Obesity is associated with balance and motor control deficits. We have recently shown that Group Ia muscle spindle afferents, the sensory arm of the muscle stretch reflex, are less responsive in mice fed a high‐fat diet. Here we test the hypothesis that reflex excitability to sensory information from Group Ia muscle spindle afferents is altered in a mouse model of diet‐induced obesity. We measured the anesthetized Hoffmann’s or H‐reflex, the electrical analog of the muscle stretch reflex. Adult mice of both sexes were fed a control diet (CD; 10% kcal from fat) or a high‐fat diet (HFD; 60% kcal from fat) for 5, 10, or 15 weeks. 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 (P = 0.16) or Hmax/Mmax ratios (P = 0.06), but RDD was significantly lower in HFD compared to CD groups (P < 0.001). Interestingly, HFD males exhibited decreased RDD compared to 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. Future studies are needed to determine whether these changes alter muscle stretch reflex strength and/or balance and to determine the underlying mechanism(s).

Obesity is a metabolic condition characterized by excess adipose tissue and chronic inflammation. It is associated with deficits in balance and motor control leading to an increased risk of falling and fall‐related injuries. These balance deficits may be partially due to alterations in the muscle stretch reflex, which helps correct motor movements and adapt to uncertain terrain. Muscle stretch is sensed by muscle spindle afferents, which then excite alpha motor neurons to cause a reflex contraction. We tested the hypothesis that spinal cord integration of sensory information from muscle spindle afferents is altered in a mouse model of diet‐induced obesity. Changes in spinal cord integration were measured using the Hoffman's or H‐reflex, the electrical analog of the muscle stretch reflex. Following electrical stimulation of the sciatic nerve, two waves of muscle contraction were recorded: the M wave caused by direct excitation of motor neuron axons and the longer latency H wave caused by reflex activation of motor neurons by muscle spindle afferents. Adult mice of both sexes were fed either a control diet (CD, 10% kcal fat; n=16 M, 8 F) or high‐fat diet (HFD, 60% kcal fat; n=15 M, 9 F) for 10 weeks. We measured three properties of the H‐reflex as indicators of excitability: (1) H latency, the time from stimulus to the peak of the H wave; (2) Hmax/Mmax, the percentage of motor neurons recruited from the stimulus of Group Ia afferents; and (3) rate‐dependent depression (RDD), the decrease in H‐reflex amplitude following high‐frequency stimulation (20 stimuli, 5 Hz). After 10 weeks, there were no significant differences in H latency (p=0.558) between groups. However, the 10‐week HFD group showed a significant increase in Hmax/Mmax (p=0.013; sex x diet p=0.570). 10 weeks of high‐fat feeding also decreased the degree of RDD (p=0.001; sex x diet p=0.797). These results suggest that obesity increases spinal cord sensitivity to sensory input from the muscle spindle afferents. A preliminary sample of male mice fed the HFD for 5‐weeks showed similar decreases in RDD (n=6 per group, p=0.033), but no changes in Hmax/Mmax (p=0.485). We are currently increasing this sample size and testing whether more severe increases in excitability are seen following longer exposures to the HFD. Future studies will also determine whether these changes in spinal cord excitability translate into changes in the strength of the muscle stretch reflex and/or balance.Support or Funding InformationThis work was supported by SJSU RSCA funds and NIGMS Grant# 4T34GM008253‐30 (MH).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.