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.

Keywords: cardiovascular control; electrical stimulation; muscle contraction; sympathetic; voluntary.

Figure 1

Experimental records from one subject during electrical stimulation of tibialis anterior (A) and during a weak voluntary contraction at a matched intensity (B). A section of the “Nerve” channel during electrical stimulation has been expanded to reveal the raw neural signal between electrical artifact and sympathetic spikes have been identified with an asterisk (^*). The “Nerve” channel during voluntary contraction has also been expanded for comparison.

Figure 2

Post-stimulus time histograms were used to measure the timing of neural spikes relative to cardiac beats (R-R intervals) of the selected period (collected in the spike train). MSNA, which is cardiac-locked, can be measured ~1200 ms after an R-R interval and the elevation of counts around this time is selected and the sum of the counts is recorded as the number of spikes during the selected period.

Figure 3

MSNA spike frequency during 1-min periods of rest, contraction, and recovery for voluntary and electrically-evoked contractions. Mean values are shown as open circles and individual values are shown as closed circles. ^*Significant main effect of time (P < 0.01). #Significant main effect of condition (P = 0.05). ^∧Significant interaction of time and condition (P < 0.01).

Figure 4

MSNA at 15 s intervals during voluntary (closed circles) and electrically-evoked (open circles) contractions. ^*Significant main effect of condition (P < 0.03). ^∧Significant interaction of time and condition (P < 0.01).

Figure 5

Individual responses of MSNA before (t = 0 s), during (t = 7.5–52.5 s) and after (t = 67.5 s) voluntary contraction.