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Exercise training and MAPK protein expression in rats with heart failure (LB521)
Author(s) -
Gomes Mariana,
Martinez Paula,
Campos Dijon,
Damatto Ricardo,
Pagan Luana,
Lima Aline,
Bonomo Camila,
Matsimbe Ana,
Juma Buanansa,
Okoshi Katashi,
Okoshi Marina
Publication year - 2014
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.28.1_supplement.lb521
Subject(s) - sed , ventricle , medicine , heart failure , cardiology , treadmill , ventricular remodeling , analysis of variance , cardiac function curve , soleus muscle , skeletal muscle , endocrinology
This study examined whether exercise training influences physical capacity, cardiac remodeling, and mitogen‐activated protein kinases (MAPK) expression in skeletal muscle of rats with pressure overload‐induced heart failure. Methods: Twenty weeks after inducing aortic stenosis (AS), Wistar rats were assigned to four groups (n=8): sham sedentary (Sed), Sham exercise (Ex), AS, and AS‐Ex. Physical training was performed 5 times per week for 8 weeks in a treadmill. Physical performance was assessed by exercise test on a treadmill with a gradual speed increase before and after the training period. Transthoracic echocardiogram was performed before and after training. Protein expression was analyzed by Western blot in soleus muscle. Statistical analyzes: ANOVA and Tukey test. Results: Before training, echocardiographic parameters did not differ between AS and AS‐Ex groups. Physical training improved functional capacity without changing cardiac structures or left ventricular function. Right ventricle weight was higher in both AS than Sham groups [Sed 0.23 (0.21‐0.24); Ex 0.26 (0.22‐0.29); AS 0.45 (0.36‐0.56); AS‐Ex 0.46 (0.40‐0.56) g]. Total p38, p‐p38 and total JNK did not differ between groups. Phosphorylated‐JNK was lower in AS‐Ex than AS group (Sed 1.00±0.17; Ex 0.95±0.17; AS 1.34±0.17; AS‐Ex 0.57±0.18; p=0.007). Conclusion: Exercise training improves physical capacity without changing left ventricular remodeling, and decreases p‐JNK in soleus muscle of heart failure rats. Support: FAPESP and CNPq.