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Cardiac Responses to Endurance Training in a Canine Model of Sudden Death
Author(s) -
MoustafaBayoumi Moustafa,
Hassanain Hamdy H,
Kirby Timothy E,
Devor Steven T,
Kukielka Monica,
Billman George E
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a395-c
Subject(s) - calcineurin , endurance training , medicine , cardiology , citrate synthase , muscle hypertrophy , protein expression , endocrinology , chemistry , enzyme , biochemistry , transplantation , gene
The present study investigated the effects of 10‐weeks of endurance training on the cardiac oxidative capacity, left ventricular wall thickness, and calcineurin A protein expression in dogs either susceptible or resistant to ventricular fibrillation. The animals were randomly assigned into four groups [susceptible trained (ST) – susceptible control (SC) –resistant trained (RT) – resistant control (RC)]. At the completion of the 10‐weeks, citrate synthase (CS) activity and calcineurin A protein expression were assayed. An echocardiogram was used to measure left ventricular (LV) systolic wall thickness. LV citrate synthase activity was significantly lower (‐40.3%) in the SC group compared to the RC group (1103.8±221.6 vs. 1848.3±194.2 μmol/mg protein/min, p < 0.05). Endurance training increased (35.5%) LV CS activity in the susceptible dogs [ST, 1711.3±138.5 vs. SC 1103.8±221.6 μmol/mg protein/min, p < 0.05] but did not alter this activity in the resistant dogs. Training also induced a significance (p < 0.025) increase in LV systolic wall thickness (ST, pre 10 ± 0.3, post 11.2 ± 0.5; RT pre 8.8 ± 0.5, post 9.8 ± 0.5 mm) but calcineurin A protein expression in the LV did not change. These data suggest that CS activity is impaired in susceptible dogs and that this deficit can be corrected by endurance training. Furthermore, endurance training can elicit ventricular hypertrophy without increasing clacineurin signaling.