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The Metaboreflex and the Peripheral Chemoreflex Interact for the Regulation of Ventilation in Patients with Chronic Heart Failure
Author(s) -
Machado Alessandro Costa,
Vianna Lauro Casqueiro,
Gomes Erika Alvarenga Correa,
Teixeira Jose Antonio Caldas,
Ribeiro Mario Luiz,
Junior Humberto Villacorta,
Nobrega Antonio Claudio Lucas,
Silva Bruno Moreira
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.728.2
Subject(s) - hyperoxia , medicine , heart failure , cardiology , peripheral chemoreceptors , ventilation (architecture) , peripheral , reflex , anesthesia , heart rate , ischemia , vasodilation , hemodynamics , ejection fraction , blood pressure , chemoreceptor , lung , mechanical engineering , receptor , engineering
Patients with chronic heart failure (CHF) tipically present exacerbated ventilation (VE) response to exercise. This phenomenon is associated with exercise intolerance and worse prognosis, and seems to be mediated, at least in part, by abnormalities in the neural control of VE, such as enhanced VE response to activation of muscle afferents sensitive to metabolites (i.e., enhanced metaboreflex), as well as enhanced VE response to inhalation of hypoxic air at rest (i.e., enhanced peripheral chemoreflex). However, the interaction between these reflexes remains unknown in CHF. Then, we sought to test the hypothesis that the activation of the metaboreflex could enhance the contribution of the peripheral chemoreflex for the regulation of VE in patients with CHF. Six men with CHF under optimal pharmacological treatment (New York Heart Association class II‐III, mean ± SD age of 55 ± 6 years and left ventricular ejection fraction (Simpson) 33.7 ± 2.9%) were submitted to 4 steady‐state cycling sessions at 60% of maximal power output for 4 minutes. Then, they recovered for 2 minutes under either 1) post exercise ischemia (PEI) plus normoxia (21% O 2 ), 2) PEI plus hyperoxia (100% O 2 ), 3) free flow plus normoxia, or 4) free flow plus hyperoxia. PEI was used to trap metabolites in the lower limbs, and, consequently, activate the metaboreflex, while hyperoxia was used to inhibit the peripheral chemoreceptors. Patients were blinded to the O 2 concentration in the inhaled air. A rebreathing circuit was used during recovery to match the end tidal partial pressure of CO 2 (PetCO 2 ) among conditions. Breath‐by‐breath data recorded at peak and throughout recovery were averaged in 20‐s windows for statistical analyses. Peak VE was similar among conditions. As expected, end tidal partial pressure of O 2 was higher during hyperoxia than normoxia throughout the recovery period. VE decayed during recovery in all conditions. Of note, hyperoxia augmented the VE decay versus normoxia at 21–40 s (hyperoxia: 16.7 ± 2.3 L/min vs. normoxia: 22.7 ± 2.9 L/min, P < 0.001) and 41–60 s (hyperoxia: 17.1 ± 1.5 L/min vs. normoxia: 20.5 ± 2.2 L/min, P = 0.01) of recovery during PEI. However, hyperoxia did not change VE decay versus normoxia during free flow recovery. Collectively, our findings indicate that the activation of the metaboreflex enhances the peripheral chemoreflex regulation of VE in patients with CHF, which confirms the interaction between these reflexes. This interaction may, consequently, mediate part of the exaggerated VE response to exercise, which is a hallmark of patients with CHF. Support or Funding Information São Paulo Research Foundation (FAPESP), National Counsel of Technological and Scientific Development (CNPq), and Research Support Foundation of the State of Rio de Janeiro (FAPERJ).