ECSS Paris 2023: OP-PN04
INTRODUCTION: Physical fatigue impairs cognitive control, with significant consequences for performance (1,2). However, it remains unclear whether fatigue-related inhibitory impairments arise from distinct catecholaminergic mechanisms and how these shape neural control dynamics. By combining pharmacological modulation and electroencephalography (EEG), this study examined whether dopaminergic and noradrenergic systems differentially influence behavioural performance and the neural stages of response execution and inhibition following physical fatigue. METHODS: Eighteen healthy adults (9 female; 23.4±2.2 years) completed a randomised, triple-blind, placebo-controlled crossover study. On separate visits, participants received methylphenidate (20 mg MPH; dopaminergic reuptake inhibitor), reboxetine (8 mg REB; selective noradrenaline reuptake inhibitor), or placebo. Physical fatigue was induced by repeated bilateral leg extensions to task failure (3). Cognitive performance was assessed pre- and post-fatigue using a Go/NoGo task. Go trials measured response speed and sustained attention; NoGo trials measured inhibitory control. Outcomes were reaction time and accuracy. EEG was recorded during cognitive task performance, and event-related potentials were derived, with N2 and P3 components quantified from frontal–central and central–parietal clusters. Sample size was supported by an a priori simulation-based sensitivity analysis for drug × time interactions. Data were analysed using mixed-effects models with subject-level random intercepts. RESULTS: Go reaction time was faster under MPH than placebo at baseline and post-fatigue (p=0.015), indicating enhanced response execution. Go accuracy declined following fatigue regardless of drug condition (p = 0.017). In NoGo trials, accuracy decreased after fatigue under placebo but was maintained under MPH, resulting in a drug × time interaction (p=0.008). At the neural level, fatigue reduced central–parietal P3 amplitude during Go trials (p=0.031), indicating diminished stimulus evaluation. In NoGo trials, MPH induced shorter frontal–central N2 latencies (p=0.038), reflecting earlier inhibitory processing. A drug × fatigue interaction was observed for frontal–central P3 latency (p = 0.047), showing that MPH prevented fatigue-related delays in later inhibitory stages. REB did not modulate behavioural or neural outcomes. CONCLUSION: By dissociating catecholaminergic contributions across neural stages of inhibition, this study provides important mechanistic evidence that dopamine is a key neurochemical for the maintenance of cognitive capacity under physical stress. These findings advance understanding of fatigue-related performance decline and inform strategies to sustain cognitive capacity under high physical demands. 1. Itagi et al. (2018), Ann Neurosci., 25(4):299-304 2. Finkenzeller et al. (2018),J Appl Physiol, 118(12):2509-2521 3. Arauz et al. (2026), Eur J Sport Sci, 26(2):e70119
Read CV Yahaira Laurisa Arenales ArauzECSS Paris 2023: OP-PN04
INTRODUCTION: Mental fatigue (MF) negatively impacts human performance. Recent studies suggest substantial interindividual variability in MF response, complicating interpretation of effects, mechanisms and management [1,2]. Yet, this is based solely on observational evidence. Moreover, while some studies have assessed the origin of this variability using features such as age, no investigation has yet assessed the combined influence of multiple internal variables. We therefore investigated the range, origin, and temporal robustness of individual MF responses. METHODS: Ninety-eight healthy subjects (33 ± 9y, 44F) completed a randomized crossover trial with familiarization, intervention and control sessions. During familiarization, 19 individual features were collected, including anthropometric (e.g., age), physical (e.g., VO₂max), cognitive (e.g., attention) and psychological (e.g., anxiety) variables. MF was induced using a 45min Stroop task; a 45min documentary served as control. Dependent variables included the MF visual analogue scale (MVAS) and GoNoGo reaction time (RT) measured pre- and post-intervention/control task, and the total distance and rate of perceived exertion (RPE) during a subsequent time trial (TT). The range of the interindividual variability was assessed using standard deviations of individual response (SDIR) and Pitman Morgan tests. Feature effects were tested using moderation analyses. Temporal robustness was assessed in 25 subjects (31 ± 8y, 10F) with an identical one year follow-up using mixed linear models and intraclass correlation coefficients (ICC). RESULTS: The SDIR indicated variability for all outcomes, but only the GoNoGo RT Pitman-Morgan test reached significance (t(98)=0.38;p<0.001). Moderation analyses revealed that baseline physical activity (p=0.033) and self-control (p=0.027) attenuated the effect of MF on TT distance. Effects on RPE were moderated by response inhibition (p=0.041), physical activity (p=0.023) and sport level (p=0.012). None of the remaining 14 features influenced the MF effect on these variables, nor did any features influence MF effects on MVAS or GoNoGo RT. Comparison from baseline to follow up revealed a small decrease in MF effect on TT distance and RPE. Only TT distance showed significant temporal robustness (ICC=0.448, p=0.011). CONCLUSION: This is the first large-scale investigation of interindividual variability in MF response. Our analyses indicated a limited amount of true variability, with a minimal influence of individual features. This indicates, together with the low temporal robustness, that the response to MF should be seen as a varying and externally influenced state, as opposed to a stable trait. This has major implications for research and practice, requiring revisions of theoretical models, management guidelines, and prior interpretations, while redirecting attention toward external influences of MF. 1.Habay, J., et al., Sports Medicine - Open, 2023. (PMID: 36808018) 2.Habay, J., et al., MSSE, 2025 (PMID: 40938104)
Read CV Jelle HabayECSS Paris 2023: OP-PN04
INTRODUCTION: Strenuous exercise causes microstructural muscle damage, leading to delayed onset muscle soreness and temporary performance loss. Improved recovery can increase training efficiency and performance in athletes, which is why novel recovery-enhancing strategies are of interest. Supplementation with cannabidiol (CBD), the non‑psychoactive compound of the cannabis plant, that exerts anti‑inflammatory and analgesic effects, might be a promising strategy. Yet, human evidence for its recovery‑enhancing potential is limited, and its effects on a muscle‑molecular level remain unknown. Therefore, this study evaluated the effect of CBD supplementation on functional performance and molecular responses in skeletal muscle tissue to a muscle damaging exercise (MDE) bout. METHODS: Ten healthy male participants completed this randomized, double-blind, placebo-controlled, crossover study in which they performed an acute bout of MDE (24x10 eccentric contractions of the knee extensors on an isokinetic dynamometer). At baseline, 24, 48, 72, and 120h following MDE, maximal isometric, concentric and eccentric voluntary contraction, jump height and perceived muscle soreness were measured. Muscle biopsies were collected at baseline and 24h following MDE and were analysed for relative protein expression by western blot. Participants received either 200mg of CBD per day or an appearance-matched placebo for nine consecutive days, beginning immediately after baseline measurements (-96h pre‑exercise) and continuing until the evening before the final test session (120h post‑exercise). RESULTS: Isometric (-19.5%), concentric (-28.9%) and eccentric strength (-28.7%), along with squat jump (-9.6%) and counter movement jump height (-8.2%), decreased following MDE (Ptime < 0.0001), without differences between conditions. The drop in performance was accompanied by an increase in perceived muscle soreness (Ptime < 0.0001). Furthermore, MDE increased the expression of the myogenic marker myogenin (+685.5%; Ptime = 0.0011) and of the anabolic marker p-mTOR (+61.0%; Ptime = 0.0001). In addition, LC3B‑I levels increased (+40.6%; Ptime = 0.0295), but other markers of autophagy and inflammation (LC3B‑II, p62, ATG5/12 and CD68) remained unchanged. Besides higher overall expression of p-mTOR in the CBD condition (35.5%; Pcondition = 0.0439), no differences in the expression of molecular markers were observed between conditions. CONCLUSION: Within the context of this study, CBD supplementation did not improve muscle soreness, muscle strength and jump performance following MDE. In addition, CBD supplementation had no effect on molecular markers of anabolism, autophagy, inflammation or regeneration in response to MDE.
Read CV Moniek SchoutenECSS Paris 2023: OP-PN04