Serum Growth Hormone Response Research Articles

Growth Hormone And Cortisol Alterations After Inhibition/stimulation Of Hpa Axis In Healthy Adults.

PURPOSE: To examine serum growth hormone (GH) and cortisol (COR) responses to a selected aerobic exercise protocol performed under inhibition or stimulation of the HPA axis in healthy male and female volunteers. METHODS: Twelve healthy volunteers (8 males, 4 females, age: 30.6 ± 4.4 yrs, body mass: 77.3 ± 12.3 kg, height: 1.77 ± 0.07 m), performed a single bout of 30 min aerobic exercise at 70%VO2 max on a treadmill, on three different conditions [control (C), HPA axis inhibition (HPA-I, induced by glucocorticoid administration), HPA axis stimulation (HPA-S, induced by ACTH administration)], following standard diet. Blood samples were collected before (t0), at the end of the exercise bout (t30), and 30 min later (t60) and serum GH and COR were measured. Two-way ANOVA was used for statistics. Data is presented as mean ± SE. RESULTS: In C condition, GH significantly increased (p < 0.001) after exercise and decreased again 30 min after exercise without reaching pre-exercise levels (0.2 ± 0.1; 5.5 ± 1.1; 1.7 ± 0.7 ng/mL; at t0, t30 and t60, respectively). COR significantly decreased 30 min after exercise (p < 0.005) (13.9 ± 1.2; 10.3 ± 1.1; 7.1 ± 1.2 μg/dL; at t0, t30 and t60, respectively). In HPA-I, GH significantly increased at the end of exercise (p < 0.05) while 30 min after exercise it decreased reaching pre-exercise levels (1.1 ± 0.3; 3.0 ± 0.6; 1.0 ± 0.2 ng/mL; at t0, t30 and t60, respectively). COR remained unchanged (p > 0.05) (0.627 ± 0.1; 0.632 ± 0.1; 0.639 ± 0.1 μg/dL; at t0, t30 and t60, respectively). Under HPA-S condition, GH significantly increased 30 min after exercise (p < 0.001) (0.3 ± 0.1; 8.9 ± 1.9; 3.1 ± 0.9 ng/mL; at t0, t30 and t60, respectively. COR significantly increased after exercise (p < 0.001) (14.7 ± 1.1; 30.7 ± 1.3; 34.6 ± 3.7 μg/dL; at t0, t30 and t60, respectively). There were no significant changes in COR between the three conditions, while COR was lower in HPA-I compared to C condition at all time points (p < 0.001). There were no significant differences between male and female participants. CONCLUSIONS: The rapid increase of GH in response to aerobic exercise is not affected by the modification of HPA axis. The specific aerobic exercise regimen influenced circulating COR yet not under exogenous inhibition of the HPA axis. Further studies will characterize how those responses are regulated by the characteristics of exercise.

Diazoxide use for neonatal hyperinsulinaemic hypoglycaemia in a low-resource setting: A Case Report

The management of neonatal hyperinsulinaemic hypoglycaemia remains a major challenge in hospitalized newborns globally. Diazoxide is one of the recommended therapeutic options. We report a late preterm, male infant of a diabetic mother who suffered severe perinatal asphyxia and had persistent hypoglycaemia requiring progressively increasing intravenous glucose concentrations to as high as 12.5 mg/kg/minute along with intravenous hydrocortisone administration. A critical sample revealed inappropriately high serum insulin, inappropriately low serum cortisol and growth hormone responses. Urinalysis was negative for ketones. With the persistence of hypoglycaemia, oral diazoxide at 5 mg/kg/day with oral hydrochlorothiazide was administered. The infant was diazoxide-responsive with complete resolution of hypoglycaemia. Diazoxide therapy was discontinued after 14 days and he was discharged after one month of admission. This report emphasizes the importance of diazoxide in the management of neonatal transient hyperinsulinaemic hypoglycaemia. The availability and cost of diazoxide, as well as the endocrine and metabolic tests, are major concerns in resource-poor settings.

A Mathematical Weibull Model to Unravel the Involvement of Acute Exercise on Serum Growth Hormone Response in Elite Male Water Polo Players

A Mathematical Weibull Model to Unravel the Involvement of Acute Exercise on Serum Growth Hormone Response in Elite Male Water Polo Players

The effect of short-term hypothyroidism on growth hormone secretory responses to growth hormone-releasing hormone (1-29) and insulin-induced hypoglycemia

Introduction: Hypothyroidism is frequently associated with growth failure. In long-standing hypothyroidism the growth hormone (GH) secretory responses to growth hormone-releasing hormone (GRH) and insulin-induced hypoglycemia are decreased. Methods: To investigate whether hypothyroidism of short duration affects pituitary GH release, we measured the serum GH response to synthetic GRH (1-29), 1g/kg body weight, given IV to six athyreotic patients during thyroxine (T4) treatment and one month after stopping T4 (short-term hypothyroid state). This served as a direct measure of pituitary somatotroph function .We also assessed the serum GH response to insulin-induced hypoglycemia in three patients as an indirect assessment of hypothalamic function. Results: We found that basal GH levels remained the same both during (euthyroid state) and after stopping T4 therapy (hypothyroid state). Peak serum GH response to GRH was significantly greater in patients while they were hypothyroid than during T4 therapy when they were euthyroid (p

An Evaluation of Growth Hormone and IGF-1 Responses in Neonates with Hyperinsulinaemic Hypoglycaemia

Background. Hyperinsulinaemic Hypoglycaemia (HH) is the most common cause of severe and persistent hypoglycemia in the neonatal period. It has been shown that the neonates with HH fail to generate adequate serum cortisol counterregulatory response to symptomatic hypoglycemia. However the role played by growth hormone (GH) and Insulin-like Growth Factor 1 (IGF-1) is not clear. Objectives. To compare the serum GH, IGF-1, and IGFBP3 responses to HH in neonates undergoing diagnostic fasting studies. Population and Methods. Data was retrospectively collected on full-term neonates who presented with severe and persistent hypoglycemia and were confirmed to have HH. Neonates born with intrauterine growth retardation or those on medical therapy (diazoxide or octreotide) were excluded. Results. 31 neonates with HH (mean gestational age: 38 weeks and mean birth weight: 3.9 kg) were included in the study. The mean age at the time of diagnostic fast was 4 weeks, the mean glucose concentration during the fast was 2.2 mmol/L (SEM ± 0.09), and the mean insulin level was 11.9 mU/L (±2.12). The mean serum GH concentration during the hypoglycaemia was 12.5 µg/L (±1.53). The mean serum IGF-1 and Insulin-like Growth Factor Binding Protein 3 (IGFBP3) levels were 29.2 ng/ml (±7.8) and 1.21 mg/L (±0.13), respectively. The mean cortisol concentration was 201 nmol/L (±33). Conclusions. Whilst the serum IGF-1 and IGFBP3 levels are relatively low during hypoglycaemia, the serum GH level does reflect an appropriate counterregulatory response to HH. The serum cortisol counterregulatory hormonal responses are blunted. Further studies are required to understand the mechanism(s) of these hormonal alterations in neonates with HH.

Retrospective Analysis Of Resistance Training-induced Strength And Hypertrophy: Separating The Wheat From The Hormone Chaff

PURPOSE: To investigate associations between purportedly anabolic acute exercise-induced hormone responses and adaptations to resistance training in a cohort with normally distributed training-induced adaptations. METHODS: Acute post-exercise serum growth hormone (GH), free testosterone (fT), cortisol, and insulin-like growth factor (IGF-1) responses were determined at the midpoint of a 12-wk resistance exercise program conducted previously. Correlations of hormonal responses with gains in lean body mass (LBM), muscle fiber cross-sectional area (CSA) and leg press strength were investigated. Dietary factors were combined with hormonal responses as independent variables in multiple regression analysis of adaptations to resistance training. RESULTS: There were no significant correlations between the exercise-induced elevation (area under the curve_AUC) of GH, fT and IGF-1 and gains in LBM or leg press strength. Significant correlations were found for cortisol AUC with change in LBM (r = 0.29, P < 0.05) and type II fiber CSA (r = 0.35, P < 0.01) as well as GH AUC and gain in fiber area (type I: r=0.36, P=0.006; type II: r= 0.28, P=0.04). Multiple regression analysis showed that increments in daily dietary protein intake and the daily consumption of dairy, but no acute hormonal response, were significant predictors in a model of change in LBM and type II fiber area. CONCLUSION: A significant association existed between GH and cortisol and fiber hypertrophy, but there was no association between any hormones and strength gains. Multiple regression analysis revealed an important role of increasing dietary protein and servings of dairy in promoting training-induced gains in LBM and fiber hypertrophy. In contrast, post-exercise elevations in endogenous hormones were relatively impotent in their predictive value for resistance training-induced hypertrophy calling into question persistent referrals, which are frequently erroneously based on pharmacological intervention studies, to their anabolic capacity. Supported by NSERC and CIHR

Hormonal Responses to Resistance Exercise after Ingestion of Carnosine and Anserine

Intramuscular carnosine buffers protons (H+) in skeletal muscle. We examined the effects of supplementation with chicken breast meat extract (CBEX) containing carnosine and anserine on hormonal responses to resistance exercise. Twenty-two men were assigned to a CBEX drink group (CBEX containing total 2 g of carnosine and anserine) (n = 14) or a placebo drink group (n = 8). The subjects ingested the prescribed drink (100 mL) twice daily for 30 days without physical training. Before and after the supplementation period, the subjects completed 5 sets of bilateral knee extension exercises (with a 90-s rest between sets). The magnitude of the increase in exercise-induced free testosterone did not change significantly after supplementation in either group. The blood lactate response to exercise was attenuated after supplementation in both groups (p < 0.05). In the CBEX group, the plasma epinephrine and norepinephrine concentrations after exercise were significantly lower after supplementation (p < 0.05). The serum growth hormone response to exercise was also reduced in the CBEX group after supplementation (delta value: 5.4 ± 1.9 ng/mL [pre] vs. 1.6 ± 0.5 ng/mL [post], p = 0.05). No significant differences in exercise-induced strength reduction (fatigue index) were observed in the 2 groups after supplementation. These results suggest that short-term supplementation with CBEX attenuates the exercise-induced epinephrine, norepinephrine, and growth hormone responses.

Arginine test is not reliable for diagnosing cerebellar multiple system atrophy

We evaluated the arginine growth hormone (GH) stimulation test for the diagnosis of cerebellar-type multiple system atrophy (MSAc) in patients with ataxia. Fourteen subjects with MSAc, 11 with idiopathic late-onset cerebellar ataxia (ILOCA), 10 with familial ataxia, and 10 healthy controls were tested. After pituitary GH deficiency was excluded, subjects underwent arginine testing. Peak serum GH response was analyzed. No significant differences in peak GH response were found between subject populations. Thirty-three percent of MSAc subjects mounted responses >10 microg/l GH. Thirty-six percent of ILOCA subjects and 40 percent of healthy controls mounted responses <4 microg/l GH. Arginine thus appears to be unreliable for the diagnosis of MSAc.

Greater growth hormone and insulin response in women than in men during repeated bouts of sprint exercise

In a previous study, sprint training has been shown to increase muscle cross-sectional area in women but not in men [Eur J Appl Physiol Occup Physiol 74 (1996) 375]. We hypothesized that sprint exercise induces a different hormonal response in women than in men. Such a difference may contribute to explaining the observed gender difference in training response. Metabolic and hormonal response to three 30-s sprints with 20-min rest between the sprints was studied in 18 physically active men and women. Accumulation of blood lactate [interaction term gender (g) x time (t): P = 0.022], and plasma ammonia (g x t: P < 0.001) after sprint exercise was greater in men. Serum insulin increased after sprint exercise more so in women than in men (g x t: P = 0.020), while plasma glucose increased in men, but not in women (g x t: P < 0.001). Serum growth hormone (GH) increased in both women and men reaching similar peak levels, but with different time courses. In women the peak serum GH level was observed after sprint 1, whereas in men the peak was observed after sprint 3 (g x t; P < 0.001). Serum testosterone tended to decrease in men and increase in women (g x t: P = 0.065). Serum cortisol increased approx. 10-15% after sprint exercise, independent of gender (time: P = 0.005). Women elicited a greater response of serum GH and insulin to sprint exercise. This may contribute to explaining the earlier observed muscle hypertrophy in women in response to sprint training.

Pituitary hypoplasia and growth hormone deficiency in a woman with glycogen storage disease type Ia: a case report

IntroductionGrowth retardation is one of the cardinal manifestations of glycogen storage disease type Ia. It is unclear which component of the growth hormone and/or insulin-like growth factor axis is primarily disrupted, and management of growth impairment in these patients remains controversial. Here we report the first case in the literature where glycogen storage disease type Ia is associated with pituitary hypoplasia and growth hormone deficiency.Case presentationA 20-year-old woman with glycogen storage disease type Ia was admitted to our endocrinology department because of growth retardation. Basal and overnight growth hormone sampling at 2-hour intervals demonstrated low levels; however, provocative testing revealed a relatively normal growth hormone response. A hypoplastic anterior pituitary with preserved growth hormone response to provocative testing suggested the possibility of growth hormone neurosecretory dysfunction and/or primary pituitary involvement.ConclusionPituitary hypoplasia may result from growth hormone-releasing hormone deficiency, a condition generally known as growth hormone neurosecretory dysfunction. It is an abnormality with a spontaneous and pulsatile secretion pattern, characterized by short stature, growth retardation and normal serum growth hormone response to provocative testing. However, in the case described in this report, a normal although relatively low growth hormone response during insulin tolerance testing and pituitary hypoplasia suggested that primary pituitary involvement or growth hormone neurosecretory dysfunction may occur in glycogen storage disease type Ia. This is a potential cause of growth failure associated with a lower somatotroph mass, and may explain the variable responsiveness to growth hormone replacement therapy in people with glycogen storage disease.

Human blood neutrophil responses to prolonged exercise with and without a thermal clamp

The purpose of this study was to investigate the effects of prolonged exercise with and without a thermal clamp on neutrophil trafficking, bacterial-stimulated neutrophil degranulation, stress hormones, and cytokine responses. Thirteen healthy male volunteers (means +/- SE: age 21 +/- 1 yr; mass 74.9 +/- 2.1 kg; maximal oxygen uptake 58 +/- 1 ml x kg(-1) x min(-1)) completed four randomly assigned, 2-h water-immersion trials separated by 7 days. Trials were exercise-induced heating (EX-H: water temperature 36 degrees C), exercise with a thermal clamp (EX-C: 24 degrees C), passive heating (PA-H: 38.5 degrees C), and control (CON: 35 degrees C). EX-H and EX-C was comprised of 2 h of deep water running at 58% maximal oxygen uptake. Blood samples were collected at pre-, post-, and 1 h postimmersion. Core body temperature was unaltered on CON, clamped on EX-C (-0.02 degrees C), and rose by 2.23 degrees C and 2.31 degrees C on EX-H and PA-H, respectively. Exercising with a thermal clamp did not blunt the neutrophilia postexercise (EX-C postexercise: 9.6 +/- 1.1 and EX-H postexercise: 9.8 +/- 1.0 x 10(9)/liter). Neutrophil degranulation decreased (P < 0.01) similarly immediately after PA-H (-21%), EX-C, and EX-H (-28%). EX-C blunted the circulating norepinephrine, cortisol, granulocyte-colony stimulating factor, and IL-6 response (P < 0.01) but not the plasma epinephrine and serum growth hormone response. These results show a similar neutrophilia and decrease in neutrophil degranulation after prolonged exercise with and without a thermal clamp. As such, the rise in core body temperature does not appear to mediate neutrophil trafficking and degranulation responses to prolonged exercise. In addition, these results suggest a limited role for cortisol, granulocyte-colony stimulating factor, and IL-6 in the observed neutrophil responses to prolonged exercise.

Provocative Stimulation of Growth Hormone: A Monozygotic Twin Study Discordant for Spinal Cord Injury

Background/Objective: A blunted growth hormone (GH) response to provocative testing and/or low levels of plasma insulin-like growth factor-1 (IGF-I) have been reported in persons with spinal cord injury (SCI). A reduction in activity of the GH-IGF-I axis may have deleterious effects on body composition and function. Provocative testing for GH stimulation was performed to determine the response in monozygotic twins that were discordant for SCI.Methods: GH stimulation testing was performed by the administration of intravenous arginine.Results: Nine SCI twins with paraplegia, a mean age of 39 ± 9 years, and duration of injury of 14 ± 9 years were studied. The twins with SCI had a significantly lower body mass index than non-SCI twins (22.5 ± 4.0 vs 25.1 ± 4.2 kg/m2; P < 0.05); percent fat mass was greater in the twins with SCI (30 ± 11 % vs 22 ± 10%; P < 0.05). Baseline serum GH was correlated with percent fat only in the SCI twins. The response to GH provocative stimulation was less in the twins with SCI: peak GH response was 5.8 ± 6.6 vs 13.0 ± 7.3 ng/mL (P < 0.05), and sum GH response was 15.7 ± 15.6 vs 30.2 ± 17.3 ng/mL (P = 0.06). Although baseline serum GH was correlated with stimulated response in the SCI twins, this relationship was not found in the non-SCI twins. Adiposity was positively related to the provocative serum GH response in twins with SCI rather than negatively related, as noted in the non-SCI twins.Conclusions: This study confirms and extends prior work that reported a reduction in stimulated GH release in persons with SCI, which was related to baseline values.

No Influence of Body Composition on Serum Growth Hormone Response to Acute Dynamic Exercise

Physical effort is a strong physiological stimulus that provokes an increase in blood growth hormone (GH) concentration. Interactions between GH and body composition are very complex. Seven athletes and seven age-matched controls completed a single 30-min bout of upright cycling exercise (5 % of VO(2max).) in order to estimate the influence of body composition on serum GH concentration during exercise. The serum GH concentration was measured in blood samples by standard immunoradiometric (IRMA) method. Anthropometric measurements were used for the calculation of body composition. There were no significant differences in total body mass or body mass index between the groups. The athletes had significantly less fat and higher bone and muscle mass. Serum GH concentration was 2.39 times higher in the athlets versus the control in the period of rest. During acute exercise, the serum GH concentration increased in both groups. No statistically significant differences between the groups in serum GH concentration were found either during the exercise or in the recovery. No correlation between body composition and serum GH concentration was found. Body composition depends on the level of physical activities but if the total body mass is in physiologycal range it does not influence the serum GH response to acute exercise.

Poor Responses to a Test Dose of Subcutaneous Octreotide Predict the Need for Adjuvant Therapy to Achieve 'Safe' Growth Hormone Levels

Somatostatin analogues are an established treatment in acromegaly. This study was designed to evaluate whether the acute serum growth hormone (GH) response to a test dose of octreotide in acromegaly predicts longer-term response to the drug at 3 years. In 23 patients, GH responses across 8 h to a subcutaneous test dose (50 microg) of octreotide were compared with GH levels after 3 years of therapy. The majority had pituitary surgery as primary therapy and at 3 years were receiving at least 600 microg octreotide daily subcutaneously or 20 mg LAR monthly intramuscularly. Seven had a test day GH Nadir of 5 mU/l or less of whom 4 achieved GH < 5 mU/l at 3 years. Sixteen had a test day nadir GH of 10 mU/l or less and of these 8 achieved GH < 5 mU/l at 3 years. Seven of the 23 had a GH Nadir >10 mU/l and of these 3 had achieved GH <5 mU/l at 3 years. However all of these 3 had received external pituitary irradiation within 4 years of the 3 year assessment, as compared with 3 of the <5 mU/l nadir group and 5 of the <10 mU/l nadir group. In patients on optimal long-term doses of octreotide for acromegaly, absence of a nadir GH <10 mU/l in the 8 h after a test dose was associated with failure to achieve GH levels associated with a normal life expectancy (5 mU/l or less) unless adjunctive external pituitary irradiation was given. As well as testing tolerability a test dose of octreotide may help in determining which patients should be offered early external pituitary irradiation or therapy with a GH receptor antagonist if surgery has failed to achieve 'safe' GH levels.

The serum growth hormone (GH) response to provocative tests is dependent on type of assay in autosomal dominant isolated GH deficiency because of an ARG(183)HIS (R183H) GH-I gene mutation.

The clinical appearance and genetic basis of familial isolated growth hormone deficiency (IGHD) are heterogeneous and are associated with at least four types of Mendelian disorders: two forms with autosomal recessive inheritance (IGHD type 1A and 1B), one with autosomal dominant inheritance (IGHD type 2), and one with X-linked inheritance (IGHD type 3) (1)(2). Recently, Deladoey et al. (3) reported a new form of IGHD type 2 in four unrelated families. These patients carried an ARG183HIS (R183H) GH-1 mutation. On the basis of in vivo and in vitro experiments, the authors reported that the R183H mutant GH peptide severely impaired GH-regulated secretion. Furthermore, this GH mutant was found to have an effect on GH receptor/GH-binding protein (GHR/GHBP) transcription identical to that of the 22-kDa GH when tested in a human hepatoma cell line (4). Human GH represents a family of proteins rather than a single hormone. Indeed, GH is among the more heterogeneous polypeptide hormones, and the proportions of immunoreactive forms in plasma vary with time after a GH secretory pulse (5). The simultaneous use of an immunoassay that detects most serum GH isoforms (total GH) and one specific for the 22-kDa GH form makes it possible to uncover changes in the pattern of secretion of GH isoforms. Moreover, discrepancies between GH immunologic and biological activities have been reported (6). It has therefore been proposed that the ratio of non-22-kDa GH to 22-kDa GH isoforms may have important implications for normal and abnormal growth (7). We studied two nonrelated patients from Argentina with severe short stature and IGHD type 2 attributable to the R183H GH-1 gene mutation and found that the evaluation of GH response to provocative tests might be misleading in these patients, depending on the type of assay used to assess …

Growth hormone responses to repeated maximal cycle ergometer exercise at different pedaling rates

The present study examined the growth hormone (GH) response to repeated bouts of maximal sprint cycling and the effect of cycling at different pedaling rates on postexercise serum GH concentrations. Ten male subjects completed two 30-s sprints, separated by 1 h of passive recovery on two occasions, against an applied resistance equal to 7.5% (fast trial) and 10% (slow trial) of their body mass, respectively. Blood samples were obtained at rest, between the two sprints, and for 1 h after the second sprint. Peak and mean pedal revolutions were greater in the fast than the slow trial, but there were no differences in peak or mean power output. Blood lactate and blood pH responses did not differ between trials or sprints. The first sprint in each trial elicited a serum GH response (fast: 40.8 +/- 8.2 mU/l, slow: 20.8 +/- 6.1 mU/l), and serum GH was still elevated 60 min after the first sprint. The second sprint in each trial did not elicit a serum GH response (sprint 1 vs. sprint 2, P < 0.05). There was a trend for serum GH concentrations to be greater in the fast trial (mean GH area under the curve after sprint 1 vs. after sprint 2: 1,697 +/- 367 vs. 933 +/- 306 min x mU(-1) x l(-1); P = 0.05). Repeated sprint cycling results in an attenuation of the GH response.

Growth Hormone Response to an Acute Bout of Resistance Exercise in Weight-Trained and Non-Weight-Trained Women

The serum growth hormone (GH) response of 6 non-weight-trained (NWT) and 6 weight-trained (WT) eumenorrehic, ovulatory women performing a heavy resistance exercise protocol (HREP) in the early follicular phase was examined. The HREP consisted of 7 different exercises and utilized a moderate resistance (10 repetition maximum) with short rest periods (1 minute). GH was evaluated preexercise, immediately postexercise, and 5, 15, 30, and 60 minutes postexercise. A significant difference was observed between groups (n = 6) for GH at preexercise, immediately, and 5 minutes postexercise (p < 0.05). The integrated area under the curve (AUC) for GH revealed no significant difference between groups (n = 6). However, after removing 2 subjects who were outliers (n = 5), significant differences in both the GH response over time (p < 0.01) and AUC GH (p < 0.01) were observed between groups. The most notable findings were that WT women demonstrated lower preexercise GH concentrations than their NWT counterparts with all subjects (n = 6; WT 2.47 ± 1.27 μg · L−1; NWT 4.99 ± 1.23 μg · L−1, p < 0.01) and with the removal of outliers (n = 5; WT 1.21 ± 0.21 μg · L−1; NWT 4.08 ± 1.0 μg · L−1p < 0.01). Additionally, the HREP elicited a greater overall GH response in the WT group (n = 5; WT 179.6 ± 59.5 μg · L−1; NWT-15.1 ± 16.7 μg · L−1) as reflected by the integrated AUC (p < 0.01). The lower preexercise GH concentrations and greater overall GH response of the WT group suggest that, in women, GH response to resistance exercise varies with training status.

Age-Sensitive Cognitive Function, Growth Hormone and Insulin-Like Growth Factor 1 Plasma Levels in Healthy Older Men

Circulating levels of growth hormone (GH) change during the process of aging. Decline of cognitive functioning with aging is also well established. In this study, we investigated whether insulin-like growth factor 1 (IGF-1) and the GH response to a challenge of GH-releasing hormone and GH-releasing peptide 6 were associated with age-sensitive cognitive functions, but not with functions that do not decline with aging, in 17 healthy male subjects aged between 66 and 76 years. In addition, relations with anthropometric measures were examined. Neuropsychological performance was scored on tests of variables not sensitive to aging (general knowledge, vocabulary, basic visual perception and reading ability), and of variables sensitive to aging (visuoconstructive ability, perceptual motor and mental processing speed, and verbal long-term memory). After correcting for education, the serum GH response was significantly associated with two age-sensitive cognitive tests (measures of mental processing speed), but with none of the tests not sensitive to aging. However, the direction of the association was opposite to the relation between IGF-1 and these cognitive tests: higher levels of GH response were associated with poorer cognitive performance, whereas higher levels of IGF-1 were associated with better performance. GH response, but not IGF-1, was inversely correlated with body mass index. The results are in accordance with previous research suggesting a disruption of the relation between IGF-1 and GH secretion in older age.

Growth Hormone Response to an Acute Bout of Resistance Exercise in Weight-Trained and Non–Weight-Trained Women

The serum growth hormone (GH) response of 6 non-weight-trained (NWT) and 6 weight-trained (WT) eumenorrehic, ovulatory women performing a heavy resistance exercise protocol (HREP) in the early follicular phase was examined. The HREP consisted of 7 different exercises and utilized a moderate resistance (10 repetition maximum) with short rest periods (1 minute). GH was evaluated preexercise, immediately postexercise, and 5, 15, 30, and 60 minutes postexercise. A significant difference was observed between groups (n = 6) for GH at preexercise, immediately, and 5 minutes postexercise (p < 0.05). The integrated area under the curve (AUC) for GH revealed no significant difference between groups (n = 6). However, after removing 2 subjects who were outliers (n = 5), significant differences in both the GH response over time (p < 0.01) and AUC GH (p < 0.01) were observed between groups. The most notable findings were that WT women demonstrated lower preexercise GH concentrations than their NWT counterparts with all subjects (n = 6; WT 2.47 ± 1.27 μg · L−1; NWT 4.99 ± 1.23 μg · L−1, p < 0.01) and with the removal of outliers (n = 5; WT 1.21 ± 0.21 μg · L−1; NWT 4.08 ± 1.0 μg · L−1p < 0.01). Additionally, the HREP elicited a greater overall GH response in the WT group (n = 5; WT 179.6 ± 59.5 μg · L−1; NWT-15.1 ± 16.7 μg · L−1) as reflected by the integrated AUC (p < 0.01). The lower preexercise GH concentrations and greater overall GH response of the WT group suggest that, in women, GH response to resistance exercise varies with training status.

Appraisal of growth hormone (GH) secretion: evaluation of a composite pharmacokinetic model that discriminates multiple components of GH input.

Criteria for a diagnosis of GH deficiency include inadequate GH secretion as assessed by provocative testing. The changes in serum GH concentration in such tests, however, do not uniformly predict treatment responses. We questioned whether the changes in serum GH have a uniform dependence among subjects on the mass of secreted GH. We simulated spontaneous GH secretory events with bolus infusions of recombinant human GH (rhGH) in 15 somatostatin-infused adult subjects. Maximum serum GH responses, the GH areas under the curve, and GH mass calculated from deconvolution techniques are all indexes of GH secretion influenced by GH clearance and distribution volume. In this group, these indexes showed a nonuniform dependence on the known GH dose. Despite somatostatin infusion, we found evidence for low level basal GH secretion with oscillatory characteristics that may have influenced the GH concentration dependence on GH dose. We then developed and evaluated a new pharmacokinetic model to account for pulsatile, basal, and oscillatory inputs to the serum GH concentration profile. The new model is comprised of three terms. The first describes plasma GH concentrations from exogenous administration of rhGH according to a one- or a two-compartment model. The second term accounts for basal GH secretion. The third is a cosinor function that describes the oscillatory pattern of basal GH. The composite pharmacokinetic model predicted plasma GH concentrations well (r2 = 0.88-0.97); pharmacokinetic and cosinor parameters had high precision and narrow 95% confidence intervals. The pharmacokinetic parameters were stable and independent. The mean values and coefficients of variance (SD/mean) of GH pharmacokinetic parameters in our 15 subjects were: clearance, 0.236 L/min (24%); volume of distribution, 3.46 L (30%); and terminal half-life, 12.3 min (37%). The values for the cosinor parameters were: basal concentration, 0.22 ng/mL (85%); amplitude, 0.758 (50%); cycle, 121 min (27%); and time shift (acrophase), 60.3 min (53.6%). During the 9-h study, clearance decreased from 0.259 +/- 0.09 to 0.214 +/- 0.06 L/min (P < 0.03), and basal concentration increased from 0.20 +/- 0.22 to 0.33 +/- 0.33 ng/mL (P < 0.5). We conclude that our model can provide useful estimates of GH pharmacokinetics in the presence of basal, oscillating, endogenous concentrations without administering a dose of radiolabeled GH. The substantial inter- and intrasubject variance in pharmacokinetic parameters between subjects negates the assumption of a uniform relationship between GH secretion and serum GH concentration and detracts from the utility of a GH concentration cut-off point in GH testing. These findings have implications to the valid appraisal of GH deficiency states, selection of rhGH treatment candidates, and physiological regulation of the GH axis.