  The mammalian circadian system comprises a network of cell-autonomous
oscillators, spanning from the central clock in the brain to peripheral clocks
in other organs. These clocks are tightly coordinated to orchestrate rhythmic
physiological and behavioral functions. Dysregulation of these rhythms is a
hallmark of aging, yet it remains unclear how age-related changes lead to more
easily disrupted circadian rhythms. Using a two-population model of coupled
oscillators that integrates the central clock and the peripheral clocks, we
derive simple mean-field equations that can capture many aspects of the rich
behavior found in the mammalian circadian system. We focus on three
age-associated effects which have been posited to contribute to circadian
misalignment: attenuated input from the sympathetic pathway, reduced
responsiveness to light, and a decline in the expression of neurotransmitters.
We find that the first two factors can significantly impede re-entrainment of
the clocks following a perturbation, while a weaker coupling within the central
clock does not affect the recovery rate. Moreover, using our minimal model, we
demonstrate the potential of using the feed-fast cycle as an effective
intervention to accelerate circadian re-entrainment. These results highlight
the importance of peripheral clocks in regulating the circadian rhythm and
provide fresh insights into the complex interplay between aging and the
resilience of the circadian system.
