Muscle metaboreflex activity after an acute session of exercise under hypoxia

Abstract

In healthy subjects, when the muscle metaboreflex (MM) is activated, mean blood pressure (MBP) increases because of a sympathetic‐induced increase in both systemic vascular resistance (SVR) and cardiac output (CO)1. Acute hypoxia vasodilation has been often reported despite the increased sympathetic tone2. We hypothesized that a single session of exercise under normobaric hypoxia (ENH) resulted in an attenuation of the MBP increment during the muscle metaboreflex activated immediately after the ENH session. 10 well trained healthy male subjects (age 34.2±11.7 yrs) participated in this study. In separate days they underwent, randomly assigned, three exercise sessions consisting of 10 min pedaling at a workload corresponding to 80% of anaerobic threshold previously assessed. In one session (TEST21%) subjects breathed normoxic air (O2 21%), in the other two tests they breathed hypoxic air with O2 concentration of 16% (TEST16%) or 13% (TEST13%) respectively. Immediately after each exercise session they underwent randomly assigned the following protocol: 1) muscle metaboreflex activation obtained by the post‐exercise muscle ischemia (PEMI) method, and 2) control exercise recovery (CER) test. Response to the metaboreflex for each cardiovascular parameter was assessed as PEMI minus CER level. Hemodynamic parameters were evaluated by impedance cardiography. Results show that SVR response was reduced during the MM after the TST13% with respect to the other two tests (−46.5±394.2 vs. +108.9±256.3 and +213.6±228.8 dynes•s‐1•cm‐5 respectively, p<0.05). However, the MBP response was similar between conditions. This because of an increased CO response which occurred during TEST13% in comparison with TEST21% and TEST16% (+421.3±545 vs. +63.2±322.9 and +128.3±238.6 ml respectively, p<0.05). It was concluded that an acute session of exercise under hypoxia is able to reduce the capacity to vasoconstrict the vascular bed during the metaboreflex activation obtained by PEMI. However, mechanisms controlling cardiovascular responses successfully defended MBP response by increasing CO which compensated for the reduced SVR increment.Support or Funding InformationThis study was supported by the University of Cagliari and the Italian Ministry of Scientific Research.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.