Exercise-Induced Elevated BDNF Level Does Not Prevent Cognitive Impairment Due to Acute Exposure to Moderate Hypoxia in Well-Trained Athletes.

Exposure to acute hypoxia causes a detrimental effect on the brain which is also manifested by a decrease in the ability to perform psychomotor tasks. Conversely, brain-derived neurotrophic factor (BDNF), whose levels are elevated in response to exercise, is a well-known factor in improving cognitive function. Therefore, the aim of our study was to investigate whether the exercise under hypoxic conditions affects psychomotor performance. For this purpose, 11 healthy young athletes performed a graded cycloergometer exercise test to volitional exhaustion under normoxia and acute mild hypoxia (FiO2 = 14.7%). Before, immediately after exercise and after a period of recovery, choice reaction time (CRT) and number of correct reactions (NCR) in relation to changes in serum BDNF were examined. Additionally, other selected factors which may modify BDNF production, i.e., cortisol (C), nitrite, catecholamines (adrenalin-A, noradrenaline-NA, dopamine-DA, serotonin-5-HT) and endothelin-1 (ET-1), were also measured. Exercise in hypoxic conditions extended CRT by 13.8% (p < 0.01) and decreased NCR (by 11.5%) compared to rest (p < 0.05). During maximal workload, NCR was lower by 9% in hypoxia compared to normoxia (p < 0.05). BDNF increased immediately after exercise in normoxia (by 29.3%; p < 0.01), as well as in hypoxia (by 50.0%; p < 0.001). There were no differences in BDNF between normoxia and hypoxia. Considering the fact that similar levels of BDNF were seen in both conditions but cognitive performance was suppressed in hypoxia, acute elevation of BDNF did not compensate for hypoxia-induced cognition impairment. Moreover, neither potentially negative effects of C nor positive effects of A, DA and NO on the brain were observed in our study.

Role of brain-derived neurotrophic factor in appetite control / Rola neurotroficznego czynnika pochodzenia mózgowego w kontroli laknienia.

It has been found that in brain areas responsible for controlling appetite brain-derived neurotrophic factor (BDNF) and TrkB receptor expression are also present. In addition to involvement in neurogenesis, neuroprotection and synaptic plasticity, BDNF has anorexigenic activity. Decreasing of BDNF levels in the brain causes uncontrolled food intake, in turn, administration of BDNF to the central nervous system (CNS) leads to weight loss in animals. BDNF may participate with other factors such as leptin, insulin, cholecystokinin or corticotropin in the regulation of food intake. In addition, BDNF can affect glucose metabolism. It was found that peripheral BDNF level is lower in anorexia compared to healthy people. Moreover, BDNF levels tend to return to basal value when body weight normalizes. The mutation in the BDNF gene could also be important in the pathogenesis of obesity, although data on the blood concentration of this neurotrophin in obese are ambiguous.

[The role of the brain-derived neurotrophic factor (BDNF) in neurodegenerative processes and in the neuroregeneration mechanisms induced by increased physical activity]. / Rola mózgowego czynnika neurotroficznego (BDNF) w procesach neurodegeneracji oraz w mechanizmach neuroregeneracji wywolanej wzmozona aktywnoscia fizyczna.

The brain-derived neurotrophic factor (BDNF) belongs to the family of neurotrophins synthesized in the central and peripheral nervous system. Several specific miRNAs (miR-1, miR-126 and miR-30a-5p) are involved in the regulation of BDNF synthesis. Its synthesis is also influenced by the SNP-Val 66Met BDNF polymorphism (rs 6265). BNDF can cross the blood brain barrier. Its role in the central and peripheral rely on regulation of important physiological functions, i.e. development and growth of neurons, the process of learning and memory, apoptosis, neurogenesis and neuroregenation through activation of TRkB and p75NTR receptors. Lowering BDNF level mediates neurodenegeration of neurons including dopaminergic neurons in Parkinson's disease. Regular long-term repeated physical exercise and/or moderate to high intensity training induces an increase level of BDNF and TrkB receptors in the brain regions responsible for motor activity, preventing neurodegeneration, especially in the.

The Impact of Acute Mild Normobaric Hypoxia and a Single Bout of Exercise to Volitional Exhaustion on Cognitive Performance in Endurance and Strength-Trained Athletes: The role of BDNF, EP-1, Catecholamines and Lactate.

The aim of the study was to examine whether a single bout of exercise to volitional exhaustion, performed under moderate normobaric hypoxia (H), would affect psychomotor performance (PP) in differently trained athletes. For this purpose, ten strength-trained (S) athletes, ten endurance-trained (E) athletes and ten healthy men leading a sedentary lifestyle as a control (C) group performed voluntarily two graded exercise tests until volitional exhaustion (EVE) under normoxia (N) and H (FiO2 = 14.7%). We measured the peripheral level of the brain derived neurotrophic factor (BDNF), choice reaction time (CRT) and the number of correct reactions (NCR) as indices of PP. Psychomotor tests were performed at rest, immediately after the EVE and 3 minutes after the EVE. Venous blood samples were collected at rest, immediately after cessation of each EVE, and 1 h after each EVE. The results showed that the EVE significantly (p < 0.05) impaired CRT under N and H, and NCR under H only in the E group. The higher WRmax in the E compared to the S and C groups was associated with a significant (p < 0.005) increase in adrenaline (A) and noradrenaline (NA). There were no significant differences between conditions (N vs. H) in the BDNF at rest and after exercise. The EVE impaired cognitive function only in the E group; higher involvement of the sympathetic nervous system, A and NA may also play a role in this phenomenon. Therefore, it can be concluded that exposure to H did not have a negative impact on CRT or NCR. Moreover, BDNF did not improve cognitive function.

Comparison of maximal lactate steady state with anaerobic threshold determined by various methods based on graded exercise test with 3-minute stages in elite cyclists.

BACKGROUND: The maximal lactate steady state (MLSS) is defined as the highest workload that can be maintained for a longer period of time without continued blood lactate (LA) accumulation. MLSS is one of the physiological indicators of aerobic performance. However, determination of MLSS requires the performance of a series of constant-intensity tests during multiple laboratory visits. Therefore, attempts are made to determine MLSS indirectly by means of anaerobic threshold (AT) evaluated during a single graded exercise test (GXT) until volitional exhaustion. The aim of our study was to verify whether AT determined by maximal deviation (Dmax), modified maximal deviation (ModDmax), baseline LA concentration + 1 mmol/l (+ 1 mmol/l), individual anaerobic threshold (IAT), onset of blood lactate accumulation (OBLA4mmol/l) and V-slope methods based on GXT with 3-min stages provide valid estimates of MLSS in elite cyclists. METHODS: Twelve elite male cyclists (71.3 ± 3.6 ml/kg/min) completed GXT (the increase by 40 W every 3 min) to establish the AT (by Dmax, ModDmax, + 1 mmol/l, IAT, OBLA4mmol/l and V-slope methods). Next, a series of 30-min constant-load tests to determine MLSS was performed. Agreement between the MLSS and workload (WR) at AT was evaluated using the Bland-Altman method. RESULTS: The analysis revealed a very high (rs > 0.90, p < 0.001) correlation between WRMLSS and WRDmax and WRIAT. The other AT methods were highly (rs > 0.70) correlated with MLSS except for OBLA4mmol/l (rs = 0.67). The Bland-Altman analysis revealed the highest agreement with MLSS for the Dmax, IAT and + 1 mmol/l methods. Mean difference between WRMLSS and WRDmax, WRIAT and WR+1mmol/l was 1.7 ± 3.9 W, 4.3 ± 7.9 W and 6.7 ± 17.2 W, respectively. Furthermore, the WRDmax and WRIAT had the lowest limits of agreement with the WRMLSS. The ModDmax and OBLA4mmol/l methods overestimated MLSS by 31.7 ± 18.5 W and 43.3 ± 17.8 W, respectively. The V-slope method underestimated MLSS by 36.2 ± 10.9 W. CONCLUSIONS: The AT determined by Dmax and IAT methods based on the cycling GXT with 3-min stages provides a high agreement with the MLSS in elite cyclists. Despite the high correlation with MLSS and low mean difference, the AT determined by + 1 mmol/l method may highly overestimate or underestimate MLSS in individual subjects. The individual MLSS cannot be properly estimated by V-slope, ModDmax and OBLA4mmol/l methods.

Acute normobaric hypoxia does not affect the simultaneous exercise-induced increase in circulating BDNF and GDNF in young healthy men: A feasibility study.

Physical exercise has a neuromodulatory effect on the central nervous system (CNS) partially by modifying expression of neuropeptides produced and secreted by neurons and glial cells, among which the best examined are brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF). Because both neurotrophins can cross the brain-blood barrier (BBB), their blood levels indirectly reflect their production in the CNS. Moreover, both neuropeptides are involved in modulation of dopaminergic and serotoninergic system function. Because limited information is available on the effects of exercise to volition exhaustion and acute hypoxia on CNS, BDNF and GDNF formation, the aims of the present study were to verify whether 1) acute exercise to exhaustion in addition to neurons also activates glial cells and 2) additional exposure to acute normobaric moderate hypoxia affects their function. In this feasibility study we measured blood concentrations of BDNF, GDNF, and neuropeptides considered as biomarkers of brain damage (bFGF, NGF, S100B, GFAP) in seven sedentary healthy young men who performed a graded exercise test to volitional exhaustion on a cycle ergometer under normoxic (N) and hypoxic conditions: 2,000 m (H2; FiO2 = 16.6%) and 3,000 m altitude (H3; FiO2 = 14.7%). In all conditions serum concentrations of both BDNF and GDNF increased immediately after cessation of exercise (p<0.01). There was no effect of condition or interaction (condition x time of measurement) and exercise on any of the brain damage biomarkers: bFGF, NGF, S100B, GFAP. Moreover, in N (0<0.01) and H3 (p<0.05) exercise caused elevated serum 5-HT concentration. The results suggest that a graded effort to volitional exhaustion in normoxia, as well as hypoxia, simultaneously activates both neurons and astrocytes. Considering that s100B, GFAP, bFGF, and NGF (produced mainly by astrocytes) are markers of brain damage, it can be assumed that a maximum effort in both conditions is safe for the CNS.

Intermittent Hypoxic Training at Lactate Threshold Intensity Improves Aiming Performance in Well-Trained Biathletes with Little Change of Cardiovascular Variables.

The main objective of this research was to evaluate the efficacy of intermittent hypoxic training (IHT) on aiming performance and aerobic capacity in biathletes. Fourteen male biathletes were randomly divided into a hypoxia group (H) (n = 7), which trained three times per week in a normobaric hypoxic environment (FiO2 = 16.5%, 2000 m a.s.l.) with lactate threshold intensity (LT) determined in hypoxia, and a control group (C) (n = 7), which exercised under normoxic conditions with LT intensity determined in normoxia. The training program included three weekly microcycles, followed by three days of recovery. The main part of the interval workout consisted of four 7 min (1st week), 8 min (2nd week), or 9 min (3rd week) running bouts at treadmill separated by 2 minutes of active recovery. After the warm-up and during the rest between the bouts, the athletes performed aiming to the target in the standing position with a sporting rifle (20 s). The results showed that the IHT caused a significant (p < 0.05) increase in retention time in the target at rest (RT9rest) by 14.4% in hypoxia, whereas RT postincremental test (RT9post) increased by 27.4% in normoxia and 26.7% in hypoxia. No significant changes in this variable were found in group C. Additionally, the capillary oxygen saturation at the end of the maximal effort (SO2capillary max) in hypoxia increased significantly (p < 0.001) by ∼4% after IHT. The maximal workload during the incremental test (WRmax) in normoxia also increased significantly (p < 0.001) by 6.3% after IHT. Furthermore, in absolute and relative values of VO2max in normoxia, there was a propensity (p < 0.07) for increasing this value by 5% in group H. In conclusion, the main findings of this study showed a significant improvement in resting and postexercise aiming performance in normoxia and hypoxia. Furthermore, the results demonstrated beneficial effects of the IHT protocol on aerobic capacity of biathletes.