Exercise training prevents development of cardiac contractile dysfunction in hypertensive TG(mREN2)27 rats

Angiotensin II (Ang II) contributes to cardiac remodeling and left ventricular (LV) dysfunction. In contrast, exercise may have beneficial effects on LV structure and function. We investigated the effects of low-intensity exercise training (ET) on in-vivo cardiac function in hypertensive TG(mREN-2)27 rats (Ren2), which develop LV hypertrophy and dysfunction. Ren2 rats and Sprague-Dawley (SD) controls (4 to 5 weeks) began treadmill exercise every day for 5 to 6 weeks. Cardiac function was evaluated by echocardiography. Cardiac output and stroke volume were increased by ET in both the 8-week-old SD and Ren2. Slope of mitral deceleration time, a noninvasive measure of diastolic function, was lower in the Ren2 rats, but not changed by ET. LV collagen deposition, as assessed by hydroxyproline assay, was not affected by rat strain or ET at 10 to 11 weeks of age. LV B-type natriuretic peptide mRNA levels were higher in the Ren2 rats (100%), but not affected by ET. Both α (∼14.5-fold) and β (∼2.5-fold) myosin heavy chain mRNA were higher in the LV of Ren2 rats (P < .05), but were not changed by ET. Low-intensity exercise training in Ren2 rats, a model of Ang-II-mediated hypertension, maintains cardiac index and stroke volume in the presence of impaired diastolic function at 8 weeks of age.