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Compensatory Effort Parallels Midbrain Deactivation during Mental Fatigue: An fMRI Study
Author(s) -
Seishu Nakagawa,
Motoaki Sugiura,
Yuko Akitsuki,
Hadi Hosseini,
Yuka Kotozaki,
Carlos Makoto Miyauchi,
Yukihito Yomogida,
Ryoichi Yokoyama,
Hikaru Takeuchi,
Ryuta Kawashima
Publication year - 2013
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0056606
Subject(s) - midbrain , neurovascular bundle , functional magnetic resonance imaging , cerebellum , audiology , neuroscience , psychology , neuroimaging , medicine , physical medicine and rehabilitation , central nervous system , anatomy
Fatigue reflects the functioning of our physiological negative feedback system, which prevents us from overworking. When fatigued, however, we often try to suppress this system in an effort to compensate for the resulting deterioration in performance. Previous studies have suggested that the effect of fatigue on neurovascular demand may be influenced by this compensatory effort. The primary goal of the present study was to isolate the effect of compensatory effort on neurovascular demand. Healthy male volunteers participated in a series of visual and auditory divided attention tasks that steadily increased fatigue levels for 2 hours. Functional magnetic resonance imaging scans were performed during the first and last quarter of the study (Pre and Post sessions, respectively). Tasks with low and high attentional load (Low and High conditions, respectively) were administrated in alternating blocks. We assumed that compensatory effort would be greater under the High-attentional-load condition compared with the Low-load condition. The difference was assessed during the two sessions. The effect of compensatory effort on neurovascular demand was evaluated by examining the interaction between load (High vs. Low) and time (Pre vs. Post). Significant fatigue-induced deactivation (i.e., Pre>Post) was observed in the frontal, temporal, occipital, and parietal cortices, in the cerebellum, and in the midbrain in both the High and Low conditions. The interaction was significantly greater in the High than in the Low condition in the midbrain. Neither significant fatigue-induced activation (i.e., Pre[PreE– PostE]) may reflect suppression of the negative feedback system that normally triggers recuperative rest to maintain homeostasis.

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