High Intensity Muscle Metaboreflex Activation Blunts Cardiopulmonary Baroreflex Control of Sympathetic Vasomotor Outflow

Abstract

Muscle sympathetic nerve activity (MSNA) is reduced during low intensity dynamic leg exercise. This reduction in MSNA has been attributed to loading of the cardiopulmonary baroreflex with increased venous return and it has been suggested that such inhibition is overridden with higher intensity exercise due to muscle metaboreflex activation. However, limited data are available regarding the interaction between the cardiopulmonary baroreflex and the muscle metaboreflex. Herein, we tested the hypothesis that cardiopulmonary baroreflex control of MSNA is attenuated when the muscle metaboreflex is strongly activated. In eight healthy young men, MSNA (right peroneal nerve), mean arterial blood pressure (MAP, Finometer), heart rate (ECG), and thoracic impedance were recorded. Graded isolation of the muscle metaboreflex was achieved by post‐exercise ischemia (PEI) following low‐ (PEI‐L), moderate‐ (PEI‐M) and high‐ (PEI‐H) intensity isometric handgrip performed at 20%, 30% and 40% maximum voluntary contraction, respectively. Lower‐body positive pressure (LBPP, +10 mmHg), to load the cardiopulmonary baroreflex, was applied at rest and during PEI. Handgrip exercise elicited intensity‐dependent increases in MSNA and MAP that were maintained during PEI indicating a graded muscle metaboreflex activation. LBPP at rest significantly decreased MSNA burst frequency and total activity (total activity: −39.5 ± 5.7%, mean ± SE, P < 0.05), while MAP was unchanged. When LBPP was applied during PEI, MSNA burst frequency and total activity decreased significantly at PEI‐L (total activity: −41.8 ± 10.6%, P < 0.05) and PEI‐M (total activity: −34.7 ± 8.6%, P < 0.05), but not at PEI‐H (total activity: −11.8 ± 8.6%, n.s., one‐way repeated measures ANOVA: F = 5.07, P < 0.05). Thoracic admittance, which was calculated from thoracic impedance as an index of central blood volume, was not changed during handgrip or PEI alone, whereas LBPP evoked similar increases in thoracic admittance during all conditions (rest: +5.4±0.8, PEI‐L: +5.8±0.5, +PEI‐M: +5.4±0.5, PEI‐H: +5.8±0.5 S·10−4, one‐way repeated measures ANOVA: F = 0.38, n.s.). These preliminary findings suggest that high intensity muscle metaboreflex activation attenuates cardiopulmonary baroreflex control of sympathetic vasomotor outflow.Support or Funding InformationNIH R01 HL127071 JSPS KAKENHI Grant Number JP16KK0201This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.