Growth Hormone Output Research Articles

Thyrotropin‐Releasing Hormone Mediates Growth Hormone Release Induced by Milk and Nursing in Neonatal Rats

Previous evidence from this laboratory suggested that growth hormone (GH) release induced by milk in vitro and by nursing in vivo from neonatal rat pituitary glands is mediated by an alternative GH-releasing factor(s) (GRF) distinct from GH-releasing hormone (GHRH(1-43) ). In the present experiments we tested whether thyrotropin-releasing hormone (TRH) could fulfil the criteria of this alternative GRF in neonatal rats. The water-soluble fraction of rat milk (infranatant, prepared by ultracentrifugation) and its methanol/acetic acid extract (milk-borne peptides) stimulated GH release from perifused pituitary glands obtained from 2-day-old rats. Dialysis of the infranatant (mol wt cut-off: 2,000) against 500 volumes of culture medium at 4°C eliminated its GH-releasing activity in the perifusion system, while the infranatant retained its full GRF-like activity when incubated at 4°C without dialysis. The milk-borne GRF eluted as a single peak and coeluted with TRH in a combined gel permeation chromatography (Sephadex G-10) and perifusion set-up. Prolactin secretion was also stimulated simultaneously with the release of GH induced either by milk or by TRH. In a stepwise C(18) reversed-phase chromatography, milk-borne GRF was highly hydrophilic and coeluted with synthetic TRH. The in vitro GH-releasing bioactivities of synthetic TRH and a milk extract purified in C(18) reversed-phase chromatography were abolished by proline-specific endopeptidase. Thus, TRH and milk-borne GRF displayed similar molecular weights, hydropathic characteristics and proteolytic enzyme resistance. In vivo, nursing (which has been reported as a potent stimulus of GH secretion even in the absence of milk-intake) increased serum GH levels in 2-day-old pups. A supramaximal dose of TRH (10 ng/g intraperitoneally) stimulated GH release in 2-day-old pups separated from their mothers for 6 h to a similar extent as nursing. Nursing-induced levels of serum GH were not further elevated by TRH. This failure of TRH to further increase serum GH levels was not due to a maximal GH output by the neonatal pituitary gland, since the GH release induced by the serotonin precursor 5-hydroxy-L-tryptophan was augmented either by TRH or by nursing. These data provide evidence that the milk-borne GRF-like activity in vitro is indistinguishable from TRH, and suggest that TRH (probably of hypothalamic origin) might be the mediator of the nursing-induced release of GH in vivo as a physiological GRF in neonatal rats.

Effect of estradiol implant on noradrenergic function and mood in menopausal subjects

The effect of the α 2-adrenoceptor agonist, clonidine, on plasma growth hormone (GH),plasma 3-methoxy-4-hydroxyphenylethyuleneglycol (MHPG), blood pressure and sedation were studied in 16 menopausal subjects before and 6 wk after a 100-mg implant of estradiol. The specific binding of tritiated yohimbine to intact platelets also was studied. Estradiol implants increased basal GH output and reduced baseline MHPG and sedation scores. However, none of the subsequent responses to clonidine were altered. Platelet yohimbine binding also was unchanged following the implant. Both observer- and self-rating scales showed a marked reduction in anxiety and depression scores. The results suggest that estradiol may alter some indices of noradrenergic function, but that the mechanism does not involve alterations in α 2-adrenoceptor sensitivity.

Diagnostic Significance of Urinary Growth Hormone Measurements in Children with Growth Failure: Correlation between Serum and Urine Growth Hormone

Twelve-h overnight urine and serum samples obtained simultaneously at 20-min intervals were assayed for growth hormone (GH). Ninety-one children, 5 to 16 y (Tanner stage 1 to 3) participated; group 1 were healthy children, group 2 were children with organic GH deficiency, and group 3 had idiopathic growth failure and normal GH stimulation tests. Serum pool GH concentrations in group 1 were similar to those in group 3 (3.3 +/- 0.3 versus 3.4 +/- 0.2 micrograms/L); group 2 had significantly lower GH concentrations (1.6 +/- 0.2 micrograms/L). Plasma IGF-I levels were significantly greater in groups 1 (14.2 +/- 2.6 nmol/L, p less than 0.001) than in groups 2 and 3 (2.6 +/- 0.5 and 5.5 +/- 0.7 nmol/L, respectively). Urinary GH (mean +/- SEM) standardized for body weight (micrograms/kg) in group 1 (0.31 +/- 0.02) was significantly greater than in group 2 (0.14 +/- 0.01) and group 3 (0.20 +/- 0.01). However, when expressed as microgram/mol creatinine, the output of GH was similar in group 1 (4.0 +/- 0.3) and group 3 (3.4 +/- 0.3); both groups had significantly greater output compared to group 2 (1.3 +/- 0.2). Urinary IGF-I (nmol/kg) in group 1 (0.22 +/- 0.02) was significantly greater than in group 2 (0.12 +/- 0.01) or group 3 (0.07 +/- 0.01). Urinary GH correlated with serum pool GH concentration (r = 0.64, p less than 0.001). Although urinary GH output reflects endogenous GH secretion, the overlap between groups 1 and 3 precludes using urinary GH measurements as a diagnostic test for GH deficiency in children with idiopathic growth failure.

Comparison of Urinary Growth Hormone and IGF-I Excretion in Small- and Appropriate-for-Gestational-Age Infants and Healthy Children

The output of urinary growth hormone (GH) and IGF-I were quantitated by RIA in 12-h urine collections obtained from infants who were preterm, small for gestational age (PT-SGA, n = 13); preterm, appropriate for gestational age (PT-AGA, n = 27); full term, small for gestational age (FT-SGA, n = 13); and full term, appropriate for gestational age (FT-AGA, n = 29); and from normal children (n = 33). The amounts of GH and IGF-I (mean +/- SEM) excreted by the PT-SGA and FT-SGA infants were not significantly lower than those excreted by the PT-AGA and FT-AGA groups, respectively [GH (micrograms/kg): PT-SGA 13.7 +/- 3.1 versus PT-AGA 14.0 +/- 2.2, FT-SGA 7.8 +/- 2.4 versus FT-AGA 6.6 +/- 1.8; IGF-I (nmol/kg): PT-SGA 0.52 +/- 0.09 versus PT-AGA 0.53 +/- 0.04, FT-SGA 0.31 +/- 0.05 versus FT-AGA 0.35 +/- 0.04]. All infant groups exhibited significantly greater outputs of urinary GH and IGF-I compared with the children (p less than 0.01). The plasma concentrations of GH in all infant groups were high, whereas the plasma IGF-I levels were low. Microalbumin and beta-2 microglobulin excretion did not correlate with urinary GH and IGF-I output. Despite the higher microalbumin output in FT babies, urinary GH and IGF-I excretion was lower in these groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Modulation of neuropeptide-stimulated pituitary hormone secretion in hatchling turtles

Neuropeptides that have relatively narrow actions on mammalian pituitary secretion may have divergent effects on pituitary hormone secretion in ectothermal vertebrates. In turtles, secretion of both thyrotropin (TSH) and growth hormone (GH) can be stimulated in vitro by thyrotropin-releasing hormone (TRH) and by members of corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GHRH) peptide families. To determine if these neuropeptides share common modes of action, and to study other potential regulators of the turtle pituitary, somatostatin-14 (SRIH) and monoamines were tested for direct effects on in vitro basal and neuropeptide-stimulated TSH and GH secretion. Pituitary glands from young turtles ( Pseudemys scripta) were cultured in the presence of 25 n M TRH, ovine CRH, or rat GHRH with or without SRIH. Glands were incubated for several 2-hr periods in medium alone or in medium containing peptides. Preincubation for 4 hr with SRIH (6 or 60 n M) significantly reduced basal and TRH-stimulated TSH and GH output (SRIH present during entire incubation). In another experiment, basal hormone secretion was reduced when SRIH (60 n M) was present only during the 2-hr basal period; however, reduction of TSH and GH responses to TRH required the presence of SRIH (60 n M) during the basal period and the period of stimulation. TSH responses to 25 n M) oCRH and GGHRH and GH responses to GGHRH were significantly reduced by preincubation with 60 n M) SRIH. The biogenic amines, dopamine (DA), serotonin (5HT), and norepinephrine (NE) (50 or 500 n M) were tested for possible direct actions on basal and neuropeptide-stimulated pituitary TSH and GH secretion. Only 5HT at the highest dose tested (500 n M) elevated TSH secretion in the absence of neuropeptides. None of the amines had any effect on neuropeptide-stimulated TSH release. In contrast, GH responses to 25 n M) TRH and GHRH were enhanced by DA (50 and 500 n M) and reduced by 5HT (500 n M) Only NE (500 n M) elevated GH secretion in the absence of neuropeptides, and NE enhanced TRH-stimulated GH secretion (NE was not tested for effects on CRH and GHRH responses). These data show that mammalian SRIH and monoamines can modify basal and neuropeptide-stimulated TSH and GH secretion in turtles. While the mechanism(s) by which the different neuropeptides stimulate the release of TSH and GH from turtle pituitaries is not known (i.e., direct or paracrine), some commonality in their mode of action seems likely, since exposure to SRIH or amines affected the responses to each of the different neuropeptides similarly. Finally, these results implicate several other brain factors in the regulation of pituitary hormone secretion in turtles.

Diagnostic Limitations of Spontaneous Growth Hormone Measurements in Normally Growing Prepubertal Children

To evaluate whether the measurement of the spontaneous overnight growth hormone secretion in prepubertal children clearly separated normal children from subjects with growth hormone deficiency, we studied 45 prepubertal normally growing children (10 with normal height and 35 with constitutional growth delay) and compared their overnight growth hormone secretion with that of a group of subjects with either isolated growth hormone deficiency or neurosecretory dysfunction. Peak growth hormone levels (greater than or equal to 10 ng/mL) following oral clonidine administration were normal in individuals with normal height, constitutional growth delay, and neurosecretory dysfunction, as was the basal somatomedin C concentration; subjects with growth hormone deficiency had low peak growth hormone levels (less than 10 ng/mL) following oral clonidine administration as well as low basal somatomedin C values. The mean 9-hour overnight growth hormone concentration, total growth hormone output, total number of nocturnal pulses, and the mean peak growth hormone response during nocturnal sampling were similar in the normal height and constitutional growth delay groups and significantly greater than those seen in subjects with either growth hormone deficiency or neurosecretory dysfunction. Twelve (26.6%) of 45 normally growing children (4 to 10 normal height and 8 of 35 constitutional growth delay), however, had low overnight growth hormone levels (less than 3 ng/mL), which overlapped results obtained in the growth hormone-deficient or neurosecretory dysfunction groups. Frequent overnight growth hormone (GH) sampling does not always separate normal-growing children from those with partial or complete GH deficiency. In our this study over one quarter of the normally growing children had overnight GH levels in the range of children with either GH deficiency or neurosecretory dysfunction. These findings, in addition to the cost and difficulty in performing this test, do not support the measurement of spontaneous GH as a routine test in short but normally growing prepubertal children.

Cachectin alters anterior pituitary hormone release by a direct action in vitro.

Cachectin (tumor necrosis factor) is a powerful macrophage hormone released during infection, which circulates in blood to produce diverse effects in the organism. We examined the effect of cachectin on release of anterior pituitary hormones from either hemipituitaries or dispersed pituitary cells incubated in vitro. The action of cachectin on dispersed cells was demonstrable only after 2 hr of incubation. With this incubation time, the protein produced a dose-related stimulation of release of adrenocorticotropin (ACTH), growth hormone (GH), and thyrotropin (TSH), but not of prolactin (Prl), from both hemipituitaries and dispersed cells. The doses required for stimulation were low in the case of hemipituitaries, usually of the order of 10(-12) M, whereas they were higher by one or two orders of magnitude with the dispersed pituitary cells. This may be related either to loss of receptors for the protein during the dispersion procedure or to the fact that in the hemipituitary system cell interactions are facilitated because the cells are close to each other. In the dispersed cell system cachectin evoked a dose-related decrease in cyclic AMP content. Incubation with somatostatin lowered the cyclic AMP content of the cells and depressed GH output without altering output of TSH or Prl. When somatostatin and cachectin were incubated together with the cells, the suppression of cyclic AMP production was abolished; TSH and Prl release were stimulated, but the action of cachectin to stimulate GH release was blocked. The stimulation of Prl release by cachectin in the presence of somatostatin may be related to the elevation of cyclic AMP, a known stimulator of Prl release. The cyclooxygenase inhibitor indomethacin nearly completely blocked the stimulatory effect of cachectin on release of GH and TSH from dispersed pituitary cells but had only a slight and nonsignificant attenuating effect on its ACTH-releasing action. These results suggest that at least part of the stimulatory action of the peptide on pituitary hormone release is brought about by prostaglandins. The failure of indomethacin to block the release of ACTH induced by cachectin suggests that other mechanisms may be involved in the release of ACTH induced by this peptide. Since the concentrations of cachectin required to stimulate pituitary hormone release are similar to those that are encountered in plasma during infection, it is likely that this direct pituitary action has pathophysiological significance.

Endocrine Aspects of Obesity

As is obvious from the previous discussions, obesity is associated with a wide variety of changes in endocrine parameters (Table 1). Some of these changes, such as the reduction in SHBG without change in serum free testosterone levels, reflect merely laboratory abnormalities that may influence interpretation of diagnostic tests but have no important physiologic relevance. Other abnormalities have major clinical impact, such as hyperestrogenemia-endometrial carcinoma and hyperlipidemia-coronary artery disease. In some cases, endocrine changes in obesity are beneficial--that is, hyperestrogenemia leading to lower incidence of osteoporosis. In other cases, such as the profound suppression of growth hormone output in obesity, the physiologic relevance is unknown. Several endocrine changes in obesity, such as the impaired response of many hormones (growth hormone, prolactin, vasopressin, corticotropin) to insulin-induced hypoglycemia and elevated endorphin levels, suggest hypothalamic dysfunction. Furthermore, the failure of all of these abnormalities to be normalized after weight reduction raises the possibility of an underlying disorder leading to both endocrine dysfunction and obesity, rather than the endocrine dysfunction being simply a consequence of the obesity. Successful elucidation of the pathogenesis of obesity, which might then lead to much needed specific treatment modalities, may be advanced if we can solve some of these puzzles.

Growth hormone (GH) responses to GH-releasing hormone in depression: Correlation with GH release following clonidine

Twenty subjects (10 patients with major depressive disorder and 10 controls matched for age, gender, and ovarian status) received 1 μg/kg synthetic human growth hormone-releasing hormone (GHRH)-44 amide as an i.v. bolus dose. Compared to controls, depressed patients showed a significant attenuation of net growth hormone (GH) responses to GHRH associated with normal basal GH concentrations. The blunted GH responses occurred in the face of significantly higher somatomedin C (Sm-C) concentrations. Comparison of GH responses after GHRH with GH output following the α 2-agonist clonidine (CLON) revealed a significant positive correlation. The concordance between GH responses after specific challenges at different levels of the GHRH-GH-somatomedin axis indicates the integrity of the hypothalamic-pituitary-somatotropic system in depression and supports the view that altered GH secretory patterns in depression may primarily be due to a suprapituitary disturbance.

Quantitation of urinary growth hormone in children with normal and abnormal growth.

Urinary growth hormone (GH) excretion was quantitated in 12-h overnight urine collections obtained from 31 control children, ages 3 to 17 yr (group 1); 21 children, ages 5 to 19 yr with GH deficiency (group 2), and 30 subjects, ages 10 to 18 yr with idiopathic growth failure and normal GH stimulation tests (group 3). The output of urinary GH was measured in one acromegalic woman. The authenticity of urinary GH, 22 kDa, was confirmed by high-performance liquid chromatography. The elution pattern of urinary GH was identical to that of biosynthetic and pituitary-derived GH. The immunoreactive profiles characterized by monoclonal immunoradiometric GH assay and standard GH radioimmunoassay were identical. The quantity of GH (mean +/- SEM per kg body weight) in group 1 (0.27 +/- 0.02 ng/kg) was significantly greater than group 2 (0.08 +/- 0.02 ng/kg) or group 3 (0.17 +/- 0.02 ng/kg, p less than 0.01). Approximately 50% of the subjects in group 3 had urinary GH measurements indistinguishable from those observed in the GH-deficient population. Twelve hypopituitary patients (group 2) excreted significantly greater amounts of urinary GH in the first 12 h after GH administration compared to the baseline period (0.41 +/- 0.07 versus 0.12 +/- 0.02 ng/kg, p less than 0.01). Markedly elevated output of urinary GH (2.0 ng/kg) was documented in one acromegalic patient. The data suggest that measurements of urinary GH may be a useful, simple, and noninvasive screening test for identifying patients with GH deficiency or excess.

Attenuated growth hormone response to growth hormone-releasing hormone in major depressive disorder

Growth hormone-releasing hormone (GHRH), recently isolated and characterized by Rivier et al. (1982), is a 44amino acid hypothalamic peptide that stimulates growth hormone (GH) release from somatotrophs. GHRH thus may help our understanding of the pathophysiology underlying the distorted regulation of growth hormone secretion linked to depression. Moreover, current research suggests that GHRH is not only a primary neuroregulator of GH secretion, but may also mediate the diurnal hypersecretion of GH (Mendlewicz et al. 1985) and the deficient GH output in response to pharmacological chal-

The effects of cranial irradiation on growth hormone secretion.

Growth hormone (GH) secretion has been studied under physiological conditions and in response to standard pharmacological stimuli in 14 children, who had previously received cranial irradiation between two and fourteen years earlier. All fourteen showed a blunted GH response to insulin hypoglycaemia and, in twelve, the GH response to arginine stimulation was also subnormal. Physiological GH secretion was studied by measuring integrated GH concentrations in 30 min blood samples collected over a 24 hour period by a continuous withdrawal pump. Compared to normal controls (n = 5), the irradiated patients showed a significant reduction in the mean integrated GH concentration (2.2: 8.8 mU/l; p less than 0.002), the total 24 hour GH output (mean 105.7 mU vs. 391.7 mU; p less than 0.002) and the mean GH output during the first six hours of sleep (mean 48.2 mU vs. 226 mU; p less than 0.002). There was no significant correlation between the maximum peak GH response to either pharmacological test and the total 24 hour GH output. Conventionally most short children undergo two provocative tests of GH release and if the GH response to one of the two tests is normal, it is usually assumed that GH production is adequate. Adopting these criteria in this study it would have been assumed incorrectly that GH production was normal in two children. Nonetheless all 14 children showed a blunted GH response to an ITT as well as a reduced total 24 hour GH output.(ABSTRACT TRUNCATED AT 250 WORDS)

Reduced pulsatile growth hormone secretion in children after therapy for acute lymphoblastic leukemia

Basal growth hormone levels were measured every 20 minutes over 24 hours in eight long-term survivors of acute lymphoblastic leukemia and in 13 age- and pubertal stage-matched normal children. Among the patients, the median total basal growth hormone output (AUC) was 43 units, compared with 341 units in the normal control group (P less than 0.001). In the patients, mean pulse amplitude (6.9 ng/ml) and frequency (4.6) over 24 hours also were reduced, compared with the control values (32 ng/ml and 8.5, P less than 0.001 and P less than 0.05, respectively). In addition, normal children secreted more GH at night (median AUC 280) than during the day (113, P less than 0.001). However, this diurnal pattern was absent in three of the patients studied. These data suggest that perturbations of spontaneous pulsatile GH secretion are common after standard therapy for ALL and may be a sensitive means of detecting therapy-related neuroendocrine damage. Blunting of spontaneous pulsatile GH secretion may contribute to the abnormalities in growth seen in children with ALL.

Alteration in both insulin release and its hypoglycemic effects in atopic bronchial asthma

In 31 patients with atopic bronchial asthma in clinical remission and in 21 healthy sex- and age-matched subjects, the responses to intravenous tolbutamide (1.0 gm) and insulin (0.1 U/kg) were studied over a period of 2 hr. In response to tolbutamide, asthmatics released significantly less insulin, but their blood glucose levels did not differ from those of controls. Asthmatics also reacted to tolbutamide-induced hypoglycemia with significantly greater output of growth hormone to blood. Following intravenous injection of insulin, the recovery of the blood glucose concentrations was significantly reduced in asthmatic patients. More economical use of insulin and increased responsiveness to its hypoglycemic action, together with the well-known reduction in hypoglycemic effects of catecholamines in bronchial asthma, might explain why asthmatics rarely develop diabetes mellitus.

Role of the gonads in hypertension-prone rats.

In a genetically hypertension-prone (S) strain of rats it was observed previously that males generally developed hypertension more rapidly on a high salt diet than did females although final pressure ultimately were similar in both sexes. A genetic study had shown that there was no sex-linkage involved in setting blood pressure levels, so it was thought that the gonads might be involved. In the present work, castration of males had no effect on blood pressure but in the females it caused a rise in pressure that could not be distinguished from that in males, both on a high and low salt diet. Castration resulted in greater growth in females than in controls, whereas it had the opposite effect in males. It was speculated that these changes were due to influences on pituitary growth hormone with castration increasing the net output of growth hormone (or enhancing receptor sensitivity to it) in the female and the opposite in the male. From the work of others, there are some data compatible with such an interpretation. Experimentally, growth hormone will induce hypertension in rats. Therefore, it is conceivable that growth hormone is involved in the increment in hypertension observed in these castrate females. Because the effect on blood pressure was observed in castrate females on both high and low NaCl diets, it was considered unlikely that the blood pressure effect was simply due to increased NaCl intake in the food associated with greater growth. It was suggested that this rise in blood pressure with cessation of ovarian function might bear on the unsettled question of "menopausal" hypertension in women: in the genetically susceptible individual an increase in growth hormone associated with declining ovarian funtion in the menopause could provide the stimulus for the appearance of hypertension some years earlier than would otherwise have been the case.

Growth hormone studies before and during catch-up growth in a child with emotional deprivation and short stature.

ABSTRACT Growth hormone response to arginine, insulin hypoglycemia and sleep was studied during separate hospitalizations in a child with emotional deprivation and short stature. During both study periods growth hormone response to arginine and hypoglycemia was low on admission to the hospital and high after 6 weeks. There was no growth hormone response to slow wave sleep in the first sleep cycle at the time of the second hospital admission but the response to sleep was normal after 6 weeks of hospitalization. These studies suggest a temporal correlation between catch-up growth and growth hormone output. The normal sleep pattern suggests that the lack of growth hormone output seen in emotional deprivation and short stature is not related to disturbed sleep.

Transorbital pituitary stalk section in primates.

✓ Pituitary stalk section through the orbit by microsurgical technique is described in eight monkeys. The use of the microscope and the approach through the optic foramen minimize incidental injury. Under these circumstances experiments designed to study neuroendocrine relationships may be carried out free of errors introduced by damage to the temporal lobe or hypothalamus. Plasma cortisol drops to very low levels, but still support life. Growth hormone output is negligible.

Assessment of growth hormone reserve: comparison of intravenous arginina and subcutaneous glucagon stimulation tests.

ABSTRACT A study was conducted to compare the effects of arginine infusion and sc glucagon injection on release of growth hormone. Twentyeight subjects received both agents on separate days and served as their own controls. Eighteen of these were tested after 48- and 72-hr fasts in order to separate any direct growth hormone stimulating effect of glucagon from the indirect response due to falling plasma glucose levels following glucagon induced hyperglycemia. Arginine was an effective agent in the majority of patients studied. There was negligible rise of plasma growth hormone in the absence of variation in plasma glucose levels after subcutaneous glucagon injection. That this failure of output of growth hormone was not due to inability to secrete it is confirmed by positive arginine induced growth hormone responses in the same individuals. Our data shows that arginine is a consistent and potent stimulus for growth hormone release, and is superior to glucagon as a test for growth hormone reserve. The occa...

The location of the chemoreceptor controlling growth hormone secretion during hypoglycemia in primates.

Monkeys were prepared with multiple, chronically implanted intracranial cannulae. Such animals when sedated with phencyclidine were found to have persistently low basal plasma growth hormone (GH) concentrations and to secrete GH and cortisol in response to insulininduced hypoglycemia and iv administered 2– deoxy—D—glucose (2DG). Microinjections of 2DG were made into many hypothalamic sites in these animals. Injections into most of the hypothalamus, including the ventro—medial nucleus, and into the third ventricle were without effect upon GH output. Unilateral microinjections of 2DG into the lateral hypothalamic area alongside the mid—part of the ventro—medial nucleus were invariably followed by a sustained rise in plasma GH comparable in magnitude and duration to that provoked by hypoglycemia. It is inferred that the chemoreceptors which control the GH secretory response to hypoglycemia are located in this area. (Endocrinology 91: 217, 197

EXERCISE AS A SCREENING TEST FOR GROWTH HORMONE RELEASE

ABSTRACT Serial exercise experiments on the same male subject and subsequent standard exercise studies on 8 men showed that it was possible to predict the timing of the output of growth hormone (GH) which resulted from exercise of sufficient severity in these normal subjects. On the basis of these observations single blood samples taken 25–30 minutes after the start of a short period of moderately severe exercise were found to contain elevated levels of GH in 89% of normal male and female subjects tested. It is suggested that this could serve as a method of screening for ability to release GH which would avoid the necessity for the usual more complex procedures.