Voluntary Wheel Running Exercise Does Not Attenuate Circadian and Cardiac Dysfunction Caused by Conditional Deletion of Bmal1

Bmal1 cardiac knockout mice exhibited cardiac hypertrophy and fibrosis with impaired systolic function.

• Conditional deletion of the Bmal1 gene in cardiac cells led to significant cardiac remodeling.
• This remodeling included both hypertrophy and fibrosis, negatively affecting heart function.
• Exercise, specifically wheel running, did not reverse the cardiac dysfunction observed in these mice.
• Disruption of the cardiac circadian clock was associated with altered systemic rhythms, including changes in activity patterns related to the light/dark cycle.
• Molecular mechanisms driving the cardiac changes remain unclear and do not involve the activation of mTOR signaling or alterations in metabolic gene expression.

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