ArticleLiterature Review

Growth hormone, arginine and exercise

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Abstract

To describe the effect of an acute bout of exercise on growth hormone responses and to discuss the effect of L-arginine supplementation on growth hormone responses. Recent studies have shown that resting growth hormone responses increase with oral ingestion of L-arginine and the dose range is 5-9 g of arginine. Within this range there is a dose-dependent increase and higher doses are not well tolerated. Most studies using oral arginine have shown that arginine alone increases the resting growth hormone levels at least 100%, while exercise can increase growth hormone levels by 300-500%. The combination of oral arginine plus exercise attenuates the growth hormone response, however, and only increases growth hormone levels by around 200% compared to resting levels. Exercise is a very potent stimulator of growth hormone release and there is considerable research documenting the dramatic growth hormone rise. At rest oral L-arginine ingestion will enhance the growth hormone response and the combination of arginine plus exercise increases growth hormone, but this increase may be less than seen with exercise alone. This diminished response is seen in both in both younger and older individuals.

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... Data from 18 clinical studies that assessed the effects of arginine alone on performance parameters [60][61][62][63][64][65][66][67][68][69][70][71][72][73][74][75] are summarized below. ...
... There was no information available concerning the quality of arginine products, nor were there controlled studies evaluating the safety of multi-ingredient formulations or studies evaluating the dose-modifying effects of other ingredients of the multi-ingredient formulations. Most of the available clinical studies of arginine [46][47][48][49][50][51][60][61][62][63][64][65][66][67][68][69][70][71][72][73][74] (not including the reports for multi-ingredient formulations) did not provide specific safety information other than a statement that no adverse effects were noted. Furthermore, spontaneous AERs involved heterogeneous populations, and several reports did not provide the subject's age, gender, medical history, concurrent medications, or amount and duration of treatment. ...
... A commonly reported adverse reaction was gastrointestinal discomfort, which was observed in some studies in concert with other findings at serving sizes ranging from 9 g/d to 30 g/d in adults. The authors 74,83 cited others' work to note that small increases in gastrointestinal discomfort may have a large impact on performance and that limiting gastrointestinal distress has been identified as an important component of sports nutrition, particularly for those who perform in ultraendurance events. 84,85 Siani et al. ...
Article
Context: Dietary supplements are widely used by military personnel and civilians for promotion of health. Objective: The objective of this evidence-based review was to examine whether supplementation with l-arginine, in combination with caffeine and/or creatine, is safe and whether it enhances athletic performance or improves recovery from exhaustion for military personnel. Data sources: Information from clinical trials and adverse event reports were collected from 17 databases and 5 adverse event report portals. Study selection: Studies and reports were included if they evaluated the safety and the putative outcomes of enhanced performance or improved recovery from exhaustion associated with the intake of arginine alone or in combination with caffeine and/or creatine in healthy adults aged 19 to 50 years. Data extraction: Information related to population, intervention, comparator, and outcomes was abstracted. Of the 2687 articles screened, 62 articles meeting the inclusion criteria were analyzed. Strength of evidence was assessed in terms of risk of bias, consistency, directness, and precision. Results: Most studies had few participants and suggested risk of bias that could negatively affect the results. l-Arginine supplementation provided little enhancement of athletic performance or improvements in recovery. Short-term supplementation with arginine may result in adverse gastrointestinal and cardiovascular effects. No information about the effects of arginine on the performance of military personnel was available. Conclusions: The available information does not support the use of l-arginine, either alone or in combination with caffeine, creatine, or both, to enhance athletic performance or improve recovery from exhaustion. Given the information gaps, an evidence-based review to assess the safety or effectiveness of multi-ingredient dietary supplements was not feasible, and therefore the development of a computational model-based approach to predict the safety of multi-ingredient dietary supplements is recommended.
... A typical western diet contains ~3-6 g·d -1 (Visek, 1986). In healthy adults, Larginine can be synthesized in sufficient quantities required for most physiological demands (Witte & Barbul, 2003;Wu & Morris, 1998);however, during periods of rapid growth, in response to a traumatic or pathologic insult, or due to the physiological demands of exercise, the requirements for L-arginine may not be met by de novo synthesis and normal dietary intake alone (Boger & Bode-Boger, 2001;Kanaley, 2008;Litte et al. 2008;Witte & Barbul, 2003). In such circumstances L-arginine supplementation may be beneficial (Kanaley, 2008). ...
... In healthy adults, Larginine can be synthesized in sufficient quantities required for most physiological demands (Witte & Barbul, 2003;Wu & Morris, 1998);however, during periods of rapid growth, in response to a traumatic or pathologic insult, or due to the physiological demands of exercise, the requirements for L-arginine may not be met by de novo synthesis and normal dietary intake alone (Boger & Bode-Boger, 2001;Kanaley, 2008;Litte et al. 2008;Witte & Barbul, 2003). In such circumstances L-arginine supplementation may be beneficial (Kanaley, 2008). ...
... This latter response was thought to be due to a down regulation of GHRH-induced GH release. Secondly, it has also been shown that acute resistance exercise (Kraemer & Ratamess, 2005;Kraemer et al. 1990) and potentially L-arginine supplementation (Kanaley, 2008) can stimulate the release of IGF-1 that is involved in an auto-negative feedback loop that reduces GH release (Collier et al. 2006;Jaffe et al. 1998). In addition, GH can directly inhibit its own release, possibly at the pituitary gland (Pontiroli et al. 1991) or via an auto-negative feedback at the level of the hypothalamus mediated by an increase in GHIH release and/or a decrease in the release of GHRH. ...
Article
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Acute resistance exercise and L-arginine have both been shown to independently elevate plasma growth hormone (GH) concentrations; however, their combined effect is controversial. The purpose was to investigate the combined effects of resistance exercise and L-arginine supplementation on plasma L-arginine, GH, GH secretagogues, and IGF-1 in strength trained participants. Fourteen strength trained males [age: 25±4 y; body mass: 81.4±9.0 kg; height: 179.4±6.9 cm; and training experience: 6.3±3.4 y] participated in a randomized double blind crossover design (separated by ~7 days). Subjects reported to the laboratory at 08:00 in a fasted state, consumed L-arginine (ARG; 0.075 g·kg-1 body mass) or a placebo (PLA) prior to performing an acute bout of resistance exercise (3 sets of 8 exercises, 10 repetitions at ~75% 1RM). Blood samples were collected at rest, before exercise, and at 0, 15, 30, 60 min of rest-recovery. The ARG condition significantly increased plasma L-arginine concentrations (~120%) while no change was detected in the PLA condition. There were no differences between conditions for GH, GH-releasing hormone, ghrelin, or IGF-1 at any time point. GH-inhibiting hormone was significantly lower in the ARG condition. However; integrated area under the curve for GH was blunted in the ARG condition (L-arginine = 288.4±368.7 vs. placebo = 487.9±482.0 min·ng·mL-1, p<0.05). L-arginine ingested prior to resistance exercise significantly elevated plasma L-arginine concentration but attenuated plasma GH in strength trained individuals despite a lower GHIH. Furthermore our data shows that the GH suppression was not due to a GH or IGF-1 induced autonegative feedback loop.
... As a physiological stress, exercise increases GHRH release and diminishes somatostatin release via adrenergic/cholinergic pathways [10,55], which further result in increased concentration of GH in the blood [53]. Exercise also stimulates liver and muscle IGF-I expression by increasing GH secretion, leading to secretion of other hormones and metabolites [25,31,44,46,54], which together improve skeletal muscle mass gain, as well as fat and glucose utilization. ...
... Our hypothesis was that the [17][18][19][20][21][22][23] protein was translated at pituitary gland stage and had being simultaneously secreted, which could result in a further increment on bloodstream concentration and not inside the somatotropic cells level. For this, we investigate the serum GH concentration and we observed that all groups had higher serum GH concentration compared to control group, indicating the Arg up regulates the pituitary GH secretion, as well demonstrated in literature [1,3,10,31,60]. We also detected enhanced Igf-I mRNA content in liver of rats subjected to Arg treatment, which reinforces Arg-induced effect on GH secretion, as previously reported by our group [15,16]. Surprisingly, Arg supplementation associated to exercise present no further effect on hepatic Igf-I mRNA expression when compared to just trained rats. ...
... Arg-supplemented animals showed a slight increment in body length and body weight, despite the greater reduction on fat mass, in accordance with previous reports [22,34]. The significant drop of the Lee index and the increased muscle mass weight observed in all experimental groups may be a response to the recognized lipolytic and protein anabolic effects of GH [31,37]. In addition to these effects, NO synthesis caused by Arg supplementation has been shown to increase fat oxidation and reducing its synthesis [28]. ...
Article
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L-Arginine has emerged as an important supplement for athletes and non-athletes in order to improve performance. Arginine has been extensively used as substrate for nitric oxide synthesis, leading to increased vasodilatation and hormonal secretion. However, the chronic consumption of arginine has been shown to impair insulin sensitivity. In the present study, we aimed to evaluate whether chronic arginine supplementation associated with exercise training would have a beneficial impact on insulin sensitivity. We, therefore, treated Wistar rats for 4weeks with arginine, associated or not with exercise training (treadmill). We assessed the somatotropic activation, by evaluating growth hormone (GH) gene expression and protein content in the pituitary, as well is GH concentration in the serum. Additionally, we evaluate whole-body insulin sensitivity, by performing an insulin tolerance test. Skeletal muscle morpho-physiological parameters were also assessed. Insulin sensitivity was impaired in the arginine-treated rats. However, exercise training reversed the negative effects of arginine. Arginine and exercise training increased somatotropic axis function, muscle mass and body weight gain. The combination arginine and exercise training further decreased total fat mass. Our results confirm that chronic arginine supplementation leads to insulin resistance, which can be reversed in the association with exercise training. We provide further evidence that exercise training is an important tool to improve whole-body metabolism.
... However, resistance training over a 12 week exercise protocol in elderly people promoted an increase in acute GH response, possibly owing to an increase ability to exert oneself (Craig et al., 1989). Thus, exercise is a potent stimulator of GH and IGF1 release and it may take a few hours to recover back to baseline levels (Kanaley, 2008). It is speculated that the mechanism responsible for exercise-induced GH release is a suppression of hypothalamic secretion of somatostatin and possibly duringhigh intensity exercise an augmented hypothalamic secretion of GHRH. ...
... It is speculated that the mechanism responsible for exercise-induced GH release is a suppression of hypothalamic secretion of somatostatin and possibly duringhigh intensity exercise an augmented hypothalamic secretion of GHRH. The primary function of GH release during exercise may be post exercise protein synthesis (Kanaley, 2008). Basal levels of IGF-1 decrease during aging (Yamamoto et al., 1991;Ruiz-Torres and Soares de Melo Kirzner, 2002;Trejo et al., 2004). ...
Article
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Alzheimer's disease (AD) is a complex, multifactorial disease with a number of leading mechanisms, including neuroinflammation, processing of amyloid precursor protein (APP) to amyloid β peptide, tau protein hyperphosphorylation, relocalization, and deposition. These mechanisms are propagated by obesity, the metabolic syndrome and type-2 diabetes mellitus. Stress, sedentariness, dietary overconsumption of saturated fat and refined sugars, and circadian derangements/disturbed sleep contribute to obesity and related metabolic diseases, but also accelerate age-related damage and senescence that all feed the risk of developing AD too. The complex and interacting mechanisms are not yet completely understood and will require further analysis. Instead of investigating AD as a mono-or oligocausal disease we should address the disease by understanding the multiple underlying mechanisms and how these interact. Future research therefore might concentrate on integrating these by " systems biology " approaches, but also to regard them from an evolutionary medicine point of view. The current review addresses several of these interacting mechanisms in animal models and compares them with clinical data giving an overview about our current knowledge and puts them into an integrated framework.
... Arginine has been shown to support protein synthesis, improve nitrogen balance and support wound healing. [9][10][11] There is a theory that consuming arginine will raise the blood level of human growth hormone (hGH) and insulin. 9 The performance advantage would be that increases in these two hormones (hGH and insulin) would help build more body mass by natural growth (accretion) and the decrease of body fat. ...
... Earlier studies were done with competitive weightlifters who have been given arginine with another amino acid or a placebo. 10,11 Insulin levels and hGH were measured daily. The researchers did not see a difference between the arginine or the placebo group. ...
... This may most likely be due to differences in sleeping and meal patterns, and it is likely to contribute to insulin resistance in FDRs, reflecting the strong association between GH and that of hyperglycemia and hyperinsulinemia [60]. It is well known that GH increased with exercise [61]. Hence, the less exercise exerted by participants during Ramadan fasting could also contribute to the observed decrease in GH levels. ...
... This slight but significant increase of insulin and insulin resistance by Ramadan fasting may be attributed to the reverse feeding schedule which causes metabolism disruption with increased caloric intake and sleep time alteration where sleep was reported to have important modulatory effects on glucose regulation, and recurrent sleep loss was associated with marked negative alterations of the parameters of glucose tolerance [70]. This reverse feeding schedule and sleep time alteration together with decreased physical activity during Ramadan results in modulatory hormonal changes due to complex interactions mediated by GH secretion during the first part of the night (in response to muscle relaxation and sleeping onset) [61] and by cortisol secretion during the second part of the night due to changes in cortisol secretory patterns (diurnal rhythm of plasma cortisol) leading to decreased glucose tolerance and increased insulin resistance [22]. Interestingly, however, insulin sensitivity (HOMA-S) was significantly decreased in both Type 2 DM and FDRs, with an observed significant decrease in β-cell function (HOMA-β) in FDRs and no change in Type 2 DM. ...
Article
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Background. In view of the association of Ramadan intermittent fasting with profound changes in lifestyle both in nondiabetic and diabetic patients, the aim of this study was to investigate the effect of Ramadan fasting on adiponectin, leptin and leptin to adiponectin ratio (LAR), growth hormone (GH), human-sensitive C-reactive protein (hs-CRP), and diabetic and metabolic syndrome factors in patients with Type 2 Diabetes Mellitus (Type 2 DM), their first-degree relatives (FDRs), and healthy controls. Methods. This cohort study involved 98 Yemeni male subjects aged 30-70 years old: 30 Type 2 DM, 37 FDRs of Type 2 diabetic patients, and 31 healthy control subjects. Subjects’ body mass index (BMI), waist circumference (WC), and blood pressure (BP) were measured, and venous blood samples were collected twice: the first samples were collected a couple of days prior to Ramadan fasting (baseline) and the second samples after 3 weeks of fasting. Results. Ramadan fasting did not affect BMI, WC, and BP in Type 2 DM and their FDRs with respect to the baseline levels prior to Ramadan, whereas triglyceride and cholesterol were borderline significantly decreased in Type 2 DM with no effect in FDRs. Fasting blood glucose was not affected in Type 2 DM but was significantly increased in FDRs and control groups, whereas glycated haemoglobin (HbA1c) was slightly decreased in Type 2 DM, FDRs, and healthy controls. C-peptide, insulin, and insulin resistance (HOMA-IR) were significantly increased in Type 2 DM and FDRs, with no effect in the control group, whereas β-cell function (HOMA-β) was significantly decreased in FDRs and controls with no change in Type 2 DM. Ramadan fasting significantly decreased GH in both FDRs and control groups, and significantly increased hs-CRP in the control with no effect in Type 2 DM and FDRs. Adiponectin was significantly decreased, and leptin and LAR were significantly increased in Type 2 DM, FDRs, and control groups. Conclusion. Ramadan intermittent fasting decreased adiponectin and increased leptin, LAR, insulin, and insulin resistance in both Type 2 DM and FDRs as well as decreased GH in both FDRs and healthy controls and increased hs-CRP in healthy controls. Moreover, Ramadan intermittent fasting neither worsens a patient’s glycemic parameters nor improves it, with the exception of a slight improvement in HbA1c in Type 2 DM, FDRs, and healthy controls. 1. Introduction Ramadan is the holiest month in the Islamic calendar, in which Muslims fast during this month by refraining from all intakes of food, water, beverages, oral medicine, and smoking from sunrise till sunset [1]. The period of fasting may vary depending on the season of the year and the geographical location of the country. Therefore, daytime fasting may vary from approximately 11-18 hours, being longer in the summer [2]. During Ramadan, food and liquid are usually consumed in two meals, in the morning before sunrise and in the evening after sunset, shifting the pattern of energy intake from daytime to the hours of darkness [3, 4]. These changes in the timing of food intake as well as in the composition of diet can alter energy metabolism, and may affect important enzymatic, hormonal, and metabolic responses and different aspects of human health [4–9]. The type and quality of food eaten during the night in Ramadan may also be different from that usually consumed during the rest of the year [10]. Ramadan intermittent fasting is a safe lifestyle modification that involves specific dietary and lifestyle modifications, such as changes in food quantity and quality, nocturnal food consumption, meal frequency, and sleep cycle as well as reduction in exercise [11–14]. Ramadan fasting has been associated with variable weight changes, ranging from a modest weight gain to weight neutrality and weight loss [15], with a reported reduction in total calorie intake in some [16], but not all populations. Different studies have reported varying impacts of Ramadan intermittent fasting on overall health [2, 17]. Several studies though inconsistent have demonstrated the effects of Ramadan fasting on biochemical markers in healthy subjects [8, 9, 18–23]; subjects with obesity [24], metabolic syndrome (MetS) [12, 25], and hypertension [26, 27]; and in patients with cardiovascular disease [10, 28] and Type 2 diabetes mellitus [16, 29–32]. Such discrepancy in the results could be attributed to several confounding factors including age, gender, ethnicity, hours of fasting, number of fasting days, climatic conditions, cultural influences, sample size, study subjects, exercise, dietary patterns, and genetic background [1, 17, 33]. Despite the above-reported discrepancies between studies, Ramadan fasting remains an interesting alternative model to investigate the beneficial effect of intermittent fasting and its potential to mitigate chronic diseases in the general population [4, 34, 35]. There is, however, a general opinion that fasting is a potential nonpharmacological intervention for improving health and increasing longevity [17]. The beneficial effects of intermittent fasting on glycaemic control, metabolism, cardiovascular risk, cancer, and life expectancy have been researched [36, 37]. Energy and glucose metabolism, appetite, and hormonal responses are changed by prolonged fasting periods, and the changes in nutritional habits also affect lipid profile and body composition during Ramadan [13, 38]. For patients with Type 2 diabetes, Ramadan fasting implies major changes in their daily routines, including mealtimes, medication frequency and doses, daily activities, and sleeping quality. Consequently, there is an increased risk of affecting metabolic control in diabetic patients for a whole month annually [20, 39]. On the other hand, several studies reported that Ramadan fasting has a positive impact on Type 2 DM [31, 40] and that Ramadan fasting is unlikely to be hazardous for well-controlled patients. In view of the association of Ramadan intermittent fasting with profound changes in lifestyle, such as altered sleeping durations and times and changes in physical activities as well as feeding patterns and restriction of food intake to night-time only, together with the existing controversial data in the literature on the effect of Ramadan fasting on metabolic and hormonal factors, this study is aimed at investigating the effect of Ramadan fasting on adipocytokines (adiponectin, leptin, and leptin/adiponectin ratio (LAR)), growth hormone (GH), human-sensitive C-reactive protein (hs-CRP) (as a marker of systemic inflammation), diabetic parameters, and metabolic syndrome factors in Type 2 DM and their first-degree relatives (FDRs) and healthy controls. 2. Methods 2.1. Subjects and Data Collection This cohort study involved 98 Yemeni male subjects aged 30-70 years old: 30 Type 2 DM patients recruited during their routine visits to the Endocrine and Diabetic Clinic of 48 Model Hospital, Sana’a, with and had been diagnosed with diabetes for at least one year and on oral hypoglycaemic drugs and desired to fast during Ramadan; 37 healthy first-degree relatives of the subjects with Type 2 DM who accompanied their diabetic patients; and 31 healthy control subjects with , who were on no medication that may affect blood glucose or lipid profile. Subjects with acute or chronic illness, or secondary diabetes mellitus due to other conditions or under immunosuppression (malignancy, renal failure, liver cirrhosis, connective tissue disease, and chronic congestive heart failure) were excluded from the study. The study was carried out in the period of June 2016 (Ramadan of 2016), and the study protocol was approved by the Institutional Review Board (IRB) of the Faculty of Medicine and Health Sciences, Sana’a University. All participants were recruited from 48 Model Hospital, Sana’a, via posters. Volunteers were approached 2 weeks before Ramadan and were given information sheets explaining the research procedure, specimen collection methods, and a written informed consent. All participants were asked to read and sign the consent form prior to the commencement of the study. Each participant was then assessed at two visits: a couple of days prior to Ramadan fasting (baseline) and a follow-up visit after 3 weeks of fasting. Baseline demographical and clinical data including age, duration of diabetes, family history of diabetes, diet and lifestyle, the current treatment regimen that the patient is following, history of hypertension, dyslipidaemia, and diabetes mellitus complications were collected from each participant. All participants were subjected to physical measurements, and fasting blood samples were obtained for laboratory analysis. The subjects’ height and weight were measured and body mass index (BMI), defined as weight (kg)/height squared (m²), was calculated. Waist circumference (WC) was measured halfway between the lower rib margin and the anterior superior iliac spine. Blood pressure (BP) measurements were taken from each patient’s right arm in the seated position by using an Omron IntelliSense Automatic Blood Pressure Monitor after 10 min of rest. Two to three successive BP readings were obtained at 5-minute intervals and averaged. Venous blood (5 ml) was collected from each individual after an overnight fast of more than 10 hours and divided into two vacuumed tubes; 4 ml was put into plain tubes for biochemical assay, and 1 ml was put into a K2EDTA tube for glycated haemoglobin (HbA1c) determination. The serum from each sample was separated within 30 minutes and aliquoted into four Eppendorfs and immediately kept at -80°C for biochemical analysis. Haemolysates were prepared immediately for HbA1c determination within 2 hours of blood collection. 2.2. Biochemical Analysis Fasting blood glucose (FBG), triglyceride (TG), total cholesterol, HDL-cholesterol (HDL-c), and LDL-cholesterol (LDL-c) were measured on an automated analyzer, the Cobas c501 (Roche Diagnostic, Germany), using the respective Roche Diagnostic kits (Mannheim, Germany). Glycated haemoglobin (HbA1c) was measured on the Cobas c501 automated analyzer (Roche Diagnostic, Germany) using a turbidimetric inhibition immunoassay. Insulin, C-peptide, and GH were measured by an electrochemiluminescence immunoassay (ECL) on an Elecsys autoanalyzer (Roche Diagnostic, Germany). Insulin resistance (HOMA-IR), insulin sensitivity (HOMA-S), and β-cell function (HOMA-β) were calculated using the Homeostasis Model Assessment (HOMA2) Calculator v2.2 which is available from the Oxford Centre for Diabetes, Endocrinology, and Metabolism [41]. Serum hs-CRP was measured by the immunoturbidimetric method (Roche Diagnostic, Germany) on the Cobas c501 automated analyzer (Roche Diagnostic, Germany). Enzyme-linked immunoassay (ELISA) kits were used to measure serum adiponectin and leptin (Société de Pharmacologie et d’Immunologie BIO, France). 2.3. Statistical Analysis The results were analyzed by the Statistical Package for the Social Sciences (SPSS) version 20 (SPSS Inc., Chicago, IL, USA), and the results were expressed as with the exception of hs-CRP (not normally distributed) which is reported as , following its log transformation. The significance and mean differences of all parameters among the three tested groups were assessed by ANOVA, whereas the significance and mean differences of all parameters prior to and during Ramadan was assessed by a paired -test. The significant interrelationships between parameters were analyzed by Pearson’s correlation, with the exception of hs-CRP which was analyzed by Spearman’s correlation. Significant differences were indicated if value was <0.05. 3. Results Table 1 shows the comparison of demographic, biochemical, and hormonal parameters between control, FDRs, and Type 2 DM subjects prior to Ramadan. In FDRs, both BMI and SBP were significantly (, ) higher by 11.6% and 7.1% as compared to the control group, whereas WC and DBP were nonsignificantly different. Triglyceride was nonsignificantly higher and total cholesterol was significantly () higher in FDRs by 7.2% and 19.5% as compared to the control group, with no significant effect on both HDL-c and LDL-c. Fasting blood glucose, HbA1c, and C-peptide were nonsignificantly higher in FDRs, whereas insulin was borderline significantly () higher by 31.8% and both HOMA-IR and HOMA-β were nonsignificantly higher by 30.3% and 16.6% than that of the control group. However, HOMA-S was significantly () lower in FDRs by 25.4% with respect to the control group. Adiponectin and GH were nonsignificantly lower in FDRs by 6% and 6.3% as compared to the control group, whereas both leptin and leptin/adiponectin ratio (LAR) were nonsignificantly higher in FDRs by 18.3% and 27% and hs-CRP was borderline significantly () higher by 35.1%. Parameters Control () FDRs () Type 2 DM () value C vs. F C vs. D F vs. D Age (years) 0.990 BMI (kg/m²) 0.028 0.004 0.701 WC (cm) 0.708 0.004 0.028 SBP (mmHg) 0.004 DBP (mmHg) 0.999 0.274 0.403 Triglyceride (mg/dl) 0.752 0.014 0.066 Cholesterol (mg/dl) 0.999 HDL-c (mg/dl) 0.465 0.810 0.858 LDL-c (mg/dl) 0.349 0.485 0.983 FBG (mmol/l) 0.937 HbA1c (%) 0.404 C-peptide (ng/ml) 0.120 Insulin (pmol/l) 0.054 HOMA-IR 0.095 HOMA-β (%) 0.127 0.064 HOMA-S (%) 0.003 GH (ng/ml) 0.565 hs-CRP (mg/l) 0.37 (0.31-0.42) 0.50 (0.40-0.59) 0.57 (0.49-0.65) 0.055 0.002 0.360 Leptin (ng/ml) 0.819 Adiponectin (IU/ml) 0.397 0.001 0.038 LAR 0.883 Data are presented as . Data are presented as geometric mean and 95% confidence interval of mean evaluated by ANOVA. C vs. F: a comparison between control and FDRs; C vs. D: a comparison between control and Type 2 DM; F vs. D: a comparison between FDRs and Type 2 DM.
... Since GH release induced by exercise is mediated by suppression of somatostatin, and L-arginine has a similar mechanism of action, the combination of both could be able to potentiate the impact of GH on protein synthesis. Although some nutritional intervention studies have shown that L-arginine alone or in combination with physical exercise may promote an increase in GH secretion, especially during the recovery period [ 60 ], there is no additional effect on protein synthesis [ 58 , 60 ]. ...
Chapter
L-Arginine (C 6 H 14 N 4 O 2 ) is nutritionally classifi ed as a conditional essential amino acid that can be commonly found in the protein component of both plants and animal foods. Over the past two decades, studies have described its role as a mediator of multiple biological processes including the release of several hormones, collagen synthesis during wound healing, antitumor activity, and immune cell responses. Typically endogenous synthesis accounts for approximately 20 % of the daily expenditure, and normal levels of L-arginine in the blood range from 40 to 100 μmol/L, which may decrease by up to 20 % in diabetes. Moreover, L-arginine is an amino acid that, through its metabolism, can impact blood fl ow and blood pressure, especially in relation to the production of nitric oxide (NO • ).
... Although the mechanisms that are at the origin of the increased concentration of arginine and ornithine in the pup plasma following the supplementation of mothers with bLF remain to be identified, it is worth noting that circulating arginine is well known to increase growth hormone secretion [46] and to further increase insulin secretion in response to increased glycemia [47]. ...
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Lactoferrin (LF) is an iron-binding protein found at relatively high concentrations in human milk. LF, which is little degraded in the infant intestinal lumen, is known to stimulate the proliferation and differentiation of the small intestine epithelial cells. The present study was designed to evaluate in the rat model the effects of bovine LF (bLF) given to the mothers during gestation and lactation on the growth of the offspring. Female Wistar rats were randomly separated into two groups of animals that received from mating and during gestation and lactation a standard diet including or not including bLF (10 g/kg of diet). The pups’ growth was determined up to postnatal day 17 (PND17), and parameters related to lean and fat mass, intestinal differentiation, intestinal barrier function, bone mineral density, osteoblast activity, and brain development were measured. In addition, metabolites in pup plasma were determined at PND17. bLF was detected in the plasma and milk of the supplemented mothers as well as in the pup plasma. Although the body weight of the pups in the two groups did not differ at birth, the pups recovered from the supplemented mothers displayed an increase body weight from PND12 up to PND17. At PND17 in the bLF group, increased small intestine epithelial cell differentiation was detected, and colon barrier function was reinforced in association with increased expression of genes coding for the tight-junction proteins. Regarding bone physiology, improved bone mineral density was measured in the pups. Lastly, the plasma metabolite analysis revealed mainly higher amino acid concentrations in the LF pups as compared to the control group. Our results support that bLF ingestion by the mother during gestation and lactation can promote pup early life development. The potential interest of supplementing the mothers with bLF in the case of risk of compromised early life development of the offspring in the context of animal and human nutrition is discussed.
... Thus, in potassium deficient animals both basal GH levels and GH response to GRF are reduced, this deficiency being corrected after potassium repletion (Flyvbjerg et al. 1991;Gil-Peña et al. 2010). In addition, potassium infusion to healthy man increases GH in plasma (Dluhy et al. 1972), and increased serum potassium and GH release have been observed after infusion of cationic amino acids or after physical exercises (Merimee et al. 1965;Hertz and Richardson 1972;Bushinsky and Gennari 1978;Massara et al. 1979;Williams et al. 1985;Bucci et al. 1990;Chromiak and Antonio 2002;Kanaley 2008;Denura et al. 2010). ...
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The administration of l-arginine hydrochloride has been used for testing pituitary secretion in humans, and as an experimental model for induction of acute pancreatitis in rats and mice. Whereas in the first case, the administration of the amino acid is associated with hiperkalemia, in the model of acute pancreatitis no data are available on possible changes in potassium homeostasis. The present study shows that the acute administration to mice of l-arginine hydrochloride or other cationic amino acids almost duplicate plasma potassium levels. This effect was associated to a marked decrease of tissue potassium in both pancreas and liver. No changes were found in other tissues. These changes cannot be ascribed to the large load of chloride ions, since similar effects were produced when l-ornithine aspartate was administered. The changes in potassium levels were dependent on the dose. The displacement of intracellular potassium from the liver and pancreas to the extracellular compartment appears to be dependent on the entry of the cationic amino acid, since the administration of an equivalent dose of alfa-difluoromethyl ornithine HCl (DFMO), a non physiological analog of l-ornithine, which is poorly taken by the tissues in comparison with the physiological cationic amino acids, did not produce any change in potassium levels in pancreas and liver. The analyses of the expression of cationic amino acid transporters (CAT) suggest that the CAT-2 transporter may be implicated in the potassium/cationic amino acid interchange in liver and pancreas. The possible physiological or pathological relevance of these findings is discussed.
... Clinical data showing also controversial findings about increasing muscle mass and weight gain in patients with tuberculosis supplemented with Arginine [56]. This ability of L-Ariginine may be related with another study that shows linkage between oral supplementation of this amino acid and increasing levels in growth hormone [57]. Studies in malnourished patients with head and neck cancer showed lower fistula rates, decreased length of hospital stay, and a trend toward improved survival, while other trials were unable to demonstrate a positive clinical outcome [58]. ...
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Caffeine, Taurine and Arginine are one of the most widely used supplements from people of all ages. There are lot of controversial information about their proper use and effects and side effects. Our goal is to determine the reasonable boundaries of using these supplements in healthy people and more important in people with socially important diseases like high blood pressure, diabetes and dementia.
... Arginine is a stimulator of growth hormone [35], and the organism stops the synthesis of arginine in order to limit the growth after 28 years of age for a human (when a body stops growing and begins its aging). ...
... Five branched-chain amino acids (BCAAs) Leu, Iso, Val, Glu and Arg were found to play critical roles in sports performance (Vary and Lynch 2007). Glu and Arg are essential acting as stimuli for growth hormone release, precursors of antioxidant glutathione that protects cells from free radical damage and modulators for the rate-limiting step of protein synthesis under certain conditions such as stress and exercise (Welbourne 1995;DiPasquale and Mauro 1997;Kanaley 2008). While the amino acid profile determines the overall nutritional quality of dietary proteins especially the concentration of individual indispensable amino acids, protein digestibility and bioavailability reflect the real protein utilization by humans (Boye et al. 2012). ...
Article
Global populations are growing and ageing, with each generation expecting a higher standard of living than their predecessor. Proteins are essential in daily diets because of their nutritional value and roles in food structure, and proteins are generally expensive. Rising awareness of food security and meeting the needs of ageing populations motivate food researchers to explore alternative protein sources and sustainable and optimized use of proteins to increase their bioavailability and digestibility. Proteins behave differently as a function of pH, ionic strength, temperature, pressure or enzymatic mechanism, prompting approaches to modify their structure and functionality. Proteins may lose their native structure and impart sensory changes as a result of processing and storage. Modified proteins are considered as value-added food ingredients, i.e. specialty proteins prepared using enzymatic reactions, hydrolysis, fermentation, heat treatment, acidification, dehydration, emulsification and ultrafiltration. Food formulation influences proteins at both molecular and macro-polymer levels. This review presents case studies from previous research and demonstrates approaches for improving protein stability, extractability and bioactivity. The need for combining protein modification and smart food formulation is highlighted. Synergies achieved between conventional ingredients and added bioactives through careful food formulation and processing are emphasized. Comprehensive characterization of chemical composition, particle size, surface activity, microstructure, freezing-thawing properties of proteins and derived foods is required, to explain structure-function relationships. Data suggest that specialty proteins will play an increasing role in current and future global food sectors. Convenient concept foods for addressing the global food security and ageing population issues are proposed.
... Início ( Nas condições experimentais utilizadas para a realização do presente estudo a SOA não foi capaz de alterar a concentração sérica de GH. Prévios estudos apresentaram resultados que indicaram que a SOA administrada isoladamente pode aumentar a secreção de GH (Collier et al., 2005;Collier, Collins, & Kanaley, 2006;Kanaley, 2008). Contudo, existem na literatura estudos em que a SOA pode apresentar um efeito dose-resposta. ...
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A Suplementação Oral de Arginina (SOA) e o exercício físico são capazes de modificar a secreção do Hormônio de Crescimento (GH), interferindo no metabolismo lipídico. O objetivo do estudo foi verificar o efeito da SOA, do exercício físico aeróbio e a combinação da suplementação com o exercício sobre a secreção de GH e metabolismo lipídico em ratos. A amostra foi composta por 40 ratos machos da linhagem Wistar, divididos em grupos Controle Sedentário (CS), Arginina Sedentário (AS), Controle treinado (CT) e Arginina Treinado (AT). O AS e AT receberam a suplementação oral de arginina em dias alternados e os CT e AT realizaram exercícios de natação por 1 hora/dia com sobrecarga equivalente à 5% do peso corporal 5 dias por semana durante 4 semanas. Em conclusão, os resultados demonstram que o treinamento físico aeróbio não alterou o metabolismo lipídico e diminuiu os valores séricos de GH e a SOA não alterou a concentração de GH em ratos Wistar.
... Of course we cannot rule out changes in GH secretory pulses that occur during the first part of sleep, which we would have missed. It is well known that GH increased with exercise [33]. Hence, the less exercise exerted by participants during the fasting month of Ramadan compared to Shaaban, could also contribute to noted changes. ...
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Background: Muslims go through strict Ramadan fasting from dawn till sunset for one month yearly. These practices are associated with disturbed feeding and sleep patterns. We recently demonstrated that, during Ramadan, circadian cortisol rhythm of Saudis is abolished, exposing these subjects to continuously increased cortisol levels. Hypothesis: Secretory patterns of other hormones and metabolic parameters associated with cortisol, and insulin resistance, might be affected during Ramadan. Protocol: Ramadan practitioners (18 males, 5 females; mean age ±SEM = 23.16±1.2 years) were evaluated before and two weeks into Ramadan. Blood was collected for measurements of endocrine and metabolic parameters at 9 am (±1 hour) and again twelve hours later. Results: In Ramadan, glucose concentration was kept within normal range, with a significant increase in the morning. Mean morning concentration of leptin was significantly higher than pre-Ramadan values (p = 0.001), in contrast to that of adiponectin, which was significantly lower (p<0.001). These changes were associated with increased insulin resistance in morning and evening. Concentrations of hsCRP were lower during Ramadan than those during regular living conditions, however, normal circadian fluctuation was abolished (p = 0.49). Even though means of liver enzymes, total bilirubin, total protein and albumin were all decreased during Ramadan, statistically lower means were only noted for GGT, total protein, and albumin (p = 0.018, 0.002 and 0.001 respectively). Discussion: Saudi Ramadan practitioners have altered adipokine patterns, typical of insulin resistance. The noted decreases of hsCRP, liver enzymes, total protein, and albumin, are most likely a result of fasting, while loss of circadian rhythmicity of hsCRP is probably due to loss of circadian cortisol rhythm. Conclusions: Modern Ramadan practices in Saudi Arabia, which are associated with evening hypercortisolism, are also characterized by altered adipokines patterns, and an abolished hsCRP circadian rhythm, all likely to increase cardiometabolic risk.
... L-arginine (2-amino-5-guanidinovaleric acid) is a conditionally essential amino acid and has been purported to be ergogenic (Bailey et al., 2010;Bescós et al., 2012b;Paddon-Jones et al., 2004). It has been suggested that L-arginine can enhance endurance exercise performance by two primary mechanisms including an enhanced secretion of endogenous growth hormone (GH: Kanaley, 2008) and as a precursor for nitric oxide (NO). First, GH may influence endurance exercise performance by enhancing lipolysis (Møller et al., 1990) and fat oxidation (Gravhølt et al., 1999). ...
Article
L-arginine may enhance endurance performance mediated by two primary mechanisms including enhanced secretion of endogenous growth hormone (GH) and as a precursor of nitric oxide (NO); however, research in trained participants has been equivocal. The purpose was to investigate the effect of acute L-arginine ingestion on the hormonal and metabolic response during submaximal exercise in trained cyclists. Fifteen aerobically trained men (age: 28 ± 5 y; body mass: 77.4 ± 9.5 kg; height: 180.9 ± 7.9 cm; VO2max: 59.6 ± 5.9 ml·kg-1·min-1) participated in a randomized, double-blind, crossover study. Subjects consumed L-arginine (ARG; 0.075 g·kg-1 body mass) or a placebo (PLA) before performing an acute bout of submaximal exercise (60 min at 80% of power output achieved at ventilatory threshold). The ARG condition significantly increased plasma L-arginine concentrations (~146%), while no change was detected in the PLA condition. There were no differences between conditions for GH, nonesterified fatty acids (NEFA), lactate, glucose, VO2, VCO2, RER, CHO oxidation, and NOx. There was reduced fat oxidation at the start of exercise (ARG: 0.36 ± 0.25 vs. PLA: 0.42 ± 0.23 g·min-1, p < .05) and an elevated plasma glycerol concentrations at the 45-min time point (ARG: 340.3 vs. PLA: 288.5 μmol·L-1, p < .05) after L-arginine consumption. In conclusion, the acute ingestion of L-arginine did not alter any hormonal, metabolic, or cardio-respiratory responses during submaximal exercise except for a small but significant increase in glycerol at the 45-min time point and a reduction in fat oxidation at the start of exercise.
... Início ( Nas condições experimentais utilizadas para a realização do presente estudo a SOA não foi capaz de alterar a concentração sérica de GH. Prévios estudos apresentaram resultados que indicaram que a SOA administrada isoladamente pode aumentar a secreção de GH (Collier et al., 2005;Collier, Collins, & Kanaley, 2006;Kanaley, 2008). Contudo, existem na literatura estudos em que a SOA pode apresentar um efeito dose-resposta. ...
Article
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The Oral Arginine Supplementation (OAS) and exercise are able to modify the secretion of the Growth Hormone (GH) that stimulates the lipid metabolism. The aim of the study was to verify the effect of the OAS, the aerobic exercise and the combination of the OAS with the aerobic exercise on the GH secretion and lipid metabolism in rats. The sample was composted for 40 male wistar rats, divided in four groups: Sedentary control (SC), sedentary arginine (SA), trained control (TC) and trained arginine (TA). The AS and AT received the oral supplementation in alternated days and the groups CT and AT realized swimming exercise for 1hour/day with overload equivalent to 5% of body mass five days per week during 4 weeks. The concentrations of GH were significantly difference between the sedentary groups (SC and AS) and (TC and AT) and the lipid metabolism did not change throughout all groups. In conclusions, aerobic physical training did not modify the lipid metabolism and diminishes the values of GH concentration and the OAS did not modify the concentration of GH in Wistar rats.
... Since GH release induced by exercise is mediated by suppression of somatostatin, and L-arginine has a similar mechanism of action, the combination of both could be able to potentiate the impact of GH on protein synthesis. Although some nutritional intervention studies have shown that L-arginine alone or in combination with physical exercise may promote an increase in GH secretion, especially during the recovery period [ 60 ], there is no additional effect on protein synthesis [ 58 , 60 ]. ...
Article
Arginine (C6H14N4O2) is nutritionally classified as a conditional essential amino acid that can be commonly found in the protein component of both plants and animal foods. Over the past two decades, studies have described its role as a mediator of multiple biological processes including the release of several hormones, collagen synthesis during wound healing, antitumor activity, and immune cell responses. Typically endogenous synthesis accounts for approximately 20 % of the daily expenditure, and normal levels of arginine in the blood range from 40 to 100 μmol/L, which may decrease by up to 20 % in diabetes. Moreover, arginine is an amino acid that, through its metabolism, can impact blood flow and blood pressure, especially in relation to the production of nitric oxide (NO•). l-arginine has pronounced glucoregulatory and insulinotropic effects, stimulating insulin secretion acutely but reducing beta cell secretory function and proliferation following chronic exposure. The effect of reducing l-arginine concentration in vivo may have profoundly negative effects on the beta cell as discussed in this chapter. In addition, pigment epithelium-derived factor (PEDF) may be considered as a novel modulator of arginine metabolism and nitric oxide generation in the beta cell. Lastly, the effects of arginine supplementation in sport and exercise are considered.
... Another study reported a substantial decline in post-exercise elbow extension (p = 0.014) and flexion peak torque (p < 0.001) after ingestion of 3 g L-Arg among physically active male and female participants [56]. The ineffectiveness of L-Arg may be related to its ability to blunt growth hormone response following exercise [78]. Resistance exercise alone is a potent stimulator of growth hormone release [79]. ...
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Consumption of amino acids L-arginine (L-Arg) and L-citrulline (L-Cit) are purported to increase nitric oxide (NO) production and improve physical performance. Clinical trials have shown relatively more favorable outcomes than not after supplementing with L-Cit and combined L-Arg and L-Cit. However, in most studies, other active ingredients such as malate were included in the supplement. Therefore, the aim of this study was to determine the efficacy of consuming standalone L-Arg, L-Cit, and their combination (in the form of powder or beverage) on blood NO level and physical performance markers. A systematic review was undertaken following PRISMA 2020 guidelines (PROSPERO: CRD42021287530). Four electronic databases (PubMed, Ebscohost, Science Direct, and Google scholar) were used. An acute dose of 0.075 g/kg of L-Arg or 6 g L-Arg had no significant increase in NO biomarkers and physical performance markers (p > 0.05). Consumption of 2.4 to 6 g/day of L-Cit over 7 to 16 days significantly increased NO level and physical performance markers (p < 0.05). Combined L-Arg and L-Cit supplementation significantly increased circulating NO, improved performance, and reduced feelings of exertion (p < 0.05). Standalone L-Cit and combined L-Arg with L-Cit consumed over several days effectively increases circulating NO and improves physical performance and feelings of exertion in recreationally active and well-trained athletes.
... A multitude of different studies (14)(15)(16)(17)(18)(19)(20)(21) have provided insight into the influence of resistance-and endurance-based exercise on immunoreactive GH concentrations, yet far fewer studies have investigated the effects of exercise perturbations on GH molecular weight (MW) variants (19,22). Regarding the latter, Wallace et al. observed that the increase, peak concentration, and disappearance differed among GH isoforms as a result of acute aerobic exercise in men (23). ...
Article
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Purpose: To determine if acute resistance exercise-induced increases in growth hormone (GH) and insulin-like growth factor-I (IGF-I) were differentially responsive for one or more molecular weight (MW) isoforms and if these responses were sex-dependent. Methods: College-aged men (n = 10) and women (n = 10) performed an acute resistance exercise test (ARET; 6 sets, 10 repetition maximum (10-RM) squat, 2-min inter-set rest). Serum aliquots from blood drawn Pre-, Mid-, and Post-ARET (0, +15, and +30-min post) were processed using High Performance Liquid Chromatography (HPLC) fractionation and pooled into 3 MW fractions (Fr.A: >60; Fr.B: 30–60; Fr.C: <30 kDa). Results: We observed a hierarchy of serum protein collected among GH fractions across all time points independent of sex (Fr.C > Fr.A > Fr.B, p ≤ 0.03). Sex × time interactions indicated that women experienced earlier and augmented increases in all serum GH MW isoform fraction pools (p < 0.05); however, men demonstrated delayed and sustained GH elevations (p < 0.01) in all fractions through +30-min of recovery. Similarly, we observed a sex-independent hierarchy among IGF-I MW fraction pools (Fr.A > Fr.B > Fr.C, p ≤ 0.01). Furthermore, we observed increases in IGF-I Fr. A (ternary complexes) in men only (p ≤ 0.05), and increases in Fr.C (free/unbound IGF-I) in women only (p ≤ 0.05) vs. baseline, respectively. Conclusions: These data indicate that the processing of GH and IGF-I isoforms from the somatotrophs and hepatocytes are differential in their response to strenuous resistance exercise and reflect both temporal and sex-related differences.
... NO has shown increased blood flow and improved muscle contraction, gas exchange, oxygen kinetics, and mitochondrial biogenesis [6,17]. Otherwise, Arg has also been shown to stimulate the release of growth hormone (GH) [18,19], which helps to promote cell growth and regulate the mobilization of fuels in the body that contributes to increase muscle mass and hypertrophy [20][21][22]. Moreover, Arg supplementation has presented a reduction of ammonia, lactate, fatty acids, and fat oxidation levels after exercise [23,24]. ...
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Nitric oxide related ergogenic aids such as arginine (Arg) have shown to impact positively on sport performance through several physiological and metabolic mechanisms. However, research results have shown to be controversial. The great differences regarding required metabolic pathways and physiological demands between aerobic and anaerobic sport disciplines could be the reasons. The aim of this systematic review and meta-analysis was to evaluate the effects of Arg supplementation on aerobic (≤VO 2 max) and anaerobic (>VO 2 max) performance. Likewise, to show the effective dose and timing of this supplementation. A structured search was carried out in accordance with PRISMA ® (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) statement and PICOS guidelines in PubMed/MEDLINE, Web of Science (WOS), and Scopus databases from inception to January 2020. Eighteen studies were included which compare Arg supplementation with placebo in an identical situation and testing its effects on aerobic and anaerobic performance tests. Trials analyzing supplementation with other supplements were removed and there was not athlete's level, gender, ethnicity, or age filters. The performed meta-analysis included 15 studies and random effects model and pooled standardized mean differences (SMD) were used according to Hedges' g. Results revealed that Arg supplementation could improve aerobic (SMD, 0.84; 95% CI, 0.12 to 1.56; magnitude of SMD (MSMD), large; I2, 89%; p = 0.02) and anaerobic (SMD, 0.24; 95% CI, 0.05 to 0.43; MSMD, small; I2, 0%; p = 0.01) performance tests. In conclusion, acute Arg supplementation protocols to improve aerobic and anaerobic performance should be adjusted to 0.15 g/kg of body weight ingested between 60-90 min before. Moreover, chronic Arg supplementation should include 1.5-2 g/day for 4-7 weeks in order to improve aerobic performance, and 10-12 g/day for 8 weeks to enhance anaerobic performance.
... Out of concern for a possible circadian effect of different exercise timing in the present relative to the preceding study [19], we included timed measurements of anabolic hormones insulin, leptin, PTH, and growth hormone and of the catabolic hormone cortisol, because secretory responses of all of these hormones are affected by exercise [25][26][27][28]. The first four support bone formation, and cortisol can block it [29][30][31][32][33]. ...
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Osteoporosis currently afflicts 8 million postmenopausal women in the US, increasing the risk of bone fractures and morbidity, and reducing overall quality of life. We sought to define moderate exercise protocols that can prevent postmenopausal osteoporosis. Our previous findings singled out higher walking speed and pre-exercise meals as necessary for suppression of bone resorption and increasing of markers of bone formation. Since both studies were amenable to alternate biomechanical, nutritional, and circadian interpretations, we sought to determine the relative importance of higher speed, momentum, speed-enhanced load, duration of impulse, and meal timing on osteogenic response. We hypothesized that: (1) 20 min of exercise one hour after eating is sufficient to suppress bone resorption as much as a 40-min impulse and that two 20 min exercise bouts separated by 7 h would double the anabolic effect; (2) early morning exercise performed after eating will be as effective as mid-day exercise for anabolic outcome; and (3) the 08:00 h 40-min. exercise uphill would be as osteogenic as the 40-min exercise downhill. Healthy postmenopausal women, 8 each, were assigned to a no-exercise condition (SED) or to 40- or 20-min exercise bouts, spaced 7 h apart, for walking uphill (40 Up and 20 Up) or downhill (40 Down and 20 Down) to produce differences in biomechanical variables. Exercise was initiated at 08:00 h one hour after eating in 40-min groups, and also 7 h later, two hours after the midday meal, in 20-min groups. Measurements were made of CICP (c-terminal peptide of type I collagen), osteocalcin (OC), and bone-specific alkaline phosphatase (BALP), markers of bone formation, and of the bone resorptive marker CTX (c-terminal telopeptide of type 1 collagen). The osteogenic ratios CICP/CTX, OC/CTX, and BALP/CTX were calculated. Only the 40-min downhill exercise of suprathreshold speed-enhanced momentum, increased the three osteogenic ratios, demonstrating the necessity of a 40-min, and inadequacy of a 20-min, exercise impulse. The failure of anabolic outcome in 40-min uphill exercise was attributed to a sustained elevation of PTH concentration, as its high morning elevation enhances the CTX circadian rhythm. We conclude that postmenopausal osteoporosis can be prevented or mitigated in sedentary women by 45 min of morning exercise of suprathreshold speed-enhanced increased momentum performed shortly after a meal while walking on level ground, or by 40-min downhill, but not 40-min uphill, exercise to avoid circadian PTH oversecretion. The principal stimulus for the anabolic effect is exercise, but the prerequisite for a pre-exercise meal demonstrates the requirement for nutrient facilitation.
... Supplementation with L-Citrulline has a dual effect by simultaneously increasing plasma levels of L-Arginine and L-Citrulline [71]. Alternatively, arginine is attributed to a growth hormone (GH) and insulin stimulating effect, while acting as a creatine precursor [72,73]. Furthermore, combined supplementation of L-Arginine plus L-Ornithine in weight lifters and body builders (strength-athletes) for 21 days stimulated (1-h post-exercise) significant increases in GH and insulin growth factor 1 (IGF-1) [74]. ...
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Multi-ingredient performance supplements (MIPS), ingested pre- or post-workout, have been shown to increase physiological level effects and integrated metabolic response on exercise. The purpose of this study was to determine the efficacy of pre-and post-training supplementation with its own MIPS, associated with CHO (1 g·kg−1) plus protein (0.3 g·kg−1) on exercise-related bench-marks across a training camp for elite cyclists. Thirty elite male cyclists participated in a randomized non-placebo-controlled trial for ten weeks assigned to one of three groups (n = 10 each): a control group treated with CHO plus protein after training (CG); a group treated with MIPS before training and a CHO plus protein after training, (PRE-MIPS); a group treated with CHO plus protein plus MIPS after training, (POST-MIPS). Performance parameters included (VO2max, peak; median and minimum power (W) and fatigue index (%)); hormonal response (Cortisol; Testosterone; and Tes-tosterone/Cortisol ratio); and muscle biomarkers (Creatine kinase (CK), Lactate dehydrogenase (LDH), and Myoglobin (Mb)) were assessed. MIPS administered before or after training (p ≤ 0.05) was significantly influential in attenuating CK, LDH, and MB; stimulating T response and modu-lating C; and improved on all markers of exercise performance. These responses were greater when MIPS was administered post-workout.
... The other possibility resides in the ability of citrulline to shift the energy metabolism to more anaerobic pathways and ameliorating mitochondria activity, through antioxidant properties [35]. Otherwise, L-Arginine has also been shown to stimulate the release of growth hormone (GH) [36,37], which is a potent anabolic agent that favors cell growth and body energetics, which promotes muscle hypertrophy [38,39]. Many effects of L-Arginine supplementation are also linked to improved carbohydrate oxidation and oxygen efficiency [40,41], with reduced exercise-induced production of ammonia, lactate, fatty acids, and fat oxidation [42,43]. ...
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Background: Ergogenic nutritional supplementation is sought by professional athletes for improving physical performance; nevertheless, scientific evidence to support the chronic use of L-Arginine among water polo players is missing. Methods: Seventeen male professional water polo players were randomly assigned to assume 5 grams per day of L-Arginine (n = 9) or placebo (n = 8) for 4 weeks. The players' fitness level was assessed in the maximal speed swimming test. Ear lobe blood samples taken before and after the effort for serum lactate content were analyzed. A speed-to-lactate ratio was generated at the baseline and after 4 weeks of treatment. We also tested the effects of L-Arginine in vitro, measuring NO production, mitochondrial respiration, and gene expression in human fibroblasts. Results: L-Arginine did not modify BMI, muscle strength, and maximal speed at 200 meters after 4 weeks. However, L-Arginine ameliorated oxidative metabolism to exercise as suggested by the statistically significant lower lactate-to-speed ratio, which was not observed in placebo-treated controls. In vitro, L-Arginine induced the expression of a key regulator of mitochondrial biogenesis (PGC1α) and genes encoding for complex I and increased the production of nitric oxide and the maximal oxygen consumption rate. Conclusions: Chronic L-Arginine is safe and effective in ameliorating the oxidative metabolism of professional water polo players, through a mechanism of enhanced mitochondrial function.
... The concentration of IGF-I tended to be greater in arginine sows. Previous studies have shown that arginine supplementation increases growth hormone levels in plasma (Kanaley, 2008), which potentially could stimulate IGF-I through the GH-IGF-I axis. It has been hypothesized that milk-borne growth factors such as IGF-I have a functional role in growth and development of neonatal organs and tissues, and there are several studies that show that oral IGF-I stimulates intestinal growth and functional maturation in newborn animals (Xu, 2003). ...
... In contrast, Fayh et al., (2007) reported that L-Arg supplementation during seven days was ineffective to augment both GH and IGF-I release in individual male adults. Kanaley (2008) fount that most studies using oral Arg have Arg alone increased the resting growth hormone levels. Possible mechanisms for the improvement in these traits may be account for that Arg stimulate GH secretion and GH induces Insulin-like Growth Factor (IGF)-1 (Le Roith et al., 2001), which in turn counteracts apoptosis similarly to Erythropoietin (EPO) and fosters proliferation and differentiation of Burst-and Colony-Forming Units-Erythroid (BFU-E, CFU-E) and myeloid progenitor and peripheral blood cells (Deicher and Walter, 2005). ...
... Moreover, arginine also has multiple functions in the body and an increased arginine concentration may be associated with several exercise adaptations including the synthesis of creatine, 38 enhanced ammonia removal during exercising, 39 and increased growth hormone secretion 40 and release. 41 Furthermore, we detected a difference in the arginine concentrations between nOR and OR. Arginine is a conditionally essential amino acid and under stressful conditions, including serious illnesses and intensive physical activity, there is elevated utilization of arginine for physiological processes. ...
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Impact statement: The diagnosis of overtraining syndrome and overreaching poses a great challenge. Military training aims at improving the physical performance of the conscripts, but an excessive training load could also lead to overreaching. This study of Finnish conscripts provides new insights into the pathophysiology of overreaching and overtraining through amino acids concentrations. In addition to confirming the possible use of plasma glutamine/glutamate concentration to indicate and predict overreaching, we made a novel finding, i.e. low alanine and arginine concentrations might have a role in performance decrement and fatigue related to overreaching. Moreover, this study is the first to show the possible association between amino acids with putative neuronal properties and overreaching. Thus, the present findings might help to detect and prevent overreaching and offer a reliable diagnostic approach. In order to avoid overreaching, military training should be planned more periodically and individually, especially during the first four weeks of military service.
... Este efecto anabólico ha llevado a la administración excesiva de GH recombinante por parte de atletas y, en consecuencia, a su clasificación como droga de abuso en el deporte (Baumann, 2012). Independientemente a la administración exógena, la secreción de GH aumenta durante la actividad física(Kanaley, 2008); es por esto, que fomentar la práctica deportiva en niños en etapa de desarrollo es una estrategia adecuada y pertinente para potenciar el crecimiento somático. En concordancia, gran parte de los estudios incluidos en esta revisión, indagan en los niveles circulantes de GH e IGF-1, en sujetos adolescentes o en edades prepuberales.La evidencia recolectada muestra que el aumento de GH es más significativo posterior a la temporada de entrenamiento; sin embargo, la magnitud del incremento de IGF-1 parece no variar luego de periodosde entrenamiento (Eliakim et al. 2013; Nemet et al. 2012). ...
Article
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Introducción: Los cambios en el patrón de secreción hormonal constituyen uno de los principales mecanismos de regulación homeostática en respuesta al ejercicio físico. Pese a que en los deportes de contacto se ha observado un aumento considerable en los marcadores séricos de estrés, la ausencia de contacto físico entre jugadores genera incertidumbre frente a la posibilidad de que la respuesta endocrina, durante la práctica del voleibol de piso, sea poco significativa. Objetivo: La presente investigación desarrolla una revisión bibliográfica de la respuesta hormonal adaptativa en voleibolistas antes, durante y posterior a sesiones de práctica de voleibol de piso, así como en condiciones basales, en comparación con sujetos sedentarios. Metodología: Se llevó a cabo una revisión bibliográfica en las bases de datos PubMed, Scopus y ScienceDirect de estudios reportados hasta junio del 2021. Resultados: Diez estudios fueron incluidos, a partir de los cuales, se observó que los voleibolistas exhiben niveles elevados de cortisol, testosterona y GH, posterior a sesiones de práctica. Los cambios en la concentración de IGF-1 al igual que el efecto del entrenamiento sobre la respuesta endocrina, mostraron resultados contradictorios. Conclusiones: Aún cuando el cortisol, la testosterona y la GH aumentan después de sesiones de juego, este incremento parece ser mayor en las primeras semanas de temporada de competencia para el cortisol, y mayor en las últimas semanas para la testosterona y la GH. Determinar si el entrenamiento regular logra modular la respuesta endocrina durante las sesiones de juego de voleibol de piso, permanece sujeto a futuras investigaciones.
... The co-administration of Ornipural ® with malathion in the current study shows significant improvement in growth rate, biochemical biomarkers, oxidative stress-related parameters, gene expression of inflammatory mediators, and histological structures of hepatic and renal tissues when compared with animals that received malathion without Ornipural ® . The observed beneficial effect of Ornipural ® on the growth rate of rats may be attributed to the presence of arginine, which is known to be one of the strongest insulin and growth hormone secretagogues [51,52]. Regarding hepato-renal and metabolic serum biochemical biomarkers, Ornipural ® markedly counteracted the adverse impact of malathion via the normalization of AST, ALT, ALP, LDH, ACP, AchE, and paraoxonase in the intoxicated group. ...
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The current study was instigated by investigating the ameliorative potential of Ornipural® solution against the hepato-renal toxicity of malathion. A total number of 35 male Wistar albino rats were divided equally into five groups. Group 1 served as control and received normal saline intraperitoneally. Group 2, the sham group, were administered only corn oil (vehicle of malathion) orally. Group 3 was orally intoxicated by malathion in corn oil at a dose of 135 mg/kg BW via intra-gastric gavage. Group 4 received malathion orally concomitantly with Ornipural® intraperitoneally. Group 5 was given Ornipural® solution in saline via intraperitoneal injection at a dose of (1 mL/kg BW). Animals received the treatment regime for 30 days. Histopathological examination revealed the harmful effect of malathion on hepatic and renal tissue. The results showed that malathion induced a significant decrease in body weight and marked elevation in the activity of liver enzymes, LDH, and ACP. In contrast, the activity of AchE and Paraoxonase was markedly decreased. Moreover, there was a significant increase in the serum content of bilirubin, cholesterol, and kidney injury markers. A significant elevation in malondialdehyde, nitric oxide (nitrite), and 8-hydroxy-2-deoxyguanosine was observed, along with a substantial reduction in antioxidant activity. Furthermore, malathion increased tumor necrosis factor-alpha, the upregulation of IL-1B, BAX, and IFN-β genes, and the downregulation of Nrf2, Bcl2, and HO-1 genes. Concurrent administration of Ornipural® with malathion attenuated the detrimental impact of malathion through ameliorating metabolic biomarkers, restoring antioxidant activity, reducing the inflammatory response, and improving pathologic microscopic alterations. It could be concluded that Ornipural® solution demonstrates hepatorenal defensive impacts against malathion toxicity at biochemical, antioxidants, molecular, and cellular levels.
... Por otro lado, a la arginina se le atribuye un efecto de estimulación de la hormona del crecimiento 373 y de la insulina, al tiempo que actúa como precursor de la creatina 374,375 . El problema es que el ejercicio por sí mismo aumenta la hormona del crecimiento más que la ingesta de arginina, y el ejercicio suplementado con arginina no incrementa la hormona del crecimiento más que el ejercicio solo 376,377 . ...
... niloticus). Arginine did better growth performance on Japanese flounder juvenile (Furuya et al., 2012) suggest that, the arginine treatment affect serum concentrations of nitrogenous and lipid signaling molecules (glycerophosphorylcholine and myoinositol) and intestinal bacterial metabolites (He et al., 2008), which increase growth hormone responses (Kanaley et al., 2008). All of these results co-relate with the results of present experiment. ...
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The present experiment was conducted for 5 weeks to investigate the effects of L-arginine on the growth performance of fingerling Nile Tilapia (Oreochrommi niloticus). Nile tilapia were stocked in aquarium and fed regularly with different dose of L-arginine and other isoenergetic diets for all the trials. Weekly sampling was carried out to evaluate body weight and length. Fingerlings having average weight and length 0.31 ± 0.01 gm and 2.71 ± 0.01 cm, respectively were fed with T 1 (SD+0.00143% L-arginine of diet+Vit-E), T 2 (SD+0.0143% L-arginine of diet+Vit-E), T 3 (SD+0.143% L-arginine of diet+Vit-E) and T 4 (SD+Vit-E) for 5 weeks. The net weight gains in T 3 (0.88 ±0.03gm) was significantly higher (p<0.01) than those of T 1 (0.72 ± 0.02gm), T 2 (0.79 ± 0.02gm) and T4 (0.66 ±0.02gm). The net length gains in T 3 (1.553 ±0.04cm) was significantly (p<0.01) higher than that of T 2 (1.480 ±0.02cm) , T 1 (1.390 ±0.01cm) and T 4 (1.290 ±0.03cm). The SGR (%/day) in treatment T3 (2.52 ±0.07) was significantly higher (p<0.01) than the treatment T1 (2.07 ± 0.04), T2 (2.26 ±0.04) and T4 (1.90 ±0.04). Significant differences (p<0.01) were observed for survival rates among various dietary treatments. The highest survival rate was found in T 3 (86.67%) and the lowest in T 4 (73.33%). The present study indicates that, supplementation of 0.143% L-arginine in feed might be a good growth indicator for mass culture of tilapia.
... niloticus). Arginine did better growth performance on Japanese flounder juvenile (Furuya et al., 2012) suggest that, the arginine treatment affect serum concentrations of nitrogenous and lipid signaling molecules (glycerophosphorylcholine and myoinositol) and intestinal bacterial metabolites (He et al., 2008), which increase growth hormone responses (Kanaley et al., 2008). All of these results co-relate with the results of present experiment. ...
Article
Full-text available
The present experiment was conducted for 5 weeks to investigate the effects of L-arginine on the growth performance of fingerling Nile Tilapia (Oreochrommi niloticus). Nile tilapia were stocked in aquarium and fed regularly with different dose of L-arginine and other isoenergetic diets for all the trials. Weekly sampling was carried out to evaluate body weight and length. Fingerlings having average weight and length 0.31 ± 0.01 gm and 2.71 ± 0.01 cm, respectively were fed with T 1 (SD+0.00143% L-arginine of diet+Vit-E), T 2 (SD+0.0143% L-arginine of diet+Vit-E), T 3 (SD+0.143% L-arginine of diet+Vit-E) and T 4 (SD+Vit-E) for 5 weeks. The net weight gains in T 3 (0.88 ±0.03gm) was significantly higher (p<0.01) than those of T 1 (0.72 ± 0.02gm), T 2 (0.79 ± 0.02gm) and T4 (0.66 ±0.02gm). The net length gains in T 3 (1.553 ±0.04cm) was significantly (p<0.01) higher than that of T 2 (1.480 ±0.02cm) , T 1 (1.390 ±0.01cm) and T 4 (1.290 ±0.03cm). The SGR (%/day) in treatment T3 (2.52 ±0.07) was significantly higher (p<0.01) than the treatment T1 (2.07 ± 0.04), T2 (2.26 ±0.04) and T4 (1.90 ±0.04). Significant differences (p<0.01) were observed for survival rates among various dietary treatments. The highest survival rate was found in T 3 (86.67%) and the lowest in T 4 (73.33%). The present study indicates that, supplementation of 0.143% L-arginine in feed might be a good growth indicator for mass culture of tilapia.
... l-arginine is also metabolized to creatinine that facilitates better muscle mass and higher anaerobic work capacity. l-arginine also helps to increase the levels of resting growth hormone, which in turns helps in gaining muscle mass (Kanaley 2008). l-Arginine soft-gel helps in reduction of menopause symptoms (Stanislavov and Rohdewald 2014). ...
Chapter
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Amino acids are used for the synthesis of body proteins and other nitrogenous metabolites in cell signaling, and as regulators of hormone secretion and nutrient metabolism. Arginine and citrulline are especially important in the control of hemodynamics and whole-body homeostasis, as both participate in multiple metabolic pathways and play vital roles in maintaining the health and integrity of skeletal and cardiac muscles. Arginine contributes to the release of growth hormone and creatine synthesis, both of which positively improve muscle mass and strength. Arginine is also required for the production of nitric oxide, which improves vascular function and regulates growth and detection of changes in mechanical loading of skeletal muscle. Indeed, arginine supplementation positively contributes to heart and muscle health as well as the maintenance of exercise capacity. Citrulline is converted into arginine in almost all cell types and thus can be used to prevent arginine and nitric oxide deficiencies under various physiological and pathological conditions. Further, citrulline aids in the detoxification of ammonia, which helps to reduce fatigue and improve exercise performance. Collectively, arginine and citrulline are crucial for enhancing sports nutrition in humans.
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Chapter
Athletic endeavors push the limits of human performance and athletes often seek ergogenic aids to gain an edge. A nutritional ergogenic aid is defined as any nutrient capable of enhancing energy utilization, including energy production, control, and efficiency (Silver, J Am Acad Orthop Surg 9:61–70, 2001). A nutritional ergogenic aid sought commonly by athletes is protein (or amino acid) supplementation (Alvares et al., Appl Physiol Nutr Metab 37:115–126, 2012; Campbell et al., J Int Soc Sports Nutr 1:35–38, 2004; Chromiak and Antonio, Nutrition 18:657–661, 2002; Paddon-Jones et al., J Nutr 134:2888S–2894S, 2004; Shao and Hathcock, Regul Toxicol Pharmacol 50:376–399, 2008). l-arginine is an amino acid that has been purported to be ergogenic and, as such, has become very popular in the food supplement industry (Alvares et al., Appl Physiol Nutr Metab 37:115–126, 2012; Campbell et al., J Int Soc Sports Nutr 1:35–38, 2004; Paddon-Jones et al., J Nutr 134:2888S–2894S, 2004; Shao and Hathcock, Regul Toxicol Pharmacol 50:376–399, 2008; McConell, Curr Opin Clin Nutr Metab Care 10:46–51, 2007; Kanaley, Curr Opin Clin Nutr Metab Care 11:50–54, 2008). Recently, Maughan et al. (J Sports Sci 29:S57–66, 2011) noted l-arginine as an emerging and growing trend among athletes.
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Previously published data (J Bone Miner Res (2005); 20: 471) did not give evidence that the administration of the nitric oxide precursor L-arginine increases bone formation and decreases bone resorption in postmenopausal women. Data of this trial were reanalysed for putative effects of L-arginine on muscle mass and muscular function. Therefore, 11 females of the former study group (n=15; age 54.5+/-4.1 years; daily oral administration of 18 g L-arginine hydrochloride (equivalent of 14.2 g L-arginine) over 6 months) and 12 females of the control group (n=15; age 55.3+/-4.4 years; daily administration of 18 g dextrose over 6 months) were analysed for biomechanical parameters (MIGF, maximal isometric grip force; PJF, peak jump force; PJP, peak jump power) and for the cross-sectional muscle area (MA) and fat area (FA) at forearm and leg (calf) measured by peripheral quantitative computed tomography. The study was performed in a double-blind design. The assessment of muscular and biomechanical parameters was undertaken before and after 6 months of L-arginine versus placebo administration. L-arginine-supplemented females had a significant increase of PJF/kg in comparison with the control group. PJP/kg, MIGF, MA and FA were not significantly influenced by the administration of L-arginine. In conclusion, the administration of L-arginine increased maximal force in mechanographic analyses and may prevent a decline of muscle force in postmenopausal women.
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The effects of intensity of run training on the pulsatile release of growth hormone (GH) were investigated in 21 eumenorrheic untrained women. The O2 consumption (VO2) at the lactate threshold (LT); fixed blood lactate concentrations (FBLC) of 2.0, 2.5, and 4.0 mM; peak VO2; maximal VO2; body composition; and pulsatile release of GH were measured. Subjects in both the at-lactate threshold (/LT, n = 9) and above-lactate threshold (greater than LT, n = 7) training groups increased VO2 at LT and FBLC of 2.0, 2.5, and 4.0 mM and VO2max after 1 yr of run training. However, the increase observed in the greater than LT group was greater than that in the /LT group (P less than 0.05). No change was observed for the control group (n = 5). No among- or within-group differences were observed for body weight, although trends for reductions in percent body fat (P less than 0.06) and fat weight (P less than 0.15) were observed in the greater than LT group, and both training groups significantly increased fat-free weight (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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It is well known that in normal adults the growth hormone (GH) response to GH-releasing hormone (GHRH) is inhibited by previous administration of the neurohormone. In 7 healthy volunteers (age 20-34 years) we studied the GH responses to two consecutive GHRH boluses (1 microgram/kg i.v. every 120 min) alone or coadministered with arginine (30 g i.v. over 30 min). The GH response to the first GHRH bolus (area under the curve, mean +/- SEM: 506.3 +/- 35.1 micrograms/l/h) was higher (p = 0.0001) than that to the second one (87.1 +/- 14.6 micrograms/l/h). The latter response was clearly increased (p = 0.0001) by coadministering arginine (980.5 +/- 257.5 micrograms/l/h). When every GHRH bolus was combined with arginine a marked potentiation of GH response to both boluses was found. However, the second combined administration of arginine and GHRH induced a GH increase which was lower compared to the first one (p = 0.016). In conclusion, our results show that arginine potentiates the GHRH-induced GH secretion preventing the lessening of somatotrope responsiveness to the neurohormone alone. As there is evidence that this phenomenon is due to an enhanced somatostatin release, these findings give further evidence of a somatostatin-suppressing effect of arginine.
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The declining activity of the growth hormone--insulin-like growth factor I (IGF-I) axis with advancing age may contribute to the decrease in lean body mass and the increase in mass of adipose tissue that occur with aging. To test this hypothesis, we studied 21 healthy men from 61 to 81 years old who had plasma IGF-I concentrations of less than 350 U per liter during a six-month base-line period and a six-month treatment period that followed. During the treatment period, 12 men (group 1) received approximately 0.03 mg of biosynthetic human growth hormone per kilogram of body weight subcutaneously three times a week, and 9 men (group 2) received no treatment. Plasma IGF-I levels were measured monthly. At the end of each period we measured lean body mass, the mass of adipose tissue, skin thickness (epidermis plus dermis), and bone density at nine skeletal sites. In group 1, the mean plasma IGF-I level rose into the youthful range of 500 to 1500 U per liter during treatment, whereas in group 2 it remained below 350 U per liter. The administration of human growth hormone for six months in group 1 was accompanied by an 8.8 percent increase in lean body mass, a 14.4 percent decrease in adipose-tissue mass, and a 1.6 percent increase in average lumbar vertebral bone density (P less than 0.05 in each instance). Skin thickness increased 7.1 percent (P = 0.07). There was no significant change in the bone density of the radius or proximal femur. In group 2 there was no significant change in lean body mass, the mass of adipose tissue, skin thickness, or bone density during treatment. Diminished secretion of growth hormone is responsible in part for the decrease of lean body mass, the expansion of adipose-tissue mass, and the thinning of the skin that occur in old age.
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Nine eumenorrheic women (age 24.11 +/- 4.28 yr) performed each of six randomly assigned heavy-resistance protocols (HREPs) on separate days during the early follicular phase of the menstrual cycle. The HREPs consisted of two series [series 1 (strength, S) and series 2 (hypertrophy, H)] of three protocols, each using identically ordered exercises controlled for load [5 vs. 10 repetitions maximum (RM)], rest period length (1 vs. 3 min), and total work (J) within each three-protocol series. Blood measures were determined pre-, mid- (after 4 of 8 exercises), and postexercise (0, 5, 15, 30, 60, 90, 120 min and 24 and 48 h). In series 1, a significant (P < 0.05) reduction in growth hormone (GH) was observed at 90 min postexercise for all three protocols. In series 2, the 10-RM protocol with 1-min rest periods (H10/1) produced significant increases above rest in GH concentrations at 0, 5, and 15 min postexercise, and the H10/1 and H5/1 protocols demonstrated significant reductions at 90 and 120 min postexercise. Cortisol demonstrated significant increases in response to the S10/3 protocol at 0 min, to the H10/1 protocol at midexercise and at 0 and 5 min postexercise, and to the H5/1 protocol at 5 and 15 min postexercise. No significant changes were observed in total insulin-like growth factor I, total testosterone, urea, or creatinine for any of the HREPs. Significant elevations in whole blood lactate and ammonia along with significant reductions in blood glucose were observed. Hormonal and metabolic blood variables measured in the early follicular phase of the menstrual cycle varied in response to different HREPs. The most dramatic increases above resting concentrations were observed with the H10/1 protocol, indicating that the more glycolytic HREPs may stimulate greater GH and cortisol increases.
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The purpose of this study was to determine whether recombinant human growth hormone (GH) administration enhances muscle protein anabolism in experienced weight lifters. The fractional rate of skeletal muscle protein synthesis and the whole body rate of protein breakdown were determined during a constant intravenous infusion of [13C]leucine in 7 young (23 +/- 2 yr; 86.2 +/- 4.6 kg) healthy experienced male weight lifters before and at the end of 14 days of subcutaneous GH administration (40 microgram.kg-1 x day-1). GH administration increased fasting serum insulin-like growth factor-I (from 224 +/- 20 to 589 +/- 80 ng/ml, P = 0.002) but did not increase the fractional rate of muscle protein synthesis (from 0.034 +/- 0.004 to 0.034 +/- 0.002%/h) or reduce the rate of whole body protein breakdown (from 103 +/- 4 to 108 +/- 5 mumol.kg-1 x h-1). These findings suggest that short-term GH treatment does not increase the rate of muscle protein synthesis or reduce the rate of whole body protein breakdown, metabolic alterations that would promote muscle protein anabolism in experienced weight lifters attempting to further increase muscle mass.
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Sixteen men completed four trials at random as follows: (Trial A) performance of a single bout of resistance exercise preceded by placebo ingestion (vitamin C); (Trial B) ingestion of 1,500 mg L-arginine and 1,500 mg L-lysine, immediately followed by exercise as in Trial A; (Trial C) ingestion of amino acids as in Trial B and no exercise; (Trial D) placebo ingestion and no exercise. Growth hormone (GH) concentrations were higher at 30, 60, and 90 min during the exercise trials (A and B) compared with the resting trials (C and D) (p < .05). No differences were noted in [GH] between the exercise trials. [GH] was significantly elevated during resting conditions 60 min after amino acid ingestion compared with the placebo trial. It was concluded that ingestion of 1,500 mg arginine and 1,500 mg lysine immediately before resistance exercise does not alter exercise-induced changes in [GH] in young men. However, when the same amino acid mixture is ingested under basal conditions, the acute secretion of GH is increased.
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Growth hormone (GH) helps maintain body composition and metabolism in adults. However, basal and peak GH decline with age. Exercise produces a physiologic GH response that is subnormal in elderly people. Arginine (Arg) infusion can augment GH secretion, but the efficacy of oral Arg to improve GH response to exercise has not been explored. We investigated whether oral Arg increases GH secretion in young and old people at rest and during exercise. Twenty young (Y: 22.1 +/- 0.9 y; SEM) and 8 old (O: 68.5 +/- 2.1 y) male and female subjects underwent three different trials following determination of their one-repetition maximum strength (1-RM); exercise only (EO; 3 sets, 8-10 reps at 85% of 1-RM; on 12 separate resistive lifts), Arg only (5.0 g), or Arg + exercise. Blood samples were collected between successive lifts, and GH (ng x ml(-1)) was determined via RIA. In Y vs O: Basal GH secreted (area under the curve) was 543.6 +/- 84.0 vs 211.5 +/- 63.0. During EO, values were 986.6 +/- 156.6 and 517.8 +/- 85.5. Both were significantly lower in the older individuals (p < .05). Oral Arg alone did not result in any increase in GH secretion at rest (310.8 +/- 73.2 vs 262.9 +/- 141.2). When Arg was coadministered during exercise, GH release was not affected in either the young or old and appeared to be blunted in the young compared to the exercise only trial in the young. Based upon these findings, we concluded that oral Arg does not stimulate GH secretion and may impair GH release during resistive exercise.
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Amenorrheic athletes exhibit a spectrum of neuroendocrine disturbances, including alterations in the GH-insulin-like growth factor I (IGF-I) axis. Whether these changes are due to exercise or amenorrhea is incompletely characterized. The present study investigates spontaneous (overnight) and exercise-stimulated GH secretion and associated IGF-binding proteins (IGFBPs) in amenorrheic (AA; n = 5), and eumenorrheic athletes ( n = 5) matched for age, percent body fat (dual energy x-ray absorptiometry), training history, and maximal oxygen consumption. Each volunteer participated in two hospital admissions consisting of a 50-min submaximal exercise bout (70% maximal oxygen consumption) and an 8-h nocturnal sampling period. Deconvolution analysis of serum GH concentration time series revealed increases in the half-life of GH (60%) and the number of secretory bursts (85%) as well as a decrease in their half-duration (50%) and the mass of GH secreted per pulse (300%) in the AA cohort. Time occupancy at elevated trough GH concentrations was significantly increased, and GH pulsatility (approximate entropy) was more irregular in the AA group. During exercise, AA exhibited a reversal of the normal relationship between IGF-I and GH, and a 4- to 5-fold blunting of stimulated peak and integrated GH secretion. Fasting levels of plasma IGF-I, IGFBP-3, and IGFBP-1 appeared to be unaffected by menstrual status. In ensemble, this phenotype of GH release in amenorrheic athletes suggests disrupted neuroregulation of episodic GH secretion, possibly reflecting decreased somatostinergic inhibition basally, and reduced GHRH output in response to exercise compared with eumenorrheic athletes. Accordingly, we postulate that the amenorrheic state, beyond the exercise experience per se, alters the neuroendocrine control of GH output in amenorrheic athletes.
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Exercise of appropriate intensity is a potent stimulus for GH and cortisol secretion. Circadian and diurnal rhythms may modulate the GH and cortisol responses to exercise, but nutrition, sleep, prior exercise patterns, and body composition are potentially confounding factors. To determine the influence of the time of day on the GH and cortisol response to acute exercise, we studied 10 moderately trained young men (24.1 +/- 1.1 yr old; maximal oxygen consumption, 47.9 +/- 1.4 mL/kg.min; percent body fat, 13.2 +/- 0.6%). After a supervised night of sleep and a standard meal 12 h before exercise, subjects exercised at a constant velocity (to elicit an initial blood lactate concentration of approximately 2.5 mmol/L) on a treadmill for 30 min on 3 separate occasions, starting at 0700, 1900, and 2400 h. Blood samples were obtained at 5-min intervals for 1 h before and 5 h after the start of exercise; subjects were not allowed to sleep during this period. Subjects were also studied on 3 control days under identical conditions without exercise. There were no significant differences with time of day in the mean blood lactate and submaximal oxygen consumption values during exercise. The differences over time in serum GH and cortisol concentrations between the exercise day and the control day were determined with 95% confidence limits for each time of day. Exercise stimulated a significant increase in serum GH concentrations over control day values for approximately 105--145 min (P < 0.05) with no significant difference in the magnitude of this response by time of day. The increase in serum GH concentrations with exercise was followed by a transient suppression of GH release (for approximately 55--90 min; P < 0.05) after exercise at 0700 and 1900 h, but not at 2400 h. Although the duration of the increase in serum cortisol concentrations after exercise was similar (approximately 150--155 min; P < 0.05) at 0700, 1900, and 2400 h, the magnitude of this increase over control day levels was greatest at 2400 h. This difference was significant for approximately 130 min and approximately 40 min compared to exercise at 1900 and 0700 h, respectively (P < 0.05). The cortisol response to exercise at 0700 h was significantly greater than that at 1900 h for about 55 min (P < 0.05). A rebound suppression of cortisol release for about 50 min (P < 0.05) was observed after exercise at 2400 h, but not 0700 or 1900 h. Both baseline (before exercise) and peak cortisol concentrations were significantly higher at 0700 h than at 1900 or 2400 h (P < 0.01). We conclude that time of day does not alter the GH response to exercise; however, the exercise-induced cortisol response is modulated by time of day.
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To evaluate the plasma leptin levels approximately 24 h post-exercise in control and type 2 diabetic subjects and to establish if observed changes in leptin concentrations were acute or chronic effects of a resistance training program. Thirty men and women (17 controls and 13 type 2, obese diabetics, age 40-55 y) had resting blood samples drawn at 08:00 h (12 h postprandial) at the beginning of the study (pre-training), 24 h after a three repetition maximal weight lifting bout (acute) and 72 h after their last training bout of 6 weeks of resistance training (chronic). The two groups were not matched with respect to body mass index and the control subjects were not normal weight. Subjects weight-trained three times a week, for 6 weeks, for 1 h, training both the upper and lower body. Serum leptin concentrations were significantly higher in the type 2 diabetics than in the control group at pre-training (41.4+/-8.9 vs 11.4+/-3.0 ng/ml, P<0.05, respectively). Compared to pre-training, the leptin levels decreased significantly (P<0.01) after acute exercise in the diabetics but not in the control subjects (diabetics 30.9+/-7.1 vs controls 10.6+/-2.6 ng/ml). Approximately 72 h after 6 weeks of exercise training, the leptin concentrations were no longer lower than the pre-training values in either group (36.9+/-8.8 vs 11.9+/-8.8 ng/ml, respectively, P=NS). When leptin concentrations were log transformed and adjusted for fat mass there were still significant changes in leptin levels over time and between the control and diabetic group (P<0.05). The type 2 diabetics showed a significant 30% reduction in resting leptin levels 24 h after a single bout of resistance exercise. This was an acute response to resistance exercise and not a chronic training effect (no difference between pre-training and chronic). The decreased resting leptin concentrations approximately 24 h post-acute exercise may be due to reduced glucose availability to the adipose tissue, particularly in the diabetic subjects. There is no chronic effect of resistance exercise on leptin concentrations.
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We previously reported that in young adult males growth hormone (GH) release is related to exercise intensity in a linear dose-response manner (Pritzlaff et al. J Appl Physiol 87: 498-504, 1999). To investigate the effects of gender and exercise intensity on GH release, eight women (24.3 +/- 1.3 yr, 171 +/- 3.2 cm height, 63.6 +/- 8.7 kg weight) were each tested on six randomly ordered occasions [1 control condition (C), 5 exercise conditions (Ex)]. Serum GH concentrations were measured in samples obtained at 10-min intervals between 0700 and 0900 (baseline) and 0900 and 1300 (Ex + recovery or C). Integrated GH concentrations (IGHC) were calculated by trapezoidal reconstruction. During Ex, subjects exercised for 30 min (0900-0930) at one of the following intensities [normalized to the lactate threshold (LT)]: 25 and 75% of the difference between LT and rest, at LT, and at 25 and 75% of the difference between LT and peak O2 uptake. No differences were observed among conditions for baseline IGHC. To determine whether total (Ex + recovery) IGHC changed with increasing exercise intensity, slopes associated with individual linear regression models were subjected to a Wilcoxon signed-rank test. To test for gender differences, data in women were compared with the previously published data in men. A Wilcoxon ranked-sums two-tailed test was used to analyze the slopes and intercepts from the regression models. Total IGHC increased linearly with increasing exercise intensity. The slope and intercept values for the relationship between total IGHC and exercise intensity were greater in women than in men. Deconvolution analysis (0700-1300 h) revealed that, regardless of gender, increasing exercise intensity resulted in a linear increase in the mass of GH secreted per pulse and summed GH production rate, with no changes in GH secretory pulse frequency or apparent half-life of elimination. Exercise reduced the half-duration of GH secretory burst in men but not in women. Gender comparisons revealed that women had greater basal (nonpulsatile) GH secretion across all conditions, more frequent GH secretory pulses, a greater GH secretory pulse amplitude, a greater production rate, and a trend for a greater mass of GH secreted per pulse than men. We conclude that, in young adults, the GH secretory response to exercise is related to exercise intensity in a linear dose-response pattern. For each incremental increase in exercise intensity, the fractional stimulation of GH secretion is greater in women than in men.
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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.
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Cholinergic and opioid pathways have been implicated as mediators of the increased growth hormone (GH) release observed during exercise. This study compared the GH responses induced by a moderate-intensity exercise bout during treatment with placebo (Plac), the opioid receptor antagonist naltrexone (Nalt), the indirect cholinergic agonist pyridostigmine (PD), or a combination of the two drugs (P + N). Ten active males served as subjects (age, 25.1 +/- 0.6 yr; wt, 79.7 +/- 2.5 kg; % body fat, 14.9 +/- 1.4; peak oxygen consumption, 46.2 +/- 2.7 ml.kg-1 x min-1). Blood samples were drawn at 5-min intervals during the 4.5-h testing period to determine the GH concentration. The testing period was divided as follows: 0600–700 h = baseline, 0700–0800 h = preexercise, 0800–0830 h = exercise, and 0830–1030 h = recovery. Drugs were administered 1 h before exercise (at 0700 h). Exercise consisted of 30 min of cycling at an individualized work load previously found to elicit a blood lactate concentration of 2.5 mM. Heart rate, oxygen consumption, blood lactate, and blood glucose were measured throughout the exercise period. Results indicated that neither the resting GH concentration nor the metabolic parameters during exercise were altered by the treatments. Peak serum GH concentration was not significantly altered by the treatments (range 7.3 +/- 2.0 to 12.6 +/- 4.4 micrograms/l).(ABSTRACT TRUNCATED AT 250 WORDS)
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Human growth hormone (GH) has a number of accepted medical uses, but has quickly become a popular ergogenic aid among athletes. The issue of performance-enhancing substances such as anabolic steroids and GH has drawn the attention of athletes, their parents, and politicians. On almost a daily basis, headlines about the status of doping in professional, international, and amateur sports seem to be more pervasive. The supraphysiologic effects of GH lead to lipolysis, with increased muscle volume. Due to the ethical limitations of studying the use of high doses of GH in isolation or combined with anabolic steroids, the scientific literature has not produced compelling results on its efficacy. GH has potential as an anti-aging drug and does lead to some improved athletic performance in isolated studies. Despite the lack of compelling data, GH seems to have developed a reputation among athletes for enhancing performance. The detection of illegal doping with GH has been the focus of a concerted international effort by the International Olympic Committee. A number of promising detection techniques may allow the detection of illicit GH use. This review on GH as an ergogenic aid includes a discussion of the basic physiology of GH and its actions, the accepted medical indications for its use, the results of scientific studies that assess whether it improves exercise performance or work capacity, and the scientific techniques under development to detect ergogenics with strong abuse potential.
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Cortisol and growth hormone (GH) are released in response to a variety of pharmacologic and physiologic stimuli. Secretion of cortisol and GH are influenced by age, gender, time of day, nutrition, sleep, body composition, and fitness level. Exercise is one of the most potent stimulators for release of these hormones. A single session of exercise of sufficient intensity will result in dramatic increases in cortisol and GH concentrations in most individuals and may take a few hours to recover back to baseline levels. Cortisol and GH are necessary for optimal exercise performance, which is most evident in chronic cortisol and GH deficiency. In deficient individuals, replacement therapy with cortisol or GH restores normal exercise performance. Exercise training can substantially alter the degree of perturbation of the hypothalamic-pituitary axis. The cortisol response pattern to exercise has been considered to be predictive of an individual's adaptation to other forms of stress. This review discusses the cortisol and GH responses to exercise, the factors affecting these responses, the mechanisms of hormone release, and the clinical implications of these physiological observations.
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Th. : Sci. : Amsterdam : (ca 1995). Références bibliogr.
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Over the past 10 years significant progress has been made in techniques for manipulating the genome of the animal. Production of transgenic mice has led to important insights into the regulation of gene expression, the molecular basis of cancer, immunology, and developmental biology. The tools necessary to generate transgenic mice are becoming widely available, making it possible to study a variety of problems. In this review a description of the strategies being used to address problems of interest in cell physiology using transgenic mice is given. Elucidation of the rules governing the regulation of gene expression now permits the targeted expression of a protein to a particular organ or cell type within an organ. Overexpression of proteins, expression of foreign or mutant proteins, mislocalization of proteins, and directed elimination of proteins are all procedures that can now be used to generate interesting animal models for physiological studies. The applications of these techniques to a variety of problems in normal and abnormal physiology are discussed in this review.
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Recent reports, based on measurements of plasma GH levels, have challenged the concept that GH secretion is dependent on sleep and not modulated by circadian rythmicity. Because plasma levels reflect not only the secretory process, but also the effects of distribution and degradation, temporal limits of active secretion and, consequently, synchrony with other physiological events cannot be accurately estimated from circulating concentrations. The present study was undertaken to examine the roles of sleep and time of day in modulating pulsatile GH secretion, using a mathematical procedure (deconvolution) allowing secretory rates to be estimated from peripheral levels. Eight young nonobese healthy men participated each in six separate 16-h studies involving either normal or delayed sleep. Plasma GH levels were measured at 15-min intervals, and GH secretory rates were calculated by deconvolution. Each individual study was preceded by one night of habituation, and sleep was polygraphically recorded in all studies. Repeated measurements of plasma insulin-like growth factor-I (IGF-I) were performed in all subjects. Deconvolution revealed the existence of approximately 20% more GH pulses than detected in the plasma profiles. Large peaks of plasma GH concentrations often reflected the occurrence of a succession of secretory pulses. The total amount of GH secreted varied 10-fold across individual studies, but the within-subject variability (32%) was less than half the across-subject variability (65%). IGF-I levels were also more reproducible for a given subject than across subjects (11% vs. 36% variability) and did not correlate with the amount of GH secreted. During normal waking hours, the GH secretory rate was similar in the evening and the morning. This secretory rate was doubled during wakefulness at times of habitual sleep and tripled during sleep, even when sleep was delayed until 0400 h. A pulse starting within 30 min after sleep onset was present in all profiles with normal sleep and in 13 of 16 profiles with delayed sleep. The amount of GH secreted in response to sleep onset was tightly correlated with the level of secretion during wakefulness (r = 0.92). Almost 70% (57 of 83) of the pulses occurring during sleep were associated with slow wave (SW) stages. The amount of GH secreted in SW-associated pulses was correlated with the amount of SW occurring during the pulse, even when sleep-onset pulses were not considered. We conclude that in normal adult men, the amount of GH secretion and the levels of IGF-I are more reproducible within than across individuals.(ABSTRACT TRUNCATED AT 400 WORDS)
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We hypothesized that circulating GH would increase only if a threshold of work intensity [corresponding to the anaerobic or lactate threshold (LT)] was exceeded. Ten healthy male volunteers (18-35 yr) first performed ramp-type progressive cycle-ergometer exercise to determine the LT and the maximal oxygen uptake. On subsequent mornings after an overnight fast, each subject performed bouts of 1, 5, and 10 min constant work rate exercise of either high intensity (above LT) or low intensity (below LT). A 1-h interval separated exercise bouts. Gas exchange (breath-by-breath), GH, immunoreactive insulin, glucose, lactate, pyruvate, and epinephrine and norepinephrine were measured at regular intervals. After the 10-min bouts of high compared with low intensity exercise, lactate was 7.2 +/- 3.7 mmol/L vs. 1.4 +/- 1.3, P less than 0.05; epinephrine was 1,113 +/- 519 pmol/L vs. 496 +/- 273, P less than 0.05; and norepinephrine was 7.89 +/- 3.45 nmole/L vs. 2.83 +/- 1.34, P less than 0.05. GH did not increase significantly from preexercise baseline during low intensity exercise (e.g., GH after 10-min low intensity exercise changed from baseline values by 1.5 +/- 2.0 micrograms/L, NS). Although lactate was elevated after 5-min of high intensity exercise, peak GH was significantly elevated (mean increase above baseline of 7.7 +/- 2.4 micrograms/L, P less than 0.05) only after 10 min of high intensity exercise (increases in 9 of 10 subjects). The GH increase occurred despite simultaneous increases in both IRI and glucose. A minimum duration of 10 min, high intensity exercise consistently increased circulating GH in adult males.
Article
Both fasting and sleep increase the secretion of human GH and, therefore, might explain its predominantly nocturnal release. To study the precise temporal relationship between GH secretory episodes and cortical activity, GH measurements and electroencephalogram sleep stage recordings were performed every 30 s for 8 h in six young male volunteers fasted for 24 h. GH was measured in two drops of whole blood, which were directly sampled into the assay tube using a continuous blood withdrawal pump and a fraction collector. Concomitant serum sampling during a GH-releasing hormone test (n = 4) revealed a high correlation (r = 0.98) between GH measurements in serum and whole blood. GH pulses were objectively identified with Cluster analysis, and GH secretion rates were calculated with a waveform-independent deconvolution algorithm. When data were analyzed as replicates with 1-min intervals, the nocturnal pulse frequency was 1.2 pulses/h. Elimination of data points demonstrated 43% and 64% reductions in the number of GH pulses detected for 5- and 20-min sampling intervals, respectively. Mean GH concentrations and secretory rates were significantly higher during stage 3 and 4 sleep compared to stage 1, 2, and rapid eye movement sleep. GH secretory rates and peripheral GH concentrations were maximally correlated with sleep stage, with lags of 4.5 and 16 min, respectively, suggesting that maximal GH release occurs within minutes of the onset of stage 3 or 4 sleep. This temporal coincidence between pituitary GH secretion and delta sleep is consistent with cortical control over hypothalamic-pituitary function.
Article
Growth hormone (GH) treatment in adults with GH deficiency increases lean body mass and thigh muscle cross-sectional area. The functional significance of this was examined by incremental cycle ergometry in 24 GH-deficient adults treated in a double-blind placebo-controlled trial with recombinant DNA human GH (rhGH) for 6 mo (0.07 U/kg body wt daily). Compared with placebo, the rhGH group increased mean maximal O2 uptake (VO2max) (+406 +/- 71 vs. +133 +/- 84 ml/min; P = 0.016) and maximal power output (+24.6 +/- 4.3 vs. +9.7 +/- 4.8 W; P = 0.047), without differences in maximal heart rate or ventilation. Forced expiratory volume in 1 s, vital capacity, and corrected CO gas transfer were within normal limits and did not change with treatment. Mean predicted VO2max, based on height and age, increased from 78.9 to 96.0% in the rhGH group (compared with 78.5 and 85.0% for placebo; P = 0.036). The anaerobic ventilatory threshold increased in the rhGH group (+159 +/- 39 vs. +1 +/- 51 ml/min; P = 0.02). The improvement in VO2max was noted when expressed per kilogram body weight but not lean body mass or thigh muscle area. We conclude that rhGH treatment in adults with GH deficiency improves and normalizes maximal exercise performance and improves submaximal exercise performance and that these changes are related to increases in lean body mass and muscle mass. Improved cardiac output may also contribute to the effect of rhGH on exercise performance.
Article
The involvement of the cholinergic system in GH secretion has recently acquired increasing importance. Data have been presented suggesting that in rats the effect of cholinergic modulation on GH secretion takes place through inhibition or stimulation of hypothalamic somatostatin (SRIF) release. To investigate further the significance of cholinergic-SRIF link and its role in the regulation of GH secretion, the action of cholinergic agonist and antagonist drugs in the GH short-loop feedback mechanism mediated by SRIF was investigated. Intracerebroventricular (i.c.v.) infusion of 0·2 or 2·0 μg GH/rat into the lateral brain ventricle of adult male rats induced a significant reduction in the GH-releasing hormone (GHRH; 2 μg/kg, i.v.)-induced peak GH rise, but only the 2·0 μg dose reduced also the GH-integrated area after administration of GHRH. This effect was absent after central administration of 20·0μg GH/rat, due probably to leakage of some GH from the cerebral ventricle into the systemic circulation. Pretreatment with cysteamine (300 mg/kg, s.c.), a known depletor of hypothalamic SRIF, or with anti-SRIF serum (0·5 ml/rat) completely counteracted the lessening of the GH response to GHRH induced by 2·0μg GH injected i.c.v. Similarly, pretreatment with the cholinergic agonist pilocarpine (3 mg/kg, i.v.) completely antagonized the inhibitory effect of central infusion of GH on the GHRH-induced GH response. Atropine (1·0 mg/kg, i.v.), a muscarinic cholinergic antagonist, strikingly inhibited the GHRH-induced GH rise, but when given in combination with i.c.v. infusion of GH there was no additive inhibitory effect. These data reinforce the idea that the GH autofeedback triggered by i.c.v. infusion of GH is mediated by enhanced SRIF release, and suggest that the hypothalamic cholinergic system plays a major role in this mechanism. J. Endocr . (1988) 117, 273–281
Article
It is known that in normal subjects repeated administration of the growth hormone-releasing factor (GRF) induces a state of partial refractoriness of the somatotropes to GRF. Studies were conducted to verify whether the cholinergic system plays a role in the mechanism(s) underlying the reduced GH responsiveness to the neuropeptide. In five healthy men, the GH response to three consecutive injections of GRF (50 micrograms iv), administered at 2 h intervals, was considerably blunted after the second and third GRF bolus. Administration of the inhibitor of cholinesterase, pyridostigmine bromide (120 mg orally) 30 min before the second GRF bolus, not only restored but greatly potentiated the GH responsiveness to the second GRF bolus. The GH response to the third GRF bolus was not apparently influenced by pre-treatment with pyridostigmine. These data reinforce the view that cholinergic neurotransmission plays an important role in the control of GH secretion in human.
Article
The effects of biosynthetic methionyl-human growth hormone (met-hGH) on body composition and endogenous secretion of growth hormone (GH) and insulin-like growth factor I (IGF-I) were studied in eight well-trained exercising adults between 22 and 33 yr of age. By the use of double-blind procedures, met-hGH (2.67 mg/0.5 ml diluent, 3 days/wk) and bacteriostatic water (placebo, 0.5 ml, 3 days/wk) were administered in a repeated-measures design that counterbalanced treatment order. Duration of each treatment was 6 wk. Subjects trained with progressive resistance exercise throughout and were maintained on a high-protein diet monitored by extensive compositional analyses of daily dietary intake records. Hydrodensitometry revealed that met-hGH significantly decreased percent body fat (%fat) and increased fat-free weight (FFW) and FFW/fat weight (FW), whereas the placebo treatment did not change any of these measures. Changes in FFW/FW correlated with the relative dose of met-hGH but did not correlate with either the peak GH response to L-dopa/arginine stimulation or IGF-I levels obtained after treatment with placebo. There were no differences between treatments in the dietary intakes of total kilocalories, protein, carbohydrates, and fat. Mean IGF-I levels were elevated after treatment with met-hGH compared with postplacebo levels. After treatment with met-hGH, five of seven subjects had a suppressed GH response to stimulation from either L-dopa/arginine or submaximal exercise. We conclude that supraphysiological doses of met-hGH will alter body composition in exercising adults in a relative dose-dependent manner and that such treatment may suppress endogenous release of GH in some individuals.
Article
Changes in plasma GH levels in response to an intravenous bolus injection of 200 micrograms GHRH-44 or 0.1 U/kg body weight regular insulin were examined in normal men who were pre-treated with 200 micrograms GHRH-44 or 0.1 U/kg body weight regular insulin 120 min in advance. The prior bolus injection of GHRH-44 inhibited the plasma GH response to the subsequent administration of GHRH-44 whereas the plasma GH response to the subsequent injection of insulin was not influenced by the prior administration of GHRH-44. The prior administration of insulin attenuated the plasma GH response to the subsequently given GHRH-44. These results suggest that desensitization of GHRH receptors in somatotrophs and/or somatostatin hypersecretion induced by increase in plasma GH levels following the prior GHRH-44 administration may be involved in the mechanism by which the prior GHRH-44 administration or insulin-induced hypoglycemia suppressed plasma GH responses to the following GHRH-44 administration. Sudden suppression of somatostatin secretion, which causes rebound of GH secretion, may occur in insulin-induced hypoglycemia.
Article
To improve the usefulness of testing pituitary function by the response of human growth hormone (HGH) to I.V. arginine loads, arginine infusions were given under a variety of conditions to healthy subjects aged 17 to 35. The minimum effective arginine load causing release of HGH was 1/6 gm per pound of body weight in men and 1/12 gm per pound of body weight in women. At each of three dosage schedules used, women responded with greater increases in plasma HGH than men. Treatment of men with diethylstilbestrol augmented their HGH response to arginine, whereas methyltestosterone pretreatment did not decrease the response in women. The HGH response to arginine was not abolished by acute hyperglycemia but was attenuated or delayed by a previous stimulus for HGH release. In the use of this test of pituitary function, it is necessary to use a proper dose of arginine, to avoid other stimuli of HGH release, and to pretreat men with estrogens.
Article
To evaluate the dynamics of GH-secretion after infusion of growth hormone releasing factor, human pancreatic growth hormone releasing factor (hpGRF ¹⁻⁴⁴ ) was infused over 2 and 5 h at a dosage of 100 μg hpGRF1-44/h into 11 healthy subjects. The infusion was started and terminated with a 50 μg hpGRF ¹⁻⁴⁴ bolus injection. In 5 subjects 200 μg TRH was given 4 h after starting the infusion. In addition, 4 healthy subjects received 50 μg hpGRF ¹⁻⁴⁴ bolus injection every 2 h. GRF, somatostatin, GH, Prl, and TSH were measured by radioimmunoassay. The initial 50 μg GRF bolus increased GH-levels in all 11 subjects with a maximum at 30 min (24.1 ± 5.1 ng/ml ± se ). However, though hpGRF ¹⁻⁴⁴ was continuously infused and GFR-levels remained elevated, GH decreased to a minimum 270 min after start of infusion (2.6 ± 0.6 ng/ml). The GH-response to the second bolus at the end of the infusion was lower compared to the first response (14.6 ± 3.4 ng/ml after 2 h and 7.6 ± 2.5 ng/ml after 5 h). TRH did not lead to a GH-increase during hpGRF ¹⁻⁴⁴ infusion though Prl and TSH rose normally. The intermittent bolus injection of 50 μg hpGRF ¹⁻⁴⁴ led to continuously decreasing GH-responses to the same GRF-dosage (I. bolus: 16.5 ± 1.6 ng/ml; II. bolus: 4.2 ± 0.8 ng/ml; III. bolus: 3.4 ± 0.5 ng/ml). No change in somatostatin levels was observed. These findings show that GRF infusion or bolus injection in short intervals does not sustain elevated GH-levels. Pituitary GH is either not readily available for continuous GRF-stimulation or GH-secretion may be antagonized by increasing portal somatostatin levels which are not reflected in the peripheral circulation.
Article
The role of acetylcholine in human GH secretion was studied with atropine, which selectively blocks cholinergic muscarinic receptors and crosses the blood-brain barrier. Paired tests were performed in 22 normal subjects divided into 4 groups. The stimuli employed were arginine (30 g/30 min, iv), clonidine (300 micrograms, orally), physical exercise for 20 min, and saline. In the second test, atropine (1 mg, im) was administered before GH stimulation. Arginine elicited a GH secretory peak of 16.6 +/- 5 ng/ml (mean +/- SEM), which was completely blocked when atropine was administered with arginine (0.9 +/- 0.1 ng/ml). Atropine did not, however, modify the PRL secretory response; peak levels after arginine and atropine plus arginine were 16.3 +/- 3.1 and 16.8 +/- 2.5 ng/ml, respectively. Clonidine elicited a GH secretory peak (11.8 +/- 2.7 ng/ml) which also was blocked by pretreatment with atropine (1.2 +/- 0.2 ng/ml). Neither clonidine nor clonidine plus atropine altered PRL secretion. GH levels also were sharply increased after physical exercise, with a peak level of 19.4 +/- 4.9 ng/ml. Atropine completely blocked exercise-induced GH secretion (2 +/- 0.9 ng/ml). Atropine alone did not modify GH or PRL values compared with saline administration. The potency of the atropine-induced suppression of GH secretion by three different stimuli, each with presumably different mechanisms of action, suggests that acetylcholine plays an important role in the regulation of GH secretion.
Article
A study was carried out in 15 male volunteers to evaluate qualitatively the secretion of growth factors following stimulation by oral amino acids. The results showed that oral administration of a combination of two amino acids (1200 mg 1-lysine plus 1200 mg 1-arginine) provoked a release of pituitary somatotropin and insulin. This phenomenon was reproducible and the growth hormone secreted in response to this stimulation had biological activity (as demonstrated by a radioreceptor assay and somatomedin induction). The effect appeared to be specific to the combination of the two amino acids; neither of the amino acids demonstrated appreciable stimulating activity when administered alone, even at the same doses.
Article
Normal aging is characterized by detrimental changes in body composition, muscle strength, and somatotropic function. Reduction in muscle strength contributes to frailty and risk for fracture in the elderly. Although older adults increase muscle strength as a result of resistance exercise training, the strength gains quickly level off, with only modest increases thereafter despite continued training. To investigate whether age-related deficits in the somatotropic axis limit the degree to which muscle strength can improve with resistance training in older individuals, we conducted a double blind, placebo-controlled exercise trial. Eighteen healthy elderly men (65-82 yr) initially underwent progressive weight training for 14 weeks to invoke a trained state. Subjects were then randomized to receive either 0.02 mg/kg BW.day recombinant human GH (rhGH) or placebo, given sc, while undertaking a further 10 weeks of strength training. Sequential measurements were made of muscle strength (one repetition maximum), body composition (dual energy x-ray absorptiometry), and circulating levels of insulin-like growth factor-I (IGF-I) and IGF-binding protein-3. For each exercise, strength increased for both groups (P = 0.0001) through 14 weeks of training, with little improvement thereafter. Increases in muscle strength ranged from 24-62% depending on the muscle group. Baseline plasma IGF-I concentrations were similar in both groups (mean +/- SEM, 106 +/- 9 micrograms/L), approximately half that observed in healthy young adults. In the rhGH group, IGF-I levels increased to 255 +/- 32 micrograms/L at week 15 and 218 +/- 21 micrograms/L at week 24 (P < 0.001). In the placebo group, IGF-I increased slightly to 119 +/- 6 micrograms/L at 24 weeks. IGF-binding protein-3 also increased in the rhGH group (P < 0.05). rhGH had no effect on muscle strength at any time, and no systematic difference in muscle strength was observed between groups throughout the study. Body weight did not change in either group, but lean body mass increased, and fat mass decreased (P < 0.05) in the rhGH group. Supplementation with rhGH does not augment the response to strength training in elderly men. These results suggest that deficits in GH secretion do not underlie the time-dependent leveling off of muscle strength seen with training in the elderly and provide no support for the popular view of GH as an ergogenic aid.
Article
To investigate whether measurements of cortisol responses to exercise are confounded by neglect of the hormone's circadian rhythm, we measured the serum and salivary cortisol responses of eight women to 40 min of 70% maximal oxygen consumption treadmill exercise beginning at 0800 and 2000. Responses were calculated relative to the usually employed preexercise concentrations and also to concentrations at the same times of another day while subjects were at rest. Compared with areas under response curves (AUCs) calculated relative to their circadian baselines, AUCs for serum and salivary cortisol calculated by reference to preexercise concentrations were underestimated (serum, P < 0.001; salivary, P < 0.01) by 93 and 84% in the morning and by 37 and 35% in the evening, respectively. Calculated by the usual preexercise baseline method, rises in serum and salivary cortisol were similarly underestimated. More accurately calculated relative to their circadian baselines, serum and salivary cortisol AUCs were similar (P = 0.63 and P = 0.37, respectively) in the morning and evening, as were their rises (P = 0.23 and P = 0.70, respectively). In future investigations of the existence and magnitude of cortisol responses, those responses must be calculated relative to the hormone's circadian baseline.
Article
An oral glutamine load was administered to nine healthy subjects to determine the effect on plasma glutamine, bicarbonate, and circulating growth hormone concentrations. Two grams glutamine were dissolved in a cola drink and ingested over a 20-min period 45 min after a light breakfast. Forearm venous blood samples were obtained at zero time and at 30-min intervals for 90 min and compared with time controls obtained 1 wk earlier. Eight of nine subjects responded to the oral glutamine load with an increase in plasma glutamine at 30 and 60 min before returning to the control value at 90 min. Ninety minutes after the glutamine administration load both plasma bicarbonate concentration and circulating plasma growth hormone concentration were elevated. These findings demonstrate that a surprisingly small oral glutamine load is capable of elevating alkaline reserves as well as plasma growth hormone.
Article
I. Introduction GRADUALLY it is being realized that GH may have important physiological functions in adult man. Until recently, GH was only used to treat short statured children with established GH deficiency (GHD), and it remains common practice to discontinue GH replacement therapy when final height is reached. From a physiological point of view, it is questionable whether this approach is appropriate since it is well known that GH secretion persists throughout life (1–5). Daily GH production reaches its maximum during puberty (3–5). Thereafter, the GH secretion rate gradually decreases with age (3). Recently, several studies have shown that GHD in adults is associated with abnormalities in body composition (6–14), metabolic derangements (15–17), and suboptimal physical performance (18–20). Since recombinant technology has solved the limitations in GH supply, policies concerning GH replacement therapy in man may now be reconsidered. The studies performed in GHD adults uniformly suggest that these patien...
Article
The effects of 6 months of replacement therapy with recombinant human GH (hGH) on physical work capacity and cardiac structure and function were investigated in 20 patients with hGH deficiency of adult onset in a double blind, placebo-controlled trial. The GH dose of 12.5 micrograms/kg BW was self-administered daily sc. Oxygen consumption (VO2), CO2 production, and ventilatory volumes were measured during exercise on a bicycle spiroergometer. M-Mode echocardiography was performed using standard techniques. The VO2 max data, expressed per kg BW (mL/min.kg BW) showed a significant increase from 23.2