Hypoxic tachycardia is not a result of increased respiratory activity in healthy subjects

New Findings What is the central question of this research? Does increased ventilation contribute to the increase in heart rate during transient exposure to hypoxia in humans? What is the main finding and its importance? Voluntary suppression of the ventilatory response to transient hypoxia does not...

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Published inExperimental physiology Vol. 104; no. 4; pp. 476 - 489
Main Authors Paleczny, Bartłomiej, Seredyński, Rafał, Tubek, Stanisław, Adamiec, Dorota, Ponikowski, Piotr, Ponikowska, Beata
Format Journal Article
LanguageEnglish
Published England John Wiley & Sons, Inc 01.04.2019
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Abstract New Findings What is the central question of this research? Does increased ventilation contribute to the increase in heart rate during transient exposure to hypoxia in humans? What is the main finding and its importance? Voluntary suppression of the ventilatory response to transient hypoxia does not affect the magnitude of the heart rate response to the stimulus. This indicates that hypoxic tachycardia is not secondary to hyperpnoea in humans. Better understanding of the physiology underlying the cardiovascular response to hypoxia might help in identification of new markers of elevated chemoreceptor activity, which has been proposed as a target in treatment of sympathetically mediated diseases. Animal data suggest that hypoxic tachycardia is secondary to hyperpnoea, and for years this observation has been extrapolated to humans, despite a lack of experimental evidence. We addressed this issue in 17 volunteers aged 29 ± 7 (SD) years. A transient hypoxia test, comprising several nitrogen‐breathing episodes, was performed twice in each subject. In the first test, the subject breathed spontaneously (spontaneous breathing). In the second test, the subject was repeatedly asked to adjust his or her depth and rate of breathing according to visual (real‐time inspiratory flow) and auditory (metronome sound) cues, respectively (controlled breathing), to maintain respiration at the resting level during nitrogen‐breathing episodes. Hypoxic responsiveness, including minute ventilation [Hyp‐VI; in liters per minute per percentage of blood oxygen saturation (SpO2)], tidal volume [Hyp‐VT; in litres per SpO2], heart rate [Hyp‐HR; in beats per minute per SpO2], systolic [Hyp‐SBP; in millimetres of mercury per SpO2] and mean blood pressure [Hyp‐MAP; in millimetres of mercury per SpO2] and systemic vascular resistance [Hyp‐SVR; in dynes seconds (centimetres)−5 per SpO2] was calculated as the slope of the regression line relating the variable to SpO2, including pre‐ and post‐hypoxic values. The Hyp‐VI and Hyp‐VT were reduced by 69 ± 25 and 75 ± 10%, respectively, in controlled versus spontaneous breathing (Hyp‐VI, −0.30 ± 0.15 versus −0.11 ± 0.09; Hyp‐VT, −0.030 ± 0.024 versus −0.007 ± 0.004; both P < 0.001). However, the cardiovascular responses did not differ between spontaneous and controlled breathing (Hyp‐HR, −0.62 ± 0.24 versus −0.71 ± 0.33; Hyp‐MAP, −0.43 ± 0.19 versus −0.47 ± 0.21; Hyp‐SVR, 9.15 ± 5.22 versus 9.53 ± 5.57; all P ≥ 0.22), indicating that hypoxic tachycardia is not secondary to hyperpnoea. Hyp‐HR was correlated with Hyp‐SVR (r = −074 and −0.80 for spontaneous and controlled breathing, respectively; both P < 0.05) and resting barosensitivity assessed with the sequence technique (r = −0.60 for spontaneous breathing; P < 0.05). This might suggest that the baroreflex mechanism is involved.
AbstractList Animal data suggest that hypoxic tachycardia is secondary to hyperpnoea, and for years this observation has been extrapolated to humans, despite a lack of experimental evidence. We addressed this issue in 17 volunteers aged 29 ± 7 (SD) years. A transient hypoxia test, comprising several nitrogen‐breathing episodes, was performed twice in each subject. In the first test, the subject breathed spontaneously (spontaneous breathing). In the second test, the subject was repeatedly asked to adjust his or her depth and rate of breathing according to visual (real‐time inspiratory flow) and auditory (metronome sound) cues, respectively (controlled breathing), to maintain respiration at the resting level during nitrogen‐breathing episodes. Hypoxic responsiveness, including minute ventilation [Hyp‐VI; in liters per minute per percentage of blood oxygen saturation (SpO2)], tidal volume [Hyp‐VT; in litres per SpO2], heart rate [Hyp‐HR; in beats per minute per SpO2], systolic [Hyp‐SBP; in millimetres of mercury per SpO2] and mean blood pressure [Hyp‐MAP; in millimetres of mercury per SpO2] and systemic vascular resistance [Hyp‐SVR; in dynes seconds (centimetres)−5 per SpO2] was calculated as the slope of the regression line relating the variable to SpO2, including pre‐ and post‐hypoxic values. The Hyp‐VI and Hyp‐VT were reduced by 69 ± 25 and 75 ± 10%, respectively, in controlled versus spontaneous breathing (Hyp‐VI, −0.30 ± 0.15 versus −0.11 ± 0.09; Hyp‐VT, −0.030 ± 0.024 versus −0.007 ± 0.004; both P < 0.001). However, the cardiovascular responses did not differ between spontaneous and controlled breathing (Hyp‐HR, −0.62 ± 0.24 versus −0.71 ± 0.33; Hyp‐MAP, −0.43 ± 0.19 versus −0.47 ± 0.21; Hyp‐SVR, 9.15 ± 5.22 versus 9.53 ± 5.57; all P ≥ 0.22), indicating that hypoxic tachycardia is not secondary to hyperpnoea. Hyp‐HR was correlated with Hyp‐SVR (r = −074 and −0.80 for spontaneous and controlled breathing, respectively; both P < 0.05) and resting barosensitivity assessed with the sequence technique (r = −0.60 for spontaneous breathing; P < 0.05). This might suggest that the baroreflex mechanism is involved.
New Findings What is the central question of this research? Does increased ventilation contribute to the increase in heart rate during transient exposure to hypoxia in humans? What is the main finding and its importance? Voluntary suppression of the ventilatory response to transient hypoxia does not affect the magnitude of the heart rate response to the stimulus. This indicates that hypoxic tachycardia is not secondary to hyperpnoea in humans. Better understanding of the physiology underlying the cardiovascular response to hypoxia might help in identification of new markers of elevated chemoreceptor activity, which has been proposed as a target in treatment of sympathetically mediated diseases. Animal data suggest that hypoxic tachycardia is secondary to hyperpnoea, and for years this observation has been extrapolated to humans, despite a lack of experimental evidence. We addressed this issue in 17 volunteers aged 29 ± 7 (SD) years. A transient hypoxia test, comprising several nitrogen‐breathing episodes, was performed twice in each subject. In the first test, the subject breathed spontaneously (spontaneous breathing). In the second test, the subject was repeatedly asked to adjust his or her depth and rate of breathing according to visual (real‐time inspiratory flow) and auditory (metronome sound) cues, respectively (controlled breathing), to maintain respiration at the resting level during nitrogen‐breathing episodes. Hypoxic responsiveness, including minute ventilation [Hyp‐VI; in liters per minute per percentage of blood oxygen saturation (SpO2)], tidal volume [Hyp‐VT; in litres per SpO2], heart rate [Hyp‐HR; in beats per minute per SpO2], systolic [Hyp‐SBP; in millimetres of mercury per SpO2] and mean blood pressure [Hyp‐MAP; in millimetres of mercury per SpO2] and systemic vascular resistance [Hyp‐SVR; in dynes seconds (centimetres)−5 per SpO2] was calculated as the slope of the regression line relating the variable to SpO2, including pre‐ and post‐hypoxic values. The Hyp‐VI and Hyp‐VT were reduced by 69 ± 25 and 75 ± 10%, respectively, in controlled versus spontaneous breathing (Hyp‐VI, −0.30 ± 0.15 versus −0.11 ± 0.09; Hyp‐VT, −0.030 ± 0.024 versus −0.007 ± 0.004; both P < 0.001). However, the cardiovascular responses did not differ between spontaneous and controlled breathing (Hyp‐HR, −0.62 ± 0.24 versus −0.71 ± 0.33; Hyp‐MAP, −0.43 ± 0.19 versus −0.47 ± 0.21; Hyp‐SVR, 9.15 ± 5.22 versus 9.53 ± 5.57; all P ≥ 0.22), indicating that hypoxic tachycardia is not secondary to hyperpnoea. Hyp‐HR was correlated with Hyp‐SVR (r = −074 and −0.80 for spontaneous and controlled breathing, respectively; both P < 0.05) and resting barosensitivity assessed with the sequence technique (r = −0.60 for spontaneous breathing; P < 0.05). This might suggest that the baroreflex mechanism is involved.
What is the central question of this research? Does increased ventilation contribute to the increase in heart rate during transient exposure to hypoxia in humans? What is the main finding and its importance? Voluntary suppression of the ventilatory response to transient hypoxia does not affect the magnitude of the heart rate response to the stimulus. This indicates that hypoxic tachycardia is not secondary to hyperpnoea in humans. Better understanding of the physiology underlying the cardiovascular response to hypoxia might help in identification of new markers of elevated chemoreceptor activity, which has been proposed as a target in treatment of sympathetically mediated diseases. Animal data suggest that hypoxic tachycardia is secondary to hyperpnoea, and for years this observation has been extrapolated to humans, despite a lack of experimental evidence. We addressed this issue in 17 volunteers aged 29 ± 7 (SD) years. A transient hypoxia test, comprising several nitrogen-breathing episodes, was performed twice in each subject. In the first test, the subject breathed spontaneously (spontaneous breathing). In the second test, the subject was repeatedly asked to adjust his or her depth and rate of breathing according to visual (real-time inspiratory flow) and auditory (metronome sound) cues, respectively (controlled breathing), to maintain respiration at the resting level during nitrogen-breathing episodes. Hypoxic responsiveness, including minute ventilation [Hyp-VI; in liters per minute per percentage of blood oxygen saturation ( )], tidal volume [Hyp-VT; in litres per ], heart rate [Hyp-HR; in beats per minute per ], systolic [Hyp-SBP; in millimetres of mercury per ] and mean blood pressure [Hyp-MAP; in millimetres of mercury per ] and systemic vascular resistance [Hyp-SVR; in dynes seconds (centimetres) per ] was calculated as the slope of the regression line relating the variable to , including pre- and post-hypoxic values. The Hyp-VI and Hyp-VT were reduced by 69 ± 25 and 75 ± 10%, respectively, in controlled versus spontaneous breathing (Hyp-VI, -0.30 ± 0.15 versus -0.11 ± 0.09; Hyp-VT, -0.030 ± 0.024 versus -0.007 ± 0.004; both P < 0.001). However, the cardiovascular responses did not differ between spontaneous and controlled breathing (Hyp-HR, -0.62 ± 0.24 versus -0.71 ± 0.33; Hyp-MAP, -0.43 ± 0.19 versus -0.47 ± 0.21; Hyp-SVR, 9.15 ± 5.22 versus 9.53 ± 5.57; all P ≥ 0.22), indicating that hypoxic tachycardia is not secondary to hyperpnoea. Hyp-HR was correlated with Hyp-SVR (r = -074 and -0.80 for spontaneous and controlled breathing, respectively; both P < 0.05) and resting barosensitivity assessed with the sequence technique (r = -0.60 for spontaneous breathing; P < 0.05). This might suggest that the baroreflex mechanism is involved.
What is the central question of this research? Does increased ventilation contribute to the increase in heart rate during transient exposure to hypoxia in humans? What is the main finding and its importance? Voluntary suppression of the ventilatory response to transient hypoxia does not affect the magnitude of the heart rate response to the stimulus. This indicates that hypoxic tachycardia is not secondary to hyperpnoea in humans. Better understanding of the physiology underlying the cardiovascular response to hypoxia might help in identification of new markers of elevated chemoreceptor activity, which has been proposed as a target in treatment of sympathetically mediated diseases.NEW FINDINGSWhat is the central question of this research? Does increased ventilation contribute to the increase in heart rate during transient exposure to hypoxia in humans? What is the main finding and its importance? Voluntary suppression of the ventilatory response to transient hypoxia does not affect the magnitude of the heart rate response to the stimulus. This indicates that hypoxic tachycardia is not secondary to hyperpnoea in humans. Better understanding of the physiology underlying the cardiovascular response to hypoxia might help in identification of new markers of elevated chemoreceptor activity, which has been proposed as a target in treatment of sympathetically mediated diseases.Animal data suggest that hypoxic tachycardia is secondary to hyperpnoea, and for years this observation has been extrapolated to humans, despite a lack of experimental evidence. We addressed this issue in 17 volunteers aged 29 ± 7 (SD) years. A transient hypoxia test, comprising several nitrogen-breathing episodes, was performed twice in each subject. In the first test, the subject breathed spontaneously (spontaneous breathing). In the second test, the subject was repeatedly asked to adjust his or her depth and rate of breathing according to visual (real-time inspiratory flow) and auditory (metronome sound) cues, respectively (controlled breathing), to maintain respiration at the resting level during nitrogen-breathing episodes. Hypoxic responsiveness, including minute ventilation [Hyp-VI; in liters per minute per percentage of blood oxygen saturation ( SpO2 )], tidal volume [Hyp-VT; in litres per SpO2 ], heart rate [Hyp-HR; in beats per minute per SpO2 ], systolic [Hyp-SBP; in millimetres of mercury per SpO2 ] and mean blood pressure [Hyp-MAP; in millimetres of mercury per SpO2 ] and systemic vascular resistance [Hyp-SVR; in dynes seconds (centimetres)-5 per SpO2 ] was calculated as the slope of the regression line relating the variable to SpO2 , including pre- and post-hypoxic values. The Hyp-VI and Hyp-VT were reduced by 69 ± 25 and 75 ± 10%, respectively, in controlled versus spontaneous breathing (Hyp-VI, -0.30 ± 0.15 versus -0.11 ± 0.09; Hyp-VT, -0.030 ± 0.024 versus -0.007 ± 0.004; both P < 0.001). However, the cardiovascular responses did not differ between spontaneous and controlled breathing (Hyp-HR, -0.62 ± 0.24 versus -0.71 ± 0.33; Hyp-MAP, -0.43 ± 0.19 versus -0.47 ± 0.21; Hyp-SVR, 9.15 ± 5.22 versus 9.53 ± 5.57; all P ≥ 0.22), indicating that hypoxic tachycardia is not secondary to hyperpnoea. Hyp-HR was correlated with Hyp-SVR (r = -074 and -0.80 for spontaneous and controlled breathing, respectively; both P < 0.05) and resting barosensitivity assessed with the sequence technique (r = -0.60 for spontaneous breathing; P < 0.05). This might suggest that the baroreflex mechanism is involved.ABSTRACTAnimal data suggest that hypoxic tachycardia is secondary to hyperpnoea, and for years this observation has been extrapolated to humans, despite a lack of experimental evidence. We addressed this issue in 17 volunteers aged 29 ± 7 (SD) years. A transient hypoxia test, comprising several nitrogen-breathing episodes, was performed twice in each subject. In the first test, the subject breathed spontaneously (spontaneous breathing). In the second test, the subject was repeatedly asked to adjust his or her depth and rate of breathing according to visual (real-time inspiratory flow) and auditory (metronome sound) cues, respectively (controlled breathing), to maintain respiration at the resting level during nitrogen-breathing episodes. Hypoxic responsiveness, including minute ventilation [Hyp-VI; in liters per minute per percentage of blood oxygen saturation ( SpO2 )], tidal volume [Hyp-VT; in litres per SpO2 ], heart rate [Hyp-HR; in beats per minute per SpO2 ], systolic [Hyp-SBP; in millimetres of mercury per SpO2 ] and mean blood pressure [Hyp-MAP; in millimetres of mercury per SpO2 ] and systemic vascular resistance [Hyp-SVR; in dynes seconds (centimetres)-5 per SpO2 ] was calculated as the slope of the regression line relating the variable to SpO2 , including pre- and post-hypoxic values. The Hyp-VI and Hyp-VT were reduced by 69 ± 25 and 75 ± 10%, respectively, in controlled versus spontaneous breathing (Hyp-VI, -0.30 ± 0.15 versus -0.11 ± 0.09; Hyp-VT, -0.030 ± 0.024 versus -0.007 ± 0.004; both P < 0.001). However, the cardiovascular responses did not differ between spontaneous and controlled breathing (Hyp-HR, -0.62 ± 0.24 versus -0.71 ± 0.33; Hyp-MAP, -0.43 ± 0.19 versus -0.47 ± 0.21; Hyp-SVR, 9.15 ± 5.22 versus 9.53 ± 5.57; all P ≥ 0.22), indicating that hypoxic tachycardia is not secondary to hyperpnoea. Hyp-HR was correlated with Hyp-SVR (r = -074 and -0.80 for spontaneous and controlled breathing, respectively; both P < 0.05) and resting barosensitivity assessed with the sequence technique (r = -0.60 for spontaneous breathing; P < 0.05). This might suggest that the baroreflex mechanism is involved.
Author Tubek, Stanisław
Ponikowska, Beata
Seredyński, Rafał
Adamiec, Dorota
Paleczny, Bartłomiej
Ponikowski, Piotr
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Issue 4
Keywords hypoxic tachycardia
peripheral chemoreflex sensitivity
transient hypoxia
controlled breathing
Language English
License 2019 The Authors. Experimental Physiology © 2019 The Physiological Society.
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Notes Funding information
Edited by: Jeremy Ward
This research was financially supported by the Ministry of Science and Higher Education (Poland)/Wroclaw Medical University, internal number: ST.A090.17.046.
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OpenAccessLink https://physoc.onlinelibrary.wiley.com/doi/pdfdirect/10.1113/EP087233
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Snippet New Findings What is the central question of this research? Does increased ventilation contribute to the increase in heart rate during transient exposure to...
What is the central question of this research? Does increased ventilation contribute to the increase in heart rate during transient exposure to hypoxia in...
Animal data suggest that hypoxic tachycardia is secondary to hyperpnoea, and for years this observation has been extrapolated to humans, despite a lack of...
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SubjectTerms Adult
Baroreceptors
Baroreflex - physiology
Blood pressure
Blood Pressure - physiology
Cardiac arrhythmia
Cardiovascular system
Chemoreceptor Cells - metabolism
Chemoreceptor Cells - physiology
controlled breathing
Female
Healthy Volunteers
Heart rate
Heart Rate - physiology
Humans
Hypoxia
Hypoxia - metabolism
Hypoxia - physiopathology
hypoxic tachycardia
Lung - metabolism
Lung - physiology
Male
Mechanical ventilation
Mercury
Oxygen - metabolism
peripheral chemoreflex sensitivity
Pulmonary Gas Exchange - physiology
Reflexes
Respiration
Tachycardia
Tachycardia - metabolism
Tachycardia - physiopathology
Tidal Volume - physiology
transient hypoxia
Vascular Resistance - physiology
Title Hypoxic tachycardia is not a result of increased respiratory activity in healthy subjects
URI https://onlinelibrary.wiley.com/doi/abs/10.1113%2FEP087233
https://www.ncbi.nlm.nih.gov/pubmed/30672622
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Volume 104
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