognized by boars as different from normal because serum testosterone decreased. Changes in LH may result from estradiol's negative effect on pituitary responsiveness to endogenous GnRH because response to exogenous GnRH was depressed by estradiol.     

Early-phase neuroendocrine responses and strength adaptations following eccentric-enhanced resistance training

The purpose of this study was to evaluate the early-phase muscular performance adaptations to 5 weeks of traditional (TRAD) and eccentric-enhanced (ECC+) progressive resistance training and to compare the acute postexercise total testosterone (TT), bioavailable testosterone (BT), growth hormone (GH), and lactate responses in TRAD- and ECC+-trained individuals. Twenty-two previously untrained men (22.1 +/- 0.8 years) completed 1 familiarization and 2 baseline bouts, 15 exercise bouts (i.e., 3 times per week for 5 weeks), and 2 postintervention testing bouts. Anthropometric and 1 repetition maximum (1RM) measurements (i.e., bench press and squat) were assessed during both baseline and postintervention testing. Following baseline testing, participants were randomized into TRAD (4 sets of 6 repetitions at 52.5% 1RM) or ECC+ (3 sets of 6 repetitions at 40% 1RM concentric and 100% 1RM eccentric) groups and completed the 5-week progressive resistance training protocols. During the final exercise bout, blood samples acquired at rest and following exercise were assessed for serum TT, BT, GH, and blood lactate. Both groups experienced similar increases in bench press (approximately 10%) and squat (approximately 22%) strength during the exercise intervention. At the conclusion of training, postexercise TT and BT concentrations increased (approximately 13% and 21%, respectively, p < 0.05) and GH concentrations increased (approximately 750-1200%, p < 0.05) acutely following exercise in both protocols. Postexercise lactate accumulation was similar between the TRAD (5.4 +/- 0.4) and ECC+ (5.6 +/- 0.4) groups; however, the ECC+ group's lactate concentrations were significantly lower than those of the TRAD group 30 to 60 minutes into recovery. In conclusion, TRAD training and ECC+ training appear to result in similar muscular strength adaptations and neuroendocrine responses, while postexercise lactate clearance is enhanced following ECC+ training.     

Changes in insulin response to glucose after exercise training in partially pancreatectomized rats

The effects of exercise training on glucose-stimulated insulin secretion (GSIS) were studied in male Sprague-Dawley rats made mildly to severely diabetic by partial pancreatectomy. Exercise trained (10 wk treadmill; T) and untrained (Unt) rats were grouped according to posttraining fed-state hyperglycemia as follows: T less than 200 and Unt less than 200 (glucose concn less than 200 mg/dl), T 200-300 and Unt 200-300 (glucose concn 200-300 mg/dl), and T greater than 300 and Unt greater than 300 (glucose concn greater than 300 mg/dl). After exercise training, hyperglycemic glucose clamps were performed in awake rats by elevation of arterial blood glucose concentration 126 mg/dl above fasting basal levels for 90 min. Exercise training significantly increased muscle citrate synthase activity. Prevailing hyperglycemia was reduced during the 10-wk exercise training period in all T rats with fed-state glucose concentrations less than 300, and only 53% of Unt rats in these groups had reduced glycemia. GSIS was significantly higher in T less than 200 [2.4 +/- 0.7 (SD) ng/ml at 90 min] than in Unt less than 200 (1.5 +/- 0.3). A similar response was found for T 200-300 (1.1 +/- 0.3 ng/dl) vs. Unt 200-300 (0.7 +/- 0.1) but not T greater than 300 (0.36 +/- 0.2) vs Unt greater than 300 (0.44 +/- 0.05). Sham-operated control rats had insulin concentrations of 6.6 +/- 1.6 ng/ml at the 90th min of the clamp. Acute exercise reduced fed-state glycemia in rats with mild-to-moderate (less than 300 mg/dl) diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Nonsteroidal substances that affect serum free testosterone

Several steroid hormones affect free testosterone (FT) levels in blood by competing with testosterone for binding sites on testosterone-binding globulin (TeBG). However, the effect of endogenous nonsteroidal substances in serum has not been reported. Some of these potential modifiers of FT were studied using equilibrium dialysis. Nonesterified fatty acids at 0.9 mM elevated FT approx 10% at pH 7.4. Investigation of the curvilinear relationship of percent FT (pFT) vs pH showed that pH-dependent changes of testosterone binding to albumin were responsible for a small linear increase in pFT with decreasing pH. The greater portion of the curvilinear increase of pFT with decreasing pH was due to fatty acids competing with testosterone for TeBG binding sites. Ketone bodies significantly affected FT (7.5% elevation) only at levels found in diabetic ketoacidosis. Sodium ions improved binding 11% when 7 mM was compared to 157 mM sodium, but physiological changes in sodium would result in only +/- 1% changes in FT. Very low levels (0.03 mM) of calcium may be essential for normal testosterone binding to TeBG since 1.0 mM EGTA raised FT by 75%. This study shows that dialysis at 37 degrees C should not be performed overnight, that thimerosol should not be used as a preservative, and that the dialysis buffer should contain physiological concentrations of sodium and calcium.     

Hypothalamic control of the post-castration rise in serum LH concentration in rams

Sexually mature rams were left intact, castrated (wethers), castrated and implanted with testosterone, or castrated, implanted with testosterone and pulse-infused every hour with LHRH. Serum concentrations of LH increased rapidly during the first week after castration and at 14 days had reached values of 13.1 +/- 2.2 ng/ml (mean +/- s.e.m.) and were characterized by a rhythmic, pulsatile pattern of secretion (1.6 +/- 0.1 pulses/h). Testosterone prevented the post-castration rise in serum LH in wethers (1.0 +/- 0.5 ng/ml; 0 pulses/h), but a castrate-type secretory pattern of LH was obtained when LHRH and testosterone were administered concurrently (10.7 +/- 0.8 ng/ml; 1.0 pulse/h). We conclude that the hypothalamus (rather than the pituitary) is a principal site for the negative feedback of androgen in rams and that an increased frequency of LHRH discharge into the hypothalamo-hypophysial portal system contributes significantly to the post-castration rise in serum LH.     

Effects of gonadotropin-releasing hormone pulse-frequency modulation on luteinizing hormone, follicle-stimulating hormone and testosterone secretion in hypothalamo/pituitary-disconnected rams

The effects of changes in pulse frequency of exogenously infused gonadotropin-releasing hormone (GnRH) were investigated in 6 adult surgically hypothalamo/pituitary-disconnected (HPD) gonadal-intact rams. Ten-minute sampling in 16 normal animals prior to HPD showed endogenous luteinizing hormone (LH) pulses occurring every 2.3 h with a mean pulse amplitude of 1.11 +/- 0.06 (SEM) ng/ml. Mean testosterone and follicle-stimulating hormone (FSH) concentrations were 3.0 +/- 0.14 ng/ml and 0.85 +/- 0.10 ng/ml, respectively. Before HPD, increasing single doses of GnRH (50-500 ng) elicited a dose-dependent rise of LH, 50 ng producing a response of similar amplitude to those of spontaneous LH pulses. The effects of varying the pulse frequency of a 100-ng GnRH dose weekly was investigated in 6 HPD animals; the pulse intervals explored were those at 1, 2, and 4 h. The pulsatile GnRH treatment was commenced 2-6 days after HPD when plasma testosterone concentrations were in the castrate range (less than 0.5 ng/ml) in all animals. Pulsatile LH and testosterone secretion was reestablished in all animals in the first 7 days by 2-h GnRH pulses, but the maximal pulse amplitudes of both hormones were only 50 and 62%, respectively, of endogenous pulses in the pre-HPD state. The plasma FSH pattern was nonpulsatile and FSH concentrations gradually increased in the first 7 days, although not to the pre-HPD range. Increasing GnRH pulse frequency from 2- to 1-hour immediately increased the LH baseline and pulse amplitude. As testosterone concentrations increased, the LH responses declined in a reciprocal fashion between Days 2 and 7. FSH concentration decreased gradually over the 7 days at the 1-h pulse frequency. Slowing the GnRH pulse to a 4-h frequency produced a progressive fall in testosterone concentrations, even though LH baselines were unchanged and LH pulse amplitudes increased transiently. FSH concentrations were unaltered during the 4-h regime. These results show that 1) the pulsatile pattern of LH and testosterone secretion in HPD rams can be reestablished by exogenous GnRH, 2) the magnitude of LH, FSH, and testosterone secretion were not fully restored to pre-HPD levels by the GnRH dose of 100 ng per pulse, and 3) changes in GnRH pulse frequency alone can influence both gonadotropin and testosterone secretion in the HPD model.     

Decreased pulsatile LH secretion in heifers superovulated with eCG or FSH

This study was designed to test the hypothesis that treatment with super-ovulatory drugs suppresses endogenous pulsatile LH secretion. Heifers (n=5/group) were superovulated with eCG (2500 IU) or FSH (equivalent to 400 mg NIH-FSH-P1), starting on Day 10 of the estrous cycle, and were injected with prostaglandin F(2alpha) on Day 12 to induce luteolysis. Control cows were injected only with prostaglandin. Frequent blood samples were taken during luteolysis (6 to 14 h after PG administration) for assay of plasma LH, estradiol, progesterone, testosterone and androstenedione. The LH pulse frequency in eCG-treated cows was significantly lower than that in control cows (2.4 +/- 0.4 & 6.4 +/- 0.4 pulses/8 h, respectively; P<0.05), and plasma progesterone (3.4 +/- 0.4 vs 1.8 +/- 0.1 ng/ml, for treated and control heifers, respectively; P<0.05) and estradiol concentrations (25.9 +/- 4.3 & 4.3 +/- 0.4 pg/ml, for treated and control heifers, respectively; P<0.05) were higher compared with those of the controls. No LH pulses were detected in FSH-treated cows, and mean LH concentrations were significantly lower than those in the controls (0.3 +/- 0.1 & 0.8 +/- 0.1, respectively; P<0.05). This suppression of LH was associated with an increase in estradiol (9.5 +/- 1.4 pg/ml; P<0.05 compared with controls) but not in progesterone concentrations (2.1 +/- 0.2 ng/ml; P>0.05 compared to controls). Both superovulatory protocols increased the ovulation rate (21.6 +/- 3.9 and 23.0 +/- 4.2, for eCG and FSH groups, respectively; P>0.05). These data demonstrate that super-ovulatory treatments decrease LH pulse frequency during the follicular phase of the treatment cycle. This could be explained by increased steroid secretion in the eCG-trated heifers but not in FSH-treated animals.     

Pituitary and gonadal function during physical exercise in the male rat

The effects of training and acute exercise on serum testosterone, luteinizing hormone (LH) and corticosterone levels and on testicular endocrine function in male rats were studied. In the first part of the study, the rats were trained progressively on a treadmill, over 8 weeks. Training did not change the basal levels of serum testosterone, LH and corticosterone, or the testicular concentrations of testosterone and its precursors progesterone and androstenedione. The levels of testicular LH (30.3 +/- 2.6 ng/g wet wt, mean +/- SEM) and lactogen (150 +/- 14 pg/g) receptors were unchanged after training. However, the capacity of testicular interstitial cell suspensions to produce cAMP and testosterone increased by 20-30% during in vitro gonadotropin stimulation. In the second part, the trained and untrained control animals underwent acute exhaustive exercise. Serum testosterone levels decreased by 74 and 42% in trained and untrained rats, respectively (P less than 0.02), and corticosterone rose by 182% in trained and 146% in untrained rats (P less than 0.01), whereas the LH level was unchanged. Testicular levels of testosterone and its precursors decreased, with the exception of unchanged androstenedione, in trained rats; the cAMP concentration was unchanged. In both trained and untrained rats, acute exercise decreased the capacity of interstitial cell suspensions to produce cAMP, whereas there were no consistent effects on testosterone production. Acute exercise had no effect on LH or lactogen receptors in testis tissue. In conclusion, training had no effect on serum or testicular androgen concentrations, but increased Leydig cell capacity to produce testosterone and cAMP. Acute exercise decreased serum and testicular testosterone concentrations without affecting serum LH. A direct inhibitory effect of the increased serum corticosterone level on the hypothalamic-pituitary level and/or testis may be the explanation for this finding.     

Effects of an anabolic treatment before puberty with trenbolone acetate-oestradiol or oestradiol alone on growth rate, testicular development and luteinizing hormone and testosterone plasma concentrations

Scrotal circumference, growth and hormonal status after prepubertal anabolic treatments were studied in 18 conventional Belgian White Blue bulls from 3 to 13 mo of age. Young bulls were assigned into three groups: six untreated (control) bulls, six bulls implanted with 140 mg trenbolone acetate + 20 mg oestradiol (Revalor; TBA-E2) and six bulls treated with 45 mg oestradiol (Compudose; E2). Mean scrotal circumference was similar in the three groups at Day O (between 13.0 +/- 0.3 cm to 13.4 +/- 0.7 cm). From Days O to 230, scrotal circumference was strongly inhibited in implanted bulls, 23.2 +/- 1.4, 21.7 +/- 1.0 cm, respectively, for TBA-E2 and E2 at Day 210, as compared with 29.5 +/- 2.2 cm in control bulls (P < 0.001). Afterwards, differences lessened gradually and no significant divergence was observed between the three groups from Day 310. Average plasma luteinizing hormone (LH) concentrations were similar in the three groups throughout the assay. Mean testosterone levels remained extremely low upto Day 150 in TBA-E2 and E2 groups (0.6 +/- 0.6, 1.2 +/- 0.7 ng/ml, respectively) before they increased abruptly and reached values observed in control bulls at Day 180 (4.0 +/- 1.9 ng/ml). The pulsatil character of LH and testosterone profiles was abolished by the anabolic treatments. Luteinizing hormone-releasing hormone (LHRH) injection was followed by an immediate and sharp increase in plasma LH concentrations in all groups at Day 0. Anabolic treatments strongly reduced LH and testosterone responses to LHRH in treated groups.     

Influence of circadian time structure on acute hormonal responses to a single bout of heavy-resistance exercise in weight-trained men

Both testosterone (T) and cortisol (C) exhibit circadian rhythmicity being highest in the morning and lowest in the evening. T is a potent stimulator of protein synthesis and may possess anti-catabolic properties within skeletal muscle, and C affects protein turnover, thereby altering the balance between hormone-mediated anabolic and catabolic activity. Physiological reactions of these hormones and training adaptations may influence the post-exercise recovery phase by modulating anabolic and catabolic processes, therefore affecting metabolic equilibrium, and may lead to intensification of catabolic processes. We investigated the effect of the circadian system on the T and C response of weight-trained men to heavy resistance exercise. Thirteen young (21.8 +/- 2.2 yr) weight-trained men (12 months training experience) performed an eight-station heavy-resistance exercise protocol on two separate occasions (AM: 06:00 h and PM: 18:00 h), completing 3 sets of 8-10 repetitions at 75% of each subject's one-repetition maximum (1-RM). Blood samples were obtained prior to, during, and following the exercise bout, and serum total T and C concentrations were determined by competitive immunoassay technique. Performing the single bout of heavy-resistance exercise in the PM as compared to the AM positively altered the C and T/C ratio hormonal response. Pre-exercise C concentrations were significantly lower (p < 0.05) in the PM session, which resulted in a lower peak value, and the accompanying increased T/C ratio suggested a reduced catabolic environment. These data demonstrate that the exercise-induced hormonal profile can be influenced by the circadian time structure toward a profile more favorable for anabolism, therefore optimizing skeletal muscle hypertrophic adaptations associated with resistance exercise.     

Effect of testosterone and bovine follicular fluid on concentrations of luteinizing hormone and follicle-stimulating hormone in plasma of castrated rams that are homozygous carriers or non-carriers of the Booroola fecundity gene.

Castrated adult FecBFecB and Fec+Fec+ Booroola rams were injected with charcoal-treated bovine follicular fluid (bFF) (a source of inhibin-like activity) or given testosterone implants to examine whether the fecundity gene (FecB) influences sensitivity to negative feedback hormones in males. Mean concentrations of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) did not differ between genotypes before treatment. In Expt 1, injections of 5 ml bFF, but not of 1 ml (each given four times at intervals of 8 h), significantly (P < 0.05) depressed concentrations of LH and FSH, but there was no effect of genotype. After treatment, gonadotrophin concentrations returned to pretreatment values and for 2-2.5 days scaled (divided by pretreatment mean) LH values (235 +/- 49 for FecBFecB and 96 +/- 26% for Fec+Fec+ rams; P < 0.05) and scaled FSH values (106 +/- 5 for FecBFecB and 85 +/- 5% for Fec+Fec+ rams; P < 0.05) were significantly higher in FecBFecB than in Fec+Fec+ rams in the group that received 5 ml bFF. Irrespective of genotype, treatment with 5 ml bFF did not reduce mean FSH to concentrations observed in testis-intact rams. In Expt 2, Silastic envelopes were implanted subdermally to give physiological or supraphysiological circulating concentrations of testosterone. Both doses significantly reduced scaled LH values in a biphasic manner, such that there was an initial suppression followed by a short-lived increase. During the initial period of suppression in the lower dose group, mean scaled LH values were significantly higher in FecBFecB than in Fec+Fec+ rams (48.3 +/- 7.5 versus 23.1 +/- 5.5%; P < 0.05). Low doses of testosterone decreased LH pulse frequency in both genotypes but decreased (P < 0.05) pulse amplitude and mean concentrations in the Fec+Fec+ animals only. In nonimplanted control rams, mean LH concentrations (in samples taken every 10 min for 12 h) were significantly lower in FecBFecB than in Fec+Fec+ rams (0.6 +/- 0.2 versus 1.3 +/- 0.1 ng ml-1; P < 0.05). The mean FSH response to testosterone was not related to genotype. These data suggest that expression of the FecB gene results in an altered sensitivity of the pituitary gland to changes in negative feedback from testicular hormones and that, irrespective of genotype, neither testosterone nor inhibin-like activity alone can fully control FSH secretion in castrated rams.     

Release of luteinizing hormone and growth hormone after recovery from maximal exercise

Pulsatile properties of luteinizing hormone (LH) and growth hormone (GH) release were evaluated in 19 eumenorrheic untrained females [mean age 31.1 +/- 1.1 yr, height 165.2 +/- 1.4 cm, weight 64.8 +/- 2.1 kg, peak oxygen uptake (Vo2) 41.6 +/- 1.4 (SE) ml.kg-1.min-1] during the early follicular phase of the menstrual cycle (days 3-4 after the onset of menses). Each subject was studied during two consecutive menstrual cycles under each of two conditions in random order: 1) no formal exercise for 72 h (C) and 2) 12-24 h after two maximal exercise bouts (peak Vo2/lactate threshold treadmill evaluation and a 3,200-m time-trial run or a maximal Vo2 inclined treadmill test) performed on consecutive days (EX). Blood sampling was performed every 10 min for 12 h. LH and GH pulsatile parameters were identified and characterized by the Cluster pulse detection algorithm. No significant differences were noted in the number of peaks, peak amplitude, interpeak interval, peak increment, or 12-h integrated concentrations between C and EX for LH or GH. We conclude that maximal exercise protocols typically used for exercise evaluation do not have an effect on the pulsatile characteristics of LH or GH release in untrained women during the early follicular phase of the menstrual cycle if 12-24 h of recovery are allowed before evaluation of the pulsatile secretion of gonadotropins or GH.     

Effects of systemic blockade of nitric oxide synthases on pulsatile LH, prolactin, and GH secretion in adult male rats.

BACKGROUND: Nitric oxide (NO) has emerged as an important neurotransmitter involved in the control of the neuroendocrine function. NO acts at hypothalamic, pituitary, and gonadal levels. Previous data from our laboratory showed that blockade of NO generation, after systemic administration of a NO synthase inhibitor (Nomega-nitro-arginine methyl ester, NAME), increased the luteinizing hormone (LH) secretion in intact and ovariectomized females, whereas a blockade of spontaneous and steroid-induced LH and prolactin surges after NO synthase inhibition has been also described. METHODS AND RESULTS: Adult male rats were implanted with chronic intra-auricular cannulae and 5 days later sampled at 15-min intervals during 6 h (10.00-16.00 h). Administration of NAME (40 mg/kg at 08.00 and 13.00 h) stimulated significantly (p < or = 0.01) the LH secretion, increasing LH pulse amplitude (0.58 +/- 0.14 vs. 0.08 +/- 0.01 ng/ml in controls), mean LH levels (0.64 +/- 0.15 vs. 0.15 +/- 0.03 ng/ml in controls), and area under curve (239 +/- 56 vs. 57 +/- 13 in controls). This effect was blocked by coadministration of sodium nitroprusside (SNP), a NO donor (0.5 mg/kg). The action of NAME was observed 3 h after administration, in contrast to the earlier response detected in female rats, and it appeared selective for LH, as prolactin and growth hormone secretion remained unchanged. Further analysis was carried out to determine whether the effect of NAME on the LH secretion was indirect and mediated by changes in testosterone release. To this end, adult male rats were decapitated 2 h after administration of NAME (40 mg/kg), SNP (0.5 mg/kg), or L-nitro-arginine methyl ester (L-AME), a substrate for NOS (1 g/kg). The serum testosterone concentrations were unchanged after NAME administration, but inhibited by SNP and L-AME. Finally, the effect of NAME and SNP on in vitro testosterone secretion was analyzed. NAME (10 mM) did not affect basal testosterone production, but inhibited the human chorionic gonadotropin stimulated testosterone secretion. CONCLUSIONS: These data strongly suggest that the stimulatory effect of NAME on LH secretion is not due to an inhibition of testosterone release and is exerted at the hypothalamic-pituitary level.     

Influence of short-term fasting on the pituitary-testicular axis in normal men

To investigate whether short-term fasting affects serum testosterone (T) in normal subjects, 10 healthy men of normal weight were studied on two occasions: after an overnight fast (8 h), and after an additional 48 h of fasting. Blood glucose declined by 22 +/- 3% between the tests (p less than 0.001). Basal serum T fell from 8.7 +/- 0.7 to 5.7 +/- 0.8 micrograms/l (p less than 0.01), and LH from 6.9 +/- 0.8 to 5.0 +/- 0.7 U/l (p less than 0.01). Serum estradiol (E2) and FSH remained unaffected. To explore possible mechanisms behind the decreased basal release of T and LH, 9 small doses of glucose were given orally at regular intervals during a 56-hour fast to 9 additional normal men to maintain blood glucose levels. These men did not experience a fall in serum T or LH. Six additional normal men were given 50 micrograms GnRH intravenously after an overnight fast, and after a fasting period of 56 h. No acute increase in T was seen after the overnight fast, but after the 56-hour fast GnRH raised serum T by 55 +/- 14% (p less than 0.02). Moreover, fasting augmented the GnRH-induced LH response by 64 +/- 15% (p less than 0.02. These results imply that: short-term fasting exerts inhibitory influence on Leydig cell function via a mechanism which might involve a reduced hypothalamic and/or pituitary stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of the type of energy supply on lh secretion, follicular growth and response to estrus synchronization treatment in feed-restricted suckler beef cows

The present experiment aimed to compare the efficiency of supplementation (+17.5 MJ Net Energy/d starting 47 +/- 4 days after calving) with concentrate (CS, maize grain, n = 10) or with forage (FS, maize silage, n = 10) in estrus-synchronized (Norgestomet implant 10 days inserted 60 +/- 4 days postpartum + PMSG at implant removal) beef cows previously restricted (47 MJ Net Energy/d, 785 g CP/d, 70% of requirements). The type of diet had no significant effect on basal LH concentrations (CS: 0.18 +/- 0.12 vs FS: 0.11+/- 0.02 ng/mL), LH pulse frequency (CS : 0.7 +/- 0.3 vs FS: 0.8 +/- 0.2 pulse/10 h), LH pulse amplitude (CS: 0.55 +/- 0.50 vs FS : 0.62 +/- 0.50 ng/mL) or estradiol (E2) concentrations (CS: 3.3 +/- 0.8 vs FS: 4.6+ /- 0.8 pg/mL) 13 days after the beginning of energy supplementation. No differences between CS and FS cows were observed for the number of small, medium and large follicles nor on the size of the largest follicle from 11 days before implant insertion to implant removal (IR). After IR, an LH surge was observed in 2 of the CS and 4 of the FS cows. The type of energy supplementation had no significant effect on LH (CS: 0.16 +/- 0.06 ng/mL vs FS 0.48 +/- 0.06 ng/mL; P > 0.05) or on estradiol concentrations (CS : 7.8 +/- 0.2 vs FS : 8.9 +/- 0.2 pg/mL, P > 0.10) measured hourly from 29 to 49 h after IR. Cows that ovulated after IR tended to have higher E2 concentrations than cows that did not ovulate (9.4 +/- 0.2 vs 6.3 +/- 0.2 pg/mL, P = 0.08). Similar ovulation and pregnancy rates were observed in CS and FS cows (CS: 6/10 vs FS: 7/10 and CS: 6/10 vs FS: 5/10 respectively, P > 0.05). To conclude, energy supplementation with forage was as effective as energy supplementation with concentrate to influence follicular growth, ovulation and pregnancy percentage after estrus synchronization treatment in diet-restricted beef cows.