Only the fastest corticospinal fibers contribute to beta corticomuscular coherence
ABSTRACTA common way to study human corticospinal transmission is with transcranial magnetic stimulation. However, this 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. A possible alternative to overcome this limitation is to study the corticospinal transmission of endogenously generated brain activity. Here we study the transmission speeds of cortical beta rhythms travelling to the muscles during steady contractions. To do this, we introduce new methods to improve delay estimates in the corticomuscular transmission of beta rhythms, and which we validate both in simulations and experimentally. Applying these approaches to experimental data from humans, we show that corticomuscular beta transmission delays are only 1-2ms longer than expected from the fastest corticospinal pathway. Simulations using realistic distributions of the conduction velocities for descending axons projecting to lower motoneurons suggest two scenarios that can explain these results: either a very small fraction of only the fastest corticospinal axons selectively transmit beta activity, or else the entire pool does. The implications that these two scenarios have for our understanding of corticomuscular interactions are discussed in the final part of this manuscript.SIGNIFICANCEWe present and validate an improved methodology to measure the delay in the transmission of cortical beta activity to tonically active muscles. The estimated corticomuscular beta transmission delays which this yields are remarkably similar to those expected from transmission in the fastest corticospinal axons. A simulation of beta transmission along a pool of corticospinal axons using a realistic distribution of fiber diameters suggests two possible mechanisms by which fast corticomuscular transmission is achieved: either a very small fraction of descending axons transmits beta activity to the muscles or, alternatively, the entire population does and natural cancellation of slow channels occurs due to the distribution of axon diameters in the corticospinal tract.