Why the study?
A progressive decline in maximum heart rate is a fundamental aspect of aging that limits aerobic capacity and functional independence, reflecting intrinsic sinoatrial node slowing.
This review summarizes the tissue, cellular, and molecular mechanisms underlying the age-related decline in maximum heart rate and sinoatrial node pacemaker activity.
May inform age-adjusted exercise testing interpretation; leaves open targeted therapies for sinoatrial node remodeling.
A progressive decline in maximum heart rate (mHR) is a fundamental aspect of aging in humans and other mammals. This decrease in mHR is independent of gender, fitness, and lifestyle, affecting in equal measure women and men, athletes and couch potatoes, spinach eaters and fast food enthusiasts. Importantly, the decline in mHR is the major determinant of the age-dependent decline in aerobic capacity that ultimately limits functional independence for many older individuals. The gradual reduction in mHR with age reflects a slowing of the intrinsic pacemaker activity of the sinoatrial node of the heart, which results from electrical remodeling of individual pacemaker cells along with structural remodeling and a blunted β-adrenergic response. In this review, we summarize current evidence about the tissue, cellular, and molecular mechanisms that underlie the reduction in pacemaker activity with age and highlight key areas for future work.
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Peters et al. (2019) studied this question.
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