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

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.

Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Jacob L Barber ◽  
Guoshuai Cai ◽  
Jeremy M Robbins ◽  
Robert E Gerszten ◽  
Prashant Rao ◽  
...  

Introduction: Regular exercise beneficially increases plasma HDL-C levels at the group level. However, variation in individual HDL-C responses to exercise highlight a need for predictive biomarkers of exercise response. Hypothesis: We hypothesized that baseline abundance of circulating proteins is predictive of HDL-C response to exercise and that identified proteins are part of a complex biological network of exercise response. Methods: We measured over 5,000 circulating proteins using an aptamer-affinity based platform (SomaScan) in 667 black and white adults from the HERITAGE Family Study. Fasting plasma HDL-C was measured at baseline and following 20 weeks of supervised endurance exercise training. To predict exercise induced changes in HDL-C using baseline abundance of circulating proteins, models were created using LASSO regression and a 70/30 training test data split with 10-fold cross validation. Biological pathways, networks, and functions involving proteins identified in predictive modeling were investigated by ingenuity pathway analysis (IPA) and integrated molecular pathway level analysis (IMPaLA). Results: Regular exercise significantly increased HDL-C in the sample by 1.5 ± 4.6 mg/dL (p<0.0001), however marked inter-individual differences in response were present (range: -19.5 to +17.4 mg/dL). LASSO regression of circulating proteins only yielded a model of 120 proteins with similar but stronger predictive power to a model of 19 clinical traits (root mean square error = 4.52 and 5.3 mg/dL respectively). LASSO regression of both clinical and proteomic predictors resulted in a final model of baseline HDL-C and 116 circulating proteins, with an improved root mean square error of 4.11 mg/dL. Furthermore, this panel of 116 proteins was able to explain 40.0% of the variance in exercise induced changes in plasma HDL-C, while clinical predictors alone (including baseline HDL-C) explained only 3.9%. Pathway analysis of these 116 proteins identified several biological processes including pathways involved in the progression towards atherosclerosis, angiogenesis, mTOR signaling, and mitochondrial fatty acid synthesis. Conclusions: Circulating proteins may allow for prediction of exercise induced changes in HDL-C. Additionally, proteins predictive of HDL-C response to exercise are associated with important biological pathways and may provide insights into the molecular mechanisms of the benefits of regular exercise.


1999 ◽  
Vol 87 (6) ◽  
pp. 2157-2167 ◽  
Author(s):  
Michael I. Lindinger ◽  
Peggy L. Horn ◽  
Simon P. Grudzien

The hypothesis was tested that exercise-induced changes in plasma composition stimulate unidirectional K+ transport ( J inK) in human red blood cells (RBCs). Ten men performed two 30-s high-intensity leg-cycling tests separated by 4 min of rest. Antecubital venous blood was sampled before exercise and at the end of the second exercise bout. RBCs were separated from true exercise plasma,42K was added to plasma, and RBC K+ transport was studied in vitro at 37°C. In the second part of the study, blood from nine healthy men studied in vitro at 37°C was used to test the hypothesis that exercise-simulated (ES) plasma stimulates net K+ transport and J inK (measured using 86Rb) in human RBCs. The J inK of resting RBCs added to true exercise plasma was 1,574 ± 200 (SE) μmol ⋅ h−1 ⋅ l−1vs. 1,236 ± 256 μmol ⋅ h−1 ⋅ l−1in true resting plasma at 2 min (controls). In true exercise and ES plasma, J inK was increased through activation of the ouabain-sensitive Na+-K+pump and the bumetanide-sensitive Na+-K+-2Cl−cotransporter. Increases in plasma osmolality and K+, H+, and epinephrine concentrations independently and in combination stimulated K+ transport into human RBCs. In a third series of experiments, in which ES plasma K+ concentration was continuously measured during the first 5 min of incubation of RBCs, a 1.6 ± 0.3 mmol/l decrease in plasma K+concentration occurred during the first 2 min. It is concluded that RBCs transport K+ at elevated rates in response to exercise-induced changes in plasma composition.


1989 ◽  
Vol 256 (1) ◽  
pp. R169-R173 ◽  
Author(s):  
A. J. Scheurink ◽  
A. B. Steffens ◽  
G. H. Dreteler ◽  
L. Benthem ◽  
R. Bruntink

The interference of the experimental conditions on the exercise-induced alterations in plasma catecholamines, plasma free fatty acids, and glucose and insulin concentrations was investigated in rats. Exercise consisted of strenuous swimming against a countercurrent (0.22 m/s) for 15 min in a pool with water of 33 degrees C. Before, during, and after swimming, blood samples were taken through a permanent heart catheter. The blood component levels in rats that were confronted with exercise for the very first time were compared with the levels in rats that were well accustomed to the exercise conditions. The very first time rats swam caused an enhanced release of epinephrine from the adrenal medulla and a reduced output of norepinephrine from the sympathetic nerve endings. Furthermore, in the first time swim group, blood glucose levels were higher and plasma free fatty acid concentrations were lower compared with the well-accustomed animals. There were no differences in plasma insulin concentrations. It is concluded that the experimental conditions may interfere considerably with the hormonal and metabolic response to exercise. Furthermore the results reinforce the idea that the two parts of the sympathoadrenal system are functionally and metabolically dissociated.


1988 ◽  
Vol 255 (4) ◽  
pp. E428-E436 ◽  
Author(s):  
J. M. Moates ◽  
D. B. Lacy ◽  
R. E. Goldstein ◽  
A. D. Cherrington ◽  
D. H. Wasserman

The role of the exercise-induced increment in epinephrine was studied in five adrenalectomized (ADX) and in six normal dogs (C). Experiments consisted of an 80-min equilibration period, a 40-min basal period, and a 150-min exercise period. ADX were studied with epinephrine replaced to basal levels during rest and to increased levels during exercise to simulate its normal rise (HE) and on a separate day with epinephrine maintained at basal levels throughout the study (BE). Cortisol was replaced during rest and exercise in ADX so as to simulate the levels seen in C. Glucose was infused as needed in ADX to maintain the glycemia evident during exercise in C. Glucose production (Ra) and utilization (Rd) were assessed isotopically. In C, epinephrine had risen by 95 +/- 25 pg/ml by the end of exercise. In HE, the increment in epinephrine (117 +/- 29 pg/ml) was similar to that seen in C, whereas in BE epinephrine fell by 18 +/- 9 pg/ml. Basal norepinephrine levels were 139 +/- 9, 260 +/- 25, and 313 +/- 33 pg/ml in C, HE, and BE, respectively. In response to exercise, norepinephrine increased by nearly twofold in all protocols. Basal and exercise-induced changes in plasma glucagon and insulin were similar in C and ADX. Ra increased similarly in C (5.3 +/- 0.6 mg.kg-1.min-1) and HE (4.9 +/- 0.6 mg.kg-1.min-1). In BE, Ra rose normally for the initial 90 min but then declined resulting in a rise of only 2.9 +/- 0.5 mg.kg-1.min-1 after 150 min of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)


1996 ◽  
Vol 81 (2) ◽  
pp. 673-678 ◽  
Author(s):  
H. W. de Gouw ◽  
Z. Diamant ◽  
E. A. Kuijpers ◽  
J. K. Sont ◽  
P. J. Sterk

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.


1991 ◽  
Vol 71 (1) ◽  
pp. 136-143 ◽  
Author(s):  
P. Bartsch ◽  
M. Maggiorini ◽  
W. Schobersberger ◽  
S. Shaw ◽  
W. Rascher ◽  
...  

A possible contribution of exercise to the fluid retention associated with acute mountain sickness (AMS) was investigated in 17 mountaineers who underwent an exercise test for 30 min on a bicycle ergometer with a constant work load of 148 +/- 9 (SE) W at low altitude (LA) and with 103 +/- 6 W 4–7 h after arrival at 4,559 m or high altitude (HA). Mean heart rates during exercise at both altitudes and during active ascent to HA were similar. Exercise-induced changes at LA did not differ significantly between the eight subjects who stayed well and the nine subjects who developed AMS during a 3-day sojourn at 4,559 m. At HA, O2 saturation before (71 +/- 2 vs. 83 +/- 2%, P less than 0.01) and during exercise (67 +/- 2 vs. 72 +/- 1%, P less than 0.025) was lower and exercise-induced increase of plasma aldosterone (617 +/- 116 vs. 233 +/- 42 pmol/l, P less than 0.025) and plasma antidiuretic hormone (23.8 +/- 14.4 vs. 3.4 +/- 1.8 pmol/l, P less than 0.05) was greater in the AMS group, whereas exercise-induced rise of plasma atrial natriuretic factor and changes of hematocrit, potassium, and osmolality in plasma were similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)


1988 ◽  
Vol 119 (3) ◽  
pp. 405-412 ◽  
Author(s):  
V. Coiro ◽  
M. Passeri ◽  
C. Davoli ◽  
A. Bacchi-Modena ◽  
L. Bianconi ◽  
...  

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.


2001 ◽  
Vol 281 (4) ◽  
pp. C1259-C1265 ◽  
Author(s):  
Karen Krzywkowski ◽  
Emil Wolsk Petersen ◽  
Kenneth Ostrowski ◽  
Jens Halkjær Kristensen ◽  
Julio Boza ◽  
...  

The purpose of this study was to investigate the possible role of glutamine in exercise-induced impairment of lymphocyte function. Ten male athletes participated in a randomized, placebo-controlled, double-blind crossover study. Each athlete performed bicycle exercise for 2 h at 75% of maximum O2consumption on 2 separate days. Glutamine or placebo supplements were given orally during and up to 2 h postexercise. The trial induced postexercise neutrocytosis that lasted at least 2 h. The total lymphocyte count increased by the end of exercise due to increase of both CD3+TCRαβ+and CD3+TCRγδ+T cells as well as CD3−CD16+CD56+natural killer (NK) cells. Concentrations of CD8+and CD4+T cells lacking CD28 and CD95 on their surface increased more than those of cells expressing these receptors. Within the CD4+cells, only CD45RA−memory cells, but not CD45RA+naive cells, increased in response to exercise. Most lymphocyte subpopulations decreased 2 h after exercise. Glutamine supplementation abolished the postexercise decline in plasma glutamine concentration but had no effect on lymphocyte trafficking, NK and lymphokine-activated killer cell activities, T cell proliferation, catecholamines, growth hormone, insulin, or glucose. Neutrocytosis was less pronounced in the glutamine-supplemented group, but it is unlikely that this finding is of any clinical significance. This study does not support the idea that glutamine plays a mechanistic role in exercise-induced immune changes.


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