Only the Fastest Corticospinal Fibers Contribute to β Corticomuscular Coherence

Human corticospinal transmission is commonly studied using brain stimulation. However, this approach is biased to activity in the fastest conducting axons. It is unclear whether conclusions obtained in this context are representative of volitional activity in mild-to-moderate contractions. An alternative to overcome this limitation may be to study the corticospinal transmission of endogenously generated brain activity. Here, we investigate in humans (N = 19; of either sex), the transmission speeds of cortical beta rhythms (similar to 20 Hz) traveling to arm (first dorsal interosseous) and leg (tibialis anterior; TA) muscles during tonic mild contractions. For this purpose, we propose two improvements for the estimation of corticomuscular beta transmission delays. First, we show that the cumulant density (cross-covariance) is more accurate than the commonly-used directed coherence to estimate transmission delays in bidirectional systems transmitting band-limited signals. Second, we show that when spiking motor unit activity is used instead of interference electromyography, corticomuscular transmission delay estimates are unaffected by the shapes of the motor unit action potentials (MUAPs). Applying these improvements, we show that descending corticomuscular beta transmission is only 1-2 ms slower than expected from the fastest corticospinal pathways. In the last part of our work, we show results from simulations using estimated distributions of the conduction velocities for descending axons projecting to lower motoneurons (from macaque histologic measurements) to suggest two scenarios that can explain fast corticomuscular transmission: either only the fastest corticospinal axons selectively transmit beta activity, or else the entire pool does. The implications of these two scenarios for our understanding of corticomuscular interactions are discussed.

Automated summary

This study investigates the transmission speeds of cortical beta rhythms to arm and leg muscles during mild contractions in humans. Two improvements for estimating corticomuscular beta transmission delays are proposed, leading to the discovery that descending corticomuscular beta transmission is only slightly slower than expected from the fastest corticospinal pathways. Simulation results suggest two possible scenarios to explain fast corticomuscular transmission, with implications for our understanding of corticomuscular interactions.