Black bears suppress their metabolism by 75% during hibernation and 50% in spring emergence, but the mechanisms regulating metabolic suppression are unknown. Studies in hibernating ground squirrels have suggested that inhibition of mitochondrial succinate dehydrogenase activity (SDH, complex II) could play a role in metabolic suppression. The goal of this study is to examine the maximal activities of SDH across different tissues and possible mechanisms underlying changes in enzymatic activity. Beyond enzymatic assays, we also conducted discovery proteomics to gain insight into possible shifts in protein abundance across different physiological states in different tissues of black bears. We hypothesized that SDH activity in kidney, liver, and skeletal muscle whole-tissue homogenate and isolated mitochondria would be decreased in hibernation but unchanged in cardiac tissue during hibernation. To test this hypothesis, we measured maximal activity of SDH in these tissues in summer, hibernating, and spring emergence bears in whole-tissue homogenates and isolated mitochondria at 37°C (n=5-10). SDH activity decreased in skeletal muscle homogenates (p= 0.018) and isolated mitochondria (p= 0.011) in hibernating black bears, while in liver (p= 0.041) and kidney (p= 0.011) SDH activity was decreased during hibernation only in homogenates, but not isolated mitochondria. Cardiac tissue showed no significant decreases across physiological states. Statistics are one-way ANOVA, posthoc Tukey and Kruskal-Wallis tests. Proteomic analysis is currently pending. Overall, our results indicate that unlike small animal hibernators, which exhibit reduced SDH activity in isolated liver and muscle mitochondria, black bears appear to only reduce isolated mitochondria SDH activity within skeletal muscle. This distinction demonstrates unique regulation of SDH in hibernating black bears compared to small animal hibernators. Research reported in this publication was supported by the Alaska Undergraduate Scholarly Activity Program, the Alaska Space Grant Program (80NSSC25M7043), and an Institutional Development Award (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health under grant number P20GM103395. The content is solely the responsibility of the authors and does not necessarily reflect the official views of the NIH. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
menon et al. (Fri,) studied this question.