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 in | Experimental physiology Vol. 104; no. 4; pp. 476 - 489 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
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. |
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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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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30672622$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1152/japplphysiol.01241.2003 10.1113/JP272075 10.1007/s10286-014-0263-9 10.1161/hc3101.093699 10.1097/00004872-200107000-00013 10.1111/sms.12619 10.1016/j.cardfail.2013.03.013 10.1161/01.RES.44.6.856 10.1152/japplphysiol.00470.2003 10.1161/01.CIR.77.2.407 10.5603/KP.a2018.0178 10.1016/0034-5687(73)90005-4 10.1152/ajpheart.00334.2016 10.1113/JP272109 10.1183/09031936.97.10010161 10.1016/j.resp.2004.05.005 10.1152/ajplegacy.1941.132.2.426 10.1152/japplphysiol.00299.2016 10.1152/ajpheart.00861.2014 10.1113/jphysiol.1958.sp006092 10.1098/rstb.1913.0006 10.1159/000195508 10.1152/jappl.1995.78.4.1522 10.1152/ajpheart.2000.279.2.H536 10.3181/00379727-76-18408 10.1113/jphysiol.2007.139204 10.1002/ejhf.641 10.1161/01.HYP.12.2.214 10.1152/japplphysiol.00553.2007 10.1152/jappl.1982.52.3.570 10.1111/j.1365-2362.1995.tb01962.x 10.1152/ajplegacy.1972.223.6.1308 10.1016/S0735-1097(00)00595-7 10.1016/j.resp.2007.01.007 10.1152/ajpheart.00746.2013 10.1152/japplphysiol.01103.2001 10.1152/physrev.1954.34.2.167 10.1016/j.jacbts.2016.06.004 10.1093/cvr/16.3.163 10.1113/jphysiol.1966.sp008036 10.1097/HJH.0b013e328350136c 10.1152/jappl.2001.90.4.1516 10.1161/01.RES.46.1.77 10.1152/jappl.1994.76.2.756 10.1111/j.1469-7793.2001.00613.x 10.1113/expphysiol.2013.075580 10.1113/EP085498 10.1111/j.1469-445X.2000.01932.x |
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Keywords | hypoxic tachycardia peripheral chemoreflex sensitivity transient hypoxia controlled breathing |
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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. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
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References | 1982; 16 2001; 90 1941; 132 1982; 52 1980; 46 2007; 583 1995; 78 1973; 17 2000; 85 1988; 77 2016; 101 2014; 24 2015; 308 2008; 104 2017; 595 2001; 104 2013; 19 1997; 10 1995; 25 2016; 311 2001; 19 1951; 76 2016; 594 2002; 93 1972; 223 2001; 537 2018; 76 2014; 99 1994; 76 1964; 146 2004; 142 2000; 279 1988; 54 1988; 12 2016; 121 1978; 234 2012; 30 2014; 306 2004; 96 2007; 157 1966; 186 2015; 25 1958; 144 1913; 203 2016; 1 1954; 34 2000; 35 2017; 19 1979; 44 e_1_2_7_5_1 e_1_2_7_3_1 e_1_2_7_9_1 e_1_2_7_19_1 e_1_2_7_17_1 e_1_2_7_15_1 e_1_2_7_13_1 e_1_2_7_43_1 e_1_2_7_11_1 e_1_2_7_45_1 e_1_2_7_47_1 e_1_2_7_26_1 e_1_2_7_49_1 e_1_2_7_28_1 e_1_2_7_50_1 e_1_2_7_25_1 e_1_2_7_31_1 e_1_2_7_23_1 e_1_2_7_33_1 e_1_2_7_21_1 e_1_2_7_35_1 e_1_2_7_37_1 e_1_2_7_39_1 e_1_2_7_6_1 e_1_2_7_4_1 e_1_2_7_8_1 e_1_2_7_18_1 e_1_2_7_16_1 e_1_2_7_40_1 e_1_2_7_2_1 e_1_2_7_14_1 e_1_2_7_42_1 e_1_2_7_12_1 e_1_2_7_44_1 e_1_2_7_10_1 e_1_2_7_46_1 Slutsky A. S. (e_1_2_7_41_1) 1978; 234 e_1_2_7_48_1 e_1_2_7_27_1 e_1_2_7_29_1 Comroe J. H. (e_1_2_7_7_1) 1964; 146 e_1_2_7_51_1 e_1_2_7_30_1 e_1_2_7_24_1 e_1_2_7_32_1 e_1_2_7_22_1 e_1_2_7_34_1 e_1_2_7_20_1 e_1_2_7_36_1 e_1_2_7_38_1 |
References_xml | – volume: 17 start-page: 302 year: 1973 end-page: 314 article-title: Ventilatory responses to transient hypoxia and hypercapnia in man publication-title: Respiration Physiology – volume: 96 start-page: 1262 year: 2004 end-page: 1269 article-title: Microneurography: How the technique developed and its role in the investigation of the sympathetic nervous system publication-title: Journal of Applied Physiology – volume: 308 start-page: H1540 year: 2015 end-page: H1546 article-title: Hypoxia increases exercise heart rate despite combined inhibition of β‐adrenergic and muscarinic receptors publication-title: American Journal of Physiology. Heart and Circulatory Physiology – volume: 34 start-page: 167 year: 1954 end-page: 201 article-title: Chemoreflexes from the heart and lungs publication-title: Physiological Reviews – volume: 19 start-page: 391 year: 2017 end-page: 400 article-title: Carotid body resection for sympathetic modulation in systolic heart failure: Results from first‐in‐man study publication-title: European Journal of Heart Failure – volume: 76 start-page: 756 year: 1994 end-page: 759 article-title: Cardiovascular and respiratory effects of adenosine in humans after pulmonary denervation publication-title: Journal of Applied Physiology – volume: 142 start-page: 13 year: 2004 end-page: 25 article-title: Cardio‐respiratory measures following isocapnic voluntary hyperventilation publication-title: Respiratory Physiology & Neurobiology – volume: 19 start-page: 408 year: 2013 end-page: 415 article-title: Clinical predictors and hemodynamic consequences of elevated peripheral chemosensitivity in optimally treated men with chronic systolic heart failure publication-title: Journal of Cardiac Failure – volume: 146 start-page: 33 year: 1964 end-page: 41 article-title: The respiratory and cardiovascular responses of temporally separated aortic and carotid bodies to cyanide, nicotine, phenyldiguanide and serotonin publication-title: Journal of Pharmacology and Experimental Therapeutics – volume: 144 start-page: 148 year: 1958 end-page: 166 article-title: The effects of stimulation of the carotid body chemoreceptors on heart rate in the dog publication-title: The Journal of Physiology – volume: 157 start-page: 12 year: 2007 end-page: 21 article-title: Adequate stimuli of the carotid body: More than an oxygen sensor? publication-title: Respiratory Physiology & Neurobiology – volume: 186 start-page: 307 year: 1966 end-page: 320 article-title: The effects of hyperventilation on the reflex cardiac response from the carotid bodies in the cat publication-title: The Journal of Physiology – volume: 10 start-page: 161 year: 1997 end-page: 166 article-title: Influence of awareness of the recording of breathing on respiratory pattern in healthy humans publication-title: European Respiratory Journal – volume: 12 start-page: 214 year: 1988 end-page: 222 article-title: Evaluation of the baroreceptor‐heart rate reflex by 24‐hour intra‐arterial blood pressure monitoring in humans publication-title: Hypertension – volume: 16 start-page: 163 year: 1982 end-page: 172 article-title: Increased sensitivity of the arterial chemoreceptor drive in young men with mild hypertension publication-title: Cardiovascular Research – volume: 104 start-page: 482 year: 2008 end-page: 489 article-title: Cardiovascular and cerebrovascular responses to acute isocapnic and poikilocapnic hypoxia in humans publication-title: Journal of Applied Physiology – volume: 121 start-page: 932 year: 2016 end-page: 943 article-title: Central command does not suppress baroreflex control of cardiac sympathetic nerve activity at the onset of spontaneous motor activity in the decerebrate cat publication-title: Journal of Applied Physiology – volume: 25 start-page: 887 year: 1995 end-page: 892 article-title: The reproducibility and comparability of tests of the peripheral chemoreflex: Comparing the transient hypoxic ventilatory drive test and the single‐breath carbon dioxide response test in healthy subjects publication-title: European Journal of Clinical Investigation – volume: 52 start-page: 570 year: 1982 end-page: 577 article-title: Modulation of human sinus node function by systemic hypoxia publication-title: Journal of Applied Physiology – volume: 24 start-page: 285 year: 2014 end-page: 296 article-title: Age‐related reflex responses from peripheral and central chemoreceptors in healthy men publication-title: Clinical Autonomic Research – volume: 76 start-page: 121 year: 1951 end-page: 124 article-title: Role of carotid chemoreceptors in hypoxic cardiac acceleration publication-title: Proceedings of the Society for Experimental Biology and Medicine – volume: 104 start-page: 544 year: 2001 end-page: 549 article-title: Peripheral chemoreceptor hypersensitivity: An ominous sign in patients with chronic heart failure publication-title: Circulation – volume: 30 start-page: 753 year: 2012 end-page: 760 article-title: Peripheral chemoreflex activation contributes to sympathetic baroreflex impairment in chronic heart failure publication-title: Journal of Hypertension – volume: 223 start-page: 1308 year: 1972 end-page: 1312 article-title: Systemic circulatory responses to hypocapnia in man publication-title: The American Journal of Physiology – volume: 35 start-page: 1462 year: 2000 end-page: 1469 article-title: Effects of controlled breathing, mental activity and mental stress with or without verbalization on heart rate variability publication-title: Journal of the American College of Cardiology – volume: 90 start-page: 1516 year: 2001 end-page: 1522 article-title: Hypoxia augments apnea‐induced peripheral vasoconstriction in humans publication-title: Journal of Applied Physiology – volume: 595 start-page: 43 year: 2017 end-page: 51 article-title: Contribution of peripheral and central chemoreceptors to sympatho‐excitation in heart failure publication-title: The Journal of Physiology – volume: 85 start-page: 227 year: 2000 end-page: 237 article-title: Body position and cardiac dynamic and chronotropic responses to steady‐state isocapnic hypoxaemia in humans publication-title: Experimental Physiology – volume: 96 start-page: 1782 year: 2004 end-page: 1787 article-title: Evidence of sustained forearm vasodilatation after brief isocapnic hypoxia publication-title: Journal of Applied Physiology – volume: 44 start-page: 856 year: 1979 end-page: 863 article-title: Effect of hypoxia on the sinoatrial node, atrium, and atrioventricular node in the rabbit heart publication-title: Circulation Research – volume: 583 start-page: 1041 year: 2007 end-page: 1048 article-title: Mechanical and neural contributions to hysteresis in the cardiac vagal limb of the arterial baroreflex publication-title: The Journal of Physiology – volume: 537 start-page: 613 year: 2001 end-page: 621 article-title: Effects of regional phentolamine on hypoxic vasodilatation in healthy humans publication-title: The Journal of Physiology – volume: 77 start-page: 407 year: 1988 end-page: 414 article-title: Mechanisms mediating the heart rate response to hypoxemia publication-title: Circulation – volume: 25 start-page: 53 year: 2015 end-page: 59 article-title: Regulation of cardiac output in hypoxia publication-title: Scandinavian Journal of Medicine & Science in Sports – volume: 93 start-page: 857 year: 2002 end-page: 864 article-title: Effect of hypoxia on arterial baroreflex control of heart rate and muscle sympathetic nerve activity in humans publication-title: Journal of Applied Physiology – volume: 279 start-page: H536 year: 2000 end-page: H541 article-title: Hyperventilation alters arterial baroreflex control of heart rate and muscle sympathetic nerve activity publication-title: American Journal of Physiology. Heart and Circulatory Physiology – volume: 76 start-page: 1426 year: 2018 end-page: 1433 article-title: Human carotid bodies as a therapeutic target: New insights from clinician perspective publication-title: Kardiologia Polska – volume: 203 start-page: 185 year: 1913 end-page: 318 article-title: Physiological observations made on Pike's Peak, Colorado, with special reference to adaptation to low barometric pressures publication-title: Philosophical Transactions of the Royal Society B: Biological Sciences – volume: 1 start-page: 313 year: 2016 end-page: 324 article-title: Unilateral carotid body resection in resistant hypertension: A safety and feasibility trial publication-title: JACC: Basic to Translational Science – volume: 132 start-page: 426 year: 1941 end-page: 436 article-title: The effect of hypoxemia on ventilation and circulation in man publication-title: The American Journal of Physiology – volume: 306 start-page: H309 year: 2014 end-page: H316 article-title: Sex differences in forearm vasoconstrictor response to voluntary apnea publication-title: American Journal of Physiology. Heart and Circulatory Physiology – volume: 46 start-page: 77 year: 1980 end-page: 83 article-title: Responses of the heart to stimulation of aortic body chemoreceptors in dogs publication-title: Circulation Research – volume: 594 start-page: 6225 year: 2016 end-page: 6240 article-title: Effects of selective carotid body stimulation with adenosine in conscious humans publication-title: The Journal of Physiology – volume: 19 start-page: 1279 year: 2001 end-page: 1287 article-title: Effect of altering conditions of the sequence method on baroreflex sensitivity publication-title: Journal of Hypertension – volume: 54 start-page: 103 year: 1988 end-page: 109 article-title: Influence of controlled breathing with diminished tidal volume on hypoxic heart rate response in man publication-title: Respiration – volume: 234 start-page: H129 year: 1978 end-page: H132 article-title: Heart rate response to isocapnic hypoxia in conscious man publication-title: The American Journal of Physiology – volume: 99 start-page: 552 year: 2014 end-page: 561 article-title: Dissociation between blood pressure and heart rate response to hypoxia after bilateral carotid body removal in men with systolic heart failure publication-title: Experimental Physiology – volume: 101 start-page: 432 year: 2016 end-page: 447 article-title: Comparing and characterizing transient and steady‐state tests of the peripheral chemoreflex in humans publication-title: Experimental Physiology – volume: 311 start-page: H1040 year: 2016 end-page: H1050 article-title: Effects of aging and coronary artery disease on sympathetic neural recruitment strategies during end‐inspiratory and end‐expiratory apnea publication-title: American Journal of Physiology. Heart and Circulatory Physiology – volume: 78 start-page: 1522 year: 1995 end-page: 1530 article-title: Role of vagal feedback from the lung in hypoxic‐induced tachycardia in humans publication-title: Journal of Applied Physiology – ident: e_1_2_7_44_1 doi: 10.1152/japplphysiol.01241.2003 – ident: e_1_2_7_45_1 doi: 10.1113/JP272075 – ident: e_1_2_7_30_1 doi: 10.1007/s10286-014-0263-9 – ident: e_1_2_7_34_1 doi: 10.1161/hc3101.093699 – ident: e_1_2_7_9_1 doi: 10.1097/00004872-200107000-00013 – ident: e_1_2_7_38_1 doi: 10.1111/sms.12619 – ident: e_1_2_7_27_1 doi: 10.1016/j.cardfail.2013.03.013 – ident: e_1_2_7_37_1 doi: 10.1161/01.RES.44.6.856 – ident: e_1_2_7_49_1 doi: 10.1152/japplphysiol.00470.2003 – ident: e_1_2_7_18_1 doi: 10.1161/01.CIR.77.2.407 – ident: e_1_2_7_47_1 doi: 10.5603/KP.a2018.0178 – ident: e_1_2_7_14_1 doi: 10.1016/0034-5687(73)90005-4 – ident: e_1_2_7_3_1 doi: 10.1152/ajpheart.00334.2016 – ident: e_1_2_7_48_1 doi: 10.1113/JP272109 – ident: e_1_2_7_16_1 doi: 10.1183/09031936.97.10010161 – ident: e_1_2_7_23_1 doi: 10.1016/j.resp.2004.05.005 – ident: e_1_2_7_2_1 doi: 10.1152/ajplegacy.1941.132.2.426 – ident: e_1_2_7_24_1 doi: 10.1152/japplphysiol.00299.2016 – ident: e_1_2_7_39_1 doi: 10.1152/ajpheart.00861.2014 – ident: e_1_2_7_8_1 doi: 10.1113/jphysiol.1958.sp006092 – ident: e_1_2_7_12_1 doi: 10.1098/rstb.1913.0006 – ident: e_1_2_7_19_1 doi: 10.1159/000195508 – ident: e_1_2_7_40_1 doi: 10.1152/jappl.1995.78.4.1522 – ident: e_1_2_7_50_1 doi: 10.1152/ajpheart.2000.279.2.H536 – volume: 234 start-page: H129 year: 1978 ident: e_1_2_7_41_1 article-title: Heart rate response to isocapnic hypoxia in conscious man publication-title: The American Journal of Physiology – volume: 146 start-page: 33 year: 1964 ident: e_1_2_7_7_1 article-title: The respiratory and cardiovascular responses of temporally separated aortic and carotid bodies to cyanide, nicotine, phenyldiguanide and serotonin publication-title: Journal of Pharmacology and Experimental Therapeutics – ident: e_1_2_7_5_1 doi: 10.3181/00379727-76-18408 – ident: e_1_2_7_43_1 doi: 10.1113/jphysiol.2007.139204 – ident: e_1_2_7_29_1 doi: 10.1002/ejhf.641 – ident: e_1_2_7_31_1 doi: 10.1161/01.HYP.12.2.214 – ident: e_1_2_7_42_1 doi: 10.1152/japplphysiol.00553.2007 – ident: e_1_2_7_13_1 doi: 10.1152/jappl.1982.52.3.570 – ident: e_1_2_7_6_1 doi: 10.1111/j.1365-2362.1995.tb01962.x – ident: e_1_2_7_35_1 doi: 10.1152/ajplegacy.1972.223.6.1308 – ident: e_1_2_7_4_1 doi: 10.1016/S0735-1097(00)00595-7 – ident: e_1_2_7_20_1 doi: 10.1016/j.resp.2007.01.007 – ident: e_1_2_7_32_1 doi: 10.1152/ajpheart.00746.2013 – ident: e_1_2_7_15_1 doi: 10.1152/japplphysiol.01103.2001 – ident: e_1_2_7_10_1 doi: 10.1152/physrev.1954.34.2.167 – ident: e_1_2_7_26_1 doi: 10.1016/j.jacbts.2016.06.004 – ident: e_1_2_7_46_1 doi: 10.1093/cvr/16.3.163 – ident: e_1_2_7_36_1 doi: 10.1113/jphysiol.1966.sp008036 – ident: e_1_2_7_11_1 doi: 10.1097/HJH.0b013e328350136c – ident: e_1_2_7_21_1 doi: 10.1152/jappl.2001.90.4.1516 – ident: e_1_2_7_17_1 doi: 10.1161/01.RES.46.1.77 – ident: e_1_2_7_25_1 doi: 10.1152/jappl.1994.76.2.756 – ident: e_1_2_7_51_1 doi: 10.1111/j.1469-7793.2001.00613.x – ident: e_1_2_7_28_1 doi: 10.1113/expphysiol.2013.075580 – ident: e_1_2_7_33_1 doi: 10.1113/EP085498 – ident: e_1_2_7_22_1 doi: 10.1111/j.1469-445X.2000.01932.x |
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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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StartPage | 476 |
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 https://www.proquest.com/docview/2200608672 https://www.proquest.com/docview/2179427839 |
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