The interaction of the peripheral and central chemoreflexes with the exercise pressor reflex: differential consequences for the cardiovascular responses to exercise
Authors: Wan Hsuan‐Yu , Weavil Joshua , Thurston Taylor , Georgescu Vincent , Hureau Thomas , Bledsoe Amber , Buys Michael , Jessop Jacob , Richardson Russell , Amann Markus 
Published: June 2021

Background

Although the exercise pressor reflex (EPR) and chemoreflexes are recognized to be powerful autonomic cardiovascular control mechanisms, the interaction of these reflexes and the resulting effect upon the circulatory response to physical activity are not clear.

Purpose

To evaluate the cardiovascular consequence of the interaction of the peripheral (PCR) and central (CCR) chemoreflexes with the EPR in exercising humans.

Method

Ten healthy volunteers (5 males, 5 females) completed two experimental sessions separated by ≥48 h. In one session, subjects performed dynamic single leg knee‐extension at 60% of peak power output for 4 min in normoxic control conditions (NormC: SaO2 ~97%, PaO2 ~92 mmHg, PaCO2 ~32 mmHg, pH ~7.39), isocapnic hypoxia (HypoC: SaO2 ~79%, PaO2 ~50 mmHg, PaCO2 ~33 mmHg, pH ~7.39), and normoxic hypercapnia (HyperC: SaO2 ~98%, PaO2 ~113, PaCO2 ~50 mmHg, pH ~7.26). In the other session, following lumbar intrathecal fentanyl administration to attenuate feedback from group III/IV leg muscle afferents, subjects repeated the same exercise characterized by similar blood gases and Hb saturations (NormF, HypoF, and HyperF). All sessions and conditions were conducted in counterbalanced order. Mean arterial blood pressure (MAP, via a radial arterial catheter), cardiac output (CO, via finger photoplethysmography) and femoral blood flow (QL, via Doppler ultrasound) were quantified continuously during exercise.

Results

Isolated activation of the EPR (i.e., ΔNormC‐NormF) significantly (p < 0.05) increased MAP (+9 ± 3 mmHg), CO (+0.7 ± 0.3 L ·min−1), QL (+0.4 ± 0.1 L ·min−1), and leg vascular conductance (LVC; +2 ± 1 ml· min−1· mmHg−1) during exercise. PCR activation alone via hypoxia (i.e., ΔHypoF‐NormF) significantly increased CO (+1.0 ± 0.4 L·min−1), QL (+0.3 ± 0.1 L· min−1), and LVC (+2 ± 1 ml ·min−1 ·mmHg−1). CCR activation alone via hypercapnia (i.e., ΔHyperF‐NormF) significantly increased MAP (+6 ± 2 mmHg), CO (+1.3 ± 0.5 L ·min−1), and QL (+0.3 ± 0.1 L· min−1). During co‐activation of the EPR and PCR (i.e., ΔHypoC‐NormF), the MAP response was significantly greater while the QL and LVC responses were significantly lower when compared with the summated responses evoked by each reflex alone (MAP: 14 ± 2 vs. 9 ± 4 mmHg; QL: 0.4 ± 0.1 vs. 0.7 ± 0.1 L· min−1; LVC: 1 ± 1 vs. 4 ± 1 ml ·min−1 ·mmHg−1); there was no difference between the observed and summated CO responses (p = 0.25). During co‐activation of the EPR and CCR (i.e., ΔHyperC‐NormF), the observed cardiovascular responses did not differ from the summated responses to the stimulation of each reflex alone (p > 0.14).

Conclusion

With predominant PCR activation, the EPR:chemoreflex interaction is hyper‐additive in terms of MAP, additive in terms of CO, and hypo‐additive in terms of QL and LVC. In contrast, with predominant CCR activation, the EPR:chemoreflex interaction is simply additive in terms of both central and peripheral hemodynamics. These findings suggest that the different modes of chemoreflexes engaged and interacting with the EPR result in substantial differences in the cardiovascular response to exercise.

Support or Funding Information

NHLBI (HL‐116579)

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