The interaction of the peripheral and central chemoreflexes with the exercise pressor reflex: differential consequences for the cardiovascular responses to exercise

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 (Norm C : S a O 2 ~97%, P a O 2 ~92 mmHg, P a CO 2 ~32 mmHg, pH ~7.39), isocapnic hypoxia (Hypo C : S a O 2 ~79%, P a O 2 ~50 mmHg, P a CO 2 ~33 mmHg, pH ~7.39), and normoxic hypercapnia (Hyper C : S a O 2 ~98%, P a O 2 ~113, P a CO 2 ~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 (Norm F , Hypo F , and Hyper F ). 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 ( Q L, via Doppler ultrasound) were quantified continuously during exercise. Results Isolated activation of the EPR (i.e., ΔNorm C ‐Norm F ) significantly ( p < 0.05) increased MAP (+9 ± 3 mmHg), CO (+0.7 ± 0.3 L ·min −1 ), Q L (+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., ΔHypo F ‐Norm F ) significantly increased CO (+1.0 ± 0.4 L·min −1 ), Q L (+0.3 ± 0.1 L· min −1 ), and LVC (+2 ± 1 ml ·min −1 ·mmHg −1 ). CCR activation alone via hypercapnia (i.e., ΔHyper F ‐Norm F ) significantly increased MAP (+6 ± 2 mmHg), CO (+1.3 ± 0.5 L ·min −1 ), and Q L (+0.3 ± 0.1 L· min −1 ). During co‐activation of the EPR and PCR (i.e., ΔHypo C ‐Norm F ), the MAP response was significantly greater while the Q L and LVC responses were significantly lower when compared with the summated responses evoked by each reflex alone (MAP: 14 ± 2 vs. 9 ± 4 mmHg; Q L : 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., ΔHyper C ‐Norm F ), 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 Q L 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 .