title: Left ventricular remodeling with exercise in hypertension.
abstract: We investigated how exercise training superimposed on chronic hypertension impacted left ventricular remodeling. Cardiomyocyte hypertrophy, apoptosis, and proliferation in hearts from female spontaneously hypertensive rats (SHRs) were examined. Four-month-old SHR animals were placed into a sedentary group (SHR-SED; n = 18) or a treadmill running group (SHR-TRD, 20 m/min, 1 h/day, 5 days/wk, 12 wk; n = 18). Age-matched, sedentary Wistar Kyoto (WKY) rats were controls (n = 18). Heart weight was greater in SHR-TRD vs. both WKY (P < 0.01) and SHR-SED (P < 0.05). Morphometric-derived left ventricular anterior, posterior, and septal wall thickness were increased in SHR-SED relative to WKY and augmented in SHR-TRD. Cardiomyocyte surface area, length, and width were increased in SHR-SED relative to WKY and further increased in SHR-TRD. Calcineurin abundance was increased in SHR-SED vs. WKY (P < 0.001) and attenuated in SHR-TRD relative to SHR-SED (P < 0.05). Protein abundance and mRNA of Akt was not different among groups. The rate of apoptosis was increased in SHR-SED relative to WKY and mitigated in SHR-TRD. The abundance of Ki-67(+) cells across groups was not statistically different across groups. The abundance of cardiac progenitor cells (c-Kit(+) cells) was increased in SHR-TRD relative to WKY. These data suggest that exercise training superimposed on hypertension augmented cardiomyocyte hypertrophy, despite attenuating calcineurin abundance. Exercise training also mitigated apoptosis in hypertension and showed a tendency to enhance the abundance of cardiac progenitor cells, resulting in a more favorable cardiomyocyte number in the exercise-trained hypertensive heart.
authors: Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
authors: Stephen C
authors: SC
authors: Kolwicz
authors: Scott M
authors: SM
authors: MacDonnell
authors: Brian F
authors: BF
authors: Renna
authors: Patricia O
authors: PO
authors: Reger
authors: Rachid
authors: R
authors: Seqqat
authors: Khadija
authors: K
authors: Rafiq
authors: Zebulon V
authors: ZV
authors: Kendrick
authors: Steven R
authors: SR
authors: Houser
authors: Abdelkarim
authors: A
authors: Sabri
authors: Joseph R
authors: JR
authors: Libonati
mesh_terms: D000818:Animals; D017209:Apoptosis; D019703:Calcineurin / Q000378:metabolism; D006332:Cardiomegaly / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D049109:Cell Proliferation; D048429:Cell Size; D002908:Chronic Disease; D004195:Disease Models, Animal; D005260:Female; D006973:Hypertension / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D020287:In Situ Nick-End Labeling; D019394:Ki-67 Antigen / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D005082:Physical Exertion; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics; D019009:Proto-Oncogene Proteins c-kit / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013234:Stem Cells / Q000378:metabolism / Q000473:pathology; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
chemical_list: D019394:Ki-67 Antigen; D012333:RNA, Messenger; D019009:Proto-Oncogene Proteins c-kit; D051057:Proto-Oncogene Proteins c-akt; D019703:Calcineurin