Carotid Chemoreflex Regulation of Post‐Exercise Cardiac Autonomic Control in Healthy Humans: Influence of Exercise Intensity
Authors: Ribeiro Indyanara C , Paula ‐ Ribeiro Marcelle , Aranda Liliane C , Silva Talita M , Ramos Roberta P , Cravo Sergio L , Nery Luiz E , Stickland Michael K , Silva Bruno M 
Published: June 2021

The recovery of cardiac autonomic control from exercise has two phases. The fast phase lasts about 60 s after exercise, and is largely dependent on the cardiac vagal reactivation. The slow phase is 300 s in duration, and is dependent on both the cardiac vagal reactivation and sympathetic withdrawal. Indexes of post‐exercise cardiac autonomic control are widely used in the clinical practice to predict morbidity and mortality. However, the mechanisms that regulate the post‐exercise cardiac autonomic control remain unclear. The carotid chemoreflex regulates cardiac autonomic control at rest, and carotid chemoreceptors are stimulated by humoral and neural signals related to exercise. As the extent of the humoral and neural responses are dependent upon exercise intensity, we hypothesized the carotid chemoreflex could regulate post‐exercise cardiac autonomic control in an exercise‐intensity‐dependent manner.

Thirteen healthy humans performed ramp incremental exercise up to either moderate‐intensity (MI; i.e., ventilatory threshold) or high‐intensity exercise (HI; i.e., 90% peak workload). Both MI and HI exercise were followed by 5 min of active recovery (i.e., unloaded cycling) while breathing, in random order, normoxia (21% of O2, control), hyperoxia (100% of O2, carotid chemoreflex inhibition) or hypoxia (12% of O2, carotid chemoreflex stimulation). Gas administration started 10 s before the onset of recovery from exercise. The fast phase of cardiac autonomic control recovery from exercise was assessed by the heart rate (HR) reduction at 60 s post‐exercise (HRR60s). The slow phase was assessed by the time constant of exponential HR decay (HRRτ) over 300 s and the HR reduction at 300 s post‐exercise (HRR300s). Fast and slow phases were assessed by the square root of mean squared differences of successive R‐R intervals of 30‐s data segments (RMSSD30s).

As compared to normoxia, hyperoxia did not change HRR60s at either exercise intensities. Hypoxia did not change HRR60s at MI, but decreased HRR60s at HI (normoxia: 29 ± 8 vs hypoxia: 17 ± 9 bpm; P < 0.01). Hyperoxia and hypoxia did not change HRRτ. Hyperoxia did not affect HRR300s, but hypoxia decreased HRR300s similarly at both exercise intensities (MI: normoxia = 32 ± 14 vs hypoxia = 26 ± 17 bpm; HI: normoxia = 55 ± 7 vs hypoxia = 48 ± 11 bpm; post hoc for gas main effect: P = 0.03). Finally, regardless of the time, hyperoxia increased RMSSD30s (MI: normoxia = 15 ± 7 vs hyperoxia = 19 ± 10 ms; HI: normoxia = 5 ± 3 vs hyperoxia = 6 ± 3 ms, post hoc for gas main effect: P < 0.01), whereas hypoxia decreased RMSSD30s (MI: hypoxia = 13 ± 9 ms vs normoxia; HI: hypoxia = 4 ± 2 vs normoxia, post hoc for gas main effect: P < 0.01) at both exercise intensities.

In conclusion, the carotid chemoreflex regulates both the fast and slow phases of post‐exercise cardiac autonomic control in healthy humans; however, only the fast phase regulation is dependent on the exercise intensity. These results suggest that sensitization of the carotid chemoreflex with exercise plays an important role for the post‐exercise cardiac vagal reactivation.

Support or Funding Information

FAPESP 2015/22198‐2; 2018/03501‐4

This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.