Abstract
The cardiac pacemaker ignites and coordinates the contraction of the whole heart, uninterruptedly, throughout our entire life. Pacemaker rate is constantly tuned by the autonomous nervous system to maintain body homeostasis. Sympathetic and parasympathetic terminals act over the pacemaker cells as the accelerator and the brake pedals, increasing or reducing the firing rate of pacemaker cells to match physiological demands. Despite the remarkable reliability of this tissue, the pacemaker is not exempt from the detrimental effects of aging. Mammals experience a natural and continuous decrease in the pacemaker rate throughout the entire lifespan. Why the pacemaker rhythm slows with age is poorly understood. Neural control of the pacemaker is remodeled from birth to adulthood, with strong evidence of age-related dysfunction that leads to a downshift of the pacemaker. Such evidence includes remodeling of pacemaker tissue architecture, alterations in the innervation, changes in the sympathetic acceleration and the parasympathetic deceleration, and alterations in the responsiveness of pacemaker cells to adrenergic and cholinergic modulation. In this review, we revisit the main evidence on the neural control of the pacemaker at the tissue and cellular level and the effects of aging on shaping this neural control.
Highlights
On average, the human heart beats 100,000 times a day
Every heartbeat starts with a subtle electrical spark inside the sinoatrial node, a small and highly specialized tissue located next to the right atrium known as the cardiac pacemaker
The slowdown of the intrinsic pacemaker rate is the main cause for the accompanying decline in maximum heart rate, playing a significant role in the loss of aerobic capacity in older adults
Summary
The human heart beats 100,000 times a day. Every heartbeat starts with a subtle electrical spark inside the sinoatrial node, a small and highly specialized tissue located next to the right atrium known as the cardiac pacemaker. Extrinsic mechanisms linked to the age-associated pacemaker slowdown include an increase in tissue fibrosis and changes in the sympathetic/parasympathetic balance. There is evidence that aging causes an important remodeling in the sympathetic and parasympathetic modulation and the response of pacemaker cells to it.
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