Effects of aerobic exercise training on cardiac renin-angiotensin system in an obese Zucker rat strain.
OBJECTIVE
Obesity and renin angiotensin system (RAS) hyperactivity are profoundly involved in cardiovascular diseases, however aerobic exercise training (EXT) can prevent obesity and cardiac RAS activation. The study hypothesis was to investigate whether obesity and its association with EXT alter the systemic and cardiac RAS components in an obese Zucker rat strain.


METHODS
THE RATS WERE DIVIDED INTO THE FOLLOWING GROUPS: Lean Zucker rats (LZR); lean Zucker rats plus EXT (LZR+EXT); obese Zucker rats (OZR) and obese Zucker rats plus EXT (OZR+EXT). EXT consisted of 10 weeks of 60-min swimming sessions, 5 days/week. At the end of the training protocol heart rate (HR), systolic blood pressure (SBP), cardiac hypertrophy (CH) and function, local and systemic components of RAS were evaluated. Also, systemic glucose, triglycerides, total cholesterol and its LDL and HDL fractions were measured.


RESULTS
The resting HR decreased (∼12%) for both LZR+EXT and OZR+EXT. However, only the LZR+EXT reached significance (p<0.05), while a tendency was found for OZR versus OZR+EXT (p = 0.07). In addition, exercise reduced (57%) triglycerides and (61%) LDL in the OZR+EXT. The systemic angiotensin I-converting enzyme (ACE) activity did not differ regardless of obesity and EXT, however, the OZR and OZR+EXT showed (66%) and (42%), respectively, less angiotensin II (Ang II) plasma concentration when compared with LZR. Furthermore, the results showed that EXT in the OZR prevented increase in CH, cardiac ACE activity, Ang II and AT2 receptor caused by obesity. In addition, exercise augmented cardiac ACE2 in both training groups.


CONCLUSIONS
Despite the unchanged ACE and lower systemic Ang II levels in obesity, the cardiac RAS was increased in OZR and EXT in obese Zucker rats reduced some of the cardiac RAS components and prevented obesity-related CH. These results show that EXT prevented the heart RAS hyperactivity and cardiac maladaptive morphological alterations in obese Zucker rats.
Laboratory of Biochemistry and Molecular Biology of Exercise, School of Physical Education and Sport, University of São Paulo, São Paulo, Brazil.
Diego Lopes Mendes
DL
Barretti
Flávio de Castro
Fde C
Magalhães
Tiago
T
Fernandes
Everton Crivoi
EC
do Carmo
Kaleizu Teodoro
KT
Rosa
Maria Claudia
MC
Irigoyen
Carlos Eduardo
CE
Negrão
Edilamar Menezes
EM
Oliveira
D000804:Angiotensin II / Q000378:metabolism; D000085962:Angiotensin-Converting Enzyme 2; D000818:Animals; D001794:Blood Pressure; D015153:Blotting, Western; D004452:Echocardiography; D006321:Heart / Q000503:physiopathology*; D006339:Heart Rate; D008297:Male; D018995:Myosin Heavy Chains / Q000378:metabolism; D009765:Obesity / Q000503:physiopathology*; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D010805:Physical Conditioning, Animal; D051381:Rats; D011924:Rats, Zucker; D060888:Real-Time Polymerase Chain Reaction; D012084:Renin-Angiotensin System; D020133:Reverse Transcriptase Polymerase Chain Reaction
D000804:Angiotensin II; D007703:Peptidyl-Dipeptidase A; C000705329:Ace2 protein, rat; D000085962:Angiotensin-Converting Enzyme 2; D018995:Myosin Heavy Chains