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PURPOSE:: To examine the influence of a selective noradrenaline reuptake inhibitor (SNRI) on the exercise-induced increase in circulating brain-derived neurotrophic factor (BDNF). METHODS:: In a double-blind, placebo-controlled, crossover design, 11 young, healthy male subjects were treated with either placebo or reboxetine. On each occasion, they performed a 60-min cycling exercise at 55% of their maximal power output (Wmax) followed by a time trial (TT) at 75% of Wmax. HR and ratings of perceived exertion were measured. Blood samples were taken at four time points. RESULTS:: An increase in serum BDNF was found after exercise without any influence of drug administration on BDNF levels. Serum BDNF returned to resting levels after 15 min of recovery. Time trial (TT) performance was significantly worse after reboxetine intake. Serum cortisol increased in both trials during and after exercise and was significantly higher in the reboxetine trial. Also, HR was increased with reboxetine intake, probably because of the sympathomimetic effect of SNRI. Midterm memory was significantly impaired after the exercise protocol without difference between reboxetine and placebo trial. CONCLUSIONS:: The administration of an SNRI has no effect on the exercise-induced increase in BDNF. However, effects were seen on serum cortisol, HR, and memory. Future research should focus on the effect of regular exercise training in combination with several reuptake inhibitors in both healthy and depressed subjects on BDNF and memory. [ABSTRACT FROM AUTHOR]

Hippocampal brain-derived neurotrophic factor (BDNF) protein is increased with exercise in rats. Monoamines seem to play a role in the regulation of BDNF, and monoamine neurotransmission is known to increase with exercise. The purpose of this study was to examine the influence of acute exercise on monoaminergic neurotransmission and BDNF protein concentrations. Hippocampal microdialysis was performed in rats that were subjected to 60 min of treadmill running at 20 m/min or rest. Two hours postexercise, the rats were killed, and the hippocampus was dissected. In experiments without microdialysis, hippocampus and serum samples were collected immediately after exercise. Exercise induced a twofold increase in hippocampal dopamine release. Noradrenaline and serotonin release were not affected. Hippocampal BDNF levels were not influenced, whether they were measured immediately or 2 h after the exercise protocol. Serum BDNF levels did not change either, but serum BDNF was negatively correlated to peripheral corticosterone concentrations, indicating a possible inhibitory reaction to the stress of running. Sixty minutes of exercise enhances dopamine release in the hippocampus of the rat in vivo. However, this increase is not associated with changes in BDNF protein levels immediately nor 2 h after the acute exercise bout. An increased corticosterone level might be the contributing factor for the absence of changes in BDNF.

Purpose: Serum brain-derived neurotrophic factor (BDNF) is known to increase with exercise. This increase is believed to originate from the brain and it is suggested that monoamines are involved in BDNF regulation. Heat exposure could influence the supposed BDNF output from the brain. Therefore, we hypothesized that administration of a selective serotonin reuptake inhibitor could influence the exercise-induced increase in BDNF, and that peripheral BDNF will be higher when exercise is performed in the heat., Methods: Eleven well-trained males performed 4 experimental trials on a cycle ergometer with citalopram or placebo treatment (20 mg in 12 h) in an environmental temperature of 18°C or 30°C. Blood samples (BDNF and cortisol) were taken at 4 time points: at rest, after 60 min at 55% W(max), after a time trial of 30 min at 75% W(max) and following 15 min of recovery. Heart rate and core temperature were measured., Results: Performance on the time trial was 20% worse in 30°C compared to 18°C (p<0.01), without influence of citalopram. Serum BDNF was found to be lower under citalopram treatment, while basal cortisol levels were increased (p<0.05). Exercise triggered an increase in both BDNF and cortisol (p<0.001). BDNF followed the same pattern as core temperature during exercise, with higher levels of both variables in 30°C. Cortisol was also increased in 30°C compared to temperate conditions (p<0.01)., Conclusion: Exercise caused a rise in serum BDNF and cortisol. This increase was enhanced with exercise in the heat. Since permeability of the blood-brain barrier increases with exercise in the heat, the hypothesis was raised that this causes a higher cerebral output of BDNF. Serotonergic stimulation did not increase peripheral BDNF, which was even lower with citalopram administration. Future research should focus on mechanisms behind BDNF increase with exercise., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Brain-derived neurotrophic factor (BDNF) is one of the neurotrophins promoting cognitive function and contributing to neurogenesis and neuroprotection. Available evidence suggests that exercise influences serum BDNF concentrations, but that the effect is transient. The purpose of this study is to determine whether a period of aerobic training, followed by a period of detraining, can influence basal serum BDNF levels in humans. Sixteen young, sedentary subjects were assigned to an experimental group (n=9) and a control group (n=7). The experimental group performed an aerobic training program during 8 weeks, followed by 8 weeks of detraining, during which subjects returned to their previous, sedentary activity level. The control group remained physically inactive during 16 weeks. In both groups, performance on short-term (Digit Span test) and mid-term memory (Recall of Images) was assessed. Aerobic training significantly increased the VO(2) peak in the experimental group, and these values returned to baseline after 8 weeks of detraining. Basal serum BDNF was not influenced by 8 weeks of aerobic training and detraining did not seem to have an effect on basal peripheral BDNF concentrations. Both training and detraining did not clearly influence short-term memory performance on the Digit Span test and no differences were present between the experimental and control group on the mid-term memory test. Future studies should focus on patient groups and elderly to further investigate the effect of training and detraining on neurotrophic factors and cognitive function, and on the effects of training and detraining on the BDNF response to acute exercise., (Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.)

The purpose of the study was to examine the acute effect of a strength training session on brain-derived neurotrophic factor and insulin-like growth factor 1. Furthermore, the influence of a 10-week strength training program on brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1 (IGF-1) resting levels and memory performance was studied. Fifteen untrained subjects followed a strength training program for 10 weeks. Eight control subjects remained physically inactive. To study the influence of an acute strength training session, blood samples were taken before and after the sixth and 30th sessions. Training effects were evaluated by taking blood samples at rest before and following the training program. Short- and mid-term memories were assessed using the digit span and a recall of images test. BDNF, IGF-1 and its binding protein (IGFBP-3) were measured in serum samples. Data were analyzed (p < 0.05) using a mixed design ANOVA model, Duncan's multiple range post hoc tests, and Pearson's correlation. A single strength training session did not influence BDNF and IGF-1 concentrations. No effect of the strength training period on BDNF, IGF-1, and IGFBP-3 was found. No correlation was found between peripheral BDNF and IGF-1. Short-term memory improved in both the experimental and control groups, but no difference between groups was present. Mid-term memory did not improve following the 10 weeks of training. A period of strength training in sedentary subjects does not significantly change the growth factors or memory function compared to a control group. Also, BDNF and IGF-1 are not acutely influenced by a training session. Further research should focus on the beneficial role of physical exercise in neurodegenerative diseases.

Exercise is known to induce a cascade of molecular and cellular processes that support brain plasticity. Brain-derived neurotrophic factor (BDNF) is an essential neurotrophin that is also intimately connected with central and peripheral molecular processes of energy metabolism and homeostasis, and could play a crucial role in these induced mechanisms. This review provides an overview of the current knowledge on the effects of acute exercise and/or training on BDNF in healthy subjects and in persons with a chronic disease or disability. A systematic and critical literature search was conducted. Articles were considered for inclusion in the review if they were human studies, assessed peripheral (serum and/or plasma) BDNF and evaluated an acute exercise or training intervention. Nine RCTs, one randomized trial, five non-randomized controlled trials, five non-randomized non-controlled trials and four retrospective observational studies were analysed. Sixty-nine percent of the studies in healthy subjects and 86% of the studies in persons with a chronic disease or disability, showed a 'mostly transient' increase in serum or plasma BDNF concentration following an acute aerobic exercise. The two studies regarding a single acute strength exercise session could not show a significant influence on basal BDNF concentration. In studies regarding the effects of strength or aerobic training on BDNF, a difference should be made between effects on basal BDNF concentration and training-induced effects on the BDNF response following an acute exercise. Only three out of ten studies on aerobic or strength training (i.e. 30%) found a training-induced increase in basal BDNF concentration. Two out of six studies (i.e. 33%) reported a significantly higher BDNF response to acute exercise following an aerobic or strength training programme (i.e. compared with the BDNF response to an acute exercise at baseline). A few studies of low quality (i.e. retrospective observational studies) show that untrained or moderately trained healthy subjects have higher basal BDNF concentrations than highly trained subjects. Yet, strong evidence still has to come from good methodological studies. Available results suggest that acute aerobic, but not strength exercise increases basal peripheral BDNF concentrations, although the effect is transient. From a few studies we learn that circulating BDNF originates both from central and peripheral sources. We can only speculate which central regions and peripheral sources in particular circulating BDNF originates from, where it is transported to and to what purpose it is used and/or stored at its final destination. No study could show a long-lasting BDNF response to acute exercise or training (i.e. permanently increased basal peripheral BDNF concentration) in healthy subjects or persons with a chronic disease or disability. It seems that exercise and/or training temporarily elevate basal BDNF and possibly upregulate cellular processing of BDNF (i.e. synthesis, release, absorption and degradation). From that point of view, exercise and/or training would result in a higher BDNF synthesis following an acute exercise bout (i.e. compared with untrained subjects). Subsequently, more BDNF could be released into the blood circulation which may, in turn, be absorbed more efficiently by central and/or peripheral tissues where it could induce a cascade of neurotrophic and neuroprotective effects.

The original central fatigue hypothesis suggested that fatigue during prolonged exercise might be due to higher 5-HT activity. Therefore, we examined the effects of acute administration of a selective 5-HT reuptake inhibitor (SSRI) on performance and thermoregulation. Eleven healthy trained male cyclists completed four experimental trials (two in 18 degrees C, two in 30 degrees C) in a double-blind randomised crossover design. Subjects ingested either a placebo (PLA: lactose 2 x 10 mg) or citalopram (CITAL 2 x 10 mg) on the evening before and the morning of the trial. Subjects cycled for 60 min at 55% W(max), immediately followed by a time trial (TT) to measure performance. The significance level was set at P < 0.05. Acute SSRI did not significantly change performance on the TT (18 degrees C P = 0.518; 30 degrees C P = 0.112). During recovery at 30 degrees C, core temperature was significantly lower in the CITAL trial (P < 0.012). At 30 degrees C heart rate was significantly lower after exercise in CITAL (P = 0.013). CITAL significantly increased cortisol concentrations at rest (P = 0.016), after the TT (P = 0.006) and after 15-min recovery (P = 0.041) at 30 degrees C. 5-HT reuptake inhibition did not cause significant reductions in performance. Core temperature was significantly lower only after the time trial in heat after CITAL administration. The present work failed to prove whether or not 5-HT has an exclusive role in the onset of centrally mediated fatigue during prolonged exercise in both normal and high ambient temperature.

Combined inhibition of dopamine (DA)/norepinephrine (NE) reuptake improves exercise performance and increases core temperature in the heat. A recent study demonstrated that this effect may primarily be related to increased DA activity. NE reuptake inhibition (NERI), however, has received little attention in humans, certainly in the heat, where central fatigue appears to be a main factor influencing performance. Therefore the present study examines the effect of NERI (reboxetine) on exercise capacity, thermoregulation, and hormonal response in normal and high temperature. Nine healthy well-trained male cyclists participated in this study. Subjects ingested either placebo (Pla; 2 x 8 mg) or reboxetine (Rebox; 2 x 8 mg). Subjects exercised in temperate (18 degrees C) or warm (30 degrees C) conditions and cycled for 60 min at 55% W(max) immediately followed by a time trial (TT; Pla18/Rebox18; Pla30/Rebox30) to measure exercise performance. Acute NERI decreased power output and consequently exercise performance in temperate (P = 0.018) and warm (P = 0.007) conditions. Resting heart rate was significantly elevated by NERI (18 degrees C: P = 0.02; 30 degrees C: P = 0.018). In Rebox18, heart rate was significantly higher than in the Pla18, while in the heat no effect of the drug treatment was reported during exercise. In Rebox30, all hormone concentrations increased during exercise, except for growth hormone (GH), which was significantly lower during exercise. In Rebox18, prolactin (PRL) concentrations were significantly elevated; GH was significantly higher at rest, but significantly lower during exercise. In conclusion, manipulation of the NE system decreases performance and modifies hormone concentrations, thereby indicating a central NE effect of the drug. These findings confirm results from previous studies that predominantly increased DA activity is important in improving performance.