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A brief morning rest period benefits cardiac repair in pressure overload hypertrophy and postmyocardial infarction
Cristine J. Reitz, … , W. Glen Pyle, Tami A. Martino
Cristine J. Reitz, … , W. Glen Pyle, Tami A. Martino
Published October 18, 2022
Citation Information: JCI Insight. 2022;7(22):e164700. https://doi.org/10.1172/jci.insight.164700.
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Research Article Cardiology

A brief morning rest period benefits cardiac repair in pressure overload hypertrophy and postmyocardial infarction

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Abstract

Rest has long been considered beneficial to patient healing; however, remarkably, there are no evidence-based experimental models determining how it benefits disease outcomes. Here, we created an experimental rest model in mice that briefly extends the morning rest period. We found in 2 major cardiovascular disease conditions (cardiac hypertrophy, myocardial infarction) that imposing a short, extended period of morning rest each day limited cardiac remodeling compared with controls. Mechanistically, rest mitigates autonomic-mediated hemodynamic stress on the cardiovascular system, relaxes myofilament contractility, and attenuates cardiac remodeling genes, consistent with the benefits on cardiac structure and function. These same rest-responsive gene pathways underlie the pathophysiology of many major human cardiovascular conditions, as demonstrated by interrogating open-source transcriptomic data; thus, patients with other conditions may also benefit from a morning rest period in a similar manner. Our findings implicate rest as a key driver of physiology, creating a potentially new field — as broad and important as diet, sleep, or exercise — and provide a strong rationale for investigation of rest-based therapy for major clinical diseases.

Authors

Cristine J. Reitz, Mina Rasouli, Faisal J. Alibhai, Tarak N. Khatua, W. Glen Pyle, Tami A. Martino

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Figure 1

Rest benefits outcomes in pressure overload–induced cardiac hypertrophy (TAC model).

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Rest benefits outcomes in pressure overload–induced cardiac hypertrophy ...
(A) Rest model and cardiac hypertrophy experimental design: mice underwent baseline echocardiography followed by transverse aortic constriction (TAC) and were randomized to control conditions (12 hour-light/12-hour dark cycle; LD 12:12) versus the rest model (12-hour light/4-hour blue light/8-hour dark; LBD 12:4:8) for up to 4 weeks. (B) Representative M-mode echocardiography at 4 weeks after TAC, showing (C) smaller left ventricular internal dimensions at diastole (LVIDd) and systole (LVIDs) and better % ejection fraction (EF) and fractional shortening (FS) in mice under the rest model. n = 11 mice/group. ***P < 0.001, unpaired, 2-tailed Student’s t test. (D) Representative images and (E) quantification of heart weight (HW) and HW/BW at 4 weeks after TAC. n = 11 mice/group. ***P < 0.001, unpaired Student’s t test. (F) Representative images and quantification of cardiomyocyte cross-sectional area at 4 weeks after TAC. n = 3 sham hearts/group, n = 5 TAC hearts/group. **P < 0.01, unpaired Student’s t test. Scale bar: 100 μm.

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