Carotid Chemoreflex Regulation of Post‐Exercise Cardiac Autonomic Control in Healthy Humans: Influence of Exercise Intensity
Bibliographic record
Abstract
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 O 2 , control), hyperoxia (100% of O 2, carotid chemoreflex inhibition) or hypoxia (12% of O 2, 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 (RMSSD 30s ). 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 RMSSD 30s (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 RMSSD 30s (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 .
Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.
How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.001 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.000 |
| Insufficient payload (model declined to judge) | 0.001 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".