Contributions of Central Command and Muscle Feedback to Sympathetic Nerve Activity in Contracting Human Skeletal Muscle

Abstract

During voluntary contractions, muscle sympathetic nerve activity (MSNA) to contracting muscles increases in proportion to force but the underlying mechanisms are not clear. To shed light on these mechanisms, particularly the influences of central command and muscle afferent feedback, the present study tested the hypothesis that MSNA is greater during voluntary compared with electrically-evoked contractions. Seven male subjects performed a series of 1-min isometric dorsiflexion contractions (left leg) separated by 2-min rest periods, alternating between voluntary and electrically-evoked contractions at similar forces (5–10% of maximum). MSNA was recorded continuously (microneurography) from the left peroneal nerve and quantified from cardiac-synchronized, negative-going spikes in the neurogram. Compared with pre-contraction values, MSNA increased by 51 ± 34% (P < 0.01) during voluntary contractions but did not change significantly during electrically-evoked contractions (−8 ± 12%, P > 0.05). MSNA analyzed at 15-s intervals revealed that this effect of voluntary contraction appeared 15–30 s after contraction onset (P < 0.01), remained elevated until the end of contraction, and disappeared within 15 s after contraction. These findings suggest that central command, and not feedback from contracting muscle, is the primary mechanism responsible for the increase in MSNA to contracting muscle. The time-course of MSNA suggests that there is a longer delay in the onset of this effect compared with its cessation after contraction.

The metaboreflex does not contribute to the increase in muscle sympathetic nerve activity to contracting muscle during static exercise in humans

“…, , Boulton et al . ). The increase in MSNA to the non‐contracting muscle did not occur until the second minute of contraction (Fig.…”

“…; Fatouleh & Macefield, ; Boulton et al . ). Moreover, measuring the average increase in the number of extracted spikes of MSNA during contraction of the muscle (51%) was similar to measuring the mean burst amplitude of the mean voltage neurogram (48%), as measured from the RMS‐processed nerve signal, whereas burst frequency increased by 22% and total MSNA by 77% (Boulton et al .…”

“…Moreover, measuring the average increase in the number of extracted spikes of MSNA during contraction of the muscle (51%) was similar to measuring the mean burst amplitude of the mean voltage neurogram (48%), as measured from the RMS‐processed nerve signal, whereas burst frequency increased by 22% and total MSNA by 77% (Boulton et al . ). In the present study, the nerve signal was shifted back in time (∼1.2–1.55 s) relative to the R‐wave of the ECG to account for central processing and conduction delays between the R‐wave and MSNA in the peroneal nerve (Fagius & Wallin, ).…”

“…More recently, we recorded MSNA to the contracting tibialis anterior muscle during brief (1 min) weak static contractions (10% MVC), comparing the increase in MSNA during volitionally‐generated and electrically‐stimulated contractions of comparable magnitude (Boulton et al . ). The results of the later study showed that MSNA only increased during volitionally‐generated contractions, supporting the conclusion that central command plays an important role.…”

“…Sympathetic vasoconstrictor drive could also be linked to muscle activity (Seals, ; Boulton et al . , ) because the perfusion demands of skeletal muscle and other organs can vary greatly and in proportion to the level of activity (Andersen & Saltin, ; Saunders et al . ; Reeder & Green, ).…”