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

• Published in: The Journal of physiology 2018-03, Vol.596 (6), p.1091-1102
• Main Authors: Boulton, Daniel, Taylor, Chloe E., Green, Simon, Macefield, Vaughan G.
• Format: Article
• Language: English
• Subjects: Ankle; Blood pressure; central command; Ischemia; metaboreflex; Muscle contraction; Neuroscience; Peroneal nerve; Reflexes; Research Paper; sympathetic
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/JP275526

Key points It is not clear how sympathetic activity to contracting muscle is controlled. We recorded muscle sympathetic nerve activity (MSNA) to the ipsilateral tibialis anterior muscle during 4 min of isometric dorsiflexion of the ankle and 6 min of post‐exercise ischaemia, which was repeated contralaterally. MSNA to the contracting muscle increased within 1 min of static exercise and returned to pre‐contraction levels at the end. Unlike the increase in MSNA seen in the non‐contracting muscle, post‐exercise ischaemia had no effect on MSNA to the contracted muscle. We conclude that central command is the primary mechanism responsible for increasing MSNA to contracting muscle and also that the metaboreflex is not expressed in contracting muscle. Both central command and metaboreflex inputs from contracting muscles increase muscle sympathetic nerve activity (MSNA) to non‐contracting muscle during sustained isometric exercise. We recently showed that MSNA to contracting muscle also increases in an intensity‐dependent manner, although whether this can be sustained by the metaboreflex is unknown. MSNA was recorded from the left common peroneal nerve and individual spikes of MSNA extracted from the nerve signal. Eleven subjects performed a series of 4 min dorsiflexions of the left ankle at 10% of maximum voluntary contraction under three conditions: without ischaemia, with 6 min of post‐exercise ischaemia, and with ischaemia during and after exercise; these were repeated in the right leg. Compared with pre‐contraction values, MSNA to the contracting muscles increased and plateaued in the first minute of contraction (50 ± 18 vs. 34 ± 10 spikes min−1, P = 0.01), returned to pre‐contraction levels within 1 min of the contraction ending and was not influenced by ischaemia during or after contraction. Conversely, MSNA to the non‐contracting muscles was not different from pre‐contraction levels in the first minute of contraction (34 ± 9 vs. 32 ± 5 spikes min−1, P = 0.48), whereas it increased each minute and was significantly greater by the second minute (44 ± 8 spikes min−1, P = 0.01). Ischaemia augmented the MSNA response to contraction (63 ± 25 spikes min−1 after 4 min, P