Obesity is associated with many co-morbidities, including impaired balance and an increased risk of falling. While the increase in weight and change in center of mass contribute to balance instability, there is growing evidence that changes in sensory function also occur during obesity. Due to the importance of muscle spindle afferent sensory information to proprioception and motor control, we tested the hypothesis that diet induced obesity could alter both muscle spindle afferent mechanosensation and motor neuron excitability to Group Ia muscle spindle afferent sensory input. For all experiments C57BL/6 mice of both sexes were fed either a control (CON; 10% kcal fat, Diet D12450J, Research Diets) or a high fat diet (HFD; 60% kcal fat, Diet D12492) for 5-15 weeks starting 4 weeks after birth. To determine whether muscle spindle afferent passive mechanosensation was affected by diet induced obesity, we used an in vitro extensor digitorum longus muscle-nerve preparation. We tested the response of individual muscle spindle afferents to ramp and hold stretch and sinusoidal vibration (CON n=10M & 11F; HFD n=12M & 11F). High fat feeding for 10 weeks led to decreased firing rates during all points of stretch measured compared to control in mice of both sexes (highest firing rate during ramp, 0.5 s and 3.5 s into hold phase of stretch; ANOVA, p<0.001 for all 3 measures). Muscle spindle afferent dynamic mechanosensation was moderately more affected in male mice, where muscle spindle afferents in high fat fed animals were less likely to entrain to vibration than controls (logistic regression, p=0.01; Elahi et al., 2018). The changes in muscle spindle afferent mechanosensation that we observed could potentially contribute to balance instability during obesity if not compensated with increased gamma motor neuron tone and/or reflex excitability. To determine whether processing of muscle spindle afferent sensory information was also altered by diet induced obesity, we measured the anesthetized Hoffmann’s or H-reflex (125 mg/kg ketamine, 12.5 mg/kg xylazine), the electrical analog of the muscle stretch reflex. Mice of both sexes were tested after 5, 10, or 15 weeks on either a CON or HFD (n=9-15/group). We used three quantitative measures of H-reflex excitability: (1) H-reflex latency; (2) the percentage of motor neurons recruited from electrical stimulation of Group Ia muscle spindle afferents (Hmax/Mmax); and (3) rate-dependent depression (RDD), the decrease in H-reflex amplitude to high frequency stimulation (20 stimuli at 5 Hz). A HFD did not significantly alter H latency (GLS, p=0.16) or Hmax/Mmax ratios (GLS, p=0.05), but RDD was significantly lower in HFD compared to CON groups (GLS, p<0.001). Interestingly, HFD males exhibited lower RDD than controls only after 5 and 10 weeks of feeding, but females showed progressive decreases in RDD that were only significant at 10 and 15 weeks on the HFD. These results suggest that high-fat feeding increases H-reflex excitability, but that there is a sex difference in the progression of these changes. Ongoing work is focused on understanding the underlying mechanism(s) of the changes we observed during high fat feeding and whether these changes alter muscle stretch reflex strength and/or balance. Future studies should investigate whether similar changes to the muscle proprioceptor system occur in humans and contribute to balance instability in individuals with obesity.