Group Ia afferents likely contribute to short-latency interlimb reflexes in the human biceps femoris muscle

Background: Ipsilateral knee (iKnee) joint rotations in seated humans elicit short-latency crossed spinal reflexes in the contralateral biceps femoris (cBF) muscle (Stevenson et al., JPhysiol., 2015). The short-latency cBF reflexes were inhibitory following iKnee extension perturbations, and facilitatory following flexion perturbations. Due to the onset latency (45 ms), spinal pathways likely mediate the reflexes. Furthermore, the same population of cBF motor units (MUs) inhibited following iKnee extension perturbations were facilitated following iKnee flexion perturbations, indicating that parallel interneuronal pathways arising from ipsilateral afferents to common motoneurons in the contralateral leg likely mediate the reflexes (Stevenson et al., JPhysiol., 2015). In the present study, we investigated which afferent pathways mediate the short-latency cBF reflexes by altering the amplitude and velocity of the iKnee rotations.
Methods: 11 seated participants (mean age: 25 ± 5 years) performed a voluntary isometric knee extension with the ipsilateral leg and contralateral knee flexion to 10% of maximum voluntary contraction (MVC). A mechanical actuator (MTS-Systems Corporation) imposed iKnee flexion or extension joint rotations with different amplitudes and velocities in blocks of 60 trials. The velocities compared were either 75 or 150°/s with an amplitude of 8°, and the amplitudes compared were 4 or 8° with a velocity of 150°/s. Intramuscular electromyography (iEMG) data for the flexion and extension perturbations were decomposed (EMGLAB, McGill et al., JNeurosci. Methods, 2005) into constituent MU action potentials (APs). The total number of APs was quantified using a 5 ms window to create peristimulus time histograms (PSTHs) for each combination of perturbation direction, amplitude, and velocity. The resulting cBF reflex amplitudes (calculated between 40-70 ms after perturbation onset) were normalized as a percentage of baseline activity (100 ms prior to perturbation onset).
Results: Across all participants, the mean background activity was not significantly different between perturbation parameters (p = 0.84). The mean amplitude of the short-latency facilitatory and inhibitory reflexes in the cBF increased with faster iKnee rotation velocities (75 vs. 150°/s) at the same 8° amplitude (p’s < 0.02). The mean cBF reflex amplitude was not significantly different with different iKnee rotation amplitudes (4 vs. 8°) at the same 150°/s velocity (p’s > 0.08).
Conclusion: Because fast conducting group Ia muscle spindle afferents are sensitive to changes in muscle stretch velocity, while group II spindle afferents are sensitive to changes in amplitude (Grey et al., JPhysiol., 2001; Matthews, Trends Neurosci., 1991), group Ia velocity sensitive muscle spindle afferents likely contribute to the short-latency crossed spinal reflexes in the cBF muscle following iKnee joint rotations. This supports the findings for the short-latency crossed responses in the human soleus muscle (Stubbs & Mrachacz-Kersting, JNeurophysiol., 2009), but is in contrast to the findings in cats, where group II afferents are the primary contributors (Jankowska, Brain Res. Rev., 2008). Moreover, these results provide further indirect evidence for the presence of spinal commissural interneurons relaying ipsilateral sensory information to contralateral motor neurons in humans (Stubbs & Mrachacz-Kersting, JNeurophysiol., 2009; Jankowska, Brain Res. Rev., 2008).
Significance Statement: This study provides further indirect evidence for the presence of spinal commissural interneurons relaying ipsilateral sensory information to contralateral motor neurons in humans, with primary contributions from group Ia muscle spindle afferents.