title: Myocardial hypoperfusion/reperfusion tolerance with exercise training in hypertension.
abstract: The purpose of this study was to examine whether exercise training, superimposed on compensated-concentric hypertrophy, could increase myocardial hypoperfusion-reperfusion (H/R) tolerance. Female Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) (age: 4 mo; N = 40) were placed into a sedentary (SED) or exercise training (TRD) group (treadmill running; 25 m/min, 1 h/day, 5 days/wk for 16 wk). Four groups were studied: WKY-SED (n = 10), WKY-TRD (n = 10), SHR-SED (n = 10), and SHR-TRD (n = 10). Blood pressure and heart rate were determined, and in vitro isolated heart performance was measured with a retrogradely perfused, Langendorff isovolumic preparation. The H/R protocol consisted of a 75% reduction in coronary flow for 17 min followed by 30 min of reperfusion. Although the rate-pressure product was significantly elevated in SHR relative to WKY, training-induced bradycardia reduced the rate-pressure product in SHR-TRD (P < 0.05) without an attenuation in systolic blood pressure. Heart-to-body weight ratio was greater in both groups of SHR vs. WKY-SED (P < 0.001). Absolute and relative myocardial tolerance to H/R was greater in WKY-TRD and both groups of SHR relative to WKY-SED (P < 0.05). Endurance training superimposed on hypertension-induced compensated hypertrophy conferred no further cardioprotection to H/R. Postreperfusion 72-kDa heat shock protein abundance was enhanced in WKY-TRD and both groups of SHR relative to WKY-SED (P < 0.05) and was highly correlated with absolute left ventricular functional recovery during reperfusion (R2= 0.86, P < 0.0001). These data suggest that both compensated hypertrophy associated with short-term hypertension and endurance training individually improved H/R and that increased postreperfusion 72-kDa heat shock protein abundance was, in part, associated with the cardioprotective phenotype observed in this study.
authors.affiliation: Department of Kinesiology, Temple Univ., 122 Pearson Hall, 1800 North Broad St., Philadelphia, PA 19122, USA.
authors.forename: Patricia O
authors.initials: PO
authors.lastname: Reger
authors.forename: Mary F
authors.initials: MF
authors.lastname: Barbe
authors.forename: Mamta
authors.initials: M
authors.lastname: Amin
authors.forename: Brian F
authors.initials: BF
authors.lastname: Renna
authors.forename: Leigh Ann
authors.initials: LA
authors.lastname: Hewston
authors.forename: Scott M
authors.initials: SM
authors.lastname: MacDonnell
authors.forename: Steven R
authors.initials: SR
authors.lastname: Houser
authors.forename: Joseph R
authors.initials: JR
authors.lastname: Libonati
mesh_terms: D000818:Animals; D001794:Blood Pressure; D006332:Cardiomegaly / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D004195:Disease Models, Animal; D005260:Female; D050884:HSP72 Heat-Shock Proteins / Q000378:metabolism; D006339:Heart Rate; D006352:Heart Ventricles / Q000378:metabolism; D006973:Hypertension / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D009200:Myocardial Contraction / Q000502:physiology; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D018487:Ventricular Dysfunction, Left / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control; D017725:Ventricular Pressure
chemical_list: D050884:HSP72 Heat-Shock Proteins