Relevant bibliographies by topics / Breathing and heart rate[Hypoxia in man]

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Academic literature on the topic 'Breathing and heart rate[Hypoxia in man]'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 February 2022

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Journal articles on the topic "Breathing and heart rate[Hypoxia in man]"

1

Kimura, Hiroshi, Yoshitake Nishibayashi, Fumiaki Hayashi, Akio Yoshida, and Yoshiyuki Honda. "Influence of Controlled Breathing with Diminished Tidal Volume on Hypoxic Heart Rate Response in Man." Respiration 54, no. 2 (1988): 103–9. http://dx.doi.org/10.1159/000195508.

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Calbet, J. A. L., R. Boushel, G. Rådegran, H. Søndergaard, P. D. Wagner, and B. Saltin. "Determinants of maximal oxygen uptake in severe acute hypoxia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 2 (February 1, 2003): R291—R303. http://dx.doi.org/10.1152/ajpregu.00155.2002.

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To unravel the mechanisms by which maximal oxygen uptake (V˙o 2 max) is reduced with severe acute hypoxia in humans, nine Danish lowlanders performed incremental cycle ergometer exercise to exhaustion, while breathing room air (normoxia) or 10.5% O2 in N2(hypoxia, ∼5,300 m above sea level). With hypoxia, exercise PaO2 dropped to 31–34 mmHg and arterial O2 content (CaO2 ) was reduced by 35% ( P < 0.001). Forty-one percent of the reduction in CaO2 was explained by the lower inspired O2 pressure (Pi O2 ) in hypoxia, whereas the rest was due to the impairment of the pulmonary gas exchange, as reflected by the higher alveolar-arterial O2 difference in hypoxia ( P < 0.05). Hypoxia caused a 47% decrease inV˙o 2 max (a greater fall than accountable by reduced CaO2 ). Peak cardiac output decreased by 17% ( P < 0.01), due to equal reductions in both peak heart rate and stroke volume ( P < 0.05). Peak leg blood flow was also lower (by 22%, P < 0.01). Consequently, systemic and leg O2 delivery were reduced by 43 and 47%, respectively, with hypoxia ( P < 0.001) correlating closely with V˙o 2 max( r = 0.98, P < 0.001). Therefore, three main mechanisms account for the reduction ofV˙o 2 max in severe acute hypoxia: 1) reduction of Pi O2 , 2) impairment of pulmonary gas exchange, and 3) reduction of maximal cardiac output and peak leg blood flow, each explaining about one-third of the loss inV˙o 2 max.
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Pal, A., M. A. Akey, R. Chatterjee, A. P. Aguila, F. Martinez, R. Aysola, and P. M. Macey. "0556 Sex-Specific Relationship Between Anxiety and Autonomic Nervous System Dysfunction in Obstructive Sleep Apnea." Sleep 43, Supplement_1 (April 2020): A213. http://dx.doi.org/10.1093/sleep/zsaa056.553.

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Abstract Introduction Cardiovascular co-morbidities in obstructive sleep apnea (OSA) are hard to treat, perhaps due to autonomic nervous system (ANS) dysfunction. In OSA, intermittent hypoxia and poor tissue oxygen perfusion damage endothelial and nervous tissue, potentially underlying the dysfunction. Moreover, OSA is strongly associated with anxiety, which is independently associated with ANS dysfunction. We assessed sex-specific relationships between anxiety and cardiovascular markers of ANS dysfunction in OSA. Methods We studied people diagnosed with OSA and healthy controls. We collected 5 minutes of wakeful resting ECG, continuous non-invasive blood pressure, and respiration data. We calculated heart rate (HR), heart rate variability (HRV; sympathetic-vagal balance related to brainstem ANS output), mean arterial blood pressure (MAP), beat-to-beat MAP variability (BPV; related to peripheral autonomic function) and breathing rate (BR). We analyzed these measures with a multivariate regression model of anxiety symptoms (generalized anxiety disorder; GAD-7 scores), sex, and group (OSA vs. control), age/BMI/AHI covariates, and Bonferroni-corrected post-hoc comparisons (p≤0.05). Results We analyzed 64 subjects (32 OSA: AHI [mean±SEM] 24±4events/hour, 12 female, age 52±21years, BMI 33±2kg/m2; 32 control: 19 female, age 46±2; BMI 26±1). We observed significant main effects of anxiety, BMI, AHI, sex on HRV, but only group on BPV; post-hoc comparisons revealed high BPV only in OSA females. Secondary analyses included classifying by anxiety symptoms (GAD-7≥5), showing only OSA females with anxiety had higher BPV. Males showed higher HRV. AHI and anxiety were positively correlated with HRV in OSA males. AHI was negatively correlated with BR in OSA females. Conclusion We observed higher anxiety associated with higher BPV in OSA, especially in females. Unexpectedly, BR was lower in OSA females; longer breaths may have led to the greater BPV. Higher HRV in males complicated by OSA severity and anxiety could be related to higher sympathetic tone. The slightly older control group may have influenced the findings. Overall, our findings suggest anxiety in OSA is associated with peripheral and centrally-mediated autonomic dysfunction, but in a sex-specific manner. Support National Institutes of Health R56-NR-017435 and RO1-HL-135562.
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Tomi, Satoko T., Ryoji Ide, and Jacopo P. Mortola. "Heart and breathing rate variability in the avian perinatal period: The chicken embryo as a model." Avian Biology Research 12, no. 1 (January 1, 2019): 13–22. http://dx.doi.org/10.1177/1758155919832137.

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We used the chicken embryo at the internal pipping phase (just after the onset of pulmonary ventilation) as a model to quantify the changes in heart rate (fH), breathing frequency (fB) and their variabilities (heart rate variability and breathing rate variability) during air breathing (21% O2) and successive 20-min periods of 15%, 10% and 5% O2 and post-hypoxic recovery. For each condition, and for both fH and fB, variability was quantified by time-domain analysis with five standard criteria; these produced qualitatively similar results, which were combined into a single variability index. In normoxia, breathing rate variability was about five times higher than heart rate variability. With 10% O2, the embryo’s oxygen consumption ([Formula: see text]) and breathing rate variability decreased while heart rate variability increased. In normoxia, respiratory sinus arrhythmia was recognisable in a minority of embryos; its average value was low (~2%) and decreased further with hypoxia. With very severe hypoxia (5% O2), in some cases, breathing stopped; when it did not, breathing rate variability was high. Within the 20-min post-hypoxia, all embryos recovered, and almost all parameters (fH, heart rate variability, fB, respiratory sinus arrhythmia and [Formula: see text]) were at the pre-hypoxic values; only breathing rate variability remained low. The possibility of simultaneous measurements of fB and fH makes the avian embryo, close to hatching, a suitable model for the investigations of heart rate variability and breathing rate variability in response to hypoxia during the transition from prenatal to postnatal life.
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5

DeBeck, Lindsay D., Stewart R. Petersen, Kelvin E. Jones, and Michael K. Stickland. "Heart rate variability and muscle sympathetic nerve activity response to acute stress: the effect of breathing." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, no. 1 (July 2010): R80—R91. http://dx.doi.org/10.1152/ajpregu.00246.2009.

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Previous research has suggested a relationship between low-frequency power of heart rate variability (HRV; LF in normalized units, LFnu) and muscle sympathetic nerve activity (MSNA). However, investigations have not systematically controlled for breathing, which can modulate both HRV and MSNA. Accordingly, the aims of this experiment were to investigate the possibility of parallel responses in MSNA and HRV (LFnu) to selected acute stressors and the effect of controlled breathing. After data were obtained at rest, 12 healthy males (28 ± 5 yr) performed isometric handgrip exercise (30% maximal voluntary contraction) and the cold pressor test in random order, and were then exposed to hypoxia (inspired fraction of O2 = 0.105) for 7 min, during randomly assigned spontaneous and controlled breathing conditions (20 breaths/min, constant tidal volume, isocapnic). MSNA was recorded from the peroneal nerve, whereas HRV was calculated from ECG. At rest, controlled breathing did not alter MSNA but decreased LFnu ( P < 0.05 for all) relative to spontaneous breathing. MSNA increased in response to all stressors regardless of breathing. LFnu increased with exercise during both breathing conditions. During cold pressor, LFnu decreased when breathing was spontaneous, whereas in the controlled breathing condition, LFnu was unchanged from baseline. Hypoxia elicited increases in LFnu when breathing was controlled, but not during spontaneous breathing. The parallel changes observed during exercise and controlled breathing during hypoxia suggest that LFnu may be an indication of sympathetic outflow in select conditions. However, since MSNA and LFnu did not change in parallel with all stressors, a cautious approach to the use of LFnu as a marker of sympathetic activity is warranted.
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Hermand, Eric, François J. Lhuissier, Aurélien Pichon, Nicolas Voituron, and Jean-Paul Richalet. "Exercising in Hypoxia and Other Stimuli: Heart Rate Variability and Ventilatory Oscillations." Life 11, no. 7 (June 28, 2021): 625. http://dx.doi.org/10.3390/life11070625.

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Periodic breathing is a respiratory phenomenon frequently observed in patients with heart failure and in normal subjects sleeping at high altitude. However, until recently, periodic breathing has not been studied in wakefulness and during exercise. This review relates the latest findings describing this ventilatory disorder when a healthy subject is submitted to simultaneous physiological (exercise) and environmental (hypoxia, hyperoxia, hypercapnia) or pharmacological (acetazolamide) stimuli. Preliminary studies have unveiled fundamental physiological mechanisms related to the genesis of periodic breathing characterized by a shorter period than those observed in patients (11~12 vs. 30~60 s). A mathematical model of the respiratory system functioning under the aforementioned stressors corroborated these data and pointed out other parameters, such as dead space, later confirmed in further research protocols. Finally, a cardiorespiratory interdependence between ventilatory oscillations and heart rate variability in the low frequency band may partly explain the origin of the augmented sympathetic activation at exercise in hypoxia. These nonlinear instabilities highlight the intrinsic “homeodynamic” system that allows any living organism to adapt, to a certain extent, to permanent environmental and internal perturbations.
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Insalaco, Giuseppe, Salvatore Romano, Adriana Salvaggio, Alberto Braghiroli, Paola Lanfranchi, Vincenzo Patruno, Oreste Marrone, Maria R. Bonsignore, Claudio F. Donner, and Giovanni Bonsignore. "Blood pressure and heart rate during periodic breathing while asleep at high altitude." Journal of Applied Physiology 89, no. 3 (September 1, 2000): 947–55. http://dx.doi.org/10.1152/jappl.2000.89.3.947.

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The ventilatory and arterial blood pressure (ABP) responses to isocapnic hypoxia during wakefulness progressively increased in normal subjects staying 4 wk at 5,050 m (Insalaco G, Romano S, Salvaggio A, Braghiroli A, Lanfranchi P, Patruno V, Donner CF, and Bonsignore G; J Appl Physiol 80: 1724–1730, 1996). In the same subjects ( n = 5, age 28–34 yr) and expedition, nocturnal polysomnography with ABP and heart rate (HR) recordings were obtained during the 1st and 4th week to study the cardiovascular effects of phasic (i.e., periodic breathing-dependent) vs. tonic (i.e., acclimatization-dependent) hypoxia during sleep. Both ABP and HR fluctuated during non-rapid eye movement sleep periodic breathing. None of the subjects exhibited an ABP increase during the ventilatory phases that correlated with the lowest arterial oxygen saturation of the preceding pauses. Despite attenuation of hypoxemia, ABP and HR behaviors during sleep in the 4th wk were similar to those in the 1st wk. Because ABP during periodic breathing in the ventilatory phase increased similarly to the ABP response to progressive hypoxia during wakefulness, ABP variations during ventilatory phases may reflect ABP responsiveness to peripheral chemoreflex sensitivity rather than the absolute value of hypoxemia, suggesting a major tonic effect of hypoxia on cardiorespiratory control at high altitude.
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Parkes, M. J. "Evaluating the Importance of the Carotid Chemoreceptors in Controlling Breathing during Exercise in Man." BioMed Research International 2013 (2013): 1–18. http://dx.doi.org/10.1155/2013/893506.

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Only the carotid chemoreceptors stimulate breathing during hypoxia in Man. They are also ideally located to warn if the brain’s oxygen supply falls, or if hypercapnia occurs. Since their discovery ~80 years ago stimulation, ablation, and recording experiments still leave 3 substantial difficulties in establishing how important the carotid chemoreceptors are in controlling breathing during exercise in Man: (i) they are in the wrong location to measure metabolic rate (but are ideally located to measure any mismatch), (ii) they receive no known signal during exercise linking them with metabolic rate and no overt mismatch signals occur and (iii) their denervation in Man fails to prevent breathing matching metabolic rate in exercise. New research is needed to enable recording from carotid chemoreceptors in Man to establish whether there is any factor that rises with metabolic rate and greatly increases carotid chemoreceptor activity during exercise. Available evidence so far in Man indicates that carotid chemoreceptors are either one of two mechanisms that explain breathing matching metabolic rate or have no importance. We still lack key experimental evidence to distinguish between these two possibilities.
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9

Siebenmann, Christoph, Camilla K. Ryrsø, Laura Oberholzer, James P. Fisher, Linda M. Hilsted, Peter Rasmussen, Niels H. Secher, and Carsten Lundby. "Hypoxia-induced vagal withdrawal is independent of the hypoxic ventilatory response in men." Journal of Applied Physiology 126, no. 1 (January 1, 2019): 124–31. http://dx.doi.org/10.1152/japplphysiol.00701.2018.

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Hypoxia increases heart rate (HR) in humans by sympathetic activation and vagal withdrawal. However, in anaesthetized dogs hypoxia increases vagal activity and reduces HR if pulmonary ventilation does not increase and we evaluated whether that observation applies to awake humans. Ten healthy males were exposed to 15 min of normoxia and hypoxia (10.5% O2), while respiratory rate and tidal volume were volitionally controlled at values identified during spontaneous breathing in hypoxia. End-tidal CO2 tension was clamped at 40 mmHg by CO2 supplementation. β-Adrenergic blockade by intravenous propranolol isolated vagal regulation of HR. During spontaneous breathing, hypoxia increased ventilation by 3.2 ± 2.1 l/min ( P = 0.0033) and HR by 8.9 ± 5.5 beats/min ( P < 0.001). During controlled breathing, respiratory rate (16.3 ± 3.2 vs. 16.4 ± 3.3 breaths/min) and tidal volume (1.05 ± 0.27 vs. 1.06 ± 0.24 l) were similar for normoxia and hypoxia, whereas the HR increase in hypoxia persisted without (8.6 ± 10.2 beats/min) and with (6.6 ± 5.6 beats/min) propranolol. Neither controlled breathing ( P = 0.80), propranolol ( P = 0.64), nor their combination ( P = 0.89) affected the HR increase in hypoxia. Arterial pressure was unaffected ( P = 0.48) by hypoxia across conditions. The hypoxia-induced increase in HR during controlled breathing and β-adrenergic blockade indicates that hypoxia reduces vagal activity in humans even when ventilation does not increase. Vagal withdrawal in hypoxia seems to be governed by the arterial chemoreflex rather than a pulmonary inflation reflex in humans. NEW & NOTEWORTHY Hypoxia accelerates the heart rate of humans by increasing sympathetic activity and reducing vagal activity. Animal studies have indicated that hypoxia-induced vagal withdrawal is governed by a pulmonary inflation reflex that is activated by the increased pulmonary ventilation in hypoxia. The present findings, however, indicate that humans experience vagal withdrawal in hypoxia even if ventilation does not increase, indicating that vagal withdrawal is governed by the arterial chemoreflex rather than a pulmonary inflation reflex.
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Engelen, Marielle, Janos Porszasz, Marshall Riley, Karlman Wasserman, Kazuhira Maehara, and Thomas J. Barstow. "Effects of hypoxic hypoxia on O2 uptake and heart rate kinetics during heavy exercise." Journal of Applied Physiology 81, no. 6 (December 1, 1996): 2500–2508. http://dx.doi.org/10.1152/jappl.1996.81.6.2500.

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Engelen, Marielle, Janos Porszasz, Marshall Riley, Karlman Wasserman, Kazuhira Maehara, and Thomas J. Barstow. Effects of hypoxic hypoxia on O2 uptake and heart rate kinetics during heavy exercise. J. Appl. Physiol. 81(6): 2500–2508, 1996.—It is unclear whether hypoxia alters the kinetics of O2 uptake (V˙o 2) during heavy exercise [above the lactic acidosis threshold (LAT)] and how these alterations might be linked to the rise in blood lactate. Eight healthy volunteers performed transitions from unloaded cycling to the same absolute heavy work rate for 8 min while breathing one of three inspired O2 concentrations: 21% (room air), 15% (mild hypoxia), and 12% (moderate hypoxia). Breathing 12% O2 slowed the time constant but did not affect the amplitude of the primary rise inV˙o 2 (period of first 2–3 min of exercise) and had no significant effect on either the time constant or the amplitude of the slowV˙o 2 component (beginning 2–3 min into exercise). Baseline heart rate was elevated in proportion to the severity of the hypoxia, but the amplitude and kinetics of increase during exercise and in recovery were unaffected by level of inspired O2. We conclude that the predominant effect of hypoxia during heavy exercise is on the early energetics as a slowed time constant forV˙o 2 and an additional anaerobic contribution. However, the sum total of the processes representing the slow component ofV˙o 2 is unaffected.
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Dissertations / Theses on the topic "Breathing and heart rate[Hypoxia in man]"

1

Khamnei, S. "Some factors affecting respiration in man." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.258344.

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Conference papers on the topic "Breathing and heart rate[Hypoxia in man]"

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Kocur, Dusan, Maria Svecova, and Jakub Demcak. "Estimation of Breathing Frequency and Heart Rate by Biometric UWB Radar." In 2018 IEEE International Conference on Systems, Man, and Cybernetics (SMC). IEEE, 2018. http://dx.doi.org/10.1109/smc.2018.00440.

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