Nearly 40% of Americans are obese. Weight gain results from a consistent imbalance between calories consumed and calories burned. Energy expended during activity is the second largest contributor to our total daily energy expenditure (EE). Uncovering ways to increase EE could yield treatments for obesity. One profound, untapped potential source for increasing EE is through muscle thermogenesis. Our lab has repeatedly shown exposing rats to predator odor (PO) induces a rapid and robust increase in muscle thermogenesis. However, it is unknown if the PO-induced thermogenic response is a general stress response, or if it is specific to predator odor. Here, we address this concern.

We surgically implanted temperature transponders into the gastrocnemius muscles of 7 female rats. Using a transponder reader, we measured the skeletal muscle temperature at multiple timepoints following 1) control odor exposure, 2) mild stress by 1 min of physical restraint, and 3) PO. We chose mild physical restraint as a stressor because gentle restraint allowed us to avoid potential heat retention.

Results showed that compared to control odor, PO, but not mild stress, induced a significant change in muscle temperature across 2hrs. These data suggest that the thermogenic response to PO in rats is mediated by brain substrates specific to predator threat rather than a generalized stress response. In other words, the response to predator threat is likely distinct from the response to other types of stressors.