Effect of physiological exercise on osteocalcin levels in subjects with adrenal incidentaloma.

AIM: In the present study, we have evaluated whether physical exercise affect low osteocalcin concentrations observed in patients with subclinical hypercortisolism. SUBJECTS AND METHODS: Sixteen patients (10 men and 6 women, age 38-55 yr) with adrenal incidentaloma were studied. Fifteen healthy volunteers matched for age (range 35-47 yr) were used as controls. Subjects were submitted to a 8-week exercise-training program with cycle-ergometer for 1 h/day 3-4 days/week at 60% of their individual VO2 max. Before and after this period, resting venous serum osteocalcin and GH concentrations were measured in the same batch. The blood sampling after 8 weeks of the training program were performed after resting for one day. All patients and controls underwent also the following endocrine evaluation: serum cortisol, plasma ACTH. RESULTS: Our results demonstrate a significant increase of osteocalcin after physical exercise and a positive correlation between osteocalcin and GH. This later might suggest a role of GH in the increased osteocalcin secretion. CONCLUSIONS: The data of the present study suggest a positive effect of physical exercise on bone metabolism in patients with adrenal incidentaloma.

Somatostatin reduces neuropeptide Y rise induced by physical exercise.

The effect of an i. v. infusion of somatostatin (SRIH) 4.1 µg/min×90 min on the basal secretion of NPY and on the NPY response to physical exercise was studied in normal men. Basal NPY secretion was not modified by SRIH infusion, whereas the NPY response to physical exercise was significantly lower in the presence of SRIH. These data suggest the involvement of a somatostatinergic mechanism in the regulation of NPY response to physical exercise.

Effect of serotonergic system on AVP secretion induced by physical exercise.

The present study was undertaken in order to establish the possible involvement of serotonergic receptors in the control of physical exercise-stimulated vasopressin secretion. Twenty-one healthy men (divided in three groups of seven) underwent bicycle-ergometer tests until exhaustion: exercise control test (n=21), exercise plus ondansetron, selective 5-HT3 antagonist (n=7), exercise plus buspirone, selective 5-HT1A receptor agonist (n=7), exercise plus sumatriptan, selective 5-HT1D receptor agonist (n=7). AVP levels, physiological and biochemical variables were measured and compared during tests. Results showed that exercise-induced AVP rise did not change after the administration of buspirone and sumatriptan. In contrast, the administration of ondansetron significantly reduced physical exercise-induced AVP rise. Mean peak levels during physical exercise were 4.9 times higher than basal values in the control test and 2.6 times higher than basal values in the ondansetron plus exercise test. These data demonstrate that 5-HT3 serotonergic receptors at least partially mediate the AVP response to physical exercise. On the other hand, 5-HT1A and 5-HT1D serotonergic receptors do not appear to be involved in the control of AVP secretion during exercise.

Naloxone decreases the inhibitory effect of ethanol on the release of arginine-vasopressin induced by physical exercise in man.

To establish whether ethanol and/or endogenous opioids play a role in the control of arginine-vasopressin (AVP) response to physical exercise, six healthy men underwent six bicycle-ergometer tests until exhaustion [exercise control test; exercise plus ethanol (50 of 110 ml proof whiskey orally), exercise plus naloxone (2 mg injected plus 5 mg infused or 4 mg injected plus 10 mg infused intravenously] or exercise plus ethanol plus naloxone). Plasma AVP levels, physiological and biochemical variables were measured during tests. Physiological and biochemical variables were similar in all tests. During the control test, exercise significantly increased plasma AVP levels, with a peak value five times higher than baseline. The AVP response to exercise was similar in the presence of naloxone, whereas it was abolished by ethanol. When ethanol tests were repeated in the presence of naloxone, at both lower and higher dose, ethanol inhibition on AVP secretion was only partial, with mean peak responses 2.5 times higher than basal values. Results indicate an ethanol involvement in regulation of the AVP response to physical exercise. Furthermore, naloxone-sensitive endogenous opioids appear to play a role in the mechanism underlying ethanol inhibitory action, but not in mediation of the AVP response to physical exercise.

Effect of naloxone on somatostatin inhibition of arginine vasopressin response to physical exercise in normal men.

To establish whether somatostatin (SRIH) and/or endogenous opioids play a role in the control of arginine-vasopressin (AVP) response to physical exercise, eight healthy men underwent four bicycle-ergometer tests until exhaustion: exercise control test; exercise plus SRIH, naloxone or SRIH plus naloxone. Serum AVP levels, physiological and biochemical variables were measured during tests. Physiological and biochemical variables were similar in all tests. During control test exercise significantly increased serum AVP levels, with a peak value 4.1 times higher than baseline. The AVP response to exercise was similar in the presence of naloxone, whereas it was significantly reduced by SRIH (AVP peak was only 2.8 times higher than baseline). When SRIH and naloxone were given together, the exercise-induced AVP rise was comparable to that observed in the control test. Results indicate a somatostatinergic involvement in the regulation of the AVP response to physical exercise. Furthermore, naloxone-sensitive endogenous opioids appear to play a role in the mechanism underlying SRIH inhibitory action, but not in mediation of the AVP response to physical exercise.

Free fatty acids inhibit adrenocorticotropin and cortisol secretion stimulated by physical exercise in normal men.

BACKGROUND: The basal circulating levels of ACTH and cortisol, but not the ACTH/cortisol response to hCRH, are significantly reduced by free fatty acid (FFA) infusion. OBJECTIVE: To verify whether FFA infusion modifies the ACTH/cortisol response to physical exercise, a well-known activator of the HPA axis at suprapituitary level. DESIGN: Exercise tests on a bicycle ergometer during infusion of a lipid-heparin emulsion (LHE) (experimental test) or normal saline (NaCl 0.9%) (control test). SETTING: Department of Cardiology at the University-Hospital. SUBJECTS: Seven healthy male subjects aged 25-33 years. INTERVENTIONS: On two mornings, at weekly intervals, LHE or saline were infused for 60 min; infusion started 10 min before exercise test on a bicycle ergometer, which lasted about 15 min. MAIN OUTCOME MEASURES: Circulating ACTH/cortisol levels and physiological variables during physical exercise. RESULTS: FFA levels (0.4 +/- 0.1 mEq/l) remained constant during control test, whereas they progressively rose (peak at 60 min, 2.7 +/- 1.0 mEq/l) during LHE infusion. Neither basal nor exercise-induced changes in physiological variables were modified by LHE infusion. Both ACTH and cortisol increased during exercise, with peak levels at 20 min and 30 min (control test: 103% and 42%, P < 0.001; experimental test: 28.5% and 18.6%, P < 0.05 higher than baseline, respectively). Both ACTH and cortisol responses were significantly lower in the experimental than in the control test (at 20 min P < 0.002 and at 30 min P < 0.05 for ACTH; at 20 min P < 0.05 and at 30 min, 40 min and 50 min P < 0.001 for cortisol). CONCLUSIONS: These data represent the first demonstration of an inhibitory action of increased circulating FFA levels on the HPA axis under stimulatory conditions (i.e. physical exercise, a challenge acting at suprapituitary level). In contrast, previous studies did not show FFA effects on the CRH-induced ACTH/cortisol response. Therefore, our data suggest negative effects of FFAs on the HPA axis at hypothalamic or higher centres in the central nervous system.

Effect of melatonin on arginine vasopressin secretion stimulated by physical exercise or angiotensin II in normal men.

The present study was undertaken in order to establish the possible involvement of melatonin in the mechanisms underlying the arginine-vasopressin (AVP) responses to physical exercise and angiotensin II (ANG II). On two mornings at least 1 week apart, normal male subjects were tested with exercise on a bicycle ergometer (the workload was gradually increased at 3-min intervals until exhaustion and lasted about 15 min in all subjects) or ANG II (60-min infusion of ANG II (Asp 1, IIe 5 angiotensin II) dissolved in 5% glucose in successively increasing doses of 4, 8, 16 ng/kg/min; each dose for 20 min). Tests were carried out with the administration of either 6 mg melatonin or placebo. Melatonin treatment neither modified the basal concentrations of AVP nor changed the AVP response to ANG II. In contrast, plasma AVP levels rose 3.6 times during exercise in the absence of melatonin, but only 2.3 times in the presence of melatonin. These data indicate an involvement of melatonin in the mechanism underlying the AVP response to physical exercise, but not ANG II, in normal men.

Opioid modulation of the gamma-aminobutyric acid-controlled inhibition of exercise-stimulated growth hormone and prolactin secretion in normal men.

The possible involvement of endogenous opioids in the gamma-aminobutyric acid-controlled (GABAergic) inhibition of growth hormone (GH) and prolactin (PRL) during physical exercise was evaluated in normal men. After fasting overnight, seven subjects were tested on four mornings at least 1 week apart. Exercise was performed on a bicycle ergometer. The workload was gradually increased at 3-min intervals until exhaustion and lasted about 15 min in all subjects. Tests were carried out under administration of placebo, the opioid antagonist naloxone (10 mg as an iv bolus injection), the GABAergic agonist sodium valproate (600 mg in three divided doses orally) or naloxone plus sodium valproate. During exercise, plasma GH and PRL levels rose 5.5- and 1.9-fold, respectively. The administration of naloxone did not modify, whereas sodium valproate significantly reduced the plasma GH and PRL rise during exercise. In the presence of sodium valproate, GH and PRL levels rose 3- and 1.5-fold, respectively, in response to exercise. When naloxone was given together with sodium valproate, both GH and PRL responses to exercise were abolished completely. These data suggest the involvement of a GABAergic mechanism in the regulation of GH and PRL responses to physical exercise in men. Furthermore, the data argue against a role of naloxone-sensitive endogenous opioids in the control of these hormonal responses to exercise, whereas they suggest a modulation by opioids of the GABAergic inhibitory action.

Role of GABA and opioids in the regulation of the vasopressin response to physical exercise in normal men.

The present study was undertaken in order to establish the possible involvement of GABAergic and/or opioid pathways in the mechanism underlying the arginine-vasopressin (AVP) response to physical exercise. After fasting overnight, seven subjects were tested on four mornings at least 1 week apart. Exercise was performed on a bicycle ergometer. The workload was gradually increased at 3 min intervals until exhaustion and lasted about 15 min in all subjects. Tests were carried out under administration of placebo, the opioid antagonist naloxone (10 mg as an i.v. bolus injection), the GABAergic agonist sodium valproate (600 mg in three divided doses orally) or naloxone plus sodium valproate. Plasma AVP levels rose 4-fold during exercise. The administration of naloxone did not modify, whereas sodium valproate completely abolished the plasma AVP rise during exercise. When naloxone was given together with sodium valproate, AVP rose 3-fold in response to exercise. These data suggest the involvement of a GABAergic mechanism in regulation of the AVP response to physical exercise in men. Furthermore, the data argue against a role of naloxone sensitive endogenous opioids in the control of AVP during exercise, whereas they suggest a partial opioid mediation of the GABAergic inhibitory action.

[The clinical significance of signal-averaged electrocardiography in hypertrophic cardiomyopathy]. / Significato clinico dell'elettrocardiogramma mediato di superficie nella cardiomiopatia ipertrofica.

We examined 44 patients (pts) with hypertrophic cardiomyopathy to evaluate the prognostic value of signal-averaged electrocardiography and its possible correlations with clinical and instrumental data. All pts (31 male, 13 female, mean age 47 +/- 15) underwent clinical examination, standard electrocardiography, M-mode and two-dimensional echocardiography, 24-72 hour dynamic electrocardiography and signal-averaged electrocardiography. The mean follow-up was 14 +/- 4 months. Signal-averaged electrocardiography was performed using a 40-250 Hz bidirectional filter. An abnormal signal-averaged electrocardiography with late potentials (filtered QRS duration greater than or equal to 120 msec and root mean square voltage in terminal 40 msec less than or equal to 20 microvolts) was detected in 5 pts (group A, 11%) while 39 pts (group B, 89%) had a normal signal-averaged electrocardiography. Ventricular tachycardia runs at dynamic ECG were present in 2 pts in group A (40%), and in 8 in group B (21%, p = NS). No statistical differences were found between the two groups for any clinical or instrumental data. During our study, one group A patient died suddenly. In detecting subjects with ventricular tachycardia runs, signal-averaged electrocardiography sensitivity was 20%, and specificity was 91%. High specificity suggests that signal-averaged electrocardiography might be used to detect pts at a lower risk for ventricular tachycardia. Further investigations are required to evaluate the predictive value of signal-averaged electrocardiography for sudden death in hypertrophic cardiomyopathy.

Reduced sensitivity to pirenzepine-induced blockade of growth hormone responses to arginine, exercise, and growth hormone-releasing hormone in type I diabetic subjects.

The present study was performed to establish whether the mechanism by which the cholinergic system influences growth hormone (GH) release was altered in type I diabetic patients. Therefore, we investigated in a dose-response fashion the inhibitory effect of the muscarinic cholinergic receptor antagonist pirenzepine on the GH responses to arginine infusion (30 g infused intravenously (IV) in 30 minutes), exercise (bicycle ergometer test at an intensity of 75 W for 30 minutes), or 1-44 GH-releasing hormone (GHRH) (1 microgram/kg in an IV bolus). In a preliminary study, IV injection of 17.5 mg pirenzepine failed to produce modification in the GH response to arginine infusion in both diabetic (N = 4) and normal subjects (N = 4), and to exercise (diabetics, N = 4; normals, N = 4). Therefore, other subjects were tested without and with 20, 25, and 30 mg pirenzepine during arginine (diabetics, N = 7; normals, N = 7) or exercise (diabetics, N = 7; normals, N = 7) tests. Each subject was tested four times. Diabetic patients presented higher GH responses to stimulation with arginine or exercise than normal controls. In both groups, pirenzepine administered at doses ranging from 20 to 30 mg produced a dose-related inhibition of the GH response to arginine and exercise, which was almost complete when 30 mg pirenzepine was administered. However, the percent inhibition produced by 20 or 25 mg pirenzepine in the arginine test and by 20 mg in the exercise test was significantly lower in the diabetic patients than in the normal controls.(ABSTRACT TRUNCATED AT 250 WORDS)

[Syndrome X]. / Il punto sulla sindrome X.

The authors reviewed the literature on X syndrome, finding criteria of inclusion/exclusion so different as to often invalidate the results. The syndrome should be diagnosed only in patients with typical anginal pain on effort relieved by nitroglycerin or rest, with perfectly regular coronary vessels and a normal resting left ventricle, without any evidence of variant angina. Other diseases must be strictly excluded (mostly at the esophageal level) and an ischemic process has to be proved by means of more than one provocative test. Interesting pathophysiological findings are the dynamic limitation of coronary flow reserve and frequent reports of a left ventricle dysfunction during stress. Whether these last findings represent an independent entity, an aspect or stage of the variant angina or the initial appearance of a cardiomyopathy, has yet to be clarified. Frequent reports of a higher prevalence of X syndrome in women have not been substantiated and could be explained by many biases.

[Acute isolated infarct of the right ventricle with an unusual hemodynamic and electrocardiographic pattern]. / Infarto acuto isolato del ventricolo destro con inusuale quadro emodinamico ed elettrocardiografico.

The Authors reports on a case of isolated infarction of the right ventricle, with electrocardiographic pattern of non-transmural anterior myocardial infarction and haemodynamic profile suggestive of important diastolic disfunction. Clinical, angiographic and haemodynamic data are discussed along with review of the literature.

[Identification using thoracic electromapping of patients with sustained postinfarct ventricular tachycardia. Preliminary results of a new method of analysis of ST-T isoarea maps]. / Identificazione mediante elettromappe toraciche di pazienti con tachicardia ventricolare sostenuta post-infartuale. Risultati preliminari di un nuovo metodo di analisi delle mappe isoaree di ST-T.

Recent studies have demonstrated that body surface maps (BSM) can be employed as non-invasive diagnostic tool for recognizing cardiac states at risk for repetitive ventricular arrhythmias in patients (pts) with old infarction. Our study reports preliminary results of a new method of statistical analysis of ST-T isoarea maps for identifying patients with post-infarction sustained ventricular tachycardia. 38 pts with previous myocardial infarction have been studied, 25 without and 13 with sustained ventricular tachycardia (VT). The two groups of pts did not differ significantly for age, site of infarction and ejection fraction. BSM have been recorded by means of an automated 35-channels instrument from 140 thoracic leads. For each lead ST-T deflection area has been calculated in microV.sec and taken as input variables for stepwise discriminant analysis which allowed identification of the integral values significantly discriminant (for F less than 0.15) between the two groups. Canonical analysis has been applied to identified values to obtain, by canonical coefficients, linear combination of the values for the highest correlation with the two groups of pts. To test the power of the method, the two groups of pts have been divided randomly in a learning set (17 pts without and 9 pts with VT) and a test set (8 pts without and 4 pts with VT).(ABSTRACT TRUNCATED AT 250 WORDS)

Nicotine from cigarette smoking enhances clonidine-induced increase of serum growth hormone concentrations in men.

In order to determine whether nicotine exerts its stimulant effect on serum concentrations of growth hormone (GH) by interacting with an adrenergic pathway, we evaluated the effect of cigarette smoking on the response of GH to the administration of clonidine, a specific alpha-adrenoceptor agonist. In six normal volunteers, clonidine significantly increased serum levels of GH. When subjects smoked two non-filter cigarettes, GH response to the alpha-adrenoceptor agonist was greatly enhanced. These findings suggest that in man nicotinic cholinergic and adrenergic mechanisms might interact in the stimulation of GH secretion.

Evaluation of oxytocin administration on luteinizing hormone and follicle-stimulating hormone response to luteinizing hormone-releasing hormone during the menstrual cycle of normal women.

In order to determine whether oxytocin modifies luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion in response to LH-releasing hormone (LH-RH), a group of normal women, 23 to 30 years of age, was studied in the follicular, periovulatory, and luteal phases. LH and FSH response to LH-RH was evaluated in the serum under control conditions and after oxytocin infusion. Oxytocin administration failed to modify LH and FSH release induced by LH-RH. These results suggest that this neuropeptide is not involved in the control of LH and FSH at the level of the anterior pituitary.