Discussion
cognitive decline
CORTEX
Most studies examining the preventive effects of exercise intervention on age-related decline in executive function have focused on cardiovascular exercise protocols such as moderate-intensity exercise. In contrast, we focused on the potential effects of exercise at very light intensity (mild exercise) based on our previous findings that even acute, mild exercise stimulates the DLPFC, which results in better executive performance [First, we expected that the ME intervention would improve executive performance by shortening SI-related RT mediated by changing task-related cortical activation in the lateral prefrontal cortex as in our previous studies [Finally, since the impact of a mild-exercise intervention on neural efficiency might differ with age, we divided our participants into two age-dependent subgroups (YA and OA) based on the median split of age in each of their respective groups (ME and Con). We observed that the intervention led to both significantly improved executive performance and significantly improved NE scores in the ME group compared to the Con group, but only for the OA subgroup. These results partially support the notion that ME intervention can stave off age-related executive decline by enhancing NE in the prefrontal cortex in older adults. However, the present findings should be interpreted carefully because our participants included people of various ages, including middle-aged, and we performed a subgroup analysis based on the median age. Therefore, long-term follow-up is necessary to determine if executive decline can be delayed or prevented altogether and whether age is a key moderator for preventing cognitive decline through exercise.Mild exercise such as walking is considered an appealing exercise prescription among exercise specialists as well as physicians in terms of feasibility and efficacy, especially for sedentary older adults. Acute mild exercise, which is considered a stress-free exercise [Tamura and colleagues (2014) demonstrated that 2 years of ME intervention improved attentional shifting ability by preventing age-related structural changes in prefrontal cortex gray matter. However, the impact of a long-term ME intervention on task-related functional plasticity in the prefrontal cortex remained unknown. To reveal the underlying functional neural substrates of ME-enhanced executive performance, we used an event-related design with fNIRS probes covering the lateral prefrontal cortex during performance of the CWST. In our previous fNIRS studies, we demonstrated that acute exercise, regardless of intensity, increased task-relevant neural activations in the prefrontal cortex in young adults [It has been previously reported that age-related decline in the efficiency of executive ability may contribute to poor cognitive task performance of older adults [While we have demonstrated that exercise-enhanced executive performance is associated with a form of functional neuroplasticity after a long-term ME intervention in older adults, it remains unknown whether and how such an exercise intervention may maintain executive brain function in the aging brain. Work in animal models has suggested that exercise-induced neurotrophins, such as brain-derived neurotrophic factor (BDNF), insulin-like growth factor I (IGF-I), and nerve growth factor (NGF), are involved in brain plasticity by increasing neuronal survival and maintenance in the face of aging [