Oxytocin reduces exercise-induced ACTH and cortisol rise in man

1988 ◽  
Vol 119 (3) ◽  
pp. 405-412 ◽  
Author(s):  
V. Coiro ◽  
M. Passeri ◽  
C. Davoli ◽  
A. Bacchi-Modena ◽  
L. Bianconi ◽  
...  
Keyword(s):  
Physical Exercise ◽  
Bolus Injection ◽  
Inhibitory Effect ◽  
Bicycle Ergometer ◽  
Endogenous Opioids ◽  
Cortisol Response ◽  
Plasma Acth ◽  
Exercise Induced ◽  
Normal Men ◽  
Response To Exercise

Abstract. The effect of oxytocin on the ACTH, cortisol, GH and PRL response to physical exercise was investigated in 6 normal men. In addition, the possible involvement of endogenous opioids in the mediation of oxytocin action was evaluated. After fasting overnight, each subject was 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 20 min in all subjects. Tests were carried out under administration of oxytocin (2000 mIU as an iv bolus injection plus 32 mIU/min per 30 min) or naloxone (10 mg as an iv bolus injection) alone; furthermore, the effect of oxytocin together with naloxone (10 mg as an iv bolus injection) was evaluated. In the remaining test, normal saline was given instead of drugs. Plasma ACTH, cortisol, PRL and GH concentrations were significantly increased by physical exercise. Administration of oxytocin, naloxone or their combination was without effect on the PRL and GH rise elicited by exercise. In contrast, the exercise-induced ACTH and cortisol response was significantly raised by naloxone and reduced by oxytocin. When oxytocin was preceded by administration of naloxone, the ACTH and cortisol response to exercise was not reduced by oxytocin. These data show that oxytocin is capable of inhibiting the rise in ACTH and cortisol, but not in GH and PRL induced by physical exercise. Since naloxone abolished the inhibitory effect of oxytocin, oxytocin action on ACTH and cortisol secretion might be supposed to be mediated by an opioid pathway. However, we cannot exclude that oxytocin and naloxone act at different sites in the hypothalamic-pituitary system.

Lack of fibrin formation in exercise-induced activation of coagulation

1979 ◽  
Vol 236 (4) ◽  
pp. H577-H579 ◽  
Author(s):  
A. Vogt ◽  
V. Hofmann ◽  
P. W. Straub
Keyword(s):  
Physical Exercise ◽  
Degradation Products ◽  
Bicycle Ergometer ◽  
Strenuous Exercise ◽  
Thrombin Time ◽  
Fibrinopeptide A ◽  
Lysis Time ◽  
Exercise Period ◽  
Euglobulin Lysis Time ◽  
Exercise Induced

Strenuous physical exercise leads to a significant shortening of blood clotting in various test systems. Such short times are also characteristic of those observed in sedentary patients with thrombosis or disseminated intravascular coagulation, and of those observed in experimental animals after thrombin infusion. The patients exhibit an increase in circulating fibrinopeptide A, which is attributed to thrombin action on circulating fibrinogen, and to an increase of fibrinogen degradation products, which is thought to indicate reactive fibrinolysis. To check whether physical exercise leads to fibrinemia, 10 healthy male volunteers were subjected to strenuous exercise on a bicycle ergometer. Blood samples were taken immediately before and on completion of the exercise period. Despite a significant shortening of the activated partial thromboplastin time, the thrombin time, and the Reptilase time, no increase of fibrinopeptide A could be demonstrated and the ethanol gelation test remained consistently negative. Simultaneously, the euglobulin lysis time was significantly shortened, whereas the fibrin(ogen) degradation products did not increase. The results indicate that the shortening of the coagulation times associated with physical exercise must be explained by mechanisms other than thrombin-mediated conversion of fibrinogen to fibrin.

Role of neutral endopeptidase in exercise-induced bronchoconstriction in asthmatic subjects

1996 ◽  
Vol 81 (2) ◽  
pp. 673-678 ◽  
Author(s):  
H. W. de Gouw ◽  
Z. Diamant ◽  
E. A. Kuijpers ◽  
J. K. Sont ◽  
P. J. Sterk
Keyword(s):  
Recovery Period ◽  
Neutral Endopeptidase ◽  
Bicycle Ergometer ◽  
Forced Expiratory Volume ◽  
Double Blind ◽  
Airway Response ◽  
Membrane Bound ◽  
Exercise Induced ◽  
Response To Exercise

The membrane-bound metalloproteinase, neutral endopeptidase (NEP), is a degrading enzyme of both bronchoconstrictor and bronchodilator peptides within the airways. To examine the role of NEP in exercise-induced bronchoconstriction (EIB) in asthmatic subjects, we used inhaled thiorphan, a NEP inhibitor, as pretreatment to a 6-min standardized exercise challenge. Thirteen clinically stable asthmatic subjects participated in this double-blind, placebo-controlled, crossover study that was performed on 2 days separated by 48 h. Thiorphan was administered by two inhalations of 0.5 ml containing 1.25 mg/ml. Subsequently, exercise was performed on a bicycle ergometer at 40–50% of predicted maximal voluntary ventilation while inhaling dry air (20 degrees C, relative humidity 6%). The airway response to exercise was measured by forced expiratory volume in 1 s (FEV1) every 3 min, up to 30 min postexercise challenge, and was expressed both as the maximal percent fall in FEV1 from baseline and as the area under the time-response curve (AUC) (0–30 min). The acute effects of both pretreatments on baseline FEV1 were not different (P > 0.2), neither was there any difference in maximal percent fall in FEV1 between thiorphan and placebo (P > 0.7). However, compared with placebo, thiorphan reduced the AUC by, on average, 26% [AUC (0–30 min, +/-SE): 213.6 +/- 47.7 (thiorphan) and 288.6 +/- 46.0%fall.h (placebo); P = 0.047]. These data indicate that NEP inhibition by thiorphan reduces EIB during the recovery period. This suggests that bronchodilator NEP substrates, such as vasoactive intestinal polypeptide or atrial natriuretic peptide, modulate EIB in patients with asthma.

The influence of naloxone on exercise-induced increase in plasma pituitary hormones and the subjectively experienced level of exhaustion in healthy males

1987 ◽  
Vol 115 (1) ◽  
pp. 125-130 ◽  
Author(s):  
Margareta Bramnert ◽  
Bernt Hökfelt
Keyword(s):  
Bolus Dose ◽  
Pituitary Hormones ◽  
Bicycle Ergometer ◽  
Pituitary Hormone ◽  
Slow Infusion ◽  
Exercise Induced ◽  
Maximal Working Capacity ◽  
Induced Changes ◽  
Response To Exercise ◽  
Healthy Males

Abstract. Opioid peptides seem to play a role as modulators of the pituitary function in man. In the present study, the effect of naloxone on exercise-induced pituitary hormone release and the subjectively experienced level of exhaustion were investigated in nine healthy males. A submaximal work test was performed on two occasions using a bicycle ergometer: 10 min on 50% of maximal working capacity (MWC), immediately followed by 10 min on 80% of MWC. Ten min before exercise, each subject received, in a single-blind randomized order, either a bolus dose of naloxone (100 μg/kg) followed by a slow infusion of naloxone (50 μg · kg−1 · h−1) or as a control a corresponding volume of the preservatives in the naloxone preparation as a bolus dose followed by an infusion of diluted preservatives. In the control studies, exercise induced a significant increase in GH, PRL, TSH and ACTH. The increase in ACTH was enhanced following naloxone. Naloxone was without effect on exercise-induced changes in GH, PRL and TSH. An increased level of exhaustion was experienced on 80% of MWC during naloxone. It is concluded that opioid receptors with a moderate sensitivity to naloxone are involved in the regulation of the ACTH response to exercise and also influence the subjectively experienced level of exhaustion.

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

1994 ◽  
Vol 131 (1) ◽  
pp. 50-55 ◽  
Author(s):  
V Coiro ◽  
R Volpi ◽  
ML Maffei ◽  
A Caiazza ◽  
G Caffarri ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Physical Exercise ◽  
Sodium Valproate ◽  
Prolactin Secretion ◽  
Endogenous Opioids ◽  
Aminobutyric Acid ◽  
Opioid Antagonist ◽  
Gamma Aminobutyric Acid ◽  
Normal Men ◽  
Plasma Gh

Coiro V, Volpi R, Maffei ML, Caiazza A, Caffarri G, Capretti L, Colla R, Chiodera P. Opioid modulation of the gamma-aminobutyric acid-controlled inhibition of exercise-stimulated growth hormone and prolactin secretion in normal men. Eur J Endocrinol 1994;131:50–5. ISSN 0804–4643 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. Vittorio Coiro, Istituto di Clinica Medica Generale e Terapia Medica, Università di Parma, via Gramsci 14, 43100 Parma, Italy

Inhibition by dexamethasone of arginine vasopressin and ACTH responses to insulin-induced hypoglycemia and cigarette smoking in normal men

1990 ◽  
Vol 123 (5) ◽  
pp. 487-492 ◽  
Author(s):  
P. Chiodera ◽  
V. Coiro
Keyword(s):  
Cigarette Smoking ◽  
Plasma Concentrations ◽  
Peak Level ◽  
Inhibitory Effect ◽  
Dexamethasone Treatment ◽  
Plasma Acth ◽  
The Mean ◽  
Normal Men ◽  
Circulating Levels ◽  
Acth Release

Abstract. Glucocorticoids are known to inhibit the AVP response to osmotic and hemodynamic stimuli in humans. In the present study, we examined whether the AVP response to other primary stimuli, such as insulin-induced hypoglycemia and cigarette smoking was sensitive to inhibition by dexamethasone. The plasma ACTH responses were also measured. Twenty-four normal men were randomly divided into 3 groups of 8 subjects. One group was tested with insulin (0.15 IU/kg in an iv bolus) and another group with cigarette smoking (2 non-filter cigarettes smoked in succession within 10 min) with and without pretreatment with dexamethasone (2 or 4 mg in an iv bolus 10 min before insulin or smoking). The third group was tested with dexamethasone alone (2 or 4 mg in an iv bolus). The administration of dexamethasone (2 or 4 mg) alone did not modify the circulating levels of AVP and ACTH at any time during the next hour. The hypoglycemic response to insulin was similar regardless of dexamethasone treatment. AVP rose sharply in response to both hypoglycemia and smoking, reaching mean peak levels at 45 and 30 min, respectively. After both stimuli, the mean peak levels of AVP were 2.25 times higher than baseline. Pretreatment with dexamethasone (2 or 4 mg) significantly decreased the AVP responses to both hypoglycemia and cigarette smoking. Following pretreatment with dexamethasone (2 or 4 mg) the AVP increments in response to hypoglycemia or cigarette smoking were only 1.7 times higher than baseline. The plasma concentrations of ACTH were strikingly increased by hypoglycemia. The mean peak level was 3.5 times higher than baseline and was reached at 45 min. Pretreatment with dexamethasone (2 or 4 mg) significantly reduced hypoglycemia-induced ACTH increase, with a mean peak response 2.8 times higher than baseline. Cigarette smoking significantly increased the plasma ACTH concentrations. The mean peak level was observed at 20 min and was 1.3 times higher than baseline. The ACTH response to smoking was not significant following pretreatment with dexamethasone (2 or 4 mg). These data show a partial inhibitory effect of dexamethasone on hypoglycemia-and cigarette smoking-stimulated AVP secretion. In addition, the data show suppression by dexamethasone of the ACTH response to cigarette smoking and confirm previous observations of a partial inhibition by glucocorticoids of hypoglycemia-induced ACTH release.

Cardiovascular responses to muscle ischemia in man--dependency on muscle mass

1978 ◽  
Vol 45 (5) ◽  
pp. 762-767 ◽  
Author(s):  
P. R. Freund ◽  
S. F. Hobbs ◽  
L. B. Rowell
Keyword(s):  
Muscle Mass ◽  
Forearm Blood Flow ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Bicycle Ergometer ◽  
Muscle Ischemia ◽  
Exercise Induced ◽  
Response To Exercise ◽  
Mass Dependent ◽  
Ischemic Muscle

We sought to determine whether the pressor response to exercise-induced muscle ischemia is related to the mass of tissue rendered ischemic. Six men repeatedly exercised for 5 min at a fixed load between 75 and 150 W (bicycle ergometer). Thirty seconds before the end of exercise, circulation to one calf, two calves, one leg, and two legs was arrested with pneumatic cuffs in successive tests with 15-min recovery periods interspersed. Each occlusion was maintained until the 3rd min of exercise recovery. During postexercise occlusion we observed 1) mean arterial pressure (MAP) was elevated in proportion to the mass of ischemic muscle, 2) forearm blood flow (FBF) was elevated during the overlap of occlusion with exercise but did not show a uniform response during the following 3 min of occlusion--either vasoconstriction or vasodilation occurred, 3) heart rate (HR) was elevated only when two legs were occluded, and 4) occlusion did not affect ventilation or endtidal CO2. We conclude that the ischemic pressor response is muscle mass-dependent. Our findings suggest that the baroreflex alters peripheral vascular resistance so as to aid in the maintenance of elevated MAP.

scholarly journals Plasma cortisol response to exercise‐induced negative energy balance is affected by protein intake

2006 ◽  
Vol 20 (5) ◽  
Author(s):  
James Philip Karl ◽  
Tracey J Smith ◽  
Matthew A Pikosky ◽  
Mona M Mathow ◽  
Ellen L Glickman ◽  
...  
Keyword(s):  
Energy Balance ◽  
Protein Intake ◽  
Plasma Cortisol ◽  
Negative Energy ◽  
Negative Energy Balance ◽  
Cortisol Response ◽  
Exercise Induced ◽  
Response To Exercise

Physical Exercise Induces Enhancement of Urokinase-Type Plasminogen Activator (u-PA) Levels in Plasma

1991 ◽  
Vol 65 (01) ◽  
pp. 082-086 ◽  
Author(s):  
G Dooijewaard ◽  
A de Boer ◽  
P N C Turion ◽  
A F Cohen ◽  
D D Breimer ◽  
...  
Keyword(s):  
Physical Exercise ◽  
Plasminogen Activator ◽  
Maximal Exercise ◽  
Normal Values ◽  
Bicycle Ergometer ◽  
Tissue Type ◽  
Healthy Male ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator ◽  
Fibrinolytic Potential

SummaryThe enhancement of the blood fibrinolytic potential by physical exercise is generally attributed to the release of tissue-type plasminogen activator (t-PA) from the vessel wall. In this study we have investigated the possible contribution of urokinase-type plasminogen activator (u-PA).Six healthy male volunteers (age 21–25 years) were screened for their ability to perform maximal exercise for their age-group for 12 min on a bicycle ergometer. Subsequently, on one occasion they were required to remain supine for 2 h (from 8.30 a. m. onwards) and on another they performed maximal exercise (from 9.00 a.m. onwards). During exercise an increase in u-PA antigen and plasmin-activatable pro-urokinase (proUK) activity, concurrent with t-PA antigen and euglobulin t-PA activity, was observed in all six volunteers, while at rest these parameters remained unaffected. Mean u-PA- and t-PA antigen increased, respectively, from 4.2 ± 1.0 ng/ml and 5.8 ± 2.1 ng/ml before exercise to 9.8 ± 3.0 ng/ml and 18.3 ± 3.8 ng/ml (peak). Mean plasminactivatable proUK activity and t-PA activity increased, respectively, from 2.1 ± 0.4 ng/ml and 0.3 ± 0.2 ng/ml before exercise to 4.3 ± 1.7 ng/ml and 7.2 ± 4.0 ng/ml (peak). The increases were statistically significant throughout (paired t-test, pre vs post, antigen P <0.005 and activity P <0.02). After cessation of exercise u-PA and t-PA declined concurrently to normal values with a 50"/" decay in about 5 min. In conclusion, we found that both u-PA antigen and plasmin-activatable proUK activity are, concurrently with t-PA, enhanced upon exercise and, therefore, we consider that u-PA also contributes to – and co-operates in – the enhancement of the blood fibrinolytic potential and activity under these conditions.

ADRENERGIC CONTROL MECHANISM FOR ACTH SECRETION IN MAN

1973 ◽  
Vol 74 (2) ◽  
pp. 263-270 ◽  
Author(s):  
Yoshikatsu Nakai ◽  
Hiroo Imura ◽  
Teruya Yoshimi ◽  
Shigeru Matsukura
Keyword(s):  
Intravenous Infusion ◽  
Human Subjects ◽  
Blocking Agent ◽  
Inhibitory Effect ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Glucose Levels ◽  
Alpha Receptors ◽  
Normal Human ◽  
Adrenergic Blocking

ABSTRACT In order to determine if an adrenergic mechanism is involved in the secretion of corticotrophin (ACTH), the effect of adrenergic-blocking or -stimulating agent on plasma ACTH, cortisol and glucose levels was studied in normal human subjects. The intravenous infusion of methoxamine, an alpha adrenergic-stimulating agent, caused a rise in plasma ACTH and cortisol. This increase in plasma ACTH and cortisol was significantly inhibited by the simultaneous administration of phentolamine, an alpha adrenergic-blocking agent, in combination with methoxamine. The intravenous infusion of propranolol, a beta adrenergic-blocking agent, caused no significant change in plasma ACTH and cortisol, although it enhanced the plasma ACTH response to insulin-induced hypoglycaemia. On the other hand, alpha adrenergicblockade by intravenous infusion of phentolamine significantly suppressed the plasma ACTH response to insulin-induced hypoglycaemia. These studies suggest a stimulatory effect of alpha receptors and a possible inhibitory effect of beta receptors on ACTH secretion in man.

Catecholamine-fuel interrelationships during exercise in fasting men

1980 ◽  
Vol 48 (1) ◽  
pp. 109-113 ◽  
Author(s):  
J. M. Pequignot ◽  
L. Peyrin ◽  
G. Peres
Keyword(s):  
Maximal Oxygen Consumption ◽  
Plasma Catecholamines ◽  
Plasma Free Fatty Acid ◽  
Work Load ◽  
Bicycle Ergometer ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Adrenergic Response ◽  
Response To Exercise

Adrenergic response to exercise and the relationships between plasma catecholamines and blood energetic substrates were studied in sedentary men after 15 h of fasting. Subjects pedaled a bicycle ergometer until exhaustion at a work load approximating 80% maximal oxygen consumption. Working ability was diminished by the fast (P less than 0.025). Resting plasma norepinephrine level was increased by fasting. During exercise plasma epinephrine (E) and norepinephrine (NE) concentrations were more elevated in fasting subjects than in fed subjects. Plasma catecholamine (CA) levels in fasting men correlated with blood glucose, blood lactate, and plasma glycerol concentrations. There was no significative correlation between CA and plasma free fatty acid (FFA) levels. The increased adrenergic activity in fasting subjects correlated with reduced endurance time. This study emphasizes the role of CA release, probably combined with other hormonal factors, in the mobilization of energy substrates during submaximal exercise.

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