scholarly journals AltitudeOmics: on the consequences of high-altitude acclimatization for the development of fatigue during locomotor exercise in humans

2013 ◽  
Vol 115 (5) ◽  
pp. 634-642 ◽  
Author(s):  
Markus Amann ◽  
Stuart Goodall ◽  
Rosie Twomey ◽  
Andrew W. Subudhi ◽  
Andrew T. Lovering ◽  
...  
Keyword(s):  
High Altitude ◽  
Muscle Fatigue ◽  
Muscle Activation ◽  
Acute Hypoxia ◽  
Central Fatigue ◽  
Constant Load ◽  
Peripheral Fatigue ◽  
Substantial Impact ◽  
Hypoxic Conditions ◽  
Exercise Induced

The development of muscle fatigue is oxygen (O2)-delivery sensitive [arterial O2 content (CaO2) × limb blood flow ( QL)]. Locomotor exercise in acute hypoxia (AH) is, compared with sea level (SL), associated with reduced CaO2 and exaggerated inspiratory muscle work (Winsp), which impairs QL, both of which exacerbate fatigue individually by compromising O2 delivery. Since chronic hypoxia (CH) normalizes CaO2 but exacerbates Winsp, we investigated the consequences of a 14-day exposure to high altitude on exercise-induced locomotor muscle fatigue. Eight subjects performed the identical constant-load cycling exercise (138 ± 14 W; 11 ± 1 min) at SL (partial pressure of inspired O2, 147.1 ± 0.5 Torr), in AH (73.8 ± 0.2 Torr), and in CH (75.7 ± 0.1 Torr). Peripheral fatigue was expressed as pre- to postexercise percent reduction in electrically evoked potentiated quadriceps twitch force (ΔQtw,pot). Central fatigue was expressed as the exercise-induced percent decrease in voluntary muscle activation (ΔVA). Resting CaO2 at SL and CH was similar, but CaO2 in AH was lower compared with SL and CH (17.3 ± 0.5, 19.3 ± 0.7, 20.3 ± 1.3 ml O2/dl, respectively). Winsp during exercise increased with acclimatization (SL: 387 ± 36, AH: 503 ± 53, CH: 608 ± 67 cmH2O·s−1·min−1; P < 0.01). Exercise at SL did not induce central or peripheral fatigue. ΔQtw,pot was significant but similar in AH and CH (21 ± 2% and 19 ± 3%; P = 0.24). ΔVA was significant in both hypoxic conditions but smaller in CH vs. AH (4 ± 1% vs. 8 ± 2%; P < 0.05). In conclusion, acclimatization to severe altitude does not attenuate the substantial impact of hypoxia on the development of peripheral fatigue. In contrast, acclimatization attenuates, but does not eliminate, the exacerbation of central fatigue associated with exercise in severe AH.

The influence of ice slushy on voluntary contraction force following exercise-induced hyperthermia

2014 ◽  
Vol 39 (7) ◽  
pp. 781-786 ◽  
Author(s):  
Catriona A. Burdon ◽  
Christopher S. Easthope ◽  
Nathan A. Johnson ◽  
Phillip G. Chapman ◽  
Helen O’Connor
Keyword(s):  
Muscle Activation ◽  
Force Production ◽  
Central Fatigue ◽  
Voluntary Contraction ◽  
Voluntary Activation ◽  
Peripheral Fatigue ◽  
Knee Extensors ◽  
Central Component ◽  
Induced Hyperthermia ◽  
Exercise Induced

This study aimed to investigate the effect of exercise-induced hyperthermia on central fatigue and force decline in exercised and nonexercised muscles and whether ingestion of ice slushy (ICE) ameliorates fatigue. Eight participants (5 males, 3 females) completed 45 s maximal voluntary isometric contractions (MVIC) with elbow flexors and knee extensors at baseline and following an exercise-induced rectal temperature (Trec) of 39.3 ± 0.2 °C. Percutaneous electrical muscle stimulation was superimposed at 15, 30 and 44 s during MVICs to assess muscle activation. To increase Trec to 39.3 °C, participants cycled at 60% maximum power output for 42 ± 11 min in 40 °C and 50% relative humidity. Immediately prior to each MVIC, participants consumed 50 g of ICE (–1 °C) or thermoneutral drink (38 °C, CON) made from 7.4% carbohydrate beverage. Participants consumed water (19 °C) during exercise to prevent hypohydration. Voluntary muscle force production and activation in both muscle groups were unchanged at Trec 39.3 °C with ICE (knee extensors: 209 ± 152 N) versus CON (knee extensors: 255 ± 157 N, p = 0.19). At Trec 39.3 °C, quadriceps mean force (232 ± 151 N) decreased versus baseline (302 ± 180 N, p < 0.001) and mean voluntary activation was also decreased (by 15% ± 11%, p < 0.001). Elbow flexor mean force decreased from 179 ± 67 N to 148 ± 65 N when Trec was increased to 39.3 °C (p < 0.001) but mean voluntary activation was not reduced at 39.3 °C (5% ± 25%, p = 0.79). After exercise-induced hyperthermia, ICE had no effect on voluntary activation or force production; however, both were reduced from baseline in the exercised muscle group. Peripheral fatigue was greater than the central component and limited the ability of an intervention designed to alter central fatigue.

Electrically-induced quadriceps fatigue in the contralateral leg impairs ipsilateral knee extensors performance

2021 ◽  
Author(s):  
Fabio Giuseppe Laginestra ◽  
Markus Amann ◽  
Emine Kirmizi ◽  
Gaia Giuriato ◽  
Chiara Barbi ◽  
...  
Keyword(s):  
Muscle Activation ◽  
Central Fatigue ◽  
Endurance Performance ◽  
Voluntary Exercise ◽  
Peripheral Fatigue ◽  
Knee Extensors ◽  
Motor Drive ◽  
Time To Exhaustion ◽  
Crossover Effect ◽  
The Impact

Muscle fatigue induced by voluntary exercise, which requires central motor drive, causes central fatigue that impairs endurance performance of a different, non-fatigued muscle. This study investigated the impact of quadriceps fatigue induced by electrically-induced (no central motor drive) contractions on single-leg knee-extension (KE) performance of the subsequently exercising ipsilateral quadriceps. On two separate occasions, eight males completed constant-load (85% of maximal power-output) KE exercise to exhaustion. In a counterbalanced manner, subjects performed the KE exercise with no pre-existing quadriceps fatigue in the contralateral leg on one day (No-PreF), while on the other day, the same KE exercise was repeated following electrically-induced quadriceps fatigue in the contralateral leg (PreF). Quadriceps fatigue was assessed by evaluating pre- to post-exercise changes in potentiated twitch force (ΔQtw,pot; peripheral-fatigue), and voluntary muscle activation (ΔVA; central-fatigue). As reflected by the 57±11% reduction in electrically-evoked pulse force, the electrically-induced fatigue protocol caused significant knee-extensors fatigue. KE endurance time to exhaustion was shorter during PreF compared to No-PreF (4.6±1.2 vs 7.7±2.4 min; p<0.01). While ΔQtw,pot was significantly larger in No-PreF compared to PreF (-60% vs -52%, p<0.05), ΔVA was greater in PreF (-14% vs -10%, p<0.05). Taken together, electrically-induced quadriceps fatigue in the contralateral leg limits KE endurance performance and the development of peripheral fatigue in the ipsilateral leg. These findings support the hypothesis that the crossover-effect of central fatigue is mainly mediated by group III/IV muscle afferent feedback and suggest that impairments associated with central motor drive may only play a minor role in this phenomenon.

Plyometric Training Does Not Affect Central and Peripheral Muscle Fatigue Differently in Prepubertal Girls and Boys

2010 ◽  
Vol 22 (4) ◽  
pp. 547-556 ◽  
Author(s):  
Albertas Skurvydas ◽  
Marius Brazaitis
Keyword(s):  
Muscle Fatigue ◽  
Central Fatigue ◽  
Quadriceps Muscle ◽  
Voluntary Activation ◽  
Peripheral Fatigue ◽  
Plyometric Training ◽  
Peripheral Muscle ◽  
Before And After ◽  
Voluntary Contractions ◽  
Prepubertal Girls

The aim of the study was to evaluate the effect of plyometric training (PT) on central and peripheral (muscle) fatigue in prepubertal girls and boys. The boys (n = 13, age 10.3 ± 0.3 years) and girls (n = 13, age, 10.2 ± 0.3 years) performed continuous 2-min maximal voluntary contractions (MVCs) before and after 16 high-intensity PT sessions. PT comprised two training sessions per week of 30 jumps in each session with 20 s between jumps. The greatest effect of PT was on excitation–contraction coupling, (twitch force increased by 323% in boys and 21% in girls) and height of a counter–movement jump (increased by 37% in boys and 38% in girls). In contrast, the quadriceps voluntary activation index, central activation ratio, and MVC did not change significantly after PT. The thickness of the quadriceps muscle increased by 9% in boys and 14% in girls after PT. In conclusion, boys and girls demonstrated similar changes in indicators of central fatigue (50–60% decrease) and peripheral fatigue (45–55% decrease) after MVC before and after PT.

scholarly journals Quadriceps Muscle Fatigue Reduces Extension and Flexion Power During Maximal Cycling

2022 ◽  
Vol 3 ◽  
Author(s):  
Steven J. O'Bryan ◽  
Janet L. Taylor ◽  
Jessica M. D'Amico ◽  
David M. Rouffet
Keyword(s):  
Muscle Fatigue ◽  
Muscle Activation ◽  
Power Production ◽  
Quadriceps Muscle ◽  
Individual Variability ◽  
Voluntary Activation ◽  
Peripheral Fatigue ◽  
Emg Activity ◽  
Pedal Force ◽  
Voluntary Contractions

Purpose: To investigate how quadriceps muscle fatigue affects power production over the extension and flexion phases and muscle activation during maximal cycling.Methods: Ten participants performed 10-s maximal cycling efforts without fatigue and after 120 bilateral maximal concentric contractions of the quadriceps muscles. Extension power, flexion power and electromyographic (EMG) activity were compared between maximal cycling trials. We also investigated the associations between changes in quadriceps force during isometric maximal voluntary contractions (IMVC) and power output (flexion and extension) during maximal cycling, in addition to inter-individual variability in muscle activation and pedal force profiles.Results: Quadriceps IMVC (−52 ± 21%, P = 0.002), voluntary activation (−24 ± 14%, P &lt; 0.001) and resting twitch amplitude (−45 ± 19%, P = 0.002) were reduced following the fatiguing task, whereas vastus lateralis (P = 0.58) and vastus medialis (P = 0.15) M-wave amplitudes were unchanged. The reductions in extension power (−15 ± 8%, P &lt; 0.001) and flexion power (−24 ± 18%, P &lt; 0.001) recorded during maximal cycling with fatigue of the quadriceps were dissociated from the decreases in quadriceps IMVC. Peak EMG decreased across all muscles while inter-individual variability in pedal force and EMG profiles increased during maximal cycling with quadriceps fatigue.Conclusion: Quadriceps fatigue induced by voluntary contractions led to reduced activation of all lower limb muscles, increased inter-individual variability and decreased power production during maximal cycling. Interestingly, power production was further reduced over the flexion phase (24%) than the extension phase (15%), likely due to larger levels of peripheral fatigue developed in RF muscle and/or a higher contribution of the quadriceps muscle to flexion power production compared to extension power during maximal cycling.

Inspiratory muscle work in acute hypoxia influences locomotor muscle fatigue and exercise performance of healthy humans

2007 ◽  
Vol 293 (5) ◽  
pp. R2036-R2045 ◽  
Author(s):  
Markus Amann ◽  
David F. Pegelow ◽  
Anthony J. Jacques ◽  
Jerome A. Dempsey
Keyword(s):  
Muscle Fatigue ◽  
Acute Hypoxia ◽  
Femoral Nerve ◽  
Inspiratory Muscle ◽  
Peripheral Fatigue ◽  
Twitch Force ◽  
Arterial Hypoxemia ◽  
Healthy Humans ◽  
Muscle Work ◽  
Hemoglobin Saturation

Our aim was to isolate the independent effects of 1) inspiratory muscle work (Wb) and 2) arterial hypoxemia during heavy-intensity exercise in acute hypoxia on locomotor muscle fatigue. Eight cyclists exercised to exhaustion in hypoxia [inspired O2 fraction (FiO2) = 0.15, arterial hemoglobin saturation (SaO2) = 81 ± 1%; 8.6 ± 0.5 min, 273 ± 6 W; Hypoxia-control (Ctrl)] and at the same work rate and duration in normoxia (SaO2 = 95 ± 1%; Normoxia-Ctrl). These trials were repeated, but with a 35–80% reduction in Wb achieved via proportional assist ventilation (PAV). Quadriceps twitch force was assessed via magnetic femoral nerve stimulation before and 2 min after exercise. The isolated effects of Wb in hypoxia on quadriceps fatigue, independent of reductions in SaO2, were revealed by comparing Hypoxia-Ctrl and Hypoxia-PAV at equal levels of SaO2 ( P = 0.10). Immediately after hypoxic exercise potentiated twitch force of the quadriceps (Qtw,pot) decreased by 30 ± 3% below preexercise baseline, and this reduction was attenuated by about one-third after PAV exercise (21 ± 4%; P = 0.0007). This effect of Wb on quadriceps fatigue occurred at exercise work rates during which, in normoxia, reducing Wb had no significant effect on fatigue. The isolated effects of reduced SaO2 on quadriceps fatigue, independent of changes in Wb, were revealed by comparing Hypoxia-PAV and Normoxia-PAV at equal levels of Wb. Qtw,pot decreased by 15 ± 2% below preexercise baseline after Normoxia-PAV, and this reduction was exacerbated by about one-third after Hypoxia-PAV (−22 ± 3%; P = 0.034). We conclude that both arterial hypoxemia and Wb contribute significantly to the rate of development of locomotor muscle fatigue during exercise in acute hypoxia; this occurs at work rates during which, in normoxia, Wb has no effect on peripheral fatigue.

Deciphering the metabolic and mechanical contributions to the exercise-induced circulatory response: insights from eccentric cycling

2007 ◽  
Vol 292 (4) ◽  
pp. R1641-R1648 ◽  
Author(s):  
Stéphane P. Dufour ◽  
Stéphane Doutreleau ◽  
Evelyne Lonsdorfer-Wolf ◽  
Eliane Lampert ◽  
Christine Hirth ◽  
...  
Keyword(s):  
Power Output ◽  
Muscle Activation ◽  
Constant Load ◽  
Emg Activity ◽  
Metabolic Demand ◽  
Mechanical Tension ◽  
Circulatory Response ◽  
Exercise Induced ◽  
Reductionist Approach ◽  
Exercise In Humans

Metabolic demand and muscle mechanical tension are closely coupled during exercise, making their respective drives to the circulatory response difficult to establish. This coupling being altered in eccentric cycling, we implemented an experimental design featuring eccentric vs. concentric constant-load cycling bouts to gain insights into the control of the exercise-induced circulatory response in humans. Heart rate (HR), stroke volume (SV), cardiac output (Q̇), oxygen uptake (V̇o2), and electromyographic (EMG) activity of quadriceps muscles were measured in 11 subjects during heavy concentric (heavy CON: 270 ± 13 W; V̇o2 = 3.59 ± 0.20 l/min), heavy eccentric (heavy ECC: 270 ± 13 W, V̇o2 = 1.17 ± 0.15 l/min), and light concentric (light CON: 70 ± 9 W, V̇o2 = 1.14 ± 0.12 l/min) cycle bouts. Using a reductionist approach, the circulatory responses observed between heavy CON vs. light CON (difference in V̇o2 and power output) was ascribed either to metabolic demand, as estimated from heavy CON vs. heavy ECC (similar power output, different V̇o2), or to muscle mechanical tension, as estimated from heavy ECC vs. light CON (similar V̇o2, different power output). 74% of the Q̇ response was determined by the metabolic demand, also accounting for 65% and 84% of HR and SV responses, respectively. Consequently, muscle mechanical tension determined 26%, 35%, and 16% of the Q̇, HR, and SV responses, respectively. Q̇ was significantly related to V̇o2 ( r2 = 0.83) and EMG activity ( r2 = 0.82; both P < 0.001). These results suggest that the exercise-induced circulatory response is mainly under metabolic control and support the idea that the level of muscle activation plays a role in the cardiovascular regulation during cycle exercise in humans.

Linear relationship between VO2max and VO2max decrement during exposure to acute hypoxia

1988 ◽  
Vol 64 (4) ◽  
pp. 1486-1492 ◽  
Author(s):  
J. Lawler ◽  
S. K. Powers ◽  
D. Thompson
Keyword(s):  
Maximal Exercise ◽  
Acute Hypoxia ◽  
Barometric Pressure ◽  
Endurance Athletes ◽  
Oxyhemoglobin Saturation ◽  
Hypoxia Exposure ◽  
Hypoxic Conditions ◽  
Significant Linear Correlation ◽  
Exercise Induced ◽  
Single Blind

The purpose of these experiments is to test the hypothesis that exercise-induced hypoxemia at sea level in highly trained athletes might be exacerbated during acute hypoxia and therefore result in correspondingly larger decrements in maximal O2 uptake (VO2max) compared with less trained individuals. Thirteen healthy male volunteers were divided into two groups according to their level of fitness: 1) trained endurance athletes (T) (n = 7), with a VO2max range of 56-75 ml.kg-1.min-1 and 2) untrained individuals (UT) (n = 6), with a VO2max range of 33-49 ml.kg-1.min-1. Subjects performed two incremental cycle ergometry tests to determine VO2max under hypoxic conditions [14% O2-86% N2, barometric pressure (PB) = 760 Torr] and normoxic conditions (21% O2-79% N2, PB = 760 Torr). Tests were single blind, randomly administered, and separated by at least 72 h. Mean percent oxyhemoglobin saturation (%SaO2) during maximal exercise under hypoxic conditions was significantly (P less than 0.05) lower in the T group (77%) compared with the UT group (86%). Furthermore, the T group exhibited larger decrements (P less than 0.05) in VO2max (normoxic-hypoxic) compared with the UT group. Finally, a significant linear correlation (r = 0.94) existed between normoxic VO2max (ml.kg-1.min-1) and delta VO2max (normoxic-hypoxic). These data suggest that highly T endurance athletes suffer more severe gas exchange impairments during acute exposure to hypoxia than UT individuals, and this may explain a portion of the observed variance in delta VO2max among individuals during acute altitude or hypoxia exposure.

scholarly journals Fatigue diminishes motoneuronal excitability during cycling exercise

2016 ◽  
Vol 116 (4) ◽  
pp. 1743-1751 ◽  
Author(s):  
Joshua C. Weavil ◽  
Simranjit K. Sidhu ◽  
Tyler S. Mangum ◽  
Russell S. Richardson ◽  
Markus Amann
Keyword(s):  
Evoked Potentials ◽  
Muscle Activation ◽  
Motor Evoked Potentials ◽  
Vastus Lateralis ◽  
Femoral Nerve ◽  
Central Fatigue ◽  
Rectus Femoris ◽  
Constant Load ◽  
Corticospinal Excitability ◽  
Cycling Exercise

Exercise-induced fatigue influences the excitability of the motor pathway during single-joint isometric contractions. This study sought to investigate the influence of fatigue on corticospinal excitability during cycling exercise. Eight men performed fatiguing constant-load (80% Wpeak; 241 ± 13 W) cycling to exhaustion during which the percent increase in quadriceps electromyography (ΔEMG; vastus lateralis and rectus femoris) was quantified. During a separate trial, subjects performed two brief (∼45 s) nonfatiguing cycling bouts (244 ± 15 and 331 ± 23W) individually chosen to match the ΔEMG across bouts to that observed during fatiguing cycling. Corticospinal excitability during exercise was quantified by transcranial magnetic, electric transmastoid, and femoral nerve stimulation to elicit motor-evoked potentials (MEP), cervicomedullary evoked potentials (CMEP), and M waves in the quadriceps. Peripheral and central fatigue were expressed as pre- to postexercise reductions in quadriceps twitch force (ΔQtw) and voluntary quadriceps activation (ΔVA). Whereas nonfatiguing cycling caused no measureable fatigue, fatiguing cycling resulted in significant peripheral (ΔQtw: 42 ± 6%) and central (ΔVA: 4 ± 1%) fatigue. During nonfatiguing cycling, the area of MEPs and CMEPs, normalized to M waves, similarly increased in the quadriceps (∼40%; P < 0.05). In contrast, there was no change in normalized MEPs or CMEPs during fatiguing cycling. As a consequence, the ratio of MEP to CMEP was unchanged during both trials ( P > 0.5). Therefore, although increases in muscle activation promote corticospinal excitability via motoneuronal facilitation during nonfatiguing cycling, this effect is abolished during fatigue. We conclude that the unaltered excitability of the corticospinal pathway from start of intense cycling exercise to exhaustion is, in part, determined by inhibitory influences on spinal motoneurons obscuring the facilitating effects of muscle activation.

scholarly journals Metabolism of asymmetric dimethylarginine in hypoxia: from bench to bedside

2020 ◽  
Vol 10 (1_suppl) ◽  
pp. 31-41 ◽  
Author(s):  
Juliane Hannemann ◽  
Julia Zummack ◽  
Jonas Hillig ◽  
Rainer Böger
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Animal Models ◽  
High Altitude ◽  
Vascular Function ◽  
Molecular Mechanisms ◽  
Asymmetric Dimethylarginine ◽  
Acute Hypoxia ◽  
Hypoxic Conditions ◽  
Pulmonary Vasoconstriction

Acute hypoxia and chronic hypoxia induce pulmonary vasoconstriction. While hypoxic pulmonary vasoconstriction is a physiological response if parts of the lung are affected, global exposure to hypoxic conditions may lead to clinical conditions like high-altitude pulmonary hypertension. Nitric oxide is the major vasodilator released from the vascular endothelium. Nitric oxide-dependent vasodilation is impaired in hypoxic conditions. Inhibition of nitric oxide synthesis is the most rapid and easily reversible molecular mechanism to regulate nitric oxide-dependent vascular function in response to physiological and pathophysiological stimuli. Asymmetric dimethylarginine is an endogenous, competitive inhibitor of nitric oxide synthase and a risk marker for major cardiovascular events and mortality. Elevated asymmetric dimethylarginine has been observed in animal models of hypoxia as well as in human cohorts under chronic and chronic intermittent hypoxia at high altitude. In lowlanders, asymmetric dimethylarginine is high in patients with pulmonary hypertension. We have recently shown that high asymmetric dimethylarginine at sea level is a predictor for high-altitude pulmonary hypertension. Asymmetric dimethylarginine is a highly regulated molecule, both by its biosynthesis and metabolism. Methylation of L-arginine by protein arginine methyltransferases was shown to be increased in hypoxia. Furthermore, the metabolism of asymmetric dimethylarginine by dimethylarginine dimethylaminohydrolases (DDAH1 and DDAH2) is decreased in animal models of hypoxia. Whether these changes are caused by transcriptional or posttranslational modifications remains to be elucidated. Current data suggest a major role of asymmetric dimethylarginine in regulating pulmonary arterial nitric oxide production in hypoxia. Further studies are needed to decipher the molecular mechanisms regulating asymmetric dimethylarginine in hypoxia and to understand their clinical significance.

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

2020 ◽  
Vol 21 (15) ◽  
pp. 5569 ◽  
Author(s):  
Zofia Piotrowicz ◽  
Małgorzata Chalimoniuk ◽  
Kamila Płoszczyca ◽  
Miłosz Czuba ◽  
Józef Langfort
Keyword(s):  
Acute Hypoxia ◽  
Negative Effects ◽  
Positive Effects ◽  
Hypoxic Conditions ◽  
Acute Elevation ◽  
Psychomotor Tasks ◽  
Exercise Induced ◽  
Response To Exercise ◽  
Cognition Impairment ◽  
The Brain

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.

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