title: Exercise training improves systolic function in hypertensive myocardium.
abstract: 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% Vo(2 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 (Akt(Pi)), Bad, phosphorylated Bad (Bad(Pi)) 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 (E(s)) in SHR vs. WKY. Exercise training corrected E(s) 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 Bad(Pi,) c-IAP, and x-IAP were significantly lower in SHR relative to WKY (P < 0.05). Exercise training increased Bad(Pi) 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.
authors.affiliation: Univ. of Pennsylvania School of Nursing, Biobehavioral and Health Sciences, Philadelphia, PA, USA. jlibonat@nursing.upenn.edu
authors.forename: Joseph R
authors.initials: JR
authors.lastname: Libonati
authors.forename: Abdelkarim
authors.initials: A
authors.lastname: Sabri
authors.forename: Canhua
authors.initials: C
authors.lastname: Xiao
authors.forename: Scott M
authors.initials: SM
authors.lastname: Macdonnell
authors.forename: Brian F
authors.initials: BF
authors.lastname: Renna
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics / Q000502:physiology; D015415:Biomarkers / Q000378:metabolism; D019703:Calcineurin / Q000235:genetics; D020169:Caspases / Q000378:metabolism; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006439:Hemodynamics; D006973:Hypertension / Q000235:genetics / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy*; D009206:Myocardium / Q000473:pathology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D015398:Signal Transduction; D013599:Systole / Q000502:physiology*
chemical_list: D015415:Biomarkers; D012333:RNA, Messenger; D019703:Calcineurin; D020169:Caspases