Exercise pressor reflex and carotid chemoreflex interaction: consequences for the cardiovascular response to exercise in healthy humans

Background Although both the exercise pressor reflex (EPR) and the carotid chemoreflex (CC) have been documented as powerful autonomic feedback mechanisms involved in the cardiovascular control during exercise, the interaction of both reflexes and the subsequent consequence for the circulatory response during physical activity remains elusive. Purpose We examined the actions and interactions of the EPR and CC on the cardiovascular response during exercise by independently and simultaneously manipulating these reflexes. Method Seven healthy volunteers completed two experimental sessions in random order. In one session, subjects performed dynamic single leg knee‐extension exercise at 60% of peak power output for 4 min, both in normoxic control conditions (Norm‐C: S a O 2 = 97%, P a O 2 = 90 mmHg) and isocapnic hypoxia (Hypo‐C: S a O 2 = 79%, P a O 2 = 42 mmHg). In the other session, following lumbar intrathecal fentanyl administration attenuating feedback from group III/IV leg muscle afferents, subjects repeated the same exercise characterized by similar blood gases and Hb saturations (Norm‐F and Hypo‐F). Mean arterial blood pressure (MAP, radial arterial catheter), cardiac output (CO, Finometer) and femoral blood flow (Q L, Doppler ultrasound) were quantified continuously during exercise. Comparisons were made between Norm‐F and Norm‐C (i.e., ΔNorm‐F/Norm‐C) and Norm‐F and Hypo‐F (i.e., ΔNorm‐F/Hypo‐F) to estimate the EPR and CC contribution to the cardiovascular responses during exercise, respectively. To determine the interaction of the reflexes, the cardiovascular responses during exercise with both the EPR and CC activated simultaneously (estimated from the differences between Norm‐F and Hypo‐C, i.e. ΔNorm‐F/Hypo‐C) were compared with the sum of the responses induced by the EPR and by the CC activation alone (i.e., calculated as ΔNorm‐F/Norm‐C + ΔNorm‐F/Hypo‐F). Results Fentanyl blockade had no effect on resting cardiovascular responses. During exercise, activation of the EPR alone (ΔNorm‐F/Norm‐C) significantly increased MAP (+11 ± 3 mmHg) and Q L (+0.5 ± 0.1 L·min − 1 ), but did not alter CO ( p = 0.41) and leg vascular conductance (LVC; p = 0.10). Activation of the CC alone (ΔNorm‐F/Hypo‐F) significantly increased CO (+1.2 ± 0.5 L·min − 1 ), Q L (+0.4 ± 0.1 L·min − 1 ), and LVC (+3 ± 1 ml·min − 1 ·mmHg − 1 ), but did not alter MAP ( p = 0.13). During co‐activation of the EPR and CC (ΔNorm‐F/Hypo‐C), the Q L and LVC responses were significantly lower than the summated responses evoked by each reflex alone (Q L : 0.5 ± 0.2 vs 0.8 ± 0.2 L·min − 1 ; LVC: 1 ± 1 vs 5 ± 1 ml·min − 1 ·mmHg − 1 ), whereas the CO and MAP responses were similar (1.5 ± 0.5 vs 1.3 ± 0.7 L·min − 1 and 15 ± 2 vs 14 ± 3 mmHg, respectively, p > 0.12). Conclusion While Q L and LVC responses to exercise undergo occlusive interaction upon co‐activation of the EPR and CC, CO and MAP responses exhibit additive interaction. Hence, when the EPR and CC are activated simultaneously, exercise‐induced increases in limb blood flow and vascular conductance are diminished, suggesting that the interaction between the two reflexes may result in augmented sympathetic vasoconstrictor tone. Support or Funding Information The authors were supported by National Heart, Lung, and Blood Institute grants (HL‐116579). This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .