Left ventricular remodeling with exercise in hypertension.
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.
Kolwicz
Stephen C
SC
Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
MacDonnell
Scott M
SM
Renna
Brian F
BF
Reger
Patricia O
PO
Seqqat
Rachid
R
Rafiq
Khadija
K
Kendrick
Zebulon V
ZV
Houser
Steven R
SR
Sabri
Abdelkarim
A
Libonati
Joseph R
JR
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
D019394:Ki-67 Antigen; D012333:RNA, Messenger; D019009:Proto-Oncogene Proteins c-kit; D051057:Proto-Oncogene Proteins c-akt; D019703:Calcineurin