Five-year changes in objectively measured cardiorespiratory fitness, physical activity, and sedentary time in mid-to-late adulthood.

This study examined 5-year changes in cardiorespiratory fitness, physical activity, and sedentary time in mid-to-late aged adults. Fifty-seven participants completed baseline and follow-up treadmill exercise tests and physical activity monitoring. We observed a 14% decline in fitness (p < 0.001), 12% decrease in physical activity (p = 0.010), and non-significant increase in sedentary time (p = 0.196). Age was negatively associated with 5-year change in physical activity (r = -0.31; p = 0.02) and this decline was strongest among APOE ε4 carriers (g = -0.75). Novelty: Cardiorespiratory fitness and physical activity significantly declined from mid-to-late adulthood, these findings were most pronounced among older adults and those with genetic risk for Alzheimer's disease.

Cardiorespiratory fitness mitigates brain atrophy and cognitive decline in adults at risk for Alzheimer's disease.

INTRODUCTION: Cardiorespiratory fitness (CRF) may mitigate Alzheimer's disease (AD) progression. This study examined the longitudinal associations of CRF with brain atrophy and cognitive decline in a late-middle-aged cohort of adults at risk for AD. METHODS: One hundred ten cognitively unimpaired adults (66% female, mean age at baseline 64.2 ± 5.7 years) completed a baseline graded treadmill exercise test, two brain magnetic resonance imaging scans (over 4.67 ± 1.17 years), and two to three cognitive assessments (over 3.26 ± 1.02 years). Linear mixed effects models examined the longitudinal associations adjusted for covariates. RESULTS: Participants with higher baseline CRF had slower annual decline in total gray matter volume (P = .013) and cognitive function (P = .048), but not hippocampal volume (P = .426). Exploratory analyses suggested these effects may be stronger among apolipoprotein E ε4 carriers. DISCUSSION: CRF is a modifiable physiological attribute that may be targeted during the preclinical phase of AD in effort to delay disease progression, perhaps most effectively among those with genetic risk.