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Characterization of regression of exercise‐induced cardiac hypertrophy
Author(s) -
Stricker Janelle C,
Nichols Cody E,
Katz Andrew,
Fancher Ibra,
Cuppett Tiffany C,
Miletti Kady,
Vasisko Corey,
Dabkowski Erinne R,
Baseler Walter A,
Hollander John M,
Morissette Michael R
Publication year - 2010
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.24.1_supplement.lb593
Subject(s) - muscle hypertrophy , medicine , protein kinase b , endocrinology , cardiology , heart failure , phosphorylation , biology , biochemistry
The heart is capable of changing size in response to changes in chronic stress or demand. Exercise and hypertension are classic examples of stimuli that promote physiologic and pathologic hypertrophy respectively. Although initially beneficial for maintaining function with increased stress, pathologic hypertrophy can progress to heart failure if the inducing stress is not mitigated. Additionally, in contrast to physiologic hypertrophy, reverse remodeling of pathologic hypertrophy is often incomplete in respect to returning to normal size and function. In order to understand the molecular mechanisms involved in the reversal of hypertrophy we subjected mice to a three‐week swim protocol followed by 0, 3, and 6 days of rest. Swim‐training induced a 25.4±2.0% (n=19, p<0.05) increase in heart weight/body weight compared to sedentary controls (n=13). Hypertrophy regressed by 31.8% and 90.0% after 3 and 6 days of rest respectively. Interestingly, western blot analysis showed an increase in cardiac LC3B II in rested mice, suggesting the involvement of autophagy in reverse remodeling. Unexpectedly the phosphorylation of Akt (308, 473), GSK3β, and S6 were not increased in rested hearts, but actually decreased in hypertrophied hearts. These data suggest that the observed increase in LC3B II is not mediated by the Akt‐mTOR pathway. Support: NCRR 5P20RR016477 (WV INBRE), NIA K01AG026337 (MRM), AHA (MRM)