Muscle Sympathetic Nerve Activity and Vascular Conductance Responses at the Onset of Arm and Leg Exercise in the Inactive Limb

Abstract

Local mechanical and metabolic factors are known to regulate the blood flow response at the onset of exercise. However, little is known regarding the contribution of muscle sympathetic nerve activity (MSNA) to this onset blood flow response. The aim of the study was to examine the MSNA and vascular conductance response to exercise anticipation and onset in the inactive leg. Two identical visits were performed on 16 participants (n = 6 female). During visit 1, hemodynamic (Finometer) and MSNA (fibular nerve microneurography) measurements were acquired during rest (1‐minute), exercise anticipation (verbal preparation, 30‐seconds), and 1 minute of rhythmic handgrip (RHG, 1:1 duty cycle, 40% MVC) and one‐legged cycling (17 ± 3% peak power output). During visit 2, hemodynamic and superficial femoral artery (SFA) blood flow (Doppler ultrasound) measurements were acquired during the same exercise modes. Leg vascular conductance was calculated as SFA mean blood flow/mean arterial pressure. Total MSNA (burst frequency x burst area) was analyzed in 15‐second moving windows (5‐second progressions), and SFA blood flow was analyzed as 5‐second time bins aligned with the last 5 seconds of each MSNA moving window; both were expressed as relative change from baseline (%). Burst frequency, burst incidence, and total MSNA (height) followed the same pattern as total MSNA (area), and thus only total MSNA (area) is presented. Significance was set as p < 0.05, and data are mean ± SE. When participants were prompted to prepare for upcoming exercise (i.e. anticipation), total MSNA decreased from baseline prior to RHG (−40 ± 6%, p < 0.001) and cycling (−20 ± 6%, p = 0.03). During anticipation of RHG, this decrease in vasoconstrictor drive was followed 5 seconds later by a trend for increased SFA vascular conductance (+24 ± 12%, p = 0.07). At the onset of exercise, total MSNA decreased during RHG (−28 ± 6%, p = 0.002) and cycling (−39 ± 7%, p = 0.009). This was followed by an increase in SFA vascular conductance during both RHG (+34 ± 12%, p = 0.02) and cycling (+34 ± 20%, p = 0.005) conditions. In the absence of mechanical or metabolic factors in the inactive limb, these data suggest that a reduction in total MSNA can contribute to the exercise hyperemia that is observed at the onset of exercise. Furthermore, the anticipatory response of MSNA suggests a partial contribution of feedforward central command in this response.Support or Funding InformationNatural Science and Engineering Research Council of CanadaOntario Ministry of Research, Innovation, and ScienceCanadian Foundation for InnovationThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.