Brain-derived neurotrophic factor concentrations in tetraplegic athletes.

STUDY DESIGN: A prospective cohort with acute tetraplegia. OBJECTIVE: The purpose of this study was to investigate acute changes in serum brain-derived neurotrophic factor (BDNF) concentrations in tetraplegic spinal cord-injured (SCI) athletes during a typical training session of wheelchair rugby. SETTINGS: German Sport University Cologne, Cologne, Germany. METHODS: Eleven male SCI (AIS A and B) athletes completed a 90-min training session: The warm-up period included continuous pushing, submaximal increasing sprints and agility drills. The main training section comprised ball handling, passing drills, scrimmage activity and tactical practice. At the end of the training session, the athletes did moderate continuous pushing as a short cool-down. Venous blood samples were taken at rest before exercise, after the warm-up period and immediately following the first part of the main training section. Serum was pipetted after 30 min of blood sample resting and a subsequent centrifugation. BDNF concentrations were measured using an enzyme immunoassay ELISA kit. RESULTS: Heart rate (P < 0.01) and lactate (P = 0.04 and P < 0.01) concentration differed significantly in warm-up and main training part in comparison with basal values at rest. At rest, BDNF concentrations were 33.2 ± 21.6 ng ml(-1), after warm up 31.9 ± 18.9 ng ml(-1) and after the training session 29.9 ± 11 ng ml(-1), without significant differences (P > 0.05). CONCLUSIONS: A typical wheelchair rugby training session does not affect basal serum BDNF concentration in elite SCI athletes. In comparison with concentrations previously reported in healthy subjects, the current values at rest were slightly higher or rather at the upper limit.

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.

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.

Executive control processes are associated with individual fitness outcomes following regular exercise training: blood lactate profile curves and neuroimaging findings.

Cardiovascular training has been associated with neuroimaging correlates of executive control functions (ECF) in seniors and children/adolescents, while complementary studies in middle-aged populations are lacking. Ascribing a prominent role to cardiorespiratory fitness improvements, most studies concentrated on training-induced gains in maximal oxygen uptake (VO2max), although other fitness indices may provide complementary information. Here, we investigated the impact of long-term sub-maximal exercise training on interference control, considering individual training-induced shifts in blood lactate profile curves (BLC) and VO2max. Twenty-three middle-aged sedentary males (M = 49 years) underwent a six-month exercise program (intervention group, IG). Additionally, 14 individuals without exercise training were recruited (control group, CG, M = 52 years). Interference control was assessed before and after the intervention, using a functional magnetic resonance imaging (fMRI) flanker paradigm. Task performance and brain activations showed no significant group-by-time interactions. However, regression analyses in the IG revealed significant associations between individual fitness gains and brain activation changes in frontal regions, which were not evident for VO2max, but for BLC. In conclusion, training-induced plasticity of ECF-related brain activity can be observed in late middle adulthood, but depends on individual fitness gains. For moderate training intensities, BLC shifts may provide sensitive markers for training-induced adaptations linked to ECF-related brain function.

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.

Energy expenditure in ball games for wheelchair users.

PURPOSE: Wheelchair sports have become popular in Germany. This is important because of the difficulty experienced by wheelchair-dependent people in maintaining cardiovascular health and fitness by daily activities. Increasing energy expenditure (EE; kcal h(-1)) is one of the most effective ways of decreasing risk of cardiovascular disease. The purpose of this study was to evaluate the EE of individuals with spinal cord injury in ball games for wheelchair-dependent persons. METHODS: Fourteen tennis players (WT), 10 basketball players (WB) and 12 rugby players (WR) completed a basal metabolism evaluation and a training test to measure respiratory parameters. RESULTS: In the basal metabolism test EE in WT was 66.8+/-12.8 kcal h(-1), in WB 62.7+/-15.0 kcal h(-1) and in WR 63.5+/-12.9 kcal h(-1). During training EE in WT was 325.8+/-73.0 kcal h(-1), in WB 374.8+/-127.1 kcal h(-1) and in WR 248.5+/-69.4 kcal h(-1). The average EE of the whole group was: 316.4+/-89.6 kcal h(-1) with a corresponding heart rate of 118.5+/-23.1 b.p.m. and a lactate concentration of 2.09+/-0.7 mmol l(-1). Statistical analysis showed significantly lower values of EE, heart rate and oxygen uptake for the WR group in comparison to the other groups. CONCLUSION: The results indicate that the additional leisure time EE of persons participating in WB and WT is sufficient to maintain fitness. This level of EE is comparable to the recommendations of the ACSM for able-bodied persons, and therefore might be sufficient to prevent the development of cardiovascular diseases.

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.