Abstract

Menopause or Estrogen deficiency increase risk of heart failure. Cardiac inflammation, apoptosis, and fibrosis were found in rats with bilateral ovariectomy or with co-mobility such as aging, diabetes, or hypertension. In current review, exercise training suppressed ovariectomy/diabetes-induced cardiac inflammatory status (decreases in Protein oxidation and TNF-α/ IL-10, increase in GSH/GSSG) as well as suppressed ovariectomy/hypertension-induced cardiac anti-oxidative stress (increases in SOD and Catalase) and inflammatory status (decreases in TNF-α, p-IKKα/ß, p-NFkB, COX-2). Exercise training suppressed ovariectomy-induced cardiac Fas dependent apoptotic pathways (decreases in t-Bid, Bad, Bax, Bak, Active Caspase 9, and Active Caspase 3) and mitochondria dependent apoptotic pathways (decreases in TNF-α, TNFR1, Fas, FADD, active Caspase 8, active Caspase 3) in ovariectomized rat models. Exercise training attenuated ovariectomy-induced cardiac fibrosis and fibrotic pathways (decreases in Collagen I, TGF-ß, p-Smad 2/3, CTGF, t-PA, MMP9).

The findings might provide one possible mechanism of exercise training on preventing heart failure in menopausal or bilateral oophorectomied women through anti-inflammatory, anti-apoptotic, and antifibrotic pathways.