Effect of plasma prolactin on sweat rate and sweat composition during exercise in men

1993 ◽  
Vol 264 (5) ◽  
pp. F816-F820
Author(s):  
P. Boisvert ◽  
G. R. Brisson ◽  
F. Peronnet
Keyword(s):  
Sweat Rate ◽  
Cycle Ergometer ◽  
Plasma Prolactin ◽  
Young Males ◽  
Low Responders ◽  
Exercise Induced ◽  
Plasma Prl ◽  
Response To Exercise ◽  
High Responders

We investigated the role of the exercise-induced elevation of plasma prolactin (PRL) concentration on sweat rate and composition during prolonged exercise in men. Two groups of healthy young males (20-26 yr old) showing a high (high responders; n = 8) or a low (low responders; n = 7) response of plasma PRL concentration to exercise were studied during a 60-min period of exercise on a cycle ergometer (65% maximum O2 consumption) in warm conditions (26.2 +/- 0.1 degrees C; 57 +/- 1% relative humidity), 1 h after receiving 1.25 mg bromocriptine (BRC) per os or a placebo. In high responders, administration of BRC totally abolished the threefold increase in plasma PRL observed in response to exercise with placebo [placebo, 10 +/- 2 (rest) and 30 +/- 2 micrograms/l (exercise); BRC, 9 +/- 1 (rest) and 8 +/- 1 microgram/l (exercise)]. The latter was associated with a significant decrease in sweat rate (2.7 +/- 0.5 to 1.9 +/- 0.3 microliter.cm-2.min-1) and a significant increase in sweat Na+ concentration (57 +/- 7 to 68 +/- 5 mmol/l). BRC also reduced the small response in plasma PRL concentration observed in low responders [placebo, 10 +/- 1 (rest) and 15 +/- 1 microgram/l (exercise); BRC, 9 +/- 1 (rest) and 7 +/- 1 microgram/l (exercise)], but this was not associated with any change in sweat rate (2.2 +/- 0.2 to 1.9 +/- 0.3 microliter.cm-2.min-1) or in sweat Na+ concentration (63 +/- 10 to 64 +/- 9 mmol/l).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of exercise on endothelium and endothelium/smooth muscle cross talk: role of exercise-induced hemodynamics

2011 ◽  
Vol 111 (1) ◽  
pp. 311-320 ◽  
Author(s):  
S. C. Newcomer ◽  
Dick H. J. Thijssen ◽  
D. J. Green
Keyword(s):  
Physical Activity ◽  
Shear Stress ◽  
Wall Stress ◽  
Beneficial Effects ◽  
Exercise Induced ◽  
Response To Exercise ◽  
And Training

Physical activity, exercise training, and fitness are associated with decreased cardiovascular risk. In the context that a risk factor “gap” exists in the explanation for the beneficial effects of exercise on cardiovascular disease, it has recently been proposed that exercise generates hemodynamic stimuli which exert direct effects on the vasculature that are antiatherogenic. In this review we briefly introduce some of the in vitro and in vivo evidence relating exercise hemodynamic modulation and vascular adaptation. In vitro data clearly demonstrate the importance of shear stress as a potential mechanism underlying vascular adaptations associated with exercise. Supporting this is in vivo human data demonstrating that exercise-mediated shear stress induces localized impacts on arterial function and diameter. Emerging evidence suggests that exercise-related changes in hemodynamic stimuli other than shear stress may also be associated with arterial remodeling. Taken together, in vitro and in vivo data strongly imply that hemodynamic influences combine to orchestrate a response to exercise and training that regulates wall stress and peripheral vascular resistance and contributes to the antiatherogenic impacts of physical activity, fitness, and training.

Use of high and low responders to novelty in rat studies on the role of the ventral striatum in radial maze performance: effects of intra-accumbens injections of sulpiride

1993 ◽  
Vol 71 (5-6) ◽  
pp. 335-342 ◽  
Author(s):  
A. R. Cools ◽  
B. Ellenbroek ◽  
D. Heeren ◽  
L. Lubbers
Keyword(s):  
Locomotor Activity ◽  
Radial Maze ◽  
Ventral Striatum ◽  
Individual Vulnerability ◽  
Low Responders ◽  
Performance Effects ◽  
Radial Maze Performance ◽  
Drug Naïve ◽  
High Responders

High and low responders to novelty (Wistar rats) were selected with the help of an open-field test and then equipped with intra-accumbens cannulae. They were then tested in a simple four-arm radial maze during 5 successive days, three trials per day, following intra-accumbens injections of distilled water or the dopaminergic D2 antagonist (±)-sulpiride. The injections were given 15 min before the first trial on each day. Both types of drug-naive rats reached the same level of performance on day 5. However, high responders made more visits, more revisits, and needed less time to make the first visit than low responders. Moreover, high responders showed their greatest increase in learning 2 days earlier than low responders. It is discussed that these differences between high and low responders are not due simply to differences in locomotor activity, but are due to a subtle, but important, difference in the mode of learning between both types. Sulpiride significantly attenuated the learning in both rat types; however, its effect in high responders was much less than that in low responders. It is suggested that the effects of sulpiride are not due to changes in locomotor activity, motivation, or perception, but are due to a learning deficit. The data are discussed in view of the genetic variation in the neurochemical and neurobiological makeup of the nucleus accumbens in both types.Key words: ventral striatum, radial maze, sulpiride, individual vulnerability.

Metabolic role of the exercise-induced increment in epinephrine in the dog

1988 ◽  
Vol 255 (4) ◽  
pp. E428-E436 ◽  
Author(s):  
J. M. Moates ◽  
D. B. Lacy ◽  
R. E. Goldstein ◽  
A. D. Cherrington ◽  
D. H. Wasserman
Keyword(s):  
Glucose Production ◽  
Plasma Glucagon ◽  
Metabolic Role ◽  
Exercise Period ◽  
Exercise Induced ◽  
Glucagon And Insulin ◽  
Induced Changes ◽  
Response To Exercise ◽  
Rest And Exercise

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)

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.

scholarly journals The Role of Autonomic Function in Exerciseinduced Endogenous Analgesia: A Case-control Study in Myalgic Encephalomyelitis⁄Chronic Fatigue Syndrome and Healthy People

2017 ◽  
Vol 3 (20;3) ◽  
pp. E389-E399 ◽  
Author(s):  
Jo Nijs
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Diastolic Blood Pressure ◽  
Chronic Fatigue ◽  
Fatigue Syndrome ◽  
Exercise Induced ◽  
Response To Exercise ◽  
Endogenous Analgesia

Background: Patients with myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) are unable to activate brain-orchestrated endogenous analgesia (or descending inhibition) in response to exercise. This physiological impairment is currently regarded as one factor explaining postexertional malaise in these patients. Autonomic dysfunction is also a feature of ME/CFS. Objectives: This study aims to examine the role of the autonomic nervous system in exerciseinduced analgesia in healthy people and those with ME/CFS, by studying the recovery of autonomic parameters following aerobic exercise and the relation to changes in self-reported pain intensity. Study Design: A controlled experimental study. Setting: The study was conducted at the Human Physiology lab of the Vrije Universiteit Brussel. Methods: Twenty women with ME/CFS- and 20 healthy, sedentary controls performed a submaximal bicycle exercise test known as the Aerobic Power Index with continuous cardiorespiratory monitoring. Before and after the exercise, measures of autonomic function (i.e., heart rate variability, blood pressure, and respiration rate) were performed continuously for 10 minutes and self-reported pain levels were registered. The relation between autonomous parameters and self-reported pain parameters was examined using correlation analysis. Results: Some relationships of moderate strength between autonomic and pain measures were found. The change (post-exercise minus pre-exercise score) in pain severity was correlated (r = .580, P = .007) with the change in diastolic blood pressure in the healthy group. In the ME/CFS group, positive correlations between the changes in pain severity and low frequency (r = .552, P = .014), and between the changes in bodily pain and diastolic blood pressure (r = .472, P = .036), were seen. In addition, in ME/CHFS the change in headache severity was inversely correlated (r = -.480, P = .038) with the change in high frequency heart rate variability. Limitations: Based on the cross-sectional design of the study, no firm conclusions can be drawn on the causality of the relations. Conclusions: Reduced parasympathetic reactivation during recovery from exercise is associated with the dysfunctional exercise-induced analgesia in ME/CFS. Poor recovery of diastolic blood pressure in response to exercise, with blood pressure remaining elevated, is associated with reductions of pain following exercise in ME/CFS, suggesting a role for the arterial baroreceptors in explaining dysfunctional exercise-induced analgesia in ME/CFS patients. Key words: Aerobic exercise, aerobic power index, autonomic nervous system, exercise-induced analgesia, exercise-induced hypoalgesia, fibromyalgia, heart rate variability, stress-induced analgesia, pain Pain

Exercise-Induced Trace Mineral Element Concentration in Regional Versus Whole-Body Wash-Down Sweat

2011 ◽  
Vol 21 (3) ◽  
pp. 233-239 ◽  
Author(s):  
Lindsay B. Baker ◽  
John R. Stofan ◽  
Henry C. Lukaski ◽  
Craig A. Horswill
Keyword(s):  
Element Concentration ◽  
Sweat Rate ◽  
Sulfate Solution ◽  
Skin Surface ◽  
Cycle Ergometer ◽  
Whole Body ◽  
Air Chamber ◽  
Local Sweat Rate ◽  
Exercise Induced ◽  
Sweat Composition

Simultaneous whole-body wash-down (WBW) and regional skin surface sweat collections were completed to compare regional patch and WBW sweat calcium (Ca), magnesium (Mg), copper (Cu), manganese (Mn), iron (Fe), and zinc (Zn) concentrations. Athletes (4 men, 4 women) cycled in a plastic open-air chamber for 90 min in the heat. Before exercise, the subjects and cycle ergometer (covered in plastic) were washed with deionized water. After the onset of sweating, sterile patches were attached to the forearm, back, chest, forehead, and thigh and removed on saturation. After exercise, the subjects and cycle ergometer were washed with 5 L of 15-mM ammonium sulfate solution to collect all sweat minerals and determine the volume of unevaporated sweat. Control trials were performed to measure mineral contamination in regional and WBW methods. Because background contamination in the collection system was high for WBW Mn, Fe, and Zn, method comparisons were not made for these minerals. After correction for minimal background contamination, WBW sweat [Ca], [Mg], and [Cu] were 44.6 ± 20.0, 9.8 ± 4.8, and 0.125 ± 0.069 mg/L, respectively, and 5-site regional (weighted for local sweat rate and body surface area) sweat [Ca], [Mg], and [Cu] were 59.0 ± 15.9, 14.5 ± 4.8, and 0.166 ± 0.031 mg/L, respectively. Five-site regional [Ca], [Mg], and [Cu] overestimated WBW by 32%, 48%, and 33%, respectively. No individual regional patch site or 5-site regional was significantly correlated with WBW sweat [Ca] (r = –.21, p = .65), [Mg] (r = .49, p = .33), or [Cu] (r = .17, p = .74). In conclusion, regional sweat [Ca], [Mg], and [Cu] are not accurate surrogates for or significantly correlated with WBW sweat composition.

scholarly journals Taming the “sleeping giant”: the role of endothelin-1 in the regulation of skeletal muscle blood flow and arterial blood pressure during exercise

2013 ◽  
Vol 304 (1) ◽  
pp. H162-H169 ◽  
Author(s):  
Zachary Barrett-O'Keefe ◽  
Stephen J. Ives ◽  
Joel D. Trinity ◽  
Garrett Morgan ◽  
Matthew J. Rossman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiovascular Response ◽  
Muscle Blood Flow ◽  
Knee Extensor ◽  
Leg Blood Flow ◽  
Arterial Blood ◽  
Before And After ◽  
Exercise Induced ◽  
Response To Exercise

The cardiovascular response to exercise is governed by a combination of vasodilating and vasoconstricting influences that optimize exercising muscle perfusion while protecting mean arterial pressure (MAP). The degree to which endogenous endothelin (ET)-1, the body's most potent vasoconstrictor, participates in this response is unknown. Thus, in eight young (24 ± 2 yr), healthy volunteers, we examined leg blood flow, MAP, tissue oxygenation, heart rate, leg arterial-venous O2 difference, leg O2 consumption, pH, and net ET-1 and lactate release at rest and during knee extensor exercise (0, 5, 10, 15, 20, and 30 W) before and after an intra-arterial infusion of BQ-123 [ET subtype A (ETA) receptor antagonist]. At rest, BQ-123 did not evoke a change in leg blood flow or MAP. During exercise, net ET-1 release across the exercising leg increased approximately threefold. BQ-123 increased leg blood flow by ∼20% across all work rates (changes of 113 ± 76, 176 ± 83, 304 ± 108, 364 ± 130, 502 ± 117, and 570 ± 178 ml/min at 0, 5, 10, 15, 20, and 30 W, respectively) and attenuated the exercise-induced increase in MAP by ∼6%. The increase in leg blood flow was accompanied by a ∼9% increase in leg O2 consumption with an unchanged arterial-venous O2 difference and deoxyhemoglobin, suggesting a decline in intramuscular efficiency after ETA receptor blockade. Together, these findings identify a significant role of the ET-1 pathway in the cardiovascular response to exercise, implicating vasoconstriction via the ETA receptor as an important mechanism for both the restraint of blood flow in the exercising limb and maintenance of MAP in healthy, young adults.

Modulation of exercise tachycardia by vasopressin in the nucleus tractus solitarii

1997 ◽  
Vol 273 (4) ◽  
pp. R1271-R1282 ◽  
Author(s):  
Daniel L. Dufloth ◽  
Mariana Morris ◽  
Lisete C. Michelini
Keyword(s):  
Brain Stem ◽  
Acute Exercise ◽  
Treadmill Exercise ◽  
Nucleus Tractus Solitarii ◽  
Male Rats ◽  
Exercise Tachycardia ◽  
Pressor Responses ◽  
Exercise Induced ◽  
Response To Exercise

Our objective was to study the role of vasopressinergic synapses at the nucleus tractus solitarii (NTS) in the modulation of exercise-induced tachycardia. We evaluated the effect of NTS administration of vasopressin (AVP) or vasopressin antagonist (AVPant) on heart rate (HR) and mean arterial pressure (MAP) responses during dynamic exercise in male rats with chronic arterial and NTS cannulas. Sedentary (S) and trained (T) animals were tested at three or four exercise levels (from 0.4 up to 1.4 km/h) after NTS injection of AVP or AVPant 20–30 min before treadmill exercise. Plasma and regional brain levels of AVP were measured in separate groups of S and T rats at rest and immediately after acute exercise. When administered into the NTS, exogenous AVP (20 pmol) caused a small but significant decrease in baseline HR and potentiated the tachycardiac response to mild to moderate exercise intensities (on average, increases of 35–46 beats/min over control tachycardic response). The potentiation of exercise tachycardia by AVP was long lasting and more pronounced in T than in S rats. Even 2 days after NTS AVP injection, there was evidence for an alteration in the HR response to exercise. Mediation by V1 receptors was supported by the blunted tachycardiac response to exercise after administration of a V1 antagonist d(CH2)5Tyr MeAVP into the NTS in both T and S rats (average reductions of 23–34 and 13–19 beats/min below control tachycardia, respectively). No changes were observed in baseline MAP or the exercise-induced pressor responses. There were specific changes in brain stem AVP levels that were related to the exercise treatment. T rats showed a marked increase in dorsal and ventral brain stem AVP content after acute exercise. There were no changes in hypothalamus, median eminence, posterior pituitary, or plasma AVP. These data indicate that vasopressinergic synapses and V1 receptors in the NTS are involved in the potentiation of tachycardic response to exercise. The vasopressinergic mechanism operates in both S and T rats, but training alters the sensitization of V1receptors by AVP.

Role of nitric oxide in the airway response to exercise in healthy and asthmatic subjects

2001 ◽  
Vol 90 (2) ◽  
pp. 586-592 ◽  
Author(s):  
H. W. F. M. De Gouw ◽  
S. J. Marshall-Partridge ◽  
H. Van der Veen ◽  
J. G. Van den Aardweg ◽  
P. S. Hiemstra ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Healthy Subjects ◽  
Geometric Mean ◽  
No Synthase ◽  
Bicycle Ergometry ◽  
Significant Difference ◽  
Airway Response ◽  
Exercise Induced ◽  
Response To Exercise

A role of nitric oxide (NO) has been suggested in the airway response to exercise. However, it is unclear whether NO may act as a protective or a stimulatory factor. Therefore, we examined the role of NO in the airway response to exercise by using N-monomethyl-l-arginine (l-NMMA, an NO synthase inhibitor), l-arginine (the NO synthase substrate), or placebo as pretreatment to exercise challenge in 12 healthy nonsmoking, nonatopic subjects and 12 nonsmoking, atopic asthmatic patients in a double-blind, crossover study. Fifteen minutes after inhalation of l-NMMA (10 mg),l-arginine (375 mg), or placebo, standardized bicycle ergometry was performed for 6 min using dry air, while ventilation was kept constant. The forced expiratory volume in 1-s response was expressed as area under the time-response curve (AUC) over 30 min. In healthy subjects, there was no significant change in AUC betweenl-NMMA and placebo treatment [28.6 ± 17.0 and 1.3 ± 20.4 (SE) for placebo and l-NMMA, respectively, P = 0.2]. In the asthmatic group, l-NMMA and l-arginine induced significant changes in exhaled NO ( P < 0.01) but had no significant effect on AUC compared with placebo (geometric mean ± SE: −204.3 ± 1.5, −186.9 ± 1.4, and −318.1 ± 1.2% · h for placebo,l-NMMA, and l-arginine, respectively, P > 0.2). However, there was a borderline significant difference in AUC between l-NMMA and l-arginine treatment ( P = 0.052). We conclude that modulation of NO synthesis has no effect on the airway response to exercise in healthy subjects but that NO synthesis inhibition slightly attenuates exercise-induced bronchoconstriction compared with NO synthase substrate supplementation in asthma. These data suggest that the net effect of endogenous NO is not inhibitory during exercise-induced bronchoconstriction in asthma.

scholarly journals Individual characteristics associated with the magnitude of heat acclimation adaptations

2021 ◽  
Author(s):  
Puck Alkemade ◽  
Nicola Gerrett ◽  
Thijs M. H. Eijsvogels ◽  
Hein A. M. Daanen
Keyword(s):  
Body Mass ◽  
Sweat Rate ◽  
Heat Acclimation ◽  
Individual Characteristics ◽  
Whole Body ◽  
Stress Tests ◽  
Adaptive Responses ◽  
Body Dimensions ◽  
Low Responders ◽  
High Responders

Abstract Purpose The magnitude of heat acclimation (HA) adaptations varies largely among individuals, but it remains unclear what factors influence this variability. This study compared individual characteristics related to fitness status and body dimensions of low-, medium-, and high responders to HA. Methods Twenty-four participants (9 female, 15 male; maximum oxygen uptake [$$\dot{{V}}$$ V ˙ O2peak,kg] 52 ± 9 mL kg−1 min−1) completed 10 daily controlled-hyperthermia HA sessions. Adaptations were evaluated by heat stress tests (HST; 35 min cycling 1.5 W  kg−1; 33 °C, 65% relative humidity) pre- and post-HA. Low-, medium-, and high responder groups were determined based on tertiles (n = 8) of individual adaptations for resting rectal temperature (Tre), exercise-induced Tre rise (ΔTre), whole-body sweat rate (WBSR), and heart rate (HR). Results Body dimensions (p > 0.3) and $$\dot{{V}}$$ V ˙ O2peak,kg (p > 0.052) did not differentiate low-, medium-, and high responders for resting Tre or ΔTre. High WBSR responders had a larger body mass and lower body surface area-to-mass ratio than low responders (83.0 ± 9.3 vs 67.5 ± 7.3 kg; 249 ± 12 vs 274 ± 15 cm2 kg−1, respectively; p < 0.005). Conversely, high HR responders had a smaller body mass than low responders (69.2 ± 6.8 vs 83.4 ± 9.4 kg; p = 0.02). $$\dot{{V}}$$ V ˙ O2peak,kg did not differ among levels of responsiveness for WBSR and HR (p > 0.3). Conclusion Individual body dimensions influenced the magnitude of sudomotor and cardiovascular adaptive responses, but did not differentiate Tre adaptations to HA. The influence of $$\dot{{V}}$$ V ˙ O2peak,kg on the magnitude of adaptations was limited.

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