Katharina Apelt-Glitz1, Fares-Alexander Alken2, Christiane Jungen3, Katharina Scherschel4, Nikolaj Klöcker5, Christian Meyer6. 1. Division of Cardiology/Angiology/Intensive Care, EVK Düsseldorf, cNEP, cardiac Neuro- and Electrophysiology Research Consortium, Düsseldorf, Germany; General Practice for Internal Medicine "Hausärzte im Stadtzentrum", Schenefeld, Germany. 2. Division of Cardiology/Angiology/Intensive Care, EVK Düsseldorf, cNEP, cardiac Neuro- and Electrophysiology Research Consortium, Düsseldorf, Germany; DZHK (German Center for Cardiovascular Research), partner site Hamburg/Kiel/Lübeck, Hamburg, Germany. Electronic address: fares.alken@gmail.com. 3. DZHK (German Center for Cardiovascular Research), partner site Hamburg/Kiel/Lübeck, Hamburg, Germany; Department of Cardiology - University Heart & Vascular Centre, University Hospital Hamburg-Eppendorf, Hamburg, Germany. 4. Division of Cardiology/Angiology/Intensive Care, EVK Düsseldorf, cNEP, cardiac Neuro- and Electrophysiology Research Consortium, Düsseldorf, Germany; DZHK (German Center for Cardiovascular Research), partner site Hamburg/Kiel/Lübeck, Hamburg, Germany. 5. Institute of Neural and Sensory Physiology, Medical Faculty and University Hospital Düsseldorf, Heinrich-Heine-University Düsseldorf, Germany. 6. Division of Cardiology/Angiology/Intensive Care, EVK Düsseldorf, cNEP, cardiac Neuro- and Electrophysiology Research Consortium, Düsseldorf, Germany; DZHK (German Center for Cardiovascular Research), partner site Hamburg/Kiel/Lübeck, Hamburg, Germany; Institute of Neural and Sensory Physiology, Medical Faculty and University Hospital Düsseldorf, Heinrich-Heine-University Düsseldorf, Germany.
Abstract
BACKGROUND: The importance of peripheral chemoreceptors for cardiorespiratory neural control is known for decades. Pure oxygen inhalation deactivates chemoreceptors and increases parasympathetic outflow. However, the relationship between autonomic nervous system (ANS) activation and resulting respiratory as well as heart rate (HR) dynamics is still not fully understood. METHODS: In young adults the impact of (1) 100 % pure oxygen inhalation (hyperoxic cardiac chemoreflex sensitivity (CHRS) testing), (2) the cold face test (CFT) and (3) the cold pressor test (CPT) on heart rate variability (HRV), hemodynamics and respiratory rate was investigated in randomized order. Baseline ANS outflow was determined assessing respiratory sinus arrhythmia via deep breathing, baroreflex sensitivity and HRV. RESULTS: Baseline ANS outflow was normal in all participants (23 ± 1 years, 7 females, 3 males). Hyperoxic CHRS testing decreased HR (after 60 ± 3 vs before 63 ± 3 min-1, p = 0.004), while increasing total peripheral resistance (1053 ± 87 vs 988 ± 76 dyne*s + m2/cm5, p = 0.02) and mean arterial blood pressure (93 ± 4 vs 91 ± 4 mm Hg, p = 0.02). HRV indicated increased parasympathetic outflow after hyperoxic CHRS testing accompanied by a decrease in respiratory rate (15 ± 1vs 19 ± 1 min-1, p = 0.001). In contrast, neither CFT nor CPT altered the respiratory rate (18 ± 1 vs 18 ± 2 min-1, p = 0.38 and 18 ± 1 vs 18 ± 1 min-1, p = 0.84, respectively). CONCLUSION: Changes in HR characteristics during deactivation of peripheral chemoreceptors but not during the CFT and CPT are related with a decrease in respiratory rate. This highlights the need of respiratory rate assessment when evaluating adaptations of cardiorespiratory chemoreceptor control.
BACKGROUND: The importance of peripheral chemoreceptors for cardiorespiratory neural control is known for decades. Pure oxygen inhalation deactivates chemoreceptors and increases parasympathetic outflow. However, the relationship between autonomic nervous system (ANS) activation and resulting respiratory as well as heart rate (HR) dynamics is still not fully understood. METHODS: In young adults the impact of (1) 100 % pure oxygen inhalation (hyperoxic cardiac chemoreflex sensitivity (CHRS) testing), (2) the cold face test (CFT) and (3) the cold pressor test (CPT) on heart rate variability (HRV), hemodynamics and respiratory rate was investigated in randomized order. Baseline ANS outflow was determined assessing respiratory sinus arrhythmia via deep breathing, baroreflex sensitivity and HRV. RESULTS: Baseline ANS outflow was normal in all participants (23 ± 1 years, 7 females, 3 males). Hyperoxic CHRS testing decreased HR (after 60 ± 3 vs before 63 ± 3 min-1, p = 0.004), while increasing total peripheral resistance (1053 ± 87 vs 988 ± 76 dyne*s + m2/cm5, p = 0.02) and mean arterial blood pressure (93 ± 4 vs 91 ± 4 mm Hg, p = 0.02). HRV indicated increased parasympathetic outflow after hyperoxic CHRS testing accompanied by a decrease in respiratory rate (15 ± 1vs 19 ± 1 min-1, p = 0.001). In contrast, neither CFT nor CPT altered the respiratory rate (18 ± 1 vs 18 ± 2 min-1, p = 0.38 and 18 ± 1 vs 18 ± 1 min-1, p = 0.84, respectively). CONCLUSION: Changes in HR characteristics during deactivation of peripheral chemoreceptors but not during the CFT and CPT are related with a decrease in respiratory rate. This highlights the need of respiratory rate assessment when evaluating adaptations of cardiorespiratory chemoreceptor control.