Plasma Epinephrine Concentrations Research Articles

Influence of plaque volume on hemodynamic response and stress hormone release in patients undergoing carotid artery stenting.

Carotid artery stenting (CAS) may cause bradycardia and hypotension due to barostimulation. The impact of periprocedural hypotension on CAS outcome remains controversial. The role of carotid plaque volume and catecholamine hormone release during CAS on hemodynamic changes has not been investigated so far. The aim of this prospective study was to evaluate if carotid artery plaque characteristics are predictive for stress hormone release or for postprocedural hemodynamic instability. In 26 patients undergoing CAS, carotid plaque volume and morphology were assessed by two- and three-dimensional (3D)-Duplex sonography prior to the procedure. Arterial plasma adrenaline, noradrenaline and renin concentrations were measured at the time of sheath insertion and 5 minutes after stent placement. ECG, heart rate, and invasive blood pressure were monitored throughout the procedure. CAS caused no significant changes in hormone release, but increasing plaque volume was related to the degree of bradycardia following stent deployment (r=0.57; P=0.01). Plaque size was not associated with postprocedural hypotension. Plaque echogenicity (echolucent, heterogeneous or echogenic) did not correlate with changes in systolic blood pressure, heart rate or catecholamine hormone release. CAS caused bradycardia in relation to plaque size, but did not cause catecholamine release which may indicate that the endovascular procedure is not associated with a relevant stress reaction.

Adrenergic and cardiac dysfunction in primary hyperparathyroidism

Primary hyperparathyroidism (PHPT) is associated with cardiovascular morbidity and premature death, but the underlying mechanisms are incompletely understood. The aim of this study was to investigate whether adrenergic dysfunction may be a contributing factor. Forty-nine patients with mild PHPT (serum calcium 2·7 ± 0·1 mM) and 48 control subjects, matched for age and sex, were examined; patients within 1 month before parathyroidectomy (PTX) and 6 months postoperatively; control subjects at inclusion. Heart rate variability (HRV) was analysed in 24-h electrocardiograms, and plasma concentrations of epinephrine and norepinephrine were measured at rest and immediately after standardized physical tests. At baseline, the patients showed, compared to the controls, reduced stress-related increase of circulating epinephrine (P < 0·05) and norepinephrine (P < 0·05). No significant change was observed 6 months after PTX. At baseline, there were no significant differences between patients and controls in HRV or heart rate, but 6 months after curative PTX, the patients showed significantly reduced HRV in both frequency and time domain, and their maximum and average heart rate had decreased (P = 0·011 and P = 0·018, respectively). The patients with the highest preoperative levels of circulating parathyroid hormone showed the greatest changes in heart rate and HRV postoperatively. This study demonstrates a previously unknown impairment of catecholamine response to physical stress in PHPT along with changes of HRV, also indicating adrenergic dysfunction. These factors should be considered in the ongoing controversy regarding the management of patients with mild 'asymptomatic' PHPT.

Chapter 16. Glucose and nutrition

Chapter 16. Glucose and nutrition

Decreased vascular endothelial growth factor response to acute hypoglycemia in type 2 diabetic patients with hypoglycemic coma

IntroductionPlasma vascular endothelial growth factor (VEGF) was shown to increase during acute hypoglycemia and could mediate rapid adaptation of the brain. In this study we examined the neuroendocrine response in patients with type 2 diabetes mellitus (T2DM) in hypoglycemic coma or with acute neuroglycopenic symptoms. MethodsWe prospectively studied 135 consecutive T2DM patients admitted for severe hypoglycemia during a 2-year period. We collected clinical variables and measured plasma concentrations of VEGF, epinephrine, norepinephrine, cortisol and growth hormone at admission and 30min afterwards. ResultsThirty two patients developed hypoglycemic coma and 103 did not lose consciousness. Median plasma VEGF level of coma patients was 3.1-fold lower at baseline than that of non-coma patients, and even 5.3-fold lower 30min afterwards. Plasma epinephrine concentration was significantly lower just at baseline in coma patients. On the contrary, there were no differences in concentrations of the other hormones. Multivariate logistic regression analysis showed that VEGF concentration (OR 0.68; CI 0.51–0.95) was a protective factor against the development of coma. ConclusionsVEGF and epinephrine responses to acute hypoglycemia are reduced in T2DM patients who develop hypoglycemic coma. An increased plasma VEGF concentration appeared to be a protective factor against the development of hypoglycemic coma.

Enhanced catecholamine release in mice expressing PKB/SGK-resistant GSK3

Glycogen synthase kinase 3 (GSK3) plays a decisive role in the regulation of multiple functions. GSK3 is phosphorylated and its activity inhibited by protein kinase B (PKB/Akt) and serum and glucocorticoid inducible kinase (SGK) isoforms, which are in turn activated by growth factors through phosphoinositide (PI) 3 kinase signaling. PI3/PKB/Akt/SGK-dependent inhibition of GSK3 is disrupted in gene-targeted knockin mice with mutated and thus PKB/SGK-resistant GSK3α,ß (gsk3 ( KI )) where the serine of the PKB/SGK phosphorylation site has been replaced by alanine. Recent experiments revealed that blood pressure is significantly higher in those mice than in wild type mice (gsk3 ( WT )). The present study was performed to elucidate the underlying cause. Blood pressure was determined with the tail cuff method, heart rate by ECG measurements, catecholamine concentrations by ELISA, and vanillylmandelic acid by high pressure liquid chromatography. As a result, blood pressure and heart rate were significantly higher in gsk3 ( KI ) than in gsk3 ( WT ) mice. The α-adrenergic blocker prazosin (1μg/g body weight, b.w.) and the ganglion blocker hexamethonium (40μg/g b.w.) decreased blood pressure to a larger extent in gsk3 ( KI ) than in gsk3 ( WT ) mice and virtually abrogated the difference between genotypes. Similarly, the β-adrenergic blocker atenolol (5μg/g b.w.) decreased the heart rate to a larger extent in gsk3 ( KI ) than in gsk3 ( WT ) mice and again dissipated the difference of heart rate between genotypes. Plasma epinephrine and norepinephrine concentrations, as well as urinary excretion of vanillylmandelic acid, were significantly higher in gsk3 ( KI ) than in gsk3 ( WT ) mice. The observations reveal a completely novel function of PKB/Akt/SGK-dependent GSK3 signaling, i.e., regulation of catecholamine release.

Case Scenario: Metastatic Pediatric Paraganglioma Presenting during the Course of an Elective Surgery

P HEOCHROMOCYTOMA and paraganglioma are neuroendocrine tumors rarely diagnosed in pediatric patients. The incidence of malignant pheochromocytoma and paraganglioma in childhood is approximately 0.02 cases per million every year. Coincidental intraoperative diagnosis of pheochromocytoma involves very high mortality rates, reaching 50%. We present a case of coincidental diagnosis of pediatric metastatic malignant paraganglioma during an elective surgical procedure. The evaluation and management of pheochromocytoma and paraganglioma are discussed.

Effects of Animal Positioning on Catecholamine and Vasopressin Levels in Pigs Undergoing Laparoscopy

Background: The aim of this study was to determine the influence of different therapeutic interventions and positions on catecholamine and vasopressin levels in the pneumoperitoneum (PN) in a porcine model. Methods: In 43 pigs, a 14-mm-Hg PN was established and plasma concentrations of epinephrine, norepinephrine and vasopressin were measured in head-up, supine and head-down positions. Additionally, the effects of the following changes were studied: (1) increase in intrathoracic blood volume (ITBV) by means of hydroxyethyl starch infusion; (2) vasodilatation induced by sodium nitroprusside, or (3) selective sympathicolysis induced by esmolol. Again, catecholamines (ELISA) and vasopressin (RIA) were determined. Results: After PN, epinephrine levels did not significantly increase in the head-up position (p = 0.075) and remained also unchanged in the supine or head-down position. Plasma norepinephrine statistically significantly decreased in the head-up position (p = 0.046). Vasopressin concentrations remained unaltered. After increased ITBV, neither catecholamine nor vasopressin concentrations changed in any body position. Application of sodium nitroprusside or esmolol caused no changes. Conclusion: Changes in endogenous catecholamine levels safely prevent cardiocirculatory instability in small pigs. Volume substitution might reduce endocrine responses to PN in the head-up position.

Cardiovascular responses to arm static exercise in men with thoracic spinal cord lesions

Isometric muscle contraction (static exercise) induces circulatory response. Static exercise in individuals with thoracic spinal cord injury (TSCI) induces cardiovascular response and blood redistribution to the non-exercising muscles. The aim of our study was to determine the circulatory response during arm static exercise in individuals with TSCI and able-bodied (AB) controls. Mean blood pressure (MBP), heart rate (HR), cardiac output (CO), leg skin blood flow (SBF), and leg muscle blood flow (MBF) were recorded noninvasively, total peripheral resistance (TPR) was estimated by dividing MBP by CO, and hormonal changes were measured before, during and after static 35% maximal voluntary contraction (MVC) of the arm flexor muscles in seven male individuals with TSCI (T7-T11) and seven age-comparable AB control (32.2 ± 7.6 and 31.0 ± 4.7 years, respectively). The 35% MVC was similar in TSCI and AB individuals (107.3 ± 28.2 and 101.0 ± 22.5 N, respectively). HR, CO, MBP, TPR, SBF and MBF increased in both groups during arm static exercise. Plasma epinephrine concentration increased during arm static exercise in AB controls only (P < 0.05). Circulation to leg muscles was similar in TSCI and AB individuals and the lack of sympathetic vasoconstriction in the paralyzed leg area did not alter the cardiovascular responses during 35% MVC of arm static exercise. We conclude that sympathetic vasoconstriction in the resting leg area did not contribute to the pressor reflex during 35% MVC of arm static exercise.

Does 20-min arm crank ergometer exercise increase plasma interleukin-6 in individuals with cervical spinal cord injury?

Interleukin-6 (IL-6) is produced by contracting skeletal muscles and then released into the circulation and considered to mediate the health benefits of exercise against chronic diseases. Individuals with spinal cord injury (SCI) are reported to be at higher risk of developing metabolic diseases. We investigated the IL-6 responses to 20-min arm crank ergometer exercise at 60% of maximum oxygen consumption in eight trained individuals with cervical SCI (CSCI) between C6 and C7, and eight able-bodied trained healthy subjects. The plasma concentrations of IL-6, adrenaline, prostaglandin E(2) and cortisol were measured before, immediately after the exercise, 1 and 2 h after exercise. At rest, the plasma adrenaline concentration was significantly lower in individuals with CSCI than in able-bodied subjects (P < 0.01). On the other hand, the concentration of IL-6 was significantly higher at rest in individuals with CSCI (2.18 ± 0.44 pg/ml, mean ± SEM) than the control (1.02 ± 0.22 pg/ml, P < 0.05). In able-bodied subjects, the plasma adrenaline concentration increased significantly immediately after the exercise (P < 0.01) and returned to the baseline level at 1 h after exercise, and the plasma IL-6 level increased significantly at 1 h after exercise (1.91 ± 0.28 pg/ml, P < 0.05) and returned to the baseline level at 2 h after exercise. In contrast, adrenaline and IL-6 levels were steady throughout the study in individuals with CSCI. The lack of exercise-related IL-6 response in individuals with CSCI could be due to muscle atrophy and sympathetic nervous system dysfunction.

Effect of indomethacin on the blood pressure and plasma catecholamine responses to acute endotoxaemia.

Injection of E. coli endotoxin (7 mg kg-1 i.v.) to pentobarbitone anaesthetized cats resulted in prolonged decrease of systemic blood pressure and increases in plasma concentrations of adrenaline, noradrenaline and 6-ketoprostaglandin (PG) F 1 alpha. Indomethacin pretreatment (10 mg kg-1 i.v.) attenuated the decrease in blood pressure following endotoxin injection. Plasma adrenaline, noradrenaline and 6-keto-PG F1 alpha were significantly lower in the indomethacin-treated cats. These data indicate that the superior haemodynamic status of the indomethacin pretreated animals exposed to endotoxic shock is not the result of potentiation of the peripheral sympathetic response.

Plasma adrenaline concentrations in rats: influence of anaesthetics and heart rate response to pronethalol

Journal Article Plasma adrenaline concentrations in rats: influence of anaesthetics and heart rate response to pronethalol Get access H G Dean, H G Dean Department of Pharmacology, School of Medicine, Leeds LS2 9NL, U.K. Search for other works by this author on: Oxford Academic Google Scholar P A Rylett P A Rylett Department of Pharmacology, School of Medicine, Leeds LS2 9NL, U.K. Search for other works by this author on: Oxford Academic Google Scholar Journal of Pharmacy and Pharmacology, Volume 27, Issue 1, January 1975, Pages 70–71, https://doi.org/10.1111/j.2042-7158.1975.tb09388.x Published: 12 April 2011 Article history Received: 26 July 1974 Published: 12 April 2011

Marked increases in plasma catecholamine concentrations precede hypotension and bradycardia caused by 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) in conscious rats

Plasma noradrenaline and adrenaline responses to 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), a selective putative 5-HT1A receptor agonist, have been studied in conscious, freely moving rats. Intravenously administered 8-OH-DPAT caused dose-related and sustained increases in plasma noradrenaline (2-fold) and adrenaline (11-fold) concentrations. Neither metergoline pretreatment (0.5 mg kg-1 i.v.) nor splanchnicectomy had any effect on the noradrenaline and adrenaline elevation caused by 8-OH-DPAT (250 micrograms kg-1 i.v.). The catecholamine responses peaked early but were still present during nadirs in blood pressure and heart rate. The discrepancy between plasma catecholamine and cardiovascular changes raises further questions about the mechanism of action of 8-OH-DPAT and supports other evidence suggesting a role for vagus stimulation in the cardiovascular effects caused by this drug.

The effects of regular endurance exercise on IL‐6 and the sympathetic nervous system

Several studies have reported that regular endurance exercise attenuated the circulating IL-6 concentration, but the underlying mechanism remained uncertain. We tested the hypothesis that the exercise-induced alteration of IL-6 would be associated with the sympathetic nervous system. Subjects were 17 young men trained in endurance exercise and 15 age-matched sedentary men. Blood sample was obtained from the brachial vein, and serum IL-6 concentration was measured by ELISA. Plasma adrenaline and noradrenaline concentration were measured as an index of sympathetic nerve activity. IL-6 was lower in the exercise-trained, than in the sedentary group (P<0.05). IL-6 was correlated with adrenaline in the trained group (r=0.63, P<0.05), but such correlation was not observed in the sedentary group. These results suggest that regular endurance exercise attenuates IL-6, which may be partly associated with sympathetic adrenergic mechanism.

Angiotensin-converting enzyme inhibition and blood pressure response during total intravenous anaesthesia for minor surgery

This study investigates whether long-term treatment with an angiotensin-converting enzyme inhibitor (ACEI) impairs the haemodynamic regulation during total intravenous anaesthesia (TIVA) for minor surgery. In a prospective, two-armed observational study, 36 patients undergoing TIVA for minor surgery were studied. Seventeen were taking ACEIs regularly but no other antihypertensive medication (ACEI group); 19 patients without any cardiovascular medication served as controls (non-ACEI group). Haemodynamic variables were measured every minute during induction and every 5 min during surgery. The plasma levels of renin, angiotensin II, vasopressin and catecholamines were measured before and 18 min after the induction of anaesthesia. The mean arterial pressure decreased to the same extent in both the groups during the induction of TIVA. There were also no differences between the groups regarding the heart rate, systolic and diastolic arterial pressure, as well as the use of vasoconstrictors, and fluids during induction and throughout surgery. In the ACEI group, the plasma renin concentration was higher at baseline and after the induction of anaesthesia presumably due to the interruption of the negative renin-angiotensin feedback loop (P<0.05). Angiotensin II increased only in the non-ACEI group (6.2 ± 2.2 before vs. 9.6 ± 3.5 pg/ml after induction; P<0.05). In both groups, the plasma norepinephrine concentration decreased after the induction of TIVA (P<0.05). Plasma vasopressin and plasma epinephrine concentrations did not change in either group. Long-term ACEI treatment does not further aggravate the blood pressure decrease under TIVA during minor surgery, provided the induction procedure is slow, the patient is kept well hydrated and vasoconstrictors are promptly applied.

Catecholamine Response to Exercise in Obese, Overweight, and Lean Adolescent Boys

The aim of this study was to examine the effect of body fat percentage on the plasma catecholamine response to a cycling sprint test (CST) in sedentary adolescent boys. In this study, 31 adolescent boys (9 obese (% body fat = 31.0% ± 3.0%), 11 overweight (% body fat = 24.0% ± 1.6%), and 11 lean (% body fat = 16.0% ± 1.9%)), matched for peak oxygen consumption, completed a CST consisting of six 6-s maximal sprints with 2 min of passive rest between each repetition. Performance of each subject was determined as the mean power output (PO(mean)) developed during the CST. Plasma lactate, epinephrine, and norepinephrine concentrations were determined successively at rest, after a 10-min warm-up, immediately after the CST, and after 20 min of passive recovery. Although groups were not different in age, height, or peak oxygen consumption (mL·kg(-1) fat-free mass·min(-1)), maximal epinephrine concentration was significantly (P < 0.05) higher in lean vs obese and was negatively correlated to body fat percentage (r = -0.60, P < 0.05). Maximal norepinephrine values were higher in lean versus overweight and obese, and a negative relationship was found between maximal norepinephrine concentration and body fat percentage (r = -0.60, P < 0.05). Maximal lactate concentration was higher in lean versus overweight and obese (14.7 ± 3.3, 10.4 ± 2.7, and 10.2 ± 2.5 mM in lean, overweight, and obese, respectively). A significant relationship was also obtained between maximal norepinephrine and maximal epinephrine values with both maximal lactate concentration (r = 0.60 and r = 0.60, P < 0.05, respectively) and PO(mean) (r = 0.65 and r = 0.6, P < 0.05). Our results show that the catecholamine response to a CST was affected by body fat percentage, with reduced epinephrine and norepinephrine values in overweight and obese adolescents.

Pulmonary Vasoconstrictive and Bronchoconstrictive Responses to Anaphylaxis Are Weakened via β2-adrenoceptor Activation by Endogenous Epinephrine in Anesthetized Rats

Patients treated with propranolol, a nonselective β-adrenoceptor antagonist, have increased incidence and severity of anaphylaxis. We determined whether β1- or β2-adrenoceptor antagonist modulated pulmonary vasoconstriction and bronchoconstriction in rat anaphylactic hypotension. Anesthetized ovalbumin-sensitized male Sprague-Dawley rats were randomly allocated to the following pretreatment groups (n = 7/group): (1) sensitized control (nonpretreatment), (2) propranolol, (3) the selective β2-adrenoceptor antagonist ICI 118,551, (4) the selective β1-adrenoceptor antagonist atenolol, and (5) adrenalectomy. Shock was induced by an intravenous injection of the antigen. Mean arterial pressure, pulmonary arterial pressure, left atrial pressure, central venous pressure, portal venous pressure, airway pressure, and aortic blood flow were continuously measured. In either sensitized control or atenolol-pretreated rats, mean arterial pressure and aortic blood flow decreased substantially, whereas pulmonary arterial pressure and airway pressure did not increase soon after antigen injection. In contrast, in rats pretreated with either propranolol, ICI 118,551, or adrenalectomy, airway pressure significantly increased by 14 cm H2O, and pulmonary arterial pressure by 7.5 mmHg after antigen injection. At 2.5 min after antigen injection, the plasma concentration of epinephrine increased 14-fold in the sensitized rats except for the adrenalectomy group. Portal venous pressure after antigen injection increased by 16 mmHg similarly in all sensitized rats. All of the sensitized control group and two of the atenolol group were alive for 60 min after antigen injection, whereas all rats of the propranolol, ICI 118,551, and adrenalectomy groups died within 50 min after antigen injection. The pulmonary vasoconstrictive and bronchoconstrictive responses to systemic anaphylaxis were weakened via β2-adrenoceptor activation by epinephrine endogenously released from the adrenal gland in the anesthetized Sprague-Dawley rats.

Changes in noxious stimulation intensity at different periods of pneumoperitoneum in gynecological laparoscopic surgery

：Objective To evaluatethe changes in noxious stimulation intensity at different periods of pneumoperitoneum ingynecological laparoscopic surgery. Methods Forty-five ASA Ⅰ orⅡ patients, aged 25-36 yr, withbody mass index 18-23 kg/m2 , undergoing elective gynecological laparoscopic surgery, wererandomly divided into 3 groups ( n = 15 each) . In group Ⅰ , anesthesia was maintained with TCI of remifentanil (target plasma concentration4-6 ng/ml) and propofol (target plasma concentration 2 μg/ml) , and theconcentrations were ad-justed according to the changes in BP and HR to maintainhemodynamics stable. Ⅱ and Ⅲ groups received inhala-tion of isoflurane (end-tidal concentration1%-2%) and TCI of remifentanil (target plasma concentration 2-4ng/ml) . TCI ofremifentanil was then stopped at 5 min before pneumoperitoneum (group Ⅱ ) or at 5 min after theend of rapid inflation (group Ⅲ ) , and isoflurane was inhaled (end-tidal concentration 1%-2% ) tomaintain anes-thesia until the end of operation in Ⅱ and Ⅲ group. Before anesthesia (T0), 5 min before pneumoperitoneum (T1), 5 and 15 min of pneumoperitoneum (T2,3), HR and MAPwere monitored and venous blood samples were taken for determination of plasma cortisol(Cor) , norepinephrine ( NE) and epinephrine ( E) concentrations. Results HR, MAP and NEand E concentrations at T2,3 , and Cor concentrations at T3 were significantly higher thanthose at T0 ingroup Ⅱ , and in group Ⅱ than in group Ⅰ(P<0.05). HR,MAP and NE and E concentrations at T2,3 ,and Cur concentrations at T3 were significantlylower in group Ⅲ than in group Ⅱ ( P < 0.05). Conclusion Theintensity of noxious stimulation is strongest during rapid inflation among the differentperiods of pneumoperitoneum in gynecological laparoscopic surgery and the depth ofanesthesia should be regulated. Key words: Pneumoperitoneum,artificial; Laparoscopy; Stress; Gynecologic surgical procedures

Hormonal Responses to Resistance Exercise after Ingestion of Carnosine and Anserine

Intramuscular carnosine buffers protons (H+) in skeletal muscle. We examined the effects of supplementation with chicken breast meat extract (CBEX) containing carnosine and anserine on hormonal responses to resistance exercise. Twenty-two men were assigned to a CBEX drink group (CBEX containing total 2 g of carnosine and anserine) (n = 14) or a placebo drink group (n = 8). The subjects ingested the prescribed drink (100 mL) twice daily for 30 days without physical training. Before and after the supplementation period, the subjects completed 5 sets of bilateral knee extension exercises (with a 90-s rest between sets). The magnitude of the increase in exercise-induced free testosterone did not change significantly after supplementation in either group. The blood lactate response to exercise was attenuated after supplementation in both groups (p < 0.05). In the CBEX group, the plasma epinephrine and norepinephrine concentrations after exercise were significantly lower after supplementation (p < 0.05). The serum growth hormone response to exercise was also reduced in the CBEX group after supplementation (delta value: 5.4 ± 1.9 ng/mL [pre] vs. 1.6 ± 0.5 ng/mL [post], p = 0.05). No significant differences in exercise-induced strength reduction (fatigue index) were observed in the 2 groups after supplementation. These results suggest that short-term supplementation with CBEX attenuates the exercise-induced epinephrine, norepinephrine, and growth hormone responses.

A Large Pheochromocytoma With Invasion of Multiple Local Organs

A Large Pheochromocytoma With Invasion of Multiple Local Organs

Significant lowering of plasma ghrelin but not des-acyl ghrelin in response to acute exercise in men

Ghrelin, an acylated peptide produced predominantly in the stomach, stimulates feeding and growth hormone (GH) secretion via interaction with the GH secretagogue receptor. Ghrelin molecules are present in two major endogenous forms, an acylated form (ghrelin) and a des-acylated form (des-acyl ghrelin). Recent studies indicated that aerobic exercise did not change plasma total ghrelin levels, however, dynamics of circulating ghrelin and des-acyl ghrelin during aerobic exercise remains unclear. The purpose of this study is to examine the effects of moderate intensity exercise on plasma ghrelin and des-acyl ghrelin concentrations, and to investigate the relationship between ghrelin molecules and other hormonal and metabolic parameters during exercise. Nine healthy males (25.2 ± 0.5 years) exercised for 60 min at 50% of their maximal oxygen consumptions. We measured the plasma concentrations of ghrelin, des-acyl ghrelin, GH, norepinephrine (NE), epinephrine (E), dopamine (DA), insulin, and glucose. Plasma ghrelin level significantly decreased during exercise, whereas plasma des-acyl ghrelin and total ghrelin levels did not change. Plasma NE, E, DA and GH levels were significantly increased during exercise. Plasma insulin level significantly decreased during exercise, and plasma glucose levels remained steady during exercise. NE, E, DA, and GH were correlated negatively with plasma ghrelin levels. These findings suggest that acute moderate exercise may suppress ghrelin release from the stomach, decrease ghrelin O-acyltransferase activity, and/or activate ghrelin utilization in peripheral tissues and that exercise-induced ghrelin suppression may be mediated by activated adrenergic system.