Insulin and physical exercise

Secretion of some pituitary hormones and sympatho-adrenal activity increase very early during exercise. Sympathetic activation is of major importance in cardiovascular adaptation, thermoregulation, etc. Furthermore among the hormonal consequences of such activation those related to insulin are capital. In animal and human subjects basal insulin level decrease during prolonged and progressive exercise. With habitual exercise, both basal and stimulated insulin levels are reduced. It seems that the reduced basal level could be due to alpha-adrenergic inhibition of the islets of Langerhans, while the reduced stimulated response could be the consequence of increased clearance. In trained subjects, in spite of reduced insulin secretion tolerance to glucose is normal due to increased sensitivity to insulin. Sensitivity to insulin is particularly enhanced at the muscular tissue level; it is accompanied by increased hexokinase and glycogen synthetase activity. As a consequence glucose uptake remains optimal at the muscular level. In the liver, both insulin sensitivity and glucokinase activity are reduced, so that glucose is spared and the muscular glycogen store can be restored. At the adipocyte level, metabolic adaptations are such that triglyceride turnover is greatly increased, favouring fuel supply and resaturation of stores.     

Influence of acute administration of human growth hormone and alpha-MSH on plasma concentrations of aldosterone, cortisol, corticosterone and growth hormone in man.

The effect of acute administration of human growth hormone (HGH) and of alpha-melanocyte stimulating hormone (alpha-MSH) on plasma aldosterone, cortisol, corticosterone and growth hormone has been studied in normal man and in patients with panhypopituitarism. There is no acute effect of exogenous HGH on plasma levels of aldosterone, cortisol and corticosterone in normal man and in patients with panhypopituitarism. The plasma level of immunoreactive HGH measured during acute HGH infusion in man does not seem to be proportional to the dose administred in our study. Alpha-MSH raises the concentartion of plasma HGH, BYT THIS STIMULATION IS NOT DOSE-DEPENDENT. Aldosterone, cortisol and corticosterone concentrations are not influenced by the elevation of HGH mediated by alpha-MSH in normal man. Although in some patients with panhypopituitarism an elevation of plasma aldosterone concenntration following alpha-MSH infusion is observed, it is unlikely that MSH is directly involved in the acute regulation of aldosterone secretion in healthy subjects.     

Elevated immunoreactive insulin concentration during spontaneous attacks in thyrotoxic periodic paralysis

It has been well documented that administration of insulin or procedures that increase endogenous insulin secretion may provoke the attack of hypokalemic periodic paralysis. However, there have been no reports on the endogenous insulin levels before and during spontaneous attack of periodic paralysis. In the present investigation we measured concentration of blood glucose, serum immunoreactive insulin (IRI), human growth hormone (HGH), Na, and K during spontaneous attacks of periodic paralysis and also after an oral load of 100 g glucose in seven thyrotoxic patients with the history of periodic paralysis. Three attacks of paralysis were observed in two patients. In one patient basal level of IRI was abnormally high, and the postglucose IRI response was exaggerated. Preceding the attack, IRI increased to 500 μU/ml from the basal level of 75 μU/ml. In the other patient it increased to 105 μU/ml from the basal level of 7 μU/ml at the onset of paralysis. Those levels observed at the onset of paralysis were abnormally high when compared to those in patients in whom no attacks were observed. HGH, blood glucose, and Na had no correlation with paralysis, although K decreased during the attack. Thus, we demonstrated for the first time that the spontaneous attack of paralysis was preceded by an increased secretion of insulin. These results suggested the following two abnormalities in thyrotoxic periodic paralysis: abnormal increase in insulin in response to glucose or dietary load, and decrease in muscle membrane potential in response to elevated insulin.     

Levels of serum sex hormones and risk factors for coronary heart disease in exercise-trained men

On the basis of previous findings, it has been hypothesized that hyperestrogenemia may be the major predisposing factor for coronary heart disease and that an elevation in the estradiol-to-testosterone ratio, or a closely related hormonal alteration, may cause the expression of risk factors for coronary heart disease. The present study was carried out to investigate whether exercise training, which has been reported to reduce risk factors for coronary heart disease, affects the serum sex hormone levels. The serum sex hormone levels, established risk factors for coronary heart disease, and physical fitness were measured in 10 men who had undergone at least six months of intensive exercise training and in 10 sedentary men of similar age. Despite evidence for a strikingly higher level of physical fitness and a lower level of risk factors in the trained group, no significant difference in mean serum estradiol level was found. Nor did three subjects from the sedentary group show a decrease in estradiol level after three to four months of exercise training. The mean estradiol-to-testosterone ratio, however, was significantly lower in the trained group and might account for the lower level of risk factors in that group. If the hypothesis is correct, exercise training may decrease established risk factors for coronary heart disease without decreasing the risk of coronary heart disease.     

The adrenocorticol stress-response in the aged male rat: Impairment of recovery from stress

To test if the adrenocortical axis of the rat loses sensitivity to negative feedback control during aging, we have examined corticosterone secretion under basal, stressed and post-stress conditions in young and in aged Fisher male rats. We find no age-related change in the speed or magnitude of the stress response or in the capacity to manifest a corticosterone response following chronic stress. However, we do observe in aging rats an elevation of basal corticosterone and an impaired capacity to adapt to and recover from stress. This latter finding is illustrated by longer latencies relative to young rats, in the return of serum corticosterone concentrations to basal values during sustained exposure to mild cold or following the end of immobilization stress. All of these deficits reflect an increased rate of corticosterone secretion during physiologically inappropriate circumstances. Such observations support the concept that there is an age-related loss of sensitivity of the brain and pituitary to the inhibitory effects of high circulating levels of corticosterone on ACTH release.     

Studies in congenital generalized lipodystrophy. IV. Effect of muscular exercise on carbohydrate and fat metabolism including plasma levels of IRI and HGH.

Two patients with congenital generalized lipodystrophy have been studied at rest, and during and after long-term exercise at different carefully measured work loads. The two patients represented different stages of diabetes development. Both patients derived most of their energy used during muscular exercise from carbohydrate, and comparatively little from fat. FFA levels remained low throughout the period of observation in contrast to normal individuals and patients with juvinile diabetes. The data presented seem to show that deposition of glucose and free fatty acids (FFA) as triglyceride, must be impaired and are not compatible with the concept of increased triglyceride turnover in the adipocytes. The fall in blood glucose concentration (BCG) was less than in normal individuals and juvenile diabetes during exercise, and the glucose tolerance remained unchanged following work stop in both patients (k-values unchanged), in contrast to normal persons and patients with juvenile diabetes. Both patients showed significant falls in circulating immuno-reactive insulin (IRI) levels during exercise irrespective of a rise or fall in BGC. Thus, the exercise itself might activate endogenous mechanisms which could, on the one hand increase the circulating BGC, and at the same time force circulating IRI to decrease, thus disturbing the well-known relationship between circulating glucose and IRI levels as has been exhibited in normal subjects. The high IRI levels, also during exercise in these patients, indicate a relative insulin resistance in the muscles, but less marked than the insulin resistance in the adipose tissue. The IRI response after glucose infusion did not change significantly with increasing work loads with one exception. Exercose did not alter significantly the human growth hormone (HGH) levels in either the diabetic or the non-diabetic patient indicating an abnormal regulation of the HGH secretion in congenital lipodystrophy.     

Exaggerated blood pressure responses to submaximal exercise in normotensive adolescents with a family history of hypertension

Twenty-four adolescent boys with a positive and 40 boys with a negative parental history of hypertension (PH+ and PH-, respectively) were studied at rest and during exercise on a bicycle ergometer at work loads ranging from 25 to 150 W. Each group was divided into fit and unfit categories on the basis of oxygen consumption at a heart rate (HR) of 150 beats/min. Blood pressure (BP) at rest averaged 114.2/68.8 mmHg in the PH+ group and 110.9/70.3 mmHg in the PH- group. Age and body weight did not differ between subgroups, although resting HR was lower in fit than in unfit subjects (P less than 0.01). Oxygen consumption increased with exercise but did not differ between groups at any work level. However, systolic BP was significantly higher in the PH+ group than in the PH- group at both 100 W (163.1 +/- 12.3 versus 156.7 +/- 12.2 mmHg) and 150 W (174.3 +/- 12.5 versus 166.6 +/- 10.4 mmHg, P less than 0.05). These results suggest that the exaggerated BP responses to exercise, characteristic of hypertensive patients, may be present in normotensive adolescents with an increased risk of developing the disorder, and may reflect pathophysiological changes that precede sustained BP elevation.     

Growth hormone response to L-Dopa in diabetes mellitus

Summary The effect of a single oral dose of 0.5 g L-Dopa on the serum levels of human growth hormone (HGH) was studied in 38 diabetics and 15 age and sex matched control subjects. The diabetics were divided into three clinical sub-groups:a) juvenile diabetics, 15;b) maturity onset diabetics, 15; andc) insulin dependent diabetics admitted in a state of ketoacidosis, 8. L-Dopa-induced HGH secretion in juvenile and maturity onset diabetics was studied before and after the control of diabetes mellitus. HGH was estimated by a homologous double antibody radioimmunoassay. The fasting serum HGH in maturity onset diabetics did not differ significantly from that of control subjects; it was significantly higher in juvenile diabetics and in ketotic diabetics during ketosis and after the control of diabetes. In juvenile diabetics the mean fasting serum HGH level decreased after the control of diabetes but was still significantly higher than in normal subjects. L-Dopa caused a significant rise in serum HGH in 14 control subjects. Among the diabetics the HGH response to L-Dopa was either absent or markedly attenuated in the uncontrolled state. After the control of diabetes a significant improvement in HGH response to L-Dopa was evident in juvenile diabetics but no improvement was seen in maturity onset diabetics. There is thus a considerable derangement in HGH secretion in diabetes mellitus. The various possibilities are discussed.     

Growth hormone isoforms release in response to physiological and pharmacological stimuli

Ten healthy subjects used to performing regular physical activity and eight subjects affected by idiopathic isolated GH deficiency (GHD) were enrolled; 22- and 20-kDa GH secretion and its biological activity were evaluated in response to pharmacological stimuli such as arginine, L-dopa or glucagon in GHD children, while the hormonal response to exercise was studied according to Bruce protocol in healthy subjects. We found a significant increase in 22- and 20-kDa GH level in healthy subjects after monitored physical exercise (MPE; basal 0.28+/-0.12 vs 7.37+/-2.08 ng/ml and basal 0.076+/-0.04 vs 0.18+/-0.05 ng/ml, respectively). Furthermore, the 22-kDa/20-kDa ratio significantly increased in children who had undergone MPE and the GH bioactivity basal mean value also increased significantly after exercise (basal 2.86+/-0.76 vs 7.64+/-1.9 ng/ml). The mean value of 22-kDa GH in GHD patients increased significantly following GH pharmacological stimulation (2.78+/-0.63 ng/ml) when compared with mean basal (0.20+/-0.11 ng/ml) value. In the GHD group the basal concentration of 20-kDa GH significantly increased following GH pharmacological stimulation (0.34+/-0.11 vs 0.72+/-0.2 ng/ml); the 22-kDa/20-kDa ratio significantly increased too. Likewise, GH bioactivity in children with GHD increased significantly after pharmacological stimulation test (basal 2.53+/-0.56 vs 7.33+/-1.26 ng/ml). Both GH isoform concentrations and their biological activity are significantly increased in healthy subjects after submaximal exercise protocol and in GHD children after pharmacological stimuli.     

Hormonal supply during physical exercise in elderly patients with ischemic heart disease

30 males, suffering from ischemic heart disease (IHD), and stable exertional angina pectoris, whose age ranged from 60 to 74 years and also 15 apparently healthy volunteers of the same age participated in the study. The IHD patients' blood displayed increased basal levels of adrenocorticotropic hormone (ACTH), cortisol, and met-enkephalins. During graded physical exercise two types of hormonal system response were established: in the first group of patients the plasma ACTH and cortisol levels were seen to rise at maximal threshold load, while in the second group the content of the above hormones declined. The first group of patients showed a less economical hemodynamic response to standard loading in comparison to the second group. A relation was found between changes in hemodynamic system and function of pituitary-adrenal system in elderly IHD patients during physical exercise. Inadequate ACTH and cortisol increase in the course of effects of stress contributed to IHD aggravation in old age, along with reduced tolerance to physical exercise. beta-Adrenoblocker, propranolol, influenced both types of hormonal response, thereby diminishing their shifts in physical stress.     

Effect of lipids on glucagon secretion in man

Animal experiments have suggested a FFA control mechanism for glucagon secretion. In man, the potent effect of FFA on HGH secretion and the similarity of the secretory control mechanisms for HGH and IRG also support a role of FFA in IRG secretion. Our studies in man in which plasma FFA were elevated by either an oral lipid emulsion (Lipomul) or an intravenous lipid suspension (Intralipid) suggest only a minor role of lipids in control of IRG secretion. Plasma FFA and triglyceride elevations did not suppress arginine- or hypoglycemia-induced plasma IRG elevations, but an inhibitory effect of Intralipid on basal plasma IRG concentrations was observed. Although nicotinic acid administration, which caused a depression in plasma FFA, did elevate plasma IRG, the IRG elevation was considered more likely a consequence of stress induced by the drug. The failure of lipids to inhibit IRG secretion at FFA concentrations inhibiting HGH secretion indicates a dissociation in the secretory control mechanisms of the two hormones.     

Ketanserin without effects on basal anterior pituitary hormone secretion in healthy subjects

The effect of ketanserin, a selective serotonin-2 (5-HT2) receptor blocking agent, on the secretion of anterior pituitary hormones was studied in 4 healthy volunteers. Ketanserin (10 mg) was administered as a slow iv injection and its effect was compared with that of saline. Ketanserin influenced neither the basal plasma levels of HGH, ACTH, TSH, LH or prolactin, nor the plasma levels of T4, T3, cortisol or glucose. Even if a single dose of ketanserin had no hormonal effects, this must also be studied after long term use.     

Pituitary and adrenal hormones in patients after myocardial infarction under ergometer load

The levels of human growth hormone (HGH), ACTH and cortisol in the plasma of 100 middle-aged men were measured by means of radioimmunoassay (12 patients in the phase of hospitalization after myocardial infarction, 47 patients in convalescence, 31 patients in post-convalescence, 10 healthy men). Twenty patients in the phase of convalescence and all patients in post-convalescence did exercises on bicycle ergometer with submaximal loading. Patients after myocardial infarction showed significantly lower basic levels of HGH than healthy persons, and the increase in the HGH level induced by exercise was significantly lower. The hormones ACTH and cortisol showed only slight differences. The secretion of the pituitary hormones, mainly HGH, seems to be altered in patients after myocardial infarction.     

Anterior pituitary function in patients with cerebrovascular disease: with special reference to growth hormone secretion in response to TRH administration (author's transl)]

HGH secretion in response to TRH was studied in patients with cerebrovascular disease in order to elucidate an influence of cerebrovascular lesions on the hypothalamus-anterior pituitary function. Blood specimens were obtained before and at the time of 10, 20, 30, 40, 60, 90 and 120 minutes after the intraveneous administration of 200 microgram of TRH in 17 patients with cerebral hemorrhage and in 8 patients with cerebral infarction. With regards to the natural fluctuations of serum HGH caused by cerebrovascular disease, the blood specimens were obrained at the time of 0, 30, 60, 90 and 120 minutes without the administration of TRH in 4 patients with cerebral hemorrhage and in 4 patients with cerebral infarction. Serum HGH was measured using the RIA method and the following results were obtained: 1) An increase in serum HGH was observed in 1 patient with cerebral hemorrhage out of 8 patients with cerebrovascular disease without TRH administration. 2) In 5 out of 17 patients with cerebral hemorrhage, an increase in serum HGH was observed following TRH administration. Three out of these 5 patients were included in the group of non-coma, and 4 out of the 5 patients were female. 3) In 2 out of 8 patients with cerebral infarction, an increase in serum HGH was observed following TRH administration.     

Dietary regulation of human growth hormone secretion

The effect of diet on the secretion of human growth hormone (HGH) was investigated in eight normal subjects—each studied before and after four separate dietary regimens. A high-carbohydrate (525 g) diet of 3600 cal containing 75 g of protein for 23 days suppressed completely arginine-initiated HGH secretion. While subjects were ingesting a control diet, the mean maximal response to arginine was 21.5 ± 3.5 mμg/ml vs. 4.6 ± 0.9 mμg/ml (p < 0.01) following the experimental diet ($\text{X}$ ± SEM). The latter value did not differ from the mean maximal HGH response occurring “spontaneously” after control infusion of saline (3.5 ± 0.9 mμg/ml). This suppression of HGH secretion appeared related to the amount of carbohydrate rather than the total caloric level. An identical pattern occurred when carbohydrate was proportionately the same, but total intake was reduced to 2300 cal. With a high-carbohydrate diet of 2300 cal, the mean maximal HGH response to arginine was 4.7 ± 1.1 mμg/ml vs. a control response of 21.4 ± 4.7 mμg/ml (p < 0.01). Twenty-four-hour secretory patterns of HGH were assessed in three subjects befor and after the high-carbohydrate diet of 2300 cal. Overall HGH secretion was reduced significantly at the termination of the 23-day experimental period in two of these three subjects. HGH secretion was, likewise, significantly reduced by high-carbohydrate diets containing less protein. The change of HGH secretion could not be related in any study to differences in plasma-free fatty acid (FFA) or glucose concentration. FFA concentrations did decline in the first 3–7 days of each experimental period, but returned to basal values 7–8 days prior to reassessment of HGH secretion. Plasma glucose concentrations did not change significantly at any time.     

Impaired counterregulatory hormonal and metabolic response to exhaustive exercise in obese subjects

A reduction of postprandial thermogenesis has been described in obesity; insulin resistance and/or decreased sympathetic nervous system activity seem to play the major role in its pathogenesis. On the other hand, a normal energy expenditure during exercise has been reported. At present, the response and the role of catecholamines in energy metabolism during exercise in obesity have not been well clarified yet. The aim of this work was to study the metabolic and hormonal changes caused by intense exercise in obesity. Nine obese subjects and ten normal weight controls were submitted to exhaustive exercise on a cycloergometer. Blood glucose, free fatty acids (FFA), glycerol, lactate, β-OH-butyrate, insulin, glucagon, plasma growth hormone (HGH), catecholamine plasma levels were assayed before and at the end of exercise, and after a recovery period. The energy cost of exercise was evaluated by indirect calorimetry. In our experiment muscular exercise did not provoke any change in blood glucose and FFA plasma levels in either of our groups. In the obese subjects the insulin plasma levels were higher than in the controls. Glucagon plasma levels did not change. The exercise responses of norepinephrine (NE) (4.28±0.74 vs 8.81±1.35 nmol/l; P<0.01), epinephrine (E) (234.21±64.18 vs 560.51±83.38 pmol/l; P<0.01) and plasma growth hormone (HGH) (134.84±58.97 vs 825.92±195.25 pmol/l; P<0.01) were significantly lower in obese subjects. At the end of exercise, the thermic effect of exercise did not differ between obese and control subjects (0.335±0.038 vs 0.425±0.040 kJ/min×kg fat-free mass. Our findings indicate that an impaired counterregulatory hormone response to exercise exists in obese subjects. The thermic effect of exercise does not seem to be affected by either the reduced catecholamine response nor insulin resistance. Received: 31 July 1996 / Accepted in revised form: 5 February 1997     

Effect of enkephalin and naloxone on gastric acid and serum gastrin and pancreatic polypeptide concentrations in humans.

The effects of a synthetic enkephalin analogue with prolonged opioid activity, D-ala-2-enkephalin (ala-enk) and naloxone given alone or in combination, on vagally, pentagastrin- and histamine-induced gastric secretion and plasma hormonal responses to vagal stimulation have been studied in healthy subjects. D-ala-2-enkephalin reduced basal gastric acid and pepsin secretion, and caused a dose-dependent inhibition of gastric secretory responses to modified sham-feeding and pentagastrin but not to histamine. It increased serum gastrin concentration and suppressed plasma pancreatic polypeptide response to modified sham-feeding. Naloxone alone at lower dose levels did not affect gastric secretion and plasma hormonal concentrations but at higher doses it reduced both basal and modified sham-feeding-induced secretion. When combined with ala-enk it reversed in part gastric secretory and plasma hormonal changes induced by this peptide during modified sham-feeding and pentagastrin stimulation. These results indicate that (1) stable enkaphalin analogue inhibits basal and vagally or pentagastrin-induced gastric secretion, and affects plasma hormonal response to vagal stimulation, at least in part, via activation of opioid receptors and (2) endogenous opioid substances may be involved in the stimulation of gastric secretion in man.     

EFFECTS OF SOMATOSTATIN ANALOGUE SMS 201–995 IN NON-INSULIN-DEPENDENT DIABETES

The 24-h hormonal and metabolic profiles obtained in five non-insulin-dependent diabetics receiving twice daily s.c. injections of the long-acting somatostatin analogue SMS 201-995 (50 micrograms) have been compared with those obtained following placebo injection. Injections were given 30 min before breakfast and the evening meal. GH secretion was not suppressed by the analogue administered in this manner. Despite suppression of serum insulin levels following breakfast and the evening meal, blood glucose levels were similar during the two study periods with no evidence of worsening in diabetic control. Prolonged suppression of plasma glucagon levels was observed and the nocturnal elevation in serum TSH levels was abolished. Free T4 levels fell significantly following the analogue but total T3 levels were unaffected. Blood alanine levels were elevated throughout the study period following SMS 201-995 but changes in lactate, pyruvate, glycerol and 3-hydroxybutyrate were minor. All five subjects suffered gastrointestinal side-effects. SMS 201-995 (50 micrograms) given twice daily before meals does not cause a deterioration in metabolic control, does not suppress 24-h GH secretion and causes significant side-effects in patients with non-insulin-dependent diabetes mellitus.     

The effect of physical training on hormonal status and exertional hormonal response in patients with chronic congestive heart failure.

BACKGROUND: Physical training improves exercise capacity in patients with chronic heart failure. It decreases plasma noradrenaline at rest, which may be prognostically favourable. The effect on atrial natriuretic peptide, another prognostic factor, and on catabolic and anabolic hormones remains unknown. Furthermore, to our knowledge, the contribution of exertional hormonal responses to the improved exercise capacity has not been evaluated. METHODS: 27 patients with stable chronic heart failure (New York Heart Association class II-III) were randomized to training (n=12) and control (n=15) groups. The training group exercised on a bicycle ergometer for 30 min three times a week for 3 months. The load corresponded to 50-60% of their peak oxygen consumption. For the next 3 months they exercised at home according to personal instructions. The control group did not change its physical activities. The levels of hormones regulating the cardiovascular system and metabolism were determined at rest and after graded maximal exercise and during exercise with constant submaximal workload. RESULTS: Submaximal exercise capacity increased significantly and peak oxygen consumption tended to improve by 12% in the training group. The plasma noradrenaline at rest tended to decrease by 19%. The plasma level of N-terminal pro atrial natriuretic peptide did not change. Serum cortisol, a catabolic hormone, was normal at baseline and remained unchanged. The serum levels of anabolic hormones, growth hormone and insulin, as well as dehydroepiandrosteronesulfate and free testosterone were within a normal range at baseline. They were not altered by training. The dehydroepiandrosteronesulfate/cortisol, and the free testosterone/cortisol ratios, reflecting anabolic/catabolic balance, did not change, either. Training resulted in a higher peak noradrenaline response during graded maximal exercise. The rise in serum cortisol during exercise tended to attenuate. CONCLUSION: Physical training, which improves exercise capacity, does not have an unfavourable effect on anabolic/catabolic balance or neurohumoral activation in patients with congestive heart failure. It decreases plasma noradrenaline at rest. Minor changes in hormonal responses during exercise emerged after physical training which unlikely contribute to the improved exercise capacity.     

Human growth hormone and prolactin during pregnancy (author's transl)]

In order to know the secretory behaviors of human growth hormone (hGH) and human prolactin (hPRL) during pregnancy, the following studies were undertaken. Twenty three normal pregnant women of every period of gestation, eighteen women of postpartum and five nonpregnant subjects volunteered for this study. After fasting overnight, these volunteers were placed at complete bed rest, and a fasting antecubital venous blood sample was drawn at 8:00 a.m. Then L-arginine, 30 g, was infused intravenously over a 30 minute period, and venous blood samples were drawn at 30, 45, 60, 90, 120, minutes after infusion. Serum hGH level was detected by hGH radioimmunoassay Kit (Dainabot) and serum hPRL concentration was measured by double-antibody radioimmunoassay system (NIH-NIAMDD). In addition, serum hCS level was measured by hCS-Kobe double-antibody radioimmunoassay system in comparison with the secretory behaviors of hGH and hPRL. 1. Serum hGH, hPRL and hCS concentrations during pregnancy. HGH concentration remained almost unchanged through the course of pregnancy, but hPRL and hCS concentrations increased with the programs of pregnancy. 2. Serum hGH and hPRL concentrations in puerperium. HGH level did not change as compared to that of nonpregnant or pregnant women. HPRL concentration maintained high level in 1-3 postpartum weeks. 3. Effect of arginine on the concentrations of serum hGH, hPRL and hCS during pregnancy. The hGH response decreased, but that of hPRL increased along with the progress of pregnancy. During the arginine loading test there was no significant change in hCS concentration. 4. Effect of arginine on the concentrations of serum hGH and hPRL in puerperium. The HGH response was suppressed at the first week of the postpartum. The response of hPRL was lower than that of late pregnancy. To summarize, hGH and hPRL have some similar biological characters, but there was a difference in secretion pattern of the two hormones during pregnancy. Reserve function of hGH secretion was suppressed, but that of hPRL secretion increased along with the progress of pregnancy. And in the third trimester of pregnancy, the difference of the secretory behavior and secretory reserve function between hGH and hPRL was prominent.