Chamber-specific regulation of cardiac myosin, gene, and protein expression in the heart of hibernating grizzly bears, Ursus arctos horribilis

Grizzly bears, Ursus arctos horribilis, tolerate extended periods of extremely low heart rate during hibernation without developing congestive heart failure or chamber dilation. I hypothesized that relative MyHC isoform ratio would be unchanged during hibernation to maintain contractility during hibernation-associated bradycardia. Myosin heavy-chain (MyHC) proteins are the primary determinates of contractility, and I report a novel shift in expression toward MyHC-alpha isoform in the left atrium during hibernation. Interestingly, mRNA expression of atrogenes and their regulatory transcription factors is not increased in concert with ventricular atrophy, although myocardial IGF-I gene expression is decreased. Proteomic analysis of seasonal protein profiles from left atria and ventricles revealed no significant differences between groups. These findings highlight chamber-specific regulation of relative MyHC expression that may serve to optimize contractility during the altered hemodynamic state of hibernation, and suggest posttranscriptional regulation of cardiac atrophy in hibernating grizzly bears.