The interplay of sleep architecture and exercise in executive function of middle-aged and older adults

Executive function decline in middle-aged and older adults is a significant public health concern, with sleep disturbances and physical inactivity being two major modifiable risk factors. Existing evidence suggests bidirectional associations between sleep and exercise, with both factors potentially influencing cognitive function. This review synthesizes current evidence on the interplay among exercise, sleep architecture, and executive function in aging populations. We first discuss the noradrenergic and adenosinergic systems as shared neuromodulatory substrates underlying the reciprocal regulation of sleep and exercise. We then review evidence linking slow-wave sleep (SWS) to exercise-induced neuroplasticity and sleep spindles to memory consolidation. The glymphatic system is presented as a sleep-dominant clearance mechanism that may interact with exercise. At the brain network level, we summarize how sleep and exercise are, respectively, associated with the dynamic balance between the central executive network and the default mode network. Furthermore, subcomponent-specific associations are examined: SWS duration correlates with inhibitory control and working memory, whereas REM sleep is linked to cognitive flexibility, and resistance or mind–body exercises show selective benefits for distinct executive domains. Nonlinear dose-timing effects are also considered, such as the optimal moderate-intensity aerobic exercise for preserving SWS and the morning exercise preference for aligning with circadian rhythms in older adults. Collectively, this review provides a theoretical basis for understanding how physical activity and sleep architecture jointly influence executive function in middle-aged and older adults. It highlights convergent physiological pathways—ranging from molecular neuromodulators and glymphatic clearance to large-scale brain network dynamics—that may guide future mechanistic studies and intervention strategies for age-related cognitive decline.