scholarly journals Acute Arginine Supplementation Is Associated with Increased Growth Hormone in Younger Healthy Males: A Randomized Controlled Trial

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 609-609
Author(s):  
John Apolzan ◽  
Jennifer Rood ◽  
Robbie Beyl ◽  
Shengping Yang ◽  
Frank Greenway ◽  
...  

Abstract Objectives Assess the effects of the amino acid arginine on growth hormone (GH), other metabolites, and mood. Arginine is reported to increase GH, but the mechanism is not known. It was hypothesized prolactin mediated this effect since it is similar in structure to GH and, like GH, is secreted by the pituitary gland. Methods Thirty physically active healthy young males (18–39 y; 18.5–25 kg/m2) were enrolled in a randomized, double-blind, placebo-controlled, crossover trial. Two days prior and 1 day following each treatment a standardized diet was provided that maintained arginine at 3–5 g/d. Arginine or placebo treatments in the form of a beverage were consumed after an overnight fast. Treatment conditions were separated by at least a one week washout period. The beverages contained either 10 g of arginine or 0 g (placebo). Blood was collected at baseline and 1.5, 3.0, and 24 hr post treatment. Plasma GH, prolactin, amino acids, glucose, insulin, triacylglycerols, thyroid hormones, sex hormone binding globulin (SHBG), testosterone, cortisol, and dehydroepiandrosterone (DHEA) were assessed. The Profile of Mood States (POMS) was administered at the same time as blood draws. Repeated measures ANOVAs were used to estimate treatment effects at each time point. Results Arginine increased plasma arginine at 1.5, 3.0, and 24 hr (P ≤ 0.001) and GH at 24 hr (P ˂ 0.05) but not other time points. Arginine increased glucose and insulin at the 1.5 and 3.0 hr (P ˂ 0.05) but not 24 hr. Arginine did not affect any other dependent measure (P > 0.05) including prolactin. When only individuals with detectable levels of GH (responders; n = 16) were analyzed separately, arginine increased GH at the 1.5 (P ˂ 0.05) but not the 3.0 or 24 hr time points. Among the responders, arginine also increased thyroid stimulating hormone (TSH) at the 24 hr time point (P ˂ 0.05) but not the 1.5 and 3.0 hr time points. Conclusions Arginine supplementation modestly increased growth hormone. Despite their similar structures, prolactin secretion was not elevated following arginine supplementation, thus another mechanism is responsible for growth hormone secretion. Funding Sources DoD and NIH P30DK072476. Views expressed are those of the authors and do not reflect official policy of the Army, DoD, or US Government.

1976 ◽  
Vol 50 (4) ◽  
pp. 241-247 ◽  
Author(s):  
J. R. Sutton ◽  
N. L. Jones ◽  
C. J. Toews

1. Seven healthy males were studied during cycle ergometer exercise at 33%, 66% and 90% of V̇o2 max. on three occasions when NH4Cl, NaHCO3 or CaCO3 (as a control substance) were administered in gelatin capsules double blind and in randomized order. Plasma growth hormone (HGH), lactic acid and hydrogen ion concentration ([H+])weremeasured at frequent intervals. 2. Ammonium chloride produced highest blood [H+] and NaHCO3 the lowest. These differences were maintained during exercise and in recovery. Plasma lactic acid concentrations were similar at rest. At 66%, 90% V̇o2 max. and recovery lactic acid was highest with NaHCO3 and lowest with NH4Cl. 3. Exercise stimulated HGH secretion in all studies and the elevation was proportional to the intensity of the exercise. NH4Cl caused a variable elevation of HGH at rest and 33% V̇o2 max. At 66% V̇o2 max., plasma HGH was significantly elevated to similar concentrations in all studies and, at 90% V̇o2 max., HGH was highest with NaHCO3. 4. An infusion of sodium l(+)-lactate producing plasma lactate concentrations of 3–5 mmol/l did not influence HGH secretion. 5. Exercise is a physiological stimulus to HGH secretion and the mechanism is independent of blood [H+] and lactate concentrations.


2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Krishna Pokharel ◽  
Mukesh Tripathi ◽  
Pramod Kumar Gupta ◽  
Balkrishna Bhattarai ◽  
Sindhu Khatiwada ◽  
...  

We assessed if the addition of melatonin to alprazolam has superior premedication effects compared to either drug alone. A prospective, double blind placebo controlled trial randomly assigned 80 adult patients (ASA 1&2) with a Visual Analogue Score (VAS) for anxiety ≥3 to receive a tablet containing a combination of alprazolam 0.5 mg and melatonin 3 mg, alprazolam 0.5 mg, melatonin 3 mg, or placebo orally 90 min before a standard anesthetic. Primary end points were change in anxiety and sedation score at 15, 30, and 60 min after premedication, and number of patients with loss of memory for the five pictures shown at various time points when assessed after 24 h. One-way ANOVA, Friedman repeated measures analysis of variance, Kruskal Wallis and chi square tests were used as relevant. Combination drug produced the maximum reduction in anxiety VAS (3 (1.0–4.3)) from baseline at 60 min (P<0.05). Sedation scores at various time points and number of patients not recognizing the picture shown at 60 min after premedication were comparable between combination drug and alprazolam alone. Addition of melatonin to alprazolam had superior anxiolysis compared with either drugs alone or placebo. Adding melatonin neither worsened sedation score nor the amnesic effect of alprazolam alone. This study was registered, approved, and released from ClinicalTrials.gov. Identifier number:NCT01486615.


1991 ◽  
Vol 35 (1) ◽  
pp. 30-34 ◽  
Author(s):  
M. Colle ◽  
P. Rosenzweig ◽  
G. Bianchetti ◽  
E. Fuseau ◽  
A. Ruffi&eacute; ◽  
...  

2004 ◽  
Vol 286 (4) ◽  
pp. R693-R698 ◽  
Author(s):  
Petra Kok ◽  
Madelon M. Buijs ◽  
Simon W. Kok ◽  
Inge H. A. P. van Ierssel ◽  
Marijke Frölich ◽  
...  

We hypothesized that a high circulating free fatty acid (FFA) concentration is involved in the pathogenesis of hyposomatotropism associated with obesity. To evaluate this hypothesis, 10 healthy premenopausal women (body mass index 33.8 ± 1.0 kg/m2) were studied in the follicular phase of their menstrual cycle at two occasions with a time interval of at least 8 wk, where body weight remained stable. Subjects were randomly assigned to treatment with either acipimox (an inhibitor of lipolysis, 250 mg orally 4 times daily) or placebo in a double-blind crossover design, starting 1 day before admission until the end of the blood sampling period. Blood samples were taken during 24 h with a sampling interval of 10 min for assessment of growth hormone (GH) concentrations, and GH secretion was estimated by deconvolution analysis. Identical methodology was used to study GH secretion in a historical control group of age-matched normal weight women. GH secretion was clearly blunted in obese women (total daily release 66 ± 10 vs. lean controls: 201 ± 23 mU·lVd-1·24 h-1, P = 0.005, where lVd is liter of distribution volume). Acipimox considerably enhanced total (113 ± 50 vs. 66 ± 10 mU·lVd-1·24 h-1, P = 0.02) and pulsatile GH secretion (109 ± 49 vs. 62 ± 30 mU·lVd-1·24 h-1, P = 0.02), but GH output remained lower compared with lean controls. Further analysis did not show any relationship between the effects of acipimox on GH secretion and regional body fat distribution. In conclusion, acipimox unleashes spontaneous GH secretion in obese women. It specifically enhances GH secretory burst mass. This might mean that lowering of systemic FFA concentrations by acipimox modulates neuroendocrine mechanisms that orchestrate the activity of the somatotropic ensemble.


1974 ◽  
Vol 77 (1_Suppl) ◽  
pp. S6 ◽  
Author(s):  
S. Raptis ◽  
H. Hirth-Schmidt ◽  
K. E. Schröder ◽  
E. F. Pfeiffer

2018 ◽  
Author(s):  
Alexey Kalinin ◽  
Natalia Strebkova ◽  
Olga Zheludkova ◽  
Maria Kareva

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