2016
DOI: 10.1249/mss.0000000000000879
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Noradrenaline Reuptake Inhibition Impairs Cortical Output and Limits Endurance Time

Abstract: These findings suggest that because of the noradrenaline reuptake inhibition, the output from the motor cortex is decreased at a greater rate than that in the PLA condition, contributing thereby to shorten endurance time.

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Cited by 27 publications
(34 citation statements)
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“…This demonstrates that altered brain neurotransmission is able to affect whole-body endurance performance and that this effect is associated with an altered RPE to power output ratio (in the case of DA, a decreased ratio). Klass et al [76] showed that muscle endurance performance is affected in a similar way. A noradrenaline reuptake inhibitor reduced endurance time by 15.6 %.…”
Section: A Potential Role For Brain Neurotransmittersmentioning
confidence: 95%
See 2 more Smart Citations
“…This demonstrates that altered brain neurotransmission is able to affect whole-body endurance performance and that this effect is associated with an altered RPE to power output ratio (in the case of DA, a decreased ratio). Klass et al [76] showed that muscle endurance performance is affected in a similar way. A noradrenaline reuptake inhibitor reduced endurance time by 15.6 %.…”
Section: A Potential Role For Brain Neurotransmittersmentioning
confidence: 95%
“…This was associated with a greater rate of supraspinal impairment and increase in RPE. Participants experienced the same intensity of intermittent contractions as harder to perform after administration of a noradrenaline reuptake inhibitor, without affecting the fatigue-related intramuscular impairments [76]. Pageaux et 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 al.…”
Section: A Potential Role For Brain Neurotransmittersmentioning
confidence: 99%
See 1 more Smart Citation
“…Operationally, it is often defined as an exercise-induced decrease in maximal voluntary activation level ( Pageaux et al, 2015 ). A mechanism that has been proposed to play a role within this kind of fatigue is for example challenged oxygenation of the brain during exercise ( Secher et al, 2008 ), but also neurochemical and thermodynamic changes of the cerebral homeostasis have been proposed to lead to central fatigue ( Kayser, 2003 ; Nybo and Secher, 2004 ; Klass et al, 2016 ). However, similarly to the proposed peripheral mechanisms of fatigue, the reductionistic pitfall to link these central mechanisms with the occurrence of exercise-induced fatigue based on the concept of a critical threshold, has to be avoided, i.e., a linear model in which increases or decreases in brain neurotransmitter concentrations cause fatigue ( Gibson and Noakes, 2004 ).…”
Section: Fatigue In Exercise Sciencementioning
confidence: 99%
“…The interaction between exercise and brain catecholamines concentrations does not only affect motivation but also the whole process of central fatigue, as dopamine (DA) and norepinephrine (NE) are vital for activation of the prefrontal cortex (PFC), which is thought to control central fatigue (Klass et al, 2016;Robertson & Marino, 2016).…”
Section: Introductionmentioning
confidence: 99%