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(Circulation. 2005;112:3115-3121.)
© 2005 American Heart Association, Inc.

Heart Failure

Cardioprotection by Intermittent Fasting in Rats

Ismayil Ahmet, MD, PhD^*; Ruiqian Wan, PhD^*; Mark P. Mattson, PhD; Edward G. Lakatta, MD; Mark Talan, MD, PhD

From the Laboratories of Cardiovascular Sciences (I.A., E.G.L., M.T.) and of Neurosciences (R.W., M.P.M.), National Institute on Aging, Intramural Research Program, National Institutes of Health, Baltimore, Md.

Correspondence to Mark I. Talan, MD, PhD, Gerontology Research Center, 5600 Nathan Shock Dr, Baltimore, MD 21224. E-mail talanm{at}grc.nia.nih.gov

Received May 20, 2005; revision received August 8, 2005; accepted August 26, 2005.

Background— Intermittent fasting (IF), a dietary regimen in which food is available only every other day, increases the life span and reduces the incidence of age-associated diseases in rodents. We have reported neuroprotective effects of IF against ischemic injury of the brain. In this study, we examined the effects of IF on ischemic injury of the heart in rats.

Methods and Results— After 3 months of IF or regular every-day feeding (control) diets started in 2-month-old rats, myocardial infarction (MI) was induced by coronary artery ligation. Twenty-four hours after MI, its size in the IF group was 2-fold smaller, the number of apoptotic myocytes in the area at risk was 4-fold less, and the inflammatory response was significantly reduced compared with the control diet group. Serial echocardiography revealed that during 10 weeks after MI (with continuation of the IF regimen), the left ventricular (LV) remodeling and MI expansion that were observed in the control diet group were absent in the IF group. In a subgroup of animals with similar MI size at 1 week after MI, further observation revealed less remodeling, better LV function, and no MI expansion in the IF group compared with the control group.

Conclusions— IF protects the heart from ischemic injury and attenuates post-MI cardiac remodeling, likely via antiapoptotic and antiinflammatory mechanisms.

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