The influence of marathon running on resting-state EEG activity: a longitudinal observational study

脑电图 静息状态功能磁共振成像 医学 心脏病学 听力学 心理学 内科学 神经科学
作者
Joanna Moussiopoulou,Benjamin Pross,Mirjam Handrack,Daniel Keeser,Oliver Pogarell,Martin Halle,Peter Falkai,Johannes Scherr,Alkomiet Hasan,Astrid Roeh
出处
期刊:European Journal of Applied Physiology [Springer Science+Business Media]
卷期号:124 (4): 1311-1321 被引量:1
标识
DOI:10.1007/s00421-023-05356-4
摘要

Abstract Physical activity (PA) has positive effects on various health aspects and neuronal functions, including neuronal plasticity. Exceeding a certain exercise frequency and duration has been associated with negative effects. Our study investigated the effects of excessive PA with a marathon run (MA) and regular PA (training and recovery phases) on electrocortical activity, as measured by electroencephalography (EEG). Thirty healthy marathon runners (26 male, 45 ± 9 yrs) were enrolled in the study. Four resting-state 32 channel EEG recordings were conducted: 12–8 weeks before MA (T-1), 14–4 days prior to MA (T0), 1–6 days after (T2), and 13–15 weeks after MA (T3). Power spectrum analyses were conducted using standardized Low-Resolution Electromagnetic Tomography (sLORETA) and included the following frequency bands: delta (1.5–6 Hz), theta (6.5–8.0 Hz), alpha1 (8.5–10 Hz), alpha2 (10.5–12.0 Hz), beta1 (12.5–18.0 Hz), beta2 (18.5–21.0 Hz), beta3 (21.5–30.0 Hz), and total power (1.5-30 Hz). Statistical nonparametric mapping showed reduced power both in the alpha-2 (log-F ratio = − 0.705, threshold log-F ratio = ± 0.685, p < 0.05) and in the delta frequency band (log-F ratio = −0.699, threshold log-F ratio = ± 0.685, p < 0.05) in frontal cortical areas after MA (T2 vs. T0). These effects diminished at long-term follow-up (T3). The results can be interpreted as correlates for subacute neuroplasticity induced by strenuous and prolonged PA. Although previous studies reported an increase in alpha frequency during and directly postexercise, the adverse observation a few days after exercise cessation suggests counterregulatory mechanisms, whose complex origin can be suspected in subcortical circuits, changes in neurotransmitter systems and modulation of affectivity.
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