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Biomedical subjects

W Hollmann

Publications and source records attributed to W Hollmann.

At least 19 recordsLinked to original sources
PubMed2005

[The analgesic effect of exercise during labor].

OBJECTIVE: The aim of this study was to test for an analgesic effect of exercise during labor. PATIENTS AND METHODS: 50 women in labor exercised continuously with moderate intensity on a bicycle ergometer for 20 minutes. During rest and exercise, they rated their pain on a visual analogue scale (VAS). Venous blood was sampled for beta-endorphin, cortisol and catecholamines during rest and directly after exercise. RESULTS: 84 percent of the women perceived uterine contractions during exercise as less painful than at rest. 76.2 percent objectified the pain relief by a reduction in VAS units 1.67 +/- 1.01. Beta-endorphin levels were much higher after exercise than at rest (P < 0.001). During exercise the fetal heart rate rose slightly within the reference range. Uterine contractions were more frequent during and after exercise than at rest (P < 0.05). CONCLUSION: Exercising on a bicycle ergometer during labor seems to be safe for the fetus, a stimulus to uterine contractions, and a source of analgesia, possibly due to the release of beta-endorphin.

Analgesia↗
PubMed2003

Plasma prolactin concentration increases after hypercapnia acidosis.

Responses of plasma prolactin (PRL) concentration to alterations in carbon dioxide pressure ( pCO(2)) induced by 4 min of rebreathing out of a bag with 6 l gas initially containing a concentration of 93% O(2) and 7% CO(2) (hypercapnia hyperoxia; HH) and 4 min of voluntary hyperventilation (VH) at a respiratory rate of 28 - 32 per minute were investigated in ten males. During rebreathing in HH, an augmentation of pCO(2) from 40.2 +/- 2.1 to 63.7 +/- 5.4 mmHg and a decrease of pH from 7.4 +/- 0.02 to 7.32 +/- 0.04 were found in capillary blood (p < 0.01). Neither breathing frequency (BF) nor plasma PRL changed during this period. After two minutes of post-rebreathing, pCO(2) and pH returned to basal values. BF increased from 2 min of rebreathing (12.4 +/- 1.9 breath/min) until 11 min of recovery period (18.1 +/- 4.9 breath/min) (p < 0.01), while plasma PRL increased from end of rebreathing (11.59 +/- 1.49 ng/dl) to 11 min of recovery period (13.63 +/- 1.97 ng/dl) (p < 0.01). In VH, hyperventilation decreased pCO (2) from 39.91 +/- 2.62 to 21.73 +/- 2.59 mmHg (p < 0.01) and increased pH from 7.39 +/- 0.04 to 7.58 +/- 0.04 (p < 0.01) in capillary blood. After four minutes of recovery from hyperventilation, pH and pCO(2) were back to their basal values. No changes in plasma PRL were found throughout VH. This present pilot study's new finding is that plasma PRL increases after hypercapnia acidosis. This indicates that acidosis-induced central chemoreflex function increases phrenic nerve activity based on serotonergic modulation, leading to an augmentation of BF. As serotonin is also the main PRL-releasing factor, this might have had the collateral effect of causing PRL release and delayed appearance in the peripheral circulation.

Acidosis↗
PubMed2001

42 years ago--development of the concepts of ventilatory and lactate threshold.

At the Third Pan-American Congress of Sport Physicians in Chicago in 1959 we reported the physiological and clinical significance of the spiroergometric determination of the aerobic-anaerobic turnover point for judging the performance of sick and healthy persons for the first time. In this context a distinction was made between a ventilatory and a lactate-related (arterial blood) method of determination. We called the former method the 'point of optimal ventilatory efficiency (PoW)', and the latter one 'endurance performance limit'. In the 1950s the clinical spiroergometric examination of patients and athletes for the determination of the aerobic performance capacity was consistently based on the measurement of the maximal oxygen uptake. As entering the individual border area of the performance capacity of a patient with, for example, cardiopulmonary disease, can provoke accidents, we started to think about a criterion in connection with submaximal work in 1954. Determination of pyruvate and lactic acid in the venous blood did not prove to be a valid parameter. If the spiroergometric values were entered into a coordinate system the most striking similarities during increasing exercise would become evident between the curve of the minute ventilation and the curve of the arterial lactate. The findings were interpreted as follows: during lower grades of performance the oxygen demand in the working muscle cells was saturated, whereas in the case of increasing exercise intensity an additional anaerobic metabolism was necessary. We termed the maximal work load which was covered nearly completely aerobically as the PoW and designated heart frequency at this point as 'pulse endurance limit'. The determination of the parameter was derived in the coordinate system with a tangent to the curve of the minute ventilation as well as to the curve of the arterial lactate. The results of patients and athletes were first published in 1959.

Anaerobic Threshold↗
PubMed2000

[Brain, psyche and physical activity].

Modern technical and biochemical methods allow investigation of hemodynamic and metabolic responses of the human brain during muscular work. Following a general introduction to the topic results from selected studies on endogenous opioid peptides, pain sensitivity and psyche, regional cerebral blood flow and cerebral glucose metabolism, amino acid transport across the blood-brain barrier, impact of physical work on the serotonergic system, influence of oxygen partial pressure on neurotransmitters and hormones during exercise, role of the brain as performance limiting factor as well as age-related changes in cerebral blood flow and hypothalamo-pituitary-adrenal/-gonadal axis function will be presented.

Adaptation, Psychological↗
PubMed2000

Anabolic steroids impair the exercise-induced growth of the cardiac capillary bed.

BACKGROUND: Concomitant application of anabolic-androgenic steroids and physical exercise can induce cardiac hypertrophy. These experiments investigate the still unknown response of the cardiac myocytes and capillaries to the combined influence of various anabolic steroids and muscular exercise. METHODS: Female SPF-NMRI mice were divided into the following groups: a) sedentary control, b) exercise (treadmill running); c) sedentary receiving Dianabol; d) exercise + Dianabol; e) exercise + Oral-Turinabol. After 3 and 6 weeks the left ventricular papillary muscles were studied morphometrically. Evaluated variables: minimal myocyte diameter, number of capillaries around a single myocyte, capillary density and intercapillary distance. RESULTS: Only the anabolic steroids + exercise groups showed a mild myocyte hypertrophy. In contrast, only exercise alone caused a significant increase of the capillary density after both experimental periods; e.g. capillary density after 6 weeks (capillaries/mm2, mean values +/- standard deviation, p < 0.05): control (4,272 +/- 287), exercise (5411 +/- 755), dianabol (4,004 +/- 333), dianabol + exercise (4,076 +/- 403), oral-turinabol + exercise (4,053 +/- 306). Moreover, unlike all other regimens, only exercise alone shortened the intercapillary distance. Finally, exercise without drugs induced the greatest increase in the number of capillaries around a single myocyte. CONCLUSIONS: Anabolic steroids combined with exercise: 1) induce mild hypertrophy of the cardiac myocytes, 2) impair the cardiac microvascular adaptation to physical conditioning. The microvascular impairment may cause a detrimental alteration of the myocardial oxygen supply, especially during muscular exercise.

Anabolic Agents↗
PubMed2000

Testosterone-propionate impairs the response of the cardiac capillary bed to exercise.

OBJECTIVE: Experimental application of anabolic-androgenic steroids and exercise training induce cardiac hypertrophy. This study quantifies for the first time, on microscopical level, the adaptation of the cardiac capillaries and myocytes to the concomitant application of testosterone-propionate and exercise training. METHODS: Female SPF-NMRI mice were studied over 3 and 6 wk. Experimental groups: (i) sedentary control (C); (ii) exercise (treadmill running, E); (iii) testosterone-propionate (TP); and (iv) testosterone-propionate+exercise (TPE). Morphometric parameters: 1) papillary muscles: capillary density, intercapillary distance, number of capillaries around a myocyte, and minimal myocyte diameter; and 2) left ventricular wall: capillary density and intercapillary distance. RESULTS: Papillary muscle: A striking suppression of the exercise-induced improvement in capillary supply occurs in the testosterone-propionate+exercise groups over 3 and 6 wk. Exercise without drugs increases significantly (P < 0.05) the capillary density, shortens significantly (P < 0.05) the intercapillary distance, whereas it increases the number of capillaries around a myocyte. These alterations are not observed in the testosterone-propionate treated sedentary animals; e.g., capillary density after 6 wk (mean values +/- standard deviation, capillaries x mm(-2)): C: 4272 +/- 287, E: 5411 +/- 758, TP: 4221 +/- 364, and TPE: 3997 +/- 397. Moreover, only in the testosterone-propionate+exercise groups occurs a mild myocyte hypertrophy after both time periods: there is a trend toward hypertrophy (P < 0.1) in comparison with the C groups and a significant hypertrophy (P < 0.05) in comparison with the E groups. CONCLUSIONS: Testosterone-propionate profoundly inhibits the exercise-induced augmented capillarization, whereas (under training conditions) it leads to a mild myocyte hypertrophy. The microvascular impairment could trigger an imbalance between the myocardial oxygen supply and demand, especially during physical exercise.

Animals↗
PubMed1999

Effect of acute and chronic exercise on plasma amino acids and prolactin concentrations and on [3H]ketanserin binding to serotonin2A receptors on human platelets.

The neurotransmitter serotonin (5-hydroxytryptamine, 5-HT) has been shown to modulate various physiological and psychological functions such as fatigue. Altered regulation of the serotonergic system has been suggested to play a role in response to exercise stress. In the present study, the influence was investigated of acute endurance exercise and short-term increase in the amount of training on the concentrations of the 5-HT precursor tryptophan (TRP), of prolactin (PRL) and of branched-chain amino acids (BCAA) in the blood, as well as on the binding of [3H]ketanserin to the serotonin-2A (5-HT2A) receptors on platelets. Nine healthy endurance-trained men were tested the day before (I) and after (II) a 9-day training programme. Samples of venous blood were drawn after an overnight fast and following 5 h of cycling. Fasted and post-exercise plasma concentrations of free TRP, BCAA and free TRP:BCAA ratio did not differ between I and II. A significant decrease of plasma BCAA (P < 0.01) and significant augmentations of plasma free TRP, free TRP:BCAA ratio and PRL (P < 0.01) were found post-exercise. The increase in plasma PRL was smaller in II compared with I. Acute endurance exercise reduced the density of platelet 5-HT2A receptor [3H]ketanserin binding sites at I and II (P < 0.05). The basal density of the binding sites and the affinity of [3H]ketanserin for these binding sites were unaffected by an increase in the amount of training. The present results support the hypothesis that acute endurance exercise may increase 5-HT availability. This was reflected in the periphery by increased concentration of the 5-HT precursor free TRP, by increased plasma PRL concentration, and by a reduction of 5-HT2A receptors on platelets. It remains to be resolved whether these alterations in the periphery occur in parallel with an increase in the availability of 5-HT in the brain.

Adult↗
PubMed1999

Blood oxygen partial pressure affects plasma prolactin concentration in humans.

Responses of plasma prolactin (PRL) concentration to acute and repeated changes in blood oxygen partial pressure (PO2a) at rest were investigated in two studies (A; B), with special reference to possible effects mediated via serotonin (5-HT) synthesis. In A, nine male subjects inhaled for 105 min gas containing different oxygen fractions for 6 days. Gas concentrations consisted of 14% (A14), 21 % (A21), 40% (A40), 60% (A60) and 80% (A80) O2 mixed with N2 as well as 100% O2 (A100). Venous and capillary blood samples were drawn before and every 15 min during gas inhalation for analysis of plasma PRL and PO2a. In B, two groups of subjects (B I; B II) were exposed to 30 min day(-1) of gas inhalation over 14 consecutive days. Gas concentration consisted for B I of 14% O2/86% N2 and for B II of 100% O2. During pre- and post-examination a baseline blood sample was drawn, followed by a neuroendocrine test of serotonergic function using a partial 5-HT1A receptor agonist (60 mg of buspirone hydrochloride). In A, each increase of inhaled oxygen fraction also resulted in higher blood POb2a. In A14, A21 and A40, plasma PRL concentrations did not change from basal level. Increases in plasma PRL concentration were found in A60 after 30 min as well as in A80 and A100 after 15 min. A higher blood PO2a induced a higher plasma PRL secretion but also an earlier decline from peak plasma PRL value despite continued inhalation of the respective oxygen concentration. During post-examination in B, basal plasma PRL concentrations were increased in B I and decreased in B II. Plasma PRL response to stimulation challenge was not affected by treatments. Thus, chronic adaptations of basal plasma PRL concentrations to decreased/increased blood PO2a were not related to up/down-regulation, respectively, of central serotonergic receptor function.

Adult↗
PubMed1999

Neuroendocrine system and mental function in sedentary and endurance-trained elderly males.

Hypothalamic-pituitary-adrenal (HPAA) and -gonadal (HPGA) axis modification and cognitive impairments have been reported in elderly subjects and related to physical training status. The aim of this study was to investigate if HPAA and HPGA regulation are altered in elderly distance runners (RUN; n = 8; age: 68.9+/-4.2 yrs; training: 65+/-20 km/wk over the last 20 yrs; means +/- SD) or are affected in elderly sedentary individuals (SED; n = 11; age: 69.1+/-2.6 yrs) by an aerobic training over 20 weeks (3 times/week, 30-60 min walking), respectively. The protocol included assessment of the hormone profile in basal non-suppressed state as well as evaluation of hormonal responses to dexamethasone (DEX, 1.5 mg) induced adrenal suppression, to post-DEX combined corticotrophin releasing hormone (CRH; 0.7 microg/kg) and luteinizing hormone releasing hormone (LHRH, 0.7 microg/kg) stimulation and to exercise challenge (30 min cycle ergometry at 65% VO2max). Mental functions influenced by HPAA and HPGA activity were also assessed in RUN and SED before (SED-PRE) and after (SED-POST) the training program. Basal and post-DEX plasma concentrations of adrenocorticotropic hormone (ACTH), cortisol (CSL), luteinizing hormone (LH), follicle stimulating hormone (FSH) and testosterone (T) did not differ between RUN and SED-PRE. Basal plasma free T concentration was significantly lower in RUN (RUN: 10.23+/-2.41 pg x ml(-1) vs. SED-PRE: 16.6+/-5.59 pg x ml(-1)). During releasing hormone challenge test after DEX administration (DEX/RH), no differences were found between RUN and SED-PRE in plasma ACTH, LH, FSH and T response. During this stimulation test, plasma CSL was significantly higher in RUN than in SED-PRE after 90 min (RUN: 5.86+/-3.65 microg x dl(-1) vs. SED-PRE: 2.74+/-2.09 microg x dl(-1)). Differences in plasma CSL concentrations between groups were not induced by 30-min exercise challenge. Basal hormone profile was not altered by training in SED. During DEX/RH only plasma ACTH concentration was significantly higher in SED-POST compared to SED-PRE. Long and short-term memory function did not differ between RUN, SED-PRE and SED-POST. Our data suggest that following post-DEX CRH/LHRH challenge elderly endurance athletes reveal-in the absence of altered peak values-a pattern of prolonged secretion of glucocorticoids. However, the high interindividual variability of plasma ACTH and CSL concentrations shows that reduced corticotropic sensitivity to negative feedback is not always induced by chronic exercise stress. Lower plasma free T concentrations in RUN compared to SED are not caused by modified LH synthesis-secretion capacity.

Adrenocorticotropic Hormone↗
PubMed1998

Hypothalamic-pituitary-adrenal and -gonadal axis function after exercise in sedentary and endurance trained elderly males.

The aim of this study was to investigate hypothalamic-pituitary-adrenal (HPAA) and -gonadal (HPGA) axis responses to post-exercise (30 min at 65% VO2max) combined corticotrophin, luteinizing hormone and thyrotrophin releasing hormone challenge (0.7 microg/ kg body mass) in elderly distance runners (DR; age: 68.9+/-4.2 year) and sedentary individuals (SI; age: 69.1+/-2.6 year). Plasma cortisol, growth hormone, prolactin, luteinizing hormone, follicle stimulating hormone and total testosterone (T) concentrations pre- and post-exercise as well as in response to stimulation did not differ between DR and SI. Plasma adrenocorticotropic hormone returned to pre-exercise level in DR 60 min and in SI 90 min post-stimulation. Free T was lower in DR at all time points. Our results do not support the notion of altered releasing hormone-stimulable HPAA and HPGA synthesis-secretion capacity in elderly males after endurance training.

Adrenal Glands↗
PubMed1998

Influence of paroxetine, branched-chain amino acids and tyrosine on neuroendocrine system responses and fatigue in humans.

Effects of a serotonin re-uptake inhibitor and oral amino acid supplementations on physical and mental performance as well as neuroendocrine variables were investigated. 10 male subjects cycled in four trials until exhaustion. Participants ingested a placebo in trial (T) I, 20 mg paroxetine in T II, 21 g branched-chain amino acids (BCAA) in T III and 20g tyrosine (TYR) in T IV. Heart rate, capillary lactate, plasma insulin, free fatty acids, glucose, serotonin and beta-endorphin did not differ in trials. Plasma ammonia increments during exercise were higher in T III. Plasma BCAA in T III and plasma TYR in T IV were increased after 30 min of exercise according to the supplemented substances. In contrast to all other trials, the ratio of plasma free TRP/BCAA did not increase in T III. Plasma TYR/BCAA was augmented in T IV and decreased in T III after 30 min of exercise, whereas it did not change in T I and II. Plasma prolactin (PRL), growth hormone, cortisol, adrenocorticotropic hormone, norepinephrine and epinephrine increased during all trials. Plasma PRL increments were higher in T IV. Exhaustion was reached earlier in T II. No significant differences were found between other trials. Drive during psychometric testing subsequent to exercise was improved in T III and IV. The results indicate that fatigue during endurance exercise was increased by pharmacological augmentation of the brain serotonergic activity. However, a reduction of 5-HT synthesis via BCAA supplementation did not affect physical fatigue. TYR administration did not alter physical performance either although plasma PRL increments suggest that changes in the monoaminergic system were induced. Precaution is necessary before assuming an ergogenic value of amino acids.

Adult↗
PubMed1997

Effect of exercise intensity on free tryptophan to branched-chain amino acids ratio and plasma prolactin during endurance exercise.

The potential of exercise-induced changes in peripheral amino acids to alter blood prolactin levels through a serotonergic system modification was investigated in 8 male athletes. In two trials, subjects (N = 8) exercised on a cycle ergometer for 5 hr. The intensity of exercise corresponded to 55% VO2max (T55) or 75% VO2max (T75), respectively. In each trial, each subject received a 25-g energy bar (111 kcal) every 60 min, as well as 300 ml of a 6% carbohydrate solution (90 kcal) every 30 min of exercise duration. Plasma glucose and insulin declined (p < or = .05) in both trials during exercise. Ammonia was augmented (p < or = .05) above the baseline concentration after 120 min in both trials. During the last 2 hr of exercise, plasma free fatty acids were higher (p < or = .05) in T75 than in T55. During this time, the plasma free TRP/BCAA ratio was also augmented (p < or = .05) in T75, while no change was induced in T55. Plasma prolactin did not change in T55, while an increase (p < or = .05) was found in T75. The findings may further support the hypothesis that during endurance exercise changes in peripheral amino acid concentration may influence prolactin response via serotonergic system modifications.

Adult↗
PubMed1997

Ergospirometry and its history.

Ergospirometry is a diagnostic procedure to continuously measure respiration and gas metabolism during ergometer exercise. It enables judgement of function and performance capacity of the cardiopulmonary system and metabolism. Ergospirometry is made up of the 2 components spirometry and ergometry. The first attempts to measure human gas metabolism while performing quantified physical work can be traced back to the year 1790. The development of procedures to measure gas metabolism and respiration as well as the construction of ergometers in the nineteenth and twentieth centuries are described. Ergospirometry and routinely performed clinical performance diagnosis were introduced in 1929, but it was not until the 1950s when the first ergospirometry apparatus which met all scientific requirements was developed. The parameters used and the physiological and pathophysiological findings by ergospirometry are given in an historical frame. Numerous medical fields have profited from the technique of ergospirometry, for example: cardiology, pneumology, sports medicine, exercise physiology, biochemistry, clinical pharmacology, surgery, orthopaedics, paediatrics and gerontology, besides such global disciplines as preventive medicine, exercise therapy and rehabilitative medicine.

Ergometry↗
PubMed1996

Effect of O2 availability on neuroendocrine variables at rest and during exercise: O2 breathing increases plasma prolactin.

Neuroendrocrine and substrate responses were investigated in eight male athletes during inhalation of either 100% O2 (HE), 14% O2 (HO) or normoxio gas (NO) before, during and after 60 min of cycle ergometry at the same absolute work rate. Concentrations of prolactin (PRL), growth hormone (GH), testosterone (T), adrenocorticotropic hormone (ACTH), cortisol (COR), adrenalin (A), noradrenalin (NA), insulin (INS), ammonia (NH3), free fatty acids, serotonin (5-HT), total protein, branched-chain amino acids (BCAA) and free tryptophan (free TRP) were determined in venous blood and lactate concentration [LA-], partial pressure of oxygen (PO2), oxygen saturation (SO2), partial pressure of carbon dioxide and pH in capillary blood. The PO2 and SO2 were augmented in HE and decreased in HO (P < or = 0.01). In HO and NO no significant changes were found for any other parameter during 30 min of rest prior to exercise. In HE, PRL increased by about 400% during this time, while NA declined (P < or = 0.01). Heart rate (HR) and [LA-] were higher during exercise in HO (P < or = 0.01). In all trials, NH3, NA, A, T, GH and ACTH increased during exercise (P < or = 0.01), while BCAA and INS declined. In comparison to NO and HE, increases of NA, A, GH, COR and ACTH were higher in HO (P < or = 0.01). The PRL in NO and COR in NO and HE did not change significantly. In HE, after the initial increase at rest, PRL declined during exercise but remained higher than in HO. Higher values for NA, A, GH, COR and ACTH in HO were likely to have reflected an augmented relative exercise intensity. Our results showed that PRL but no other hormone increased during acute exposure to hyperoxia. This PRL release was independent of exercise stress and greater than PRL augmentation during hypoxia, which was related to a higher relative exercise intensity as indicated by [LA-] and HR. Responses of plasma NH3, BCAA, free TRP and 5-HT could not explain PRL augmentation induced by the increment in blood SO2 during hyperoxia.

Adrenocorticotropic Hormone↗
PubMed1996

Alterations in plasma free tryptophan and large neutral amino acids do not affect perceived exertion and prolactin during 90 min of treadmill exercise.

It has been hypothesized that fatigue and prolactin (PRL) changes during endurance exercise are influenced by serotonin synthesis, and in turn, release. Such a change is thought to occur through an increase in blood free tryptophan (TRP) and a concomitant decrease in those large neutral amino acids (LNAA) which compete with free TRP for entry into the brain. For further investigation, 10 healthy athletes were randomly subjected to three test units (TU), each consisting of a treadmill run for 90 min. The speed was adjusted to a blood lactate level of 2 mmol/l. During the first 30 min of exercise infusions of 500 ml saline (TU I), 500 ml saline with amino acids (TU II) or 500 ml saline with 30 U heparin/kg following an oral soy oil solution given 1 h before (TU III) were administered. Rate of perceived exertion (RPE), heart rate and running speed were recorded during exercise. Venous blood samples were taken after a 10 h fast, at rest, after 10, 50 and 90 min of exercise as well as 10 and 30 min post-exercise. PRL, insulin, glucose, ammonia, lactate, triglycerides (TG), free fatty acids (FFA) and amino acids were determined in each sample. No significant differences were found in RPE. PRL increased (p < 0.01) in all TU. TG and heparin administration resulted in an increase (p <0.01) in FFA, which correlated (p < 0.01) with free TRP and the ratio of free TRP/TRP. Artificial increase in free TRP in TU III did not affect plasma PRL level. The amino acid infusion in TU II induced an increase in LNAA but had no significant effect on PRL. PRL and ammonia peaked at the end of exercise. We conclude that neither exercise-induced PRL secretion nor RPE are affected by changes in circulating free TRP and LNAA under the present conditions.

Adult↗
PubMed1996

Increased prolactin response to hyperoxia at rest and during endurance exercise.

Neuroendocrine responses were investigated in 8 male athletes before, during and after 60 min of bicycle ergometry at an intensity corresponding to 1.5 mmol/l blood lactate in an incremental bicycle test. Hyperoxic gas (HE: 100% O2), hypoxic gas (HO: 14% O2, 86% N2) or normoxic gas (NO) were inhaled continuously during exercise as well as for 30 min before and after. During exercise, prolactin (PRL) increased in HO while it did not change significantly in NO. Only HE induced a PRL increase (400%) during 30 min of rest before exercise. PRL decreased in HE during exercise but remained higher than in HO. Growth hormone (GH), ACTH and norepinephrine (NE) did not increase in a similar pattern during HE. In comparison to NO and HE, increase of NE, GH and ACTH was significantly higher in HO, NE declined significantly in HE before exercise. Our results demonstrate that only PRL is affected by acute exposure to hyperoxia. Changes in inhibition of the dopaminergic system might contribute to augmentation of PRL before exercise. The exact underlying mechanisms are yet unknown.

Adult↗
PubMed1995

Amino acid metabolism in tennis and its possible influence on the neuroendocrine system.

To investigate amino acid metabolism during endurance exercise as well as its influence on plasma prolactin (PRL) we subjected eight nationally ranked tennis players (mean(s.d.) age 25.6(2.8) years, mean(s.d.) weight 83.9(5.7) kg, mean(s.d.) height 184.4(4.6) cm) to 4h of continuous tournament tennis. Venous and capillary blood samples were taken before and after the exercise. Amino acids were measured by HPLC-fluorescence detection as o-phthalaldehyde derivatives; nonesterified fatty acids (NEFA), ammonia, total protein, glucose insulin and PRL by enzymatic methods. Exercise caused a decline of branched-chain amino acids (BCAA) by 28(14)%. Elevation of NEFA resulted in a significant mean(s.d.) increase of free tryptophan (TRP) (9.7(2.6) [pmol/microliter] vs 17.8(6.4) [pmol/microliter]. The mean(s.d.) ratio of free TRP:BCAA increased by 165%(90) which favours entry of free TRP into the brain. However, PRL did not change significantly. We conclude that during long-lasting interval sports BCAA contribute as energy substrates. Alterations in competition of amino acids at the blood-brain barrier favour entry of free TRP into the brain. PRL changes cannot be explained by the increase in plasma level of free TRP or the ratio of free TRP:BCAA.

Adult↗