Exercise training improves systolic function in hypertensive myocardium
The general purpose of this study was to test the effect of exercise training on the left ventricular (LV) pressure-volume relationship (LV/PV) and apoptotic signaling markers in normotensive and hypertensive hearts. Four-month-old female normotensive Wistar-Kyoto rats (WKY; n = 37) and spontaneously hypertensive rats (SHR; n = 38) were assigned to a sedentary (WKY-SED, n = 21; SHR-SED, n = 19) or treadmill-trained (WKY-TRD, n = 16; SHR-TRD, n = 19) group (∼60% V̇o2 peak, 60 min/day, 5 days/wk, 12 wk). Ex vivo LV/PV were established in isovolumic Langendorff-perfused hearts, and LV levels of Akt, phosphorylated Akt (AktPi), Bad, phosphorylated Bad (BadPi) c-IAP, x-IAP, calcineurin, and caspases 3, 8, and 9 were measured. Heart-to-body weight ratio was increased in SHR vs. WKY ( P < 0.05), concomitant with increased calcineurin mRNA ( P < 0.05). There was a rightward shift in the LV/PV ( P < 0.05) and a reduction in systolic elastance (Es) in SHR vs. WKY. Exercise training corrected Es in SHR ( P < 0.05) but had no effect on the LV/PV in WKY. Caspase 3 was increased in SHR-SED relative to WKY-SED, while BadPi, c-IAP, and x-IAP were significantly lower in SHR relative to WKY ( P < 0.05). Exercise training increased BadPi in both WKY and SHR but did not alter caspase 9 activity in either group. While caspase 3 activity was increased with training in WKY ( P < 0.05), it was unchanged with training in SHR. We conclude that moderate levels of regular aerobic exercise attenuate systolic dysfunction early in the compensatory phase of hypertrophy, and that a differential phenotypical response to moderate-intensity exercise exists between WKY and SHR.