Greater Growth Hormone Response Research Articles

Differences in cortical and pituitary activity in response to hypoglycaemia and cognitive testing in healthy men with different basal activity of the renin-angiotensin system

High renin-angiotensin system (RAS) activity has been associated with a high risk of severe hypoglycaemia in patients with type 1 diabetes and with cognitive deterioration during experimental hypoglycaemia in healthy subjects. The aim of this study was to describe possible differences in cerebral activity during hypoglycaemia and cognitive testing in two groups of healthy men with different basal RAS activity. Ten healthy men with high RAS activity and 10 with low activity underwent six oxygen-15-labelled water positron emission tomography scans: twice during normoglycaemia, twice during insulin-induced hypoglycaemia and twice during post-hypoglycaemia. During the scans, the subjects performed a computer-based reaction time test. Occipital areas were consistently more activated in the low RAS group than in the high RAS group throughout all three conditions. During normoglycaemia, the frontal region was more activated in the low RAS group than in the high RAS group. During hypoglycaemia, the high RAS group was more activated in the pituitary gland than the low RAS group. Basal RAS activity influenced cerebral activity. Low RAS was associated with more pronounced cortical activation in all glycaemic conditions. High RAS was associated with pituitary activation during hypoglycaemia and post-hypoglycaemia, and this was associated with a greater growth hormone response.

Comparison between voluntary and stimulated contractions of the quadriceps femoris for growth hormone response and muscle damage

This study aimed to compare voluntary and stimulated exercise for changes in muscle strength, growth hormone (GH), blood lactate, and markers of muscle damage. Nine healthy men had two leg press exercise bouts separated by 2 wk. In the first bout, the quadriceps muscles were stimulated by biphasic rectangular pulses (75 Hz, duration 400 mus, on-off ratio 6.25-20 s) with current amplitude being consistently increased throughout 40 contractions at maximal tolerable level. In the second bout, 40 voluntary isometric contractions were performed at the same leg press force output as the first bout. Maximal voluntary isometric strength was measured before and after the bouts, and serum GH and blood lactate concentrations were measured before, during, and after exercise. Serum creatine kinase (CK) activity and muscle soreness were assessed before, immediately after, and 24, 48, and 72 h after exercise. Maximal voluntary strength decreased significantly (P < 0.05) after both bouts, but the magnitude of the decrease was significantly (P < 0.05) greater for the stimulated contractions (-22%) compared with the voluntary contractions (-9%). Increases in serum GH and lactate concentrations were significantly (P < 0.05) larger after the stimulation compared with the voluntary exercise. Increases in serum CK activity and muscle soreness were also significantly (P < 0.05) greater for the stimulation than voluntary exercise. It was concluded that a single bout of electrical stimulation exercise resulted in greater GH response and muscle damage than voluntary exercise.

Oral arginine attenuates the growth hormone response to resistance exercise

This study investigated the combined effect of resistance exercise and arginine ingestion on spontaneous growth hormone (GH) release. Eight healthy male subjects were studied randomly on four separate occasions [placebo, arginine (Arg), placebo + exercise (Ex), arginine + exercise (Arg+Ex)]. Subjects had blood sampled every 10 min for 3.5 h. After baseline sampling (30 min), subjects ingested a 7-g dose of arginine or placebo (blinded, randomly assigned). On the exercise days, the subject performed 3 sets of 9 exercises, 10 repetitions at 80% one repetition maximum. Resting GH concentrations were similar on each study day. Integrated GH area under the curve was significantly higher on the Ex day (508.7 +/- 169.6 min.ng/ml; P < 0.05) than on any of the other study days. Arg+Ex (260.5 +/- 76.8 min.ng/ml) resulted in a greater response than the placebo day but not significantly greater than the Arg day. The GH half-life and half duration were not influenced by the stimulus administered. The GH secretory burst mass was larger, but not significantly, on the Arg, Ex, and Arg+Ex day than the placebo day. Endogenous GH production rate (Ex > Arg+Ex > Arg > placebo) was greater on the Ex and Arg+Ex day than on the placebo day (P < 0.05) but there were no differences between the Ex and Arg+Ex day. Oral arginine alone (7 g) stimulated GH release, but a greater GH response was seen with exercise alone. The combined effect of arginine before exercise attenuates the GH response. Autonegative feedback possibly causes a refractory period such that when the two stimuli are presented there will be suppression of the somatotrope.

Similar hormonal responses to concentric and eccentric muscle actions using relative loading

Conventional resistance exercise is performed using sequential concentric (CON) and eccentric (ECC) contractions, utilizing the same muscle load. Thus, relative to maximal CON and ECC resistance, the ECC contraction is loaded to a lesser degree. We have recently shown that at the same absolute load, CON contractions are associated with greater growth hormone (GH) but similar total testosterone (TT) and free testosterone (FT) responses compared with ECC contractions and attributed the larger GH response to greater relative CON loading. In the present study, we have examined the same endocrine parameters to six different upper and lower body exercises using relative loading rather than absolute loading, hypothesizing that GH responses would be similar for CON and ECC actions, but TT and FT responses would be greater after ECC contractions. Seven young men with recreational weight training experience completed an ECC and CON muscle contraction trial on two different occasions in a counterbalanced fashion. The exercises consisted of four sets of 10 repetitions of lat pull-down, leg press, bench press, leg extension, military press, and leg curl exercises at 65% of an ECC or CON 1-RM with 90 s between sets and exercises. CON and ECC actions were performed at the same speed. ECC 1-RMs were considered to be 120% of the CON 1-RM for the same exercise. Blood samples were collected before, immediately after, and 15 min after the exercise. GH significantly increased across both trials but was not different between the two trials. Total testosterone was not significantly altered in response to either trial; however, free testosterone concentrations increased in response to both ECC and CON trials. Data suggest that CON and ECC muscle contractions produce similar GH, T, and free testosterone responses with the same relative loading.

Growth hormone response to the insulin tolerance and clonidine tests in type 1 diabetes

The insulin tolerance test (ITT) is regarded the gold standard for assessing growth hormone (GH) release in adult patients with suspected GH deficiency. Some of these patients also have diabetes mellitus. There are contradictory reports regarding the GH response to ITT in type 1 diabetic patients with varying degrees of metabolic control. This is also true for the clonidine test. We studied ten patients with uncomplicated type 1 diabetes mellitus during periods of poor and improved metabolic control and compared them with ten healthy control subjects. The GH secretion was assessed by an ITT with an insulin infusion of 2.5 mU/kg/min and an intravenous clonidine test. The GH response to ITT was similar during poor and improved metabolic control (mean +/- SEM) (AUC 2327 +/- 616 vs. 2649 +/- 508 microg/l x min) and did not differ from the response in control subjects (AUC 2587 +/- 343 microg/1 x min). The clonidine test induced a significantly greater GH response during poor than during improved metabolic control in the diabetic patients (AUC 2598 +/- 492 vs. 1508 +/- 368 microg/l x min, p < 0.05); this response was greater than in the control subjects (670 +/- 226 x microg/l x min, p < 0.005 vs. improved metabolic control). Thus, the GH response to ITT is similar in diabetic patients with varying degrees of metabolic control and healthy subjects, while the GH response to the clonidine test is higher in the type 1 diabetic patients than in healthy controls.

Enhanced GABAb receptor-mediated transmission in alcohol-dependence syndrome

We have studied the GABAb receptor-mediated neurotransmissions of alcoholic patients by administering baclofen 10 mg orally and measuring the growth hormone (GH) response. There was a minimal GH response to the baclofen in one of eight control subjects and a greater GH response in 11 of the 16 alcoholic patients. There is thus evidence for increased transmission at the GABAb receptor in detoxified patients with alcohol-dependence syndrome.

Hypothalamic control of growth hormone (GH) secretion in type I diabetic men: effect of the combined administration of GH-releasing hormone and hexarelin, a novel GHRP-6 analog.

Insulin dependent (type I) diabetic patients show abnormal growth hormone (GH) secretion. Hexarelin is an analog of GHRP-6 which releases GH in part via somatostatin inhibition. The aim of our study was to evaluate the effects of hexarelin and GHRH, administered either alone or in combination, on GH secretion in 10 type I diabetic and 7 normal men. All the subjects were administered: 1) human GHRH (1-29) NH2 100 micrograms i.v. bolus at 0 min; 2) hexarelin 100 micrograms i.v. bolus at 0 min; 3) hexarelin 100 micrograms + hGHRH 100 micrograms i.v. bolus at 0 min. In type I diabetic patients significantly greater GH responses to GHRH and hexarelin have been observed with normal subjects. Hexarelin caused a significantly (p < 0.05) greater GH response as compared to GHRH in both diabetic and control subjects. After the administration of hexarelin+GHRH, a significant increase in both GH absolute and peak levels as compared to hexarelin or GHRH alone was found in all the subjects. However, the GH responses to the combined stimuli were not significantly different in diabetics as compared to normals; moreover, the interaction of GHRH and hexarelin was synergistic in controls and additive in diabetics. We hypothesize that a reduction in the hypothalamic somatostatin inhibitory tone combined with increased pituitary GH production may be responsible for the pattern of the GH responses to hexarelin and GHRH observed in our type I diabetic patients.

Growth hormone response to acute growth hormone releasing hormone administration in uraemic patients on haemodialysis.

To examine the response of growth hormone (GH) to growth hormone releasing factor (GHRF) in patients on haemodialysis, we performed the acute GHRF test (50 micrograms administered intravenously as a bolus) in 10 uraemic male patients on haemodialysis and eight normal controls. Each patient was tested before and after a haemodialysis session (at 08.30 and 12.30). Controls were tested on the same time schedule. At 08.30, patients had significantly greater basal and peak GH values (2.5 +/- 0.6 and 27.8 +/- 5.5 micrograms/l) than controls (0.68 +/- and 11.5 +/- 4 micrograms/l). After the haemodialysis session, basal and peak values declined significantly (P less than 0.01) in the uraemic group (0.5 +/- 0.03 and 3.1 +/- 1.1 micrograms/l), whereas the controls did not show such a change in the 12.30 test. Basal and intratest glycaemic values were comparable both before and after haemodialysis. After dialysis test results did not change either with the use of glucose-free dialysate or with bicarbonate buffer. Uraemic patients display a greater GH response to GHRF injection than normal subjects, and this response decreases after haemodialysis. The degree of reduction has no relationship with either glycaemia or the dialysate buffer. We suggest that other GH secretion regulating factors are altered by the haemodialysis procedure.

Increased growth hormone response to clonidine in 6-hydroxydopamine-treated rats.

Alpha 2-adrenergic receptors mediate adrenergic stimulation of growth hormone (GH) secretion in the rat. The GH response to the alpha 2-adrenergic agonist clonidine has thus been used as an index of alpha 2-adrenergic receptor responsiveness. Pharmacologic manipulations known to upregulate alpha 2-adrenergic receptor sensitivity would then be expected to result in an enhancement of the GH response to clonidine. To test this hypothesis, rats were injected in the lateral ventricle with either 6-hydroxydopamine or sterile saline. One month following the lesion, urethane-anesthetized rats from each group were administered clonidine or saline. Venous samples for plasma GH were drawn prior to or following the clonidine or saline administration. Rats administered clonidine had greater GH responses than those administered saline within either the lesioned or nonlesioned groups. The GH response to clonidine was significantly greater in the lesioned group than in the nonlesioned group. As 6-hydroxydopamine pretreatment upregulates alpha 2-adrenergic receptors, these results support the validity of the use of the GH response to clinidine as an index of alpha 2-adrenergic receptor responsiveness.