Abstract

A delay in the post‐exercise recovery heart rate is a strong predictor of mortality that may be mediated by autonomic nervous system dysfunction (e.g., impaired parasympathetic reactivation and/or augmented sympathetic nerve activity, SNA). We tested the hypothesis that augmented SNA during exercise recovery would delay the rate of post‐exercise heart rate decay compared to a control condition (CTL). Twenty‐two healthy adults (13 f; 22 ± 2 yrs; peak VO2 = 47 ± 7.4 mL/kg/min; BMI = 23.4 kg/m2) performed heavy‐intensity exercise above the ventilatory threshold at 90 ± 6% peak heart rate for 5 min during CTL (no SNA augmentation) and during an experimental (EXP) condition. The EXP condition entailed SNA augmentation via the muscle metaboreflex following 2 min of bilateral isometric handgrip exercise at 30–40% maximal voluntary contraction during cycle ergometry exercise. Bilateral circulatory occlusion was performed during the last 1 min of exercise and continued during 4 min of recovery. Post‐exercise heart rate kinetics were analyzed using paired t‐tests and significant differences were determined when P < 0.05. There was no difference in end‐exercise heart rate (last 1 min) between CTL (159 ± 3 beats/min) and EXP (158 ± 3 beats/min, P = 0.592), amplitude of heart rate recovery between CTL (−61 ± 2 beats/min) and EXP (−64 ± 2 beats/min, P = 0.178), or end recovery heart rate between CTL (98 ± 3 beats/min) and EXP (94 ± 3 beats/min, P = 0.068). There was a significant difference in heart rate kinetics between CTL (57 ± 3 s) and EXP (69 ± 5 s, P = 0.009). These findings suggest that augmented SNA may modulate a delay in the recovery time for heart rate following heavy intensity exercise.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call