Echocardiographic and biochemical analysis of cardiac function and injury among female amateur runners post-marathon.

BACKGROUND: Numerous studies with male amateur runners have determined negative changes in their cardiac function/of their myocard following long endurance loads. This study aims to examine such potential changes in women, specifically, after running a marathon. METHODS: A total of 18 female amateur runners (39.5 ± 10.5 years) were examined before (T1), immediately after (T2) and 24 h post-marathon (T3). An echocardiography was performed using Tissue Doppler (TD) imaging. In addition, the concentration of cardiac troponin T (cTnT) and the activity of the myocardial muscle creatine kinase (CK-MB) were determined at T1 and T2. RESULTS: The echocardiographic parameters revealed impairment of the diastolic function, without, however, documenting a diastolic dysfunction (in accordance with the classification of Nagueh (J Am Soc Echocardiogr, 22:107-33, 2009)). The ratio of blood flow velocity through the mitral valve during early versus late diastole (MV E/A ratio), for example, decreased. The values measured at T3 were similar to those measured at T1. The ratio of early transmitral diastolic filling velocity and of the transmitral diastolic filling velocity by TD imaging (MV E/E') did not indicate any change from T1 to T2, but a significant increase at T3 (in comparison with T1). The systolic function (measured by the left ventricular ejection fraction) did not change significantly. The cTnT concentration and CK-MB activity were significantly higher in T2 than in T1. CONCLUSION: The data collected does not provide any solid evidence of pathological changes in the cardiac function of female amateur runners post-marathon, although the lab values indicate a strongly increased myocardial stimulation.

The spirografic oxygen deficit: its role in cardiopulmonary exercise testing.

The increase in oxygen uptake > 100 ml · min-1 during steady state exercise when elevating the inspired fractional air content (FinO2) from 0.21-1.00 defines the "spirografic oxygen deficit" (SOD). The purpose of this study was 2-fold: 1) determine the SOD at different exercise intensities in healthy participants and 2) investigate if a correlation exists among key variables of cardiopulmonary exercise testing. 12 men (24±2 yrs; 183±4 cm; 83.5±5.3 kg) performed cycle tests to determine maximal power output (Pmax), the power output at the first (PVT1) and the second ventilatory threshold (PVT2), at 4 mmol · l-1 blood lactate (P4) and lactate threshold (PLT). When cycling at 30, 40, 50, 60, 70 and 80% Pmax, the FinO2 was increased from 0.21-1.00 after 5 min to assess the power output at the SOD and at which blood lactate increased > 1 mmol∙L-1 (PLLAC). The SOD occurred at 70% Pmax accompanied by increased blood lactate concentration (p<0.01). The PSOD correlated with PLACC (p=0.05; r=0.61), but not with PVT1, PVT2, P4, or PLT (best p=0.29; highest r=0.39). In conclusion, the SOD may represent a non-invasive tool for evaluating submaximal endurance performance, especially when evaluating the peripheral contribution to performance.

Influences of exercise and training on the circulating concentration of prolactin in humans.

Physical activity has an impact on several endocrine functions. During exercise, certain endocrine adjustments are required to maintain the homeostasis. It is well known that, depending on the intensity and duration, exercise stimulates the release of the hormone prolactin (PRL). After the cessation of acute exercise, this effect persist and continues during the recovery period. Chronic exercise can affect the PRL basal concentration and/or the PRL response to acute exercise. The main functions of PRL are associated with the maintenance of homeostasis and processes of reproduction. A role for PRL also has been recognised as an important regulator of cellular proliferation. The present review examines the exercise-induced acute or adaptive responses of PRL secretion. It is also hypothesised that increased concentrations of PRL during exercise could play an important role for neuroplasticity as a result of involvement of the hormone in the neurogenesis in subventricular zone of the adult brain.

pH buffering does not influence BDNF responses to exercise.

The influence of acidosis on brain-derived neurotrophic factor (BDNF) was examined by buffering pH changes during 10 min of continuous low intensity (LIE) and following high intensity cycling exercise to exhaustion (HIE). 11 athletes participated in 2 trials separated by 1 week. Individuals received either a placebo infusion (isotonic saline) or an isotonic sodium bicarbonate infusion before and during exercise. Blood samples were drawn at rest, after LIE and after HIE, as well as 3, 6, 10 and 15 min post exercise. During placebo trial, HIE induced a profound decrease (p<0.01) of capillary blood bicarbonate concentration (HCO3-), pH, base excess (BE) and pCO2. Higher (p<0.01) HCO3-, pH and BE were found during bicarbonate infusion and post exercise in comparison to the placebo trial. Exercise induced an identical increase of blood lactate concentration in both trials. Serum BDNF concentration was increased (p<0.01) at the end of HIE and remained elevated until 3 min post exercise in both trials. The present study suggests that during HIE lactate might have an acidosis-independed impact on BDNF secretion because buffering of blood gases, that attenuate the fall of pH but not the accumulation of lactic acid, failed to alter the exercise-induced increase of BDNF.

Effect of resistance exercise on serum levels of growth factors in humans.

Studies have shown that, depending on intensity, endurance exercise increases neurotrophins and thereby induces neuroplasticity. However, data on the effect of acute resistance exercise at different intensities on neurotrophins is not yet available. Thus, we conducted 2 trials to determine the serum concentrations of brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF), and insulin-like growth factor (IGF-1) before and after a low or high intensity resistance exercise in 11 healthy humans. Exercise load was related to 3 repetitions of maximal effort isokinetic work involving knee extension under alternating concentric and eccentric conditions for muscle work at a velocity of 60°s-1 registered during a familiarization session. The torque angle diagrams from these 3 repetitions were averaged and displayed as target curves in the test sessions, the intensity of resistance exercise was set at 40% (trial: R1) or 110% (trial: R2) of the averaged individual maximal effort curve, respectively. After resistance exercise, serum IGF-1 was increased significantly (p<0.01) by 28% in R1 and 16% in R2 compared to pre-exercise levels. Resistance exercise did not increase serum VEGF at any time point. Serum BDNF increased during exercise compared to post-exercise, but did not achieve significant difference from pre-exercise values. The present study shows that either low or high resistance exercise increases levels of IGF-1, but not of BDNF or VEGF. This finding is of importance for health promotion by means of resistance exercise because circulating serum IGF-1 has been demonstrated to mediate positive effects of exercise on brain functions.

Effects of strength and endurance training on brain-derived neurotrophic factor and insulin-like growth factor 1 in humans.

Blood neurotrophins like insulin-like growth factor (IGF-1) and brain-derived neurotrophic factor (BDNF) are discussed to mediate health benefits of physical activity in humans. The aim of the study was to analyze the training effects of moderate endurance training (Em) and strength training with high loads (Sh) on blood plasma concentrations of IGF-1 and BDNF in humans. Venous blood samples were obtained from 27 healthy students, randomly assigned to an Em, Sh, and a control group, before and after a 12-week training intervention. Sh resulted in an increase in isometric (14.5%) and dynamic (8.3%) strength of the knee extensor muscles in the Sh group and Em led to a significant increase in the endurance performance in the Em group (p<0.05). IGF-1 basal plasma concentrations decreased (p<0.05) after the intervention in all groups. There were no significant changes for BDNF. Despite specific functional adaptations induced by Em and Sh there are no correspondingly different adaptations in the basal blood concentrations of the neurotrophins IGF-1 and BDNF. Additionally, exercise per se does not result in changes in basal plasma concentrations of BDNF, suggesting that the mode of the exercise programme is a decisive factor.

Impact of exercise on neuroplasticity-related proteins in spinal cord injured humans.

The present study investigated the effects of exercise on the serum concentrations of brain-derived neurotrophic factor (BDNF), insulin-like growth factor 1 (IGF-1), prolactin (PRL) and cortisol (COR) in 11 chronically spinal cord-injured athletes. In these subjects BDNF concentration at rest was sixfold higher compared with the concentrations reported earlier in able-bodied persons, while IGF-1, PRL and COR were within normal range. Ten minutes of moderate intensity handbiking (54% of the maximal heart rate) during a warm-up period (W) induced an increase (P<0.05) of BDNF of approximately 1.5-fold from basal level at rest, while a decrease to basal level was found after an immediately succeeding handbiking time trial (89% of the maximal heart rate) over the marathon distance of 42 km (M). An increase (P<0.01) of serum IGF-1 was found after W and this levels remained elevated (P<0.01) until the end of M. W had no significant effects on the serum PRL and COR, however, M induced an increase (P<0.01) of both hormones. This is the first study showing elevated BDNF concentrations at rest in spinal cord-injured athletes. Furthermore, short moderate intensity handbiking but not immediately following long lasting high intensity handbiking further increases serum BDNF concentrations. IGF-1 response to exercise differs to BDNF response as this neuroplasticity-related protein remains elevated during the long lasting physical demand with high intensity. The augmented PRL concentration suggests that a possible mechanism by which exercise promotes neuroplasticity might be the activation of neural serotonergic pathways as 5-HT is the main PRL releasing factor. Elevated COR concentrations after M are unlikely to be deleterious to neuroplasticity as COR concentrations remain within the physiological range. The present study suggests that exercise might be beneficial to enhance neuroprotection and neuroplasticity, thereby improving recovery after spinal cord injury.

Intense exercise increases adenosine concentrations in rat brain: implications for a homeostatic sleep drive.

Intense exercise and sleep deprivation affect the amount of homeostatically regulated slow wave sleep in the subsequent sleep period. Since brain energy metabolism plays a decisive role in the regulation of behavioral states, we determined the concentrations of nucleotides and nucleosides: phosphocreatine, creatine, ATP, ADP, AMP, adenosine, and inosine after moderate and exhaustive treadmill exercise as well as 3 and 5 h of sleep deprivation and sleep in the rat brain using the freeze-clamp technique. High intensity exercise resulted in a significant increase of the sleep-promoting substance adenosine. In contrast, following sleep, inosine and adenosine levels declined considerably, with an accompanied increase of ADP after 3 h and ATP after 5 h. Following 3 h and 5 h sleep deprivation, ADP and ATP did not differ significantly, whereas inosine increased during the 3 and 5-h period. The concentrations of AMP, creatine and phosphocreatine remained unchanged between experimental conditions. The present results are in agreement with findings from other authors and suggest that depletion of cerebral energy stores and accumulation of the sleep promoting substance adenosine after high intensity exercise may play a key role in homeostatic sleep regulation, and that sleep may play an essential role in replenishment of high-energy compounds.

[The analgesic effect of exercise during labor]. / Der analgetische Effekt von körperlicher Aktivität auf Wehen unter der Geburt.

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.

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.

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.

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.

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.

[Brain, psyche and physical activity]. / Gehirn, Psyche und körperliche Aktivität.

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.

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.

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.

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.

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.

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.