The hibernation phenomenon captures biological as well as clinical interests to understand how organs adapt. We studied how hibernating grizzly bears (Ursus arctos horribilis) tolerate extremely low heart rates without developing cardiac chamber dilation. We evaluated cardiac filling function in unanesthetized grizzly bears by echocardiography during the active and hibernating period. We also investigated both collagen and titin expression in the myocardium of active and hibernating grizzly bears. Heart rates were reduced from 84 bpm in active bears to 19 bpm in hibernating bears. Diastolic volume, stroke volume and left ventricular ejection fraction were not different. However, left ventricular muscle mass was significantly lower in the hibernating bears 300 ± 12 compared to 402 ± 14 grams (p = 0.003). Early ventricular filling deceleration times were shorter during hibernation, 106.4 ± 14 compared to 143.2 ± 20 ms (p = 0.002) suggesting increased ventricular stiffness. Collagen type I and III comparisons did not reveal differences between the two groups of bears. In contrast, expression of titin was altered by a significant upregulation of the stiffer N2B isoform at the expense of the more compliant N2BA isoform. The mean ratio of N2BA to N2B titin was 0.73 ± 0.07 in the active bears and decreased to 0.42 ± 0.03 (p = 0.006) in the hibernating bears. The upregulation of stiff N2B cardiac titin is a likely explanation for the increased ventricular stiffness revealed by echocardiography and we propose that it plays a role in preventing chamber dilation in hibernating grizzly bears.