Central Command, but not the Muscle Metaboreflex, is Responsible for Intensity‐Dependent Increases in Muscle Sympathetic Nerve Activity to Contracting Muscle during High‐Intensity Static Isometric Exercise in Humans

Abstract

Post‐exercise ischaemia has been used to demonstrate muscle metaboreflex‐mediated increases in muscle sympathetic nerve activity (MSNA) to an inactive limb during static isometric exercise. In contrast, we have previously shown a rapid centrally‐mediated increase in MSNA to a contracting leg during sustained isometric exercise, which promptly returned to resting levels at the cessation of exercise despite the presence of post‐exercise muscle ischaemia of the ipsilateral limb. However, these observations have been made during relatively low‐intensity exercise. The present study tested the hypothesis that central command, but not the muscle metaboreflex, increases MSNA to the contracting muscle during sustained isometric contractions even at higher intensities. MSNA was recorded continuously (microneurography) from the right common peroneal nerve. Twelve subjects (seven males, five females) performed two‐minute ankle dorsiflexions at 10, 20, 30, 40 and 50% of maximum voluntary contraction (MVC) ipsilateral to the MSNA recording, which was immediately followed by six minutes of post‐exercise ischaemia. There was at least six minutes rest between contractions. MSNA was analysed by measuring negative‐going cardiac‐locked sympathetic spikes from the raw neurogram. Compared with MSNA at rest (82 ± 5 spikes/min), MSNA to contracting muscle increased in an intensity‐dependent manner within one‐minute of contraction at 10 %MVC (145 ± 27 spikes/min, P=0.04), 20 %MVC (219 ± 28 spikes/min, P=0.002), 30 %MVC (480 ± 92 spikes/min, P=0.002), 40 %MVC (716 ± 185 spikes/min, P=0.01) and 50 %MVC (934 ± 275 spikes/min, P=0.02). Blood pressure increased in an intensity‐dependent manner during contractions up to 50 %MVC (76 ± 5 vs 93 ± 7 mmHg, P=0.02). Within one‐minute after each contraction MSNA returned close to resting levels even in the presence of post‐exercise ischaemia. These findings indicate that central command, and not the metaboreflex, is responsible for the increase in MSNA to contracting muscle during sustained isometric contractions, even at intensities up to 50% of MVC.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.