Recent studies have demonstrated a need for understanding the effects of physical activity on neurological processes in ME/CFS, specifically the central autonomic network (CAN) that controls the peripheral autonomic nervous system (ANS).
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Numerous clinical conditions include fatigue as part of their etiology (Ropper & Samuels, 2009) and the symptom sequelae of postexertional malaise (PEM) are widely recognized as the most debilitating and unrelenting feature of ME/CFS.
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The ANS, in coordination with the neuroendocrine system, regulates the cascading physiological events which serve as primary mediators of stress and arousal (McEwen et al., 2015). Operating synergistically with the CNS, the ANS promotes physiological stability through adaptive response to ever-changing internal and external demands.
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The CAN is a set of interconnected regions involved in top-down homeostatic control (Benarroch, 2012; Mo et al., 2019) of the peripheral ANS in coordination with intricate neuroimmune responses (Benarroch, 2019; Morrison & Nakamura, 2019) and arousal responses (Saper, 2002), emphasizing its potential importance in ANS-related disease.
The structures of the CAN were recently confirmed in a comprehensive meta-analysis of 43 task-based studies using the activation likelihood estimation (Turkeltaub et al., 2002), a widely used technique for showing the convergence of activated brain areas across different experiments.
Many cortical regions were reportedly involved in cognitive, affective, and sensorimotor tasks for initiating autonomic outflow with neuroendocrine responses of the hypothalamus and 1) upper brainstem nuclei which regulate pain modulation and stress responses, 2) lower brainstem nuclei which control circulation, respiration, and GI function, and 3) spinal level reflex centers.
The present study examined the cortical regions of the CAN using exact low-resolution electromagnetic tomography (eLORETA), an inverse solution that estimates cortical current density from EEG signals recorded at the scalp.
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The main objective of this pilot study was to quantify the effects of physical exertion on CAN function in ME/CFS using an isometric handgrip task.
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Resting-state qEEG data were collected from all participants during 3 separate time points: 1) before handgrip, 2) immediately after handgrip, and 3) 24 hours later. Thus, the discrepancy between CAN function at pre vs. posthandgrip exercise was used to quantify PEM.
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The principal finding was a significant time and frequency-dependent pattern of CAN perturbation in the patient group, relative to the HC group. Baseline current density in the patient group was significantly lower in the Alpha and Beta frequency bands, but marginally higher in the Delta band.
At Time 2 (posthandgrip), significant physiological changes emerged within both groups: ME/CFS current density was reduced, while HC current density was elevated. This discrepancy between groups occurred in all frequency bands, except Delta.
After 24 hours, however, the difference between groups became more pronounced.The ME/CFS group showed a greater reduction in current density whereas the HCs had further increased across all frequency bands.
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Together, these results are consistent with the characteristic stamina loss and behavioral worsening of symptoms in PEM after 24 hours and they extend previous investigations showing aberrant CNS signaling followed by fatigue-inducing voluntary motor tasks.
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However, this was a pilot study intended to provide groundwork for a larger scale study without sample size limitations. Thus, given the small sample size of each group, the differences found here must be interpreted with caution.
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We recognize that eLORETA source estimations are restricted to cortical regions of interest and several subcortical regions of the CAN (thalamus, red nucleus, cerebellum) were excluded from the analyses.
