Department of Functional Brain Imaging, Institute of Development, Aging and Cancer, (IDAC), Tohoku University, Sendai, Japan.
PLoS One. 2013;8(2):e56606. doi: 10.1371/journal.pone.0056606. Epub 2013 Feb 14.
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<Post), nor its interaction with factor Load, was identified. The observed midbrain deactivation ([PreH - PostH]>[PreE- PostE]) may reflect suppression of the negative feedback system that normally triggers recuperative rest to maintain homeostasis.
疲劳反映了我们生理负反馈系统的功能，该系统防止我们过度工作。然而，当感到疲劳时，我们常常试图抑制这个系统，以弥补由此导致的表现下降。先前的研究表明，疲劳对神经血管需求的影响可能受到这种代偿努力的影响。本研究的主要目的是分离代偿努力对神经血管需求的影响。健康的男性志愿者参与了一系列视觉和听觉分散注意力任务，这些任务在 2 小时内逐渐增加疲劳水平。在研究的第一和最后四分之一（分别为 Pre 和 Post 期）进行功能磁共振成像扫描。在交替的块中管理低和高注意力负荷的任务（分别为 Low 和 High 条件）。我们假设在高注意力负荷条件下，代偿努力会比低负荷条件下更大。在两个阶段评估差异。通过检查负荷（高与低）与时间（预与后）之间的相互作用，评估代偿努力对神经血管需求的影响。在 High 和 Low 条件下，在前额、颞叶、枕叶和顶叶皮层、小脑和中脑都观察到了显著的疲劳诱导去激活（即 Pre>Post）。在中脑，这种相互作用在 High 条件下明显大于 Low 条件。在中脑，既没有显著的疲劳诱导激活（即 Pre<Post），也没有发现其与负荷因素的相互作用。观察到的中脑去激活（[PreH - PostH]>[PreE- PostE]）可能反映了对负反馈系统的抑制，该系统通常会触发恢复性休息以维持体内平衡。
