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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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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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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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Finley, John P., and C. Kelly. "Heart rate and respiratory patterns in mild hypoxia in unanaesthetized newborn mammals." Canadian Journal of Physiology and Pharmacology 64, no. 2 (February 1, 1986): 122–24. http://dx.doi.org/10.1139/y86-018.
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The heart rate and respiratory patterns in hypoxia are not well documented in unanaesthetized intact newborn animals. We studied heart rate and respiratory patterns during quiet sleep in 17% inspired O2 in 31 unanaesthetized newborns of five species: lamb, piglet, puppy, kitten, and rabbit. There was no significant change in mean heart rate and respiratory rate with hypoxia for any species. Brief apneas greater than 5 s were frequent (5–8/h), both in 21 and 17% O2 only in lambs and puppies. No sustained periodic breathing was induced by hypoxia. Thus, mild hypoxia has little steady-state effect on heart rate and respiratory rate and pattern in these unanaesthetized newborns. These findings are compatible with depressed chemoreceptor threshold, but indicate a remarkably mature respiratory pattern in full-term newborns of these species.
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Cooper, D. M., D. H. Wasserman, M. Vranic, and K. Wasserman. "Glucose turnover in response to exercise during high- and low-FIO2 breathing in man." American Journal of Physiology-Endocrinology and Metabolism 251, no. 2 (August 1, 1986): E209—E214. http://dx.doi.org/10.1152/ajpendo.1986.251.2.e209.
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The purpose of this study was to assess whether breathing high or low concentrations of O2 could affect glucose turnover during exercise in man. Ten healthy subjects performed two constant work-rate exercise tests, one when the fraction of inspired O2 (FIO2) was 0.15 and the other at the same work rate but when the FIO2 was 0.80. The work rate for each subject was chosen so that blood lactate would be elevated during hypoxia, but would be lower during hyperoxia. Glucose appearance (Ra) and disappearance (Rd) were measured using the primed, constant infusion of [3-3H]glucose. Although the work rate was the same during hypoxia and hyperoxia in each subject, hypoxic exercise was accompanied by a significantly larger rest to exercise increase in Rd (delta Rd) compared with hyperoxia by 265%. Similarly, delta Ra was greater during hypoxia than during hyperoxia by 188%. Lactate to pyruvate ratios were significantly higher during hypoxic exercise suggesting a shift in the cell redox to a more reduced state. Insulin and glucagon were not affected by the FIO2, but both epinephrine and norepinephrine were increased during hypoxic exercise, which may explain the increase in Ra. The regulation of blood glucose during exercise in vivo appears to be dependent on the availability of oxygen to the working muscle cells.
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Kaijser, L., J. Pernow, B. Berglund, J. Grubbstrom, and J. M. Lundberg. "Neuropeptide Y release from human heart is enhanced during prolonged exercise in hypoxia." Journal of Applied Physiology 76, no. 3 (March 1, 1994): 1346–49. http://dx.doi.org/10.1152/jappl.1994.76.3.1346.
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To evaluate the effect of hypoxemia on cardiac release of neuropeptide Y-like immunoreactivity (NPY-LI) and norepinephrine (NE), arterial and coronary sinus blood was sampled and coronary sinus blood flow was measured by thermodilution in nine healthy volunteers at rest and during supine cycle ergometer exercise while they breathed air and 12% O2, which reduced arterial O2 saturation to approximately 68%. Five subjects started to exercise for 30 min breathing air and continued for 30 min breathing 12% O2; four subjects breathed 12% O2 and air in the reverse order. The load was adjusted to give the same heart rate during O2 and air breathing. No significant cardiac net release of NPY-LI or NE was seen at rest. Exercise induced release of NPY-LI and NE. The net release of NPY-LI was 0.7 +/- 0.4 pmol/min during air breathing (average 12 and 30 min) and 2.8 +/- 0.6 pmol/min during 12% O2 breathing. The difference was not influenced by the order of the breathing periods. The NE coronary sinus-arterial difference was not significantly different between 12% O2 and air breathing, whereas the net release was significantly larger during 12% O2 breathing (0.6 +/- 0.1 vs. 0.4 +/- 0.1 nmol/min). Thus, NPY is released with NE from the heart during exercise. Arterial hypoxemia seems to be an additional stimulus of preferential NPY release.
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Chau, Andrew, and Brian J. Koos. "Metabolic and cardiorespiratory responses to hypoxia in fetal sheep: adenosine receptor blockade." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 6 (June 1, 1999): R1805—R1811. http://dx.doi.org/10.1152/ajpregu.1999.276.6.r1805.
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8-Phenyltheophylline (PT), a potent and specific inhibitor of adenosine receptors, was infused intra-arterially into unanesthetized fetal sheep to determine the role of adenosine in hypoxic inhibition of fetal breathing. PT in normoxic fetuses increased heart rate and the incidence of low-voltage electrocortical activity, rapid eye movements (REM), and breathing. Mean breath amplitude increased by 44%. Hypoxia (preductal arterial[Formula: see text] = 14 Torr) induced a metabolic acidemia, a transient bradycardia, and hypertension while virtually eliminating REM and breathing. PT administration during hypoxia enhanced the metabolic acidemia, blocked the bradycardia and hypertension, increased the incidence of REM and breathing, and elevated mean breath amplitude. The results indicate that 1) adenosine is involved in fetal glycolytic and cardiovascular responses to hypoxia, 2) activation of central adenosine receptors mediates about one-half the inhibitory effects of hypoxia on REM and breathing, and 3) the depression of breathing may critically depend on a hypoxia-induced reduction in phasic REM sleep.
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Galletly, D. C., P. D. Tobin, B. J. Robinson, and T. Corfiatis. "Effect of Inhalation of 30% Nitrous Oxide on Spectral Components of Heart Rate Variability in Conscious man." Clinical Science 85, no. 4 (October 1, 1993): 389–92. http://dx.doi.org/10.1042/cs0850389.
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1. Periodicities in cardiac interbeat interval may be resolved into discrete frequency components by applying Fourier analysis to heart rate time series. Low-frequency components (<0.15 Hz) are believed to be under parasympathetic and sympathetic control, whereas a higher frequency component in phase with respiration is believed to be entirely parasympathetic. The ratio of the power in the low-/high-frequency spectrum gives an estimate of sympathetic/para-sympathetic balance. 2. This study examined, using heart rate variability spectral analysis, the cardiac autonomic effects of breathing 30% N2O in normal subjects. While supine, the inhalation of N2O caused a significant fall in high-frequency power and a rise in the low-/high-frequency spectrum. During air breathing, tilting caused a significant rise in the mean blood pressure, heart rate, low-frequency power and low-/high-frequency spectrum. During N2O breathing, tilting caused a rise in the heart rate and the mean blood pressure, but no significant alteration in the power of individual spectral components. During tilting, the heart rate, the low-frequency and low-/high-frequency spectrum were less when breathing N2O than when breathing air. 3. These observations are consistent with the effect of N2O being an enhanced sympathetic balance of sinoatrial control, with the primary effect being through reduced parasympathetic tone. Enhanced sympathetic dominance of heart rate variability was seen on standing while subjects breathed air, but this effect was blunted with N2O.
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Rocha, P. L., and L. G. S. Branco. "Seasonal changes in the cardiovascular, respiratory and metabolic responses to temperature and hypoxia in the bullfrog rana catesbeiana." Journal of Experimental Biology 201, no. 5 (March 1, 1998): 761–68. http://dx.doi.org/10.1242/jeb.201.5.761.
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We assessed seasonal variations in the effects of temperature on hypoxia-induced alterations in the bullfrog Rana catesbeiana by measuring the heart rate, arterial blood pressure, breathing frequency, metabolic rate, blood gas levels, acid-base status and plasma glucose concentration. Regardless of the season, decreased body temperature was accompanied by a reduction in heart and breathing frequencies. Lower temperatures caused a significant decrease in arterial blood pressure during all four seasons. Hypoxia-induced changes in breathing frequency were proportional to body temperature and were more pronounced during winter, less so during spring and autumn and even smaller during summer. Season had no effect on the relationship between hypoxia and heart rate. At any temperature tested, the rate of oxygen consumption had a tendency to be highest during summer and lowest during winter, but the difference was significant only at 35 degrees C. The PaO2 and pH values showed no significant change during the year, but PaCO2 was almost twice as high during winter than in summer and spring, indicating increased plasma bicarbonate levels. Lower temperatures were accompanied by decreased plasma glucose levels, and this effect was greater during summer and smaller during autumn. Hypoxia-induced hyperglycaemia was influenced by temperature and season. During autumn and winter, plasma glucose level remained elevated regardless of temperature, probably to avoid dehydration and/or freezing. In winter, the bullfrog may be exposed not only to low temperatures but also to hypoxia. These animals show temperature-dependent responses that may be beneficial since at low body temperatures the set-points of most physiological responses to hypoxia are reduced, regardless of the season. <P>
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LUNDBY, Carsten, Peter MØLLER, Inge-Lis KANSTRUP, and Niels Vidiendal OLSEN. "Heart rate response to hypoxic exercise: role of dopamine D2-receptors and effect of oxygen supplementation." Clinical Science 101, no. 4 (September 14, 2001): 377–83. http://dx.doi.org/10.1042/cs1010377.
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This study examined the effects of dopamine D2-receptor blockade on the early decrease in maximal heart rate at high altitude (4559m). We also attempted to clarify the time-dependent component of this reduction and the extent to which it is reversed by oxygen breathing. Twelve subjects performed two consecutive maximal exercise tests, without and with oxygen supplementation respectively, at sea level and after 1, 3 and 5 days at altitude. On each study day, domperidone (30mg; n = 6) or no medication (n = 6) was given 1h before the first exercise session. Compared with sea level, hypoxia progressively decreased the maximal heart rate from day 1 and onwards; also, hypoxia by itself increased plasma noradrenaline levels after maximal exercise. Domperidone further increased maximal noradrenaline concentrations, but had no effect on maximal heart rate. On each study day at altitude, oxygen breathing completely reversed the decrease in maximal heart rate to values not different from those at sea level. In conclusion, dopamine D2-receptor blockade with domperidone demonstrates that hypoxic exercise in humans activates D2-receptors, resulting in a decrease in circulating levels of noradrenaline. However, dopamine D2-receptors are not involved in the hypoxia-induced decrease in the maximal heart rate. These data suggest that receptor uncoupling, and not down-regulation, of cardiac adrenoreceptors, is responsible for the early decrease in heart rate at maximal hypoxic exercise.
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Koos, B. J., and K. Matsuda. "Fetal breathing, sleep state, and cardiovascular responses to adenosine in sheep." Journal of Applied Physiology 68, no. 2 (February 1, 1990): 489–95. http://dx.doi.org/10.1152/jappl.1990.68.2.489.
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The possibility that adenosine mediates hypoxic inhibition of fetal breathing and eye movements was tested in nine chronically catheterized fetal sheep (0.8 term). Intracarotid infusion of adenosine (0.25 +/- 0.03 mg.min-1.kg-1) for 1 h to the fetus increased heart rate and hemoglobin concentration but did not significantly affect mean arterial pressure or blood gases. As with hypoxia, adenosine decreased the incidence of rapid eye movements by 55% and the incidence of breathing by 77% without significantly affecting the incidence of low-voltage electrocortical activity. However, with longer (9 h) administration, the incidence of breathing and eye movements returned to normal during the adenosine infusion. Intravenous infusion of theophylline, an adenosine receptor antagonist, prevented most of the reduction in the incidence of breathing and eye movements normally seen during severe hypoxia (delta arterial PO2 = -10 Torr). It is concluded that 1) adenosine likely depresses fetal breathing and eye movements during hypoxia and 2) downregulation of adenosine receptors may contribute to the adaptation of breathing and eye movements during prolonged hypoxia.
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Van Eyck, Annelies, Kim Van Hoorenbeeck, Benedicte Y. De Winter, Luc Van Gaal, Wilfried De Backer, and Stijn L. Verhulst. "Sleep disordered breathing and autonomic function in overweight and obese children and adolescents." ERJ Open Research 2, no. 4 (October 2016): 00038–2016. http://dx.doi.org/10.1183/23120541.00038-2016.
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Obstructive sleep apnoea (OSA), common in children with obesity, is associated with cardiovascular morbidity. Autonomic dysfunction has been suggested to be a key player in the development of these complications. We investigated the relationship between obesity, OSA and sympathetic activity in children.191 children with obesity were included and distributed into two groups: 131 controls and 60 with OSA. Beat-to-beat RR interval data were extracted from polysomnography for heart rate variability analysis. Urinary free cortisol levels were determined.Urinary free cortisol did not differ between groups and was not associated with OSA, independent of the level of obesity. Differences in heart rate variability measures were found: mean RR interval decreased with OSA, while low/high-frequency band ratio and mean heart rate increased with OSA. Heart rate variability measures correlated with OSA, independent of obesity parameters and age: oxygen desaturation index correlated with mean heart rate (r=0.19, p=0.009) and mean RR interval (r= −0.18, p=0.02), while high-frequency bands and low/high-frequency band ratio correlated with arterial oxygen saturation measured by pulse oximetry (SpO2) (r= −0.20, p=0.008 and r= −0.16, p=0.04) andSpO2nadir (r=0.23, p=0.003 and r= −0.19, p=0.02).These results suggest that sympathetic heart activity is increased in children with obesity and OSA. Measures of hypoxia were related to increased sympathetic tone, suggesting that intermittent hypoxia is involved in autonomic dysfunction.
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Dominelli, Paolo B., Sarah E. Baker, Chad C. Wiggins, Glenn M. Stewart, Pavol Sajgalik, John R. A. Shepherd, Shelly K. Roberts, et al. "Dissociating the effects of oxygen pressure and content on the control of breathing and acute hypoxic response." Journal of Applied Physiology 127, no. 6 (December 1, 2019): 1622–31. http://dx.doi.org/10.1152/japplphysiol.00569.2019.
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Arterial oxygen tension and oxyhemoglobin saturation ([Formula: see text]) decrease in parallel during hypoxia. Distinguishing between changes in oxygen tension and oxygen content as the relevant physiological stimulus for cardiorespiratory alterations remains challenging. To overcome this, we recruited nine individuals with hemoglobinopathy manifesting as high-affinity hemoglobin [HAH; partial pressure at 50% [Formula: see text] (P50) = 16 ± 0.4 mmHg] causing greater [Formula: see text] at a given oxygen partial pressure compared with control subjects ( n = 12, P50 = 26 ± 0.4 mmHg). We assessed ventilatory and cardiovascular responses to acute isocapnic hypoxia, iso-oxic hypercapnia, and 20 min of isocapnic hypoxia (arterial Po2 = 50 mmHg). Blood gas alterations were achieved with dynamic end-tidal forcing. When expressed as a function of the logarithm of oxygen partial pressure, ventilatory sensitivity to hypoxia was not different between groups. However, there was a significant difference when expressed as a function of [Formula: see text]. Conversely, the rise in heart rate was blunted in HAH subjects when expressed as a function of partial pressure but similar when expressed as a function of [Formula: see text]. Ventilatory sensitivity to hypercapnia was not different between groups. During sustained isocapnic hypoxia, the rise in minute ventilation was similar between groups; however, heart rate was significantly greater in the controls during 3 to 9 min of exposure. Our results support the notion that oxygen tension, not content, alters cellular Po2 in the chemosensors and drives the hypoxic ventilatory response. Our study suggests that in addition to oxygen partial pressure, oxygen content may also influence the heart rate response to hypoxia. NEW & NOTEWORTHY We dissociated the effects of oxygen content and pressure of cardiorespiratory regulation studying individuals with high-affinity hemoglobin (HAH). During hypoxia, the ventilatory response, expressed as a function of oxygen tension, was similar between HAH variants and controls; however, the rise in heart rate was blunted in the variants. Our work supports the notion that the hypoxic ventilatory response is regulated by oxygen tension, whereas cardiovascular regulation may be influenced by arterial oxygen content and tension.
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O'Hagan, K. P., L. B. Bell, and P. S. Clifford. "Effects of pulmonary denervation on renal sympathetic and heart rate responses to hypoxia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 269, no. 4 (October 1, 1995): R923—R929. http://dx.doi.org/10.1152/ajpregu.1995.269.4.r923.
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We hypothesized that the renal sympathetic nerve activity (RSNA) response to hypoxia is attenuated because of stimulation of pulmonary receptors by the increase in ventilation. RSNA was measured during 20 min of severe hypoxia (8% O2) in conscious New Zealand White rabbits with intact lung innervation and in rabbits with surgical denervation of the lungs (LDX). LDX decreased resting breathing frequency but had no effect on resting mean arterial pressure (MAP), heart rate (HR), or RSNA. In intact rabbits, 4 min of hypoxia resulted in elevated RSNA (from 14 +/- 2 to 29 +/- 3% of smoke-elicited maximum), bradycardia (delta-65 +/- 12 beats/min), and no change in MAP (delta 2 +/- 2 mmHg). Bradycardia diminished with time, but elevated RSNA was maintained throughout the 20-min exposure. LDX enhanced the initial bradycardia (delta-113 +/- 11 beats/min, P < 0.01) but had no effect on the RSNA response (35 +/- 2% of maximum) to hypoxia. LDX did not alter steady-state responses of HR or RSNA, but MAP declined over time (-11 +/- 2 mmHg). These results suggest that in conscious rabbits pulmonary receptors have a minor influence on control of sympathetic activity to viscera during severe hypoxemia.
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OHYABU, YOSHIO, MIDORI SATO, and YOSHIYUKI HONDA. "ENHANCED VENTILATORY AND HEART RATE RESPONSIVENESS TO HYPOXIA DURING MODERATE EXERCISE IN MAN." Japanese Journal of Physical Fitness and Sports Medicine 37, no. 1 (1988): 93–99. http://dx.doi.org/10.7600/jspfsm1949.37.93.
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Reeves, J. T., B. M. Groves, J. R. Sutton, P. D. Wagner, A. Cymerman, M. K. Malconian, P. B. Rock, P. M. Young, and C. S. Houston. "Operation Everest II: preservation of cardiac function at extreme altitude." Journal of Applied Physiology 63, no. 2 (August 1, 1987): 531–39. http://dx.doi.org/10.1152/jappl.1987.63.2.531.
Full textAbstract:
Hypoxia at high altitude could depress cardiac function and decrease exercise capacity. If so, impaired cardiac function should occur with the extreme, chronic hypoxemia of the 40-day simulated climb of Mt. Everest (8,840 m, barometric pressure of 240 Torr, inspiratory O2 pressure of 43 Torr). In the five of eight subjects having resting and exercise measurements at the barometric pressures of 760 Torr (sea level), 347 Torr (6,100 m), 282 Torr (7,620 m), and 240 Torr, heart rate for a given O2 uptake was higher with more severe hypoxia. Slight (6 beats/min) slowing of the heart rate occurred only during exercise at the lowest barometric pressure when arterial blood O2 saturations were less than 50%. O2 breathing reversed hypoxemia but never increased heart rate, suggesting that hypoxic depression of rate, if present, was slight. For a given O2 uptake, cardiac output was maintained. The decrease in stroke volume appeared to reflect decreased ventricular filling (i.e., decreased right atrial and wedge pressures). O2 breathing did not increase stroke volume for a given filling pressure. We concluded that extreme, chronic hypoxemia caused little or no impairment of cardiac rate and pump functions.
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Mendoza, James P., Rachael J. Passafaro, Santhosh M. Baby, Alex P. Young, James N. Bates, Benjamin Gaston, and Stephen J. Lewis. "Role of nitric oxide-containing factors in the ventilatory and cardiovascular responses elicited by hypoxic challenge in isoflurane-anesthetized rats." Journal of Applied Physiology 116, no. 11 (June 1, 2014): 1371–81. http://dx.doi.org/10.1152/japplphysiol.00842.2013.
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Exposure to hypoxia elicits changes in mean arterial blood pressure (MAP), heart rate, and frequency of breathing (fr). The objective of this study was to determine the role of nitric oxide (NO) in the cardiovascular and ventilatory responses elicited by brief exposures to hypoxia in isoflurane-anesthetized rats. The rats were instrumented to record MAP, heart rate, and fr and then exposed to 90 s episodes of hypoxia (10% O2, 90% N2) before and after injection of vehicle, the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME), or the inactive enantiomer d-NAME (both at 50 μmol/kg iv). Each episode of hypoxia elicited a decrease in MAP, bidirectional changes in heart rate (initial increase and then a decrease), and an increase in fr. These responses were similar before and after injection of vehicle or d-NAME. In contrast, the hypoxia-induced decreases in MAP were attenuated after administration of l-NAME. The initial increases in heart rate during hypoxia were amplified whereas the subsequent decreases in heart rate were attenuated in l-NAME-treated rats. Finally, the hypoxia-induced increases in fr were virtually identical before and after administration of l-NAME. These findings suggest that NO factors play a vital role in the expression of the cardiovascular but not the ventilatory responses elicited by brief episodes of hypoxia in isoflurane-anesthetized rats. Based on existing evidence that NO factors play a vital role in carotid body and central responses to hypoxia in conscious rats, our findings raise the novel possibility that isoflurane blunts this NO-dependent signaling.
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MacCormack, T. J., R. S. McKinley, R. Roubach, V. M. F. Almeida-Val, A. L. Val, and W. R. Driedzic. "Changes in ventilation, metabolism, and behaviour, but not bradycardia, contribute to hypoxia survival in two species of Amazonian armoured catfish." Canadian Journal of Zoology 81, no. 2 (February 1, 2003): 272–80. http://dx.doi.org/10.1139/z03-003.
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Amazonian armoured catfishes exhibit substantial cardiac hypoxia tolerance, but little is known concerning organismal cardiorespiratory, metabolic, and behavioural responses to low oxygen levels. This study assessed the general mechanisms used by two species of armoured catfish, Glyptoperichthyes gibbceps and Liposarcus pardalis, to survive the frequent periods of hypoxia encountered in the Amazon River. The gill ventilation rate (fv) and heart rate (fh) were studied under controlled hypoxia in aquaria and under natural hypoxia in a simulated pond. Glyptoperichthyes gibbceps were fitted with radiotelemetry tags and held in field cages to study their habits of depth selection and air breathing. When denied aerial respiration under hypoxia in aquaria, G. gibbceps increased fv, but neither they nor L. pardalis exhibited alterations in fh. An increase in fvwas initially observed in G. gibbceps during pond hypoxia before aerial respiration was initiated and fvdeclined. Glyptoperichthyes gibbceps were hyperglycaemic under normoxia, and extremely large increases in plasma glucose and lactate concentrations were observed under hypoxia. Field studies confirmed their nocturnal behaviour and showed that air breathing increased at night, regardless of dissolved oxygen concentration. Our results show that armoured catfishes preferentially up-regulate fvand anaerobic metabolism and exhibit no bradycardia during hypoxia.
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Liu, Chun, Quentin P. P. Croft, Swati Kalidhar, Jerome T. Brooks, Mari Herigstad, Thomas G. Smith, Keith L. Dorrington, and Peter A. Robbins. "Dexamethasone mimics aspects of physiological acclimatization to 8 hours of hypoxia but suppresses plasma erythropoietin." Journal of Applied Physiology 114, no. 7 (April 1, 2013): 948–56. http://dx.doi.org/10.1152/japplphysiol.01414.2012.
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Dexamethasone ameliorates the severity of acute mountain sickness (AMS) but it is unknown whether it obtunds normal physiological responses to hypoxia. We studied whether dexamethasone enhanced or inhibited the ventilatory, cardiovascular, and pulmonary vascular responses to sustained (8 h) hypoxia. Eight healthy volunteers were studied, each on four separate occasions, permitting four different protocols. These were: dexamethasone (20 mg orally) beginning 2 h before a control period of 8 h of air breathing; dexamethasone with 8 h of isocapnic hypoxia (end-tidal Po2 = 50 Torr); placebo with 8 h of air breathing; and placebo with 8 h of isocapnic hypoxia. Before and after each protocol, the following were determined under both euoxic and hypoxic conditions: ventilation; pulmonary artery pressure (estimated using echocardiography to assess maximum tricuspid pressure difference); heart rate; and cardiac output. Plasma concentrations of erythropoietin (EPO) were also determined. Dexamethasone had no early (2-h) effect on any variable. Both dexamethasone and 8 h of hypoxia increased euoxic values of ventilation, pulmonary artery pressure, and heart rate, together with the ventilatory sensitivity to acute hypoxia. These effects were independent and additive. Eight hours of hypoxia, but not dexamethasone, increased the sensitivity of pulmonary artery pressure to acute hypoxia. Dexamethasone, but not 8 h of hypoxia, increased both cardiac output and systemic arterial pressure. Dexamethasone abolished the rise in EPO induced by 8 h of hypoxia. In summary, dexamethasone enhances ventilatory acclimatization to hypoxia. Thus, dexamethasone in AMS may improve oxygenation and thereby indirectly lower pulmonary artery pressure.
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Xue, Yong, Jun Yang, Yutao Feng, Yubin Zhou, Yufei Qin, Yang Li, Yuwen Li, Qiushi Ren, Chengyu Liu, and Zhengtao Cao. "Effects of Mindful Breathing on Rapid Hypoxia Preacclimatization Training." Journal of Medical Imaging and Health Informatics 10, no. 3 (March 1, 2020): 718–23. http://dx.doi.org/10.1166/jmihi.2020.2923.
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Rapid exposure at high altitude is likely to cause Acute Mountain Sickness (AMS) of different levels. This paper designs a "quick acclimatization" method to make the volunteers adapt to 3,600 meters (m) after 2-day training and 3,900 m after 3-day training. Especially, we investigate the effects of mindful breathing on rapid hypoxia preacclimatization training. 8 young male volunteers were randomly divided into one treatment group and one control group. Peripheral Saturation of Oxygen (SpO2), Heart Rate (HR) and Respiratory Rate (RR) were recorded from the beginning to the end. We find that: (1) Hypoxic Preacclimatization Training Scheme (HPTS): at 3600 m, the increment of SpO2 was 3.18% after 2-day training (P < 0.01); at 3900 m, 8 volunteers got obviously higher SpO2 (2.65%, P < 0.05) and lower HR (–5.31 bpm, P < 0.05) after 3-day training. (2) Mindful Breathing Training Scheme (MBTS): at 3,600 m, the treatment group obtained better SpO2 level (2.21%) with obviously lower HR (–7.1 bpm) and unobvious higher RR (2.85 br/min) than control group after 2-day training; at 3900 m, the treatment group did not show a significant difference after 3-day training. Besides, the treatment group exhibited a comprehensive better performance over the control group at night, which obtained a higher SpO2 with lower HR and lower RR. In the comparison of different altitudes, the two groups had similar RR while the treatment group had a higher SpO2 (P < 0.05) and a lower HR (P < 0.001). In the dynamic comparison during mindful breathing training, SpO2 occurred remarkable differences: P < 0.05 every 15 minutes started from the 45th minute. We conclude that HPTS successfully helped volunteers adapt to the setting altitude in a short time. MBTS can induce significant phenomenon of sustained gain effect. It can effectively increase the acclimatization speed to quickly return to lower HR and RR and obtain higher SpO2. MBTS can enable beginners without any experience of mindfulness and breathing training to initially stimulate the trend of "energy-saving" acclimatization in 2–3 days.
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Robinson, K. A., and E. M. Haymes. "Metabolic effects of exposure to hypoxia plus cold at rest and during exercise in humans." Journal of Applied Physiology 68, no. 2 (February 1, 1990): 720–25. http://dx.doi.org/10.1152/jappl.1990.68.2.720.
Full textAbstract:
To determine effects on metabolic responses, subjects were exposed to four environmental conditions for 90 min at rest followed by 30 min of exercise: breathing room air with an ambient temperature of 25 degrees C (NN); breathing room air with an ambient temperature of 8 degrees C (NC); hypoxia (induced by breathing 12% O2 in N2) with a neutral temperature (HN); and hypoxia in the cold (HC). Hypoxia increased heart rate (HR), systolic blood pressure (SBP), pulmonary ventilation (VE), respiratory exchange ratio (R), blood lactate, and perceived exertion during exercise while depressing rectal temperature (Tre) and O2 uptake (VO2). Cold exposure elevated SBP, diastolic blood pressure (DBP), VE, VO2, blood glucose, and blood glycerol but decreased HR, Tre, and R. Shivering and DBP were higher and Tre was lower in HC compared with NC. HR, SBP, VE, R, and lactate tended to be higher in HC compared with NC, whereas VO2 and blood glycerol tended to be depressed. These results suggest that cold exposure during hypoxia results in an increased reliance on shivering for thermogenesis at rest whereas, during exercise, heat loss is accelerated.
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Del Rio, Rodrigo, Noah J. Marcus, and Harold D. Schultz. "Inhibition of hydrogen sulfide restores normal breathing stability and improves autonomic control during experimental heart failure." Journal of Applied Physiology 114, no. 9 (May 1, 2013): 1141–50. http://dx.doi.org/10.1152/japplphysiol.01503.2012.
Full textAbstract:
Cardiovascular autonomic imbalance and breathing instability are major contributors to the progression of heart failure (CHF). Potentiation of the carotid body (CB) chemoreflex has been shown to contribute to these effects. Hydrogen sulfide (H2S) recently has been proposed to mediate CB hypoxic chemoreception. We hypothesized that H2S synthesis inhibition should decrease CB chemoreflex activation and improve breathing stability and autonomic function in CHF rats. Using the irreversible inhibitor of cystathione γ-lyase dl-propargylglycine (PAG), we tested the effects of H2S inhibition on resting breathing patterns, the hypoxic and hypercapnic ventilatory responses, and the hypoxic sensitivity of CB chemoreceptor afferents in rats with CHF. In addition, heart rate variability (HRV) and systolic blood pressure variability (SBPV) were calculated as an index of autonomic function. CHF rats, compared with sham rats, exhibited increased breath interval variability and number of apneas, enhanced CB afferent discharge and ventilatory responses to hypoxia, decreased HRV, and increased low-frequency SBPV. Remarkably, PAG treatment reduced the apnea index by 90%, reduced breath interval variability by 40–60%, and reversed the enhanced hypoxic CB afferent and chemoreflex responses observed in CHF rats. Furthermore, PAG treatment partially reversed the alterations in HRV and SBPV in CHF rats. Our results show that PAG treatment restores breathing stability and cardiac autonomic function and reduces the enhanced ventilatory and CB chemosensory responses to hypoxia in CHF rats. These results support the idea that PAG treatment could potentially represent a novel pathway to control sympathetic outflow and breathing instability in CHF.
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TANAKA, M., S. TAKAISHI, T. OHDAIRA, T. KOBAYASHI, R. MARUYAMA, B. AHN, A. MASUDA, S. MASUYAMA, and Y. HONDA. "Dependence of Biphasic Heart Rate Response to Sustained Hypoxia on Magnitude of Ventilation in Man." Japanese Journal of Physiology 42, no. 6 (1992): 865–75. http://dx.doi.org/10.2170/jjphysiol.42.865.
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Halliwill, John R., and Christopher T. Minson. "Cardiovagal regulation during combined hypoxic and orthostatic stress: fainters vs. nonfainters." Journal of Applied Physiology 98, no. 3 (March 2005): 1050–56. http://dx.doi.org/10.1152/japplphysiol.00871.2004.
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We tested the hypothesis that individual differences in the effect of acute hypoxia on the cardiovagal arterial baroreflex would determine individual susceptibility to hypoxic syncope. In 16 healthy, nonsmoking, normotensive subjects (8 women, 8 men, age 20–33 yr), we assessed orthostatic tolerance with a 20-min 60° head-upright tilt during both normoxia and hypoxia (breathing 12% O2). On a separate occasion, we assessed baroreflex control of heart rate (cardiovagal baroreflex gain) using the modified Oxford technique during both normoxia and hypoxia. When subjects were tilted under hypoxic conditions, 5 of the 16 developed presyncopal signs or symptoms, and the 20-min tilt had to be terminated. These “fainters” had comparable cardiovagal baroreflex gain to “nonfainters” under both normoxic and hypoxic conditions (normoxia, fainters: −1.2 ± 0.2, nonfainters: −1.0 ± 0.2 beats·min−1·mmHg−1, P = 0.252; hypoxia, fainters: −1.3 ± 0.2, nonfainters: −1.0 ± 0.1 beats·min−1·mmHg−1, P = 0.208). Furthermore, hypoxia did not alter cardiovagal baroreflex gain in either group (both P > 0.8). It appears from these observations that hypoxic syncope results from the superimposed vasodilator effects of hypoxia on the cardiovascular system and not from a hypoxia-induced maladjustment in baroreflex control of heart rate.
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Leuenberger, Urs A., J. Cullen Hardy, Michael D. Herr, Kristen S. Gray, and Lawrence I. Sinoway. "Hypoxia augments apnea-induced peripheral vasoconstriction in humans." Journal of Applied Physiology 90, no. 4 (April 1, 2001): 1516–22. http://dx.doi.org/10.1152/jappl.2001.90.4.1516.
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Obstructive apnea and voluntary breath holding are associated with transient increases in muscle sympathetic nerve activity (MSNA) and arterial pressure. The contribution of changes in blood flow relative to the contribution of changes in vascular resistance to the apnea-induced transient rise in arterial pressure is unclear. We measured heart rate, mean arterial blood pressure (MAP), MSNA (peroneal microneurography), and femoral artery blood velocity ( V FA, Doppler) in humans during voluntary end-expiratory apnea while they were exposed to room air, hypoxia (10.5% inspiratory fraction of O2), and hyperoxia (100% inspiratory fraction of O2). Changes from baseline of leg blood flow (Q˙) and vascular resistance (R) were estimated from the following relationships: Q˙ ∝ V FA, corrected for the heart rate, and R ∝ MAP/Q˙. During apnea, MSNA rose; this rise in MSNA was followed by a rise in MAP, which peaked a few seconds after resumption of breathing. Responses of MSNA and MAP to apnea were greatest during hypoxia and smallest during hyperoxia ( P < 0.05 for both compared with room air breathing). Similarly, apnea was associated with a decrease in Q˙ and an increase in R. The decrease in Q˙ was greatest during hypoxia and smallest during hyperoxia (−25 ± 3 vs. −6 ± 4%, P < 0.05), and the increase in R was the greatest during hypoxia and the least during hyperoxia (60 ± 8 vs. 21 ± 6%, P < 0.05). Thus voluntary apnea is associated with vasoconstriction, which is in part mediated by the sympathetic nervous system. Because apnea-induced vasoconstriction is most intense during hypoxia and attenuated during hyperoxia, it appears to depend at least in part on stimulation of arterial chemoreceptors.
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Piazza, Tiziana, Anne Marie Lauzon, and Jacopo P. Mortola. "Time course of adaptation to hypoxia in newborn rats." Canadian Journal of Physiology and Pharmacology 66, no. 1 (January 1, 1988): 152–58. http://dx.doi.org/10.1139/y88-027.
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In newborn rats after a few minutes of hypoxia, ventilation is similar to the normoxic value. Nevertheless, after a few days in hypoxia, newborn rats have a sustained hyperventilation. In this study we examined the time course of the newborn rat's adaptation to hypoxia. Measurements of body size, hematocrit, lung and heart mass, and breathing pattern have been performed on newborn rats exposed to hypoxia (10% O2) for different time intervals from 4 to 60 h (hypoxic, H), and on same-age rats growing in air (controls, C). Ventilation measured by flow plethysmography was increased in H rats above the C value from about 8 h; this was due to a higher breathing rate and, from 24 h, also to a larger tidal volume. During the early hours of hypoxia, oxygen consumption measured manometrically was about 50% of C, while after 3 days in hypoxia it was almost like the C value. These observations indicate that the lack of sustained hyperventilation, characteristic of the newborn's acute exposure to hypoxia, is an immediate but transient phenomenon that is resolved after a few hours, and suggest a tight link between metabolic and ventilatory hypoxic responses. Body weight of H rats was less than in C, owing to an immediate decrease below the prehypoxic value. Dry heart and lung weight changed in proportion with the rest of the body during the first 36–48 h of hypoxia, then they increased disproportionately more. Hence, these temporal changes suggest that the large heart and lung weight – body weight ratios of the chronic hypoxic animals result from their smaller body mass and the stimulated growth of cardiac and pulmonary tissues.
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Zerbini, Livio, Alfredo Brighenti, Barbara Pellegrini, Lorenzo Bortolan, Tommaso Antonetti, and Federico Schena. "Effects of acute hypoxia on the oxygen uptake kinetics of older adults during cycling exercise." Applied Physiology, Nutrition, and Metabolism 37, no. 4 (August 2012): 744–52. http://dx.doi.org/10.1139/h2012-048.
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Pulmonary oxygen uptake, heart rate (HR), and deoxyhemoglobin (HHb) kinetics were studied in a group of older adults exercising in hypoxic conditions. Fourteen healthy older adults (aged 66 ± 6 years) performed 4 exercise sessions that consisted of (i) an incremental test to exhaustion on a cycloergometer while breathing normoxic room air (fractional inspired oxygen (FiO2) = 20.9% O2); (ii) an incremental test to exhaustion on a cycloergometer while breathing hypoxic room air (FiO2 = 15% O2); (iii) 3 repeated square wave cycling exercises at moderate intensity while breathing normoxic room air; and (iv) 3 repeated square wave cycling exercises at moderate intensity while breathing hypoxic room air. During all exercise sessions, pulmonary gas exchange was measured breath-by-breath; HHb was determined on the vastus lateralis muscle by near-infrared spectroscopy; and HR was collected beat-by-beat. The pulomary oxygen uptake kinetics became slower in hypoxia (31 ± 9 s) than in normoxia (27 ± 7 s) because of an increased mismatching between O2 delivery to O2 utilization at the level of the muscle. The HR and HHb kinetics did not change between hypoxia and normoxia,
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Giesbrecht, G. G., A. Puddy, M. Ahmed, M. Younes, and N. R. Anthonisen. "Exercise endurance and arterial desaturation in normobaric hypoxia with increased chemosensitivity." Journal of Applied Physiology 70, no. 4 (April 1, 1991): 1770–74. http://dx.doi.org/10.1152/jappl.1991.70.4.1770.
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We studied whether exercise endurance under normobaric hypoxia can be enhanced by increasing hypoxic ventilatory sensitivity with almitrine bismesylate (ALM). On both ALM and placebo (PL) days, resting subjects breathed a hypoxic gas mixture (an inspired O2 fraction of 10.4-13.2%), which lowered resting arterial O2 saturation (SaO2) to 80%. After 15 min of rest there was a 3-min warm-up period of exercise at 50 W (light) on a cycle ergometer, followed by a step increase in load to 60% of the previously determined maximum power output with room-air breathing (moderate), which was maintained until exhaustion. With PL, SaO2 decreased rapidly with the onset of exercise and continued to fall slowly during moderate exercise, averaging 71.0 +/- 1.8% (SE) at exhaustion. With ALM, saturation did not differ from PL during air breathing but significantly exceeded SaO2 with PL, by 3.4% during resting hypoxia, by 4.0% at the start of exercise, and by 5.9% at exhaustion. Ventilation was not affected by ALM during air breathing and was slightly, although not significantly, increased during hypoxic rest and exercise. ALM was associated with an increased heart rate during room air breathing but not during hypoxia. Endurance time was 20.6 +/- 1.6 min with ALM and 21.3 +/- 0.9 min with PL. During hypoxic exercise, the potential benefit of greater saturation with ALM is apparently offset by other unidentified factors.
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Furilla, R. A., and D. R. Jones. "The contribution of nasal receptors to the cardiac response to diving in restrained and unrestrained redhead ducks (Aythya americana)." Journal of Experimental Biology 121, no. 1 (March 1, 1986): 227–38. http://dx.doi.org/10.1242/jeb.121.1.227.
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In restrained redhead ducks, forced submergence caused heart rate to fall from 100 +/− 3 beats min-1 (mean +/− S.E.M., N = 12) to a stable underwater rate of 35 +/− 4 beats min-1 (N = 12) within 5 s after submergence. Bradycardia was unaffected by breathing oxygen before a dive, but was virtually eliminated by local anaesthesia of the narial region. In contrast, in a dabbling duck (Anas platyrhynchos) bradycardia in short dives was eliminated by breathing oxygen before a dive. In unrestrained diving, on a man-made pond, heart rate in redheads diving voluntarily (y) was related to pre-dive heart rate (x) by the equation y = 76 + 0.29 +/− 0.05x +/− 17 (r2 = 0.71). Chasing, to induce submergence, had variable effects on this relationship. Local anaesthesia of the narial region inhibited voluntary diving but heart rates in chase-induced dives after nasal blockade were significantly higher, by 10–30%, than those obtained from untreated ducks in chase-induced dives. Breathing oxygen before voluntary dives had no apparent effect on heart rate after 2–5 s submergence. Voluntary head submersion by dabbling ducks caused no change in heart rate. We conclude that nasal receptors make only a minor contribution to cardiac responses in unrestrained dives, compared with forced dives, in diving ducks. Furthermore, these results show that little can be learned about cardiac responses in free diving ducks from studies of forced dives in dabblers or divers.
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Smatresk, N. J., M. L. Burleson, and S. Q. Azizi. "Chemoreflexive responses to hypoxia and NaCN in longnose gar: evidence for two chemoreceptor loci." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 251, no. 1 (July 1, 1986): R116—R125. http://dx.doi.org/10.1152/ajpregu.1986.251.1.r116.
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Interactions between internal and external O2 stimulus levels were assessed by measuring the ventilatory and cardiovascular responses to varying water (PWO2) and air bladder (PabO2) O2 levels and intravascular NaCN in anesthetized spontaneously ventilating Lepisosteus osseus. As PWO2 fell, air-breathing frequency (fab) increased. Buccal pressure amplitude (Pb) also increased as PWO2 fell from hyperoxia to normoxia, but hypoxic water depressed Pb. The PO2 in the ventral aorta (VA) fell as PabO2 fell, which stimulated fab and Pb when the gar was in normoxic or hyperoxic water. Thus gill ventilation and air breathing were normally controlled by both internal and external O2 levels, but aquatic hypoxia uniformly depressed gill ventilation regardless of changes in PabO2 levels. Heart rate and blood pressure were unaffected by these changes. NaCN stimulated hypoxic reflexes and bradycardia more quickly when given into the VA or conus than when given into the dorsal aorta. The animals appear to possess internal chemoreceptors that set the level of hypoxic drive and external chemoreceptors that inhibit gill ventilation and shift the ventilatory emphasis from water to air breathing.
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HEDRICK, M. S., M. L. BURLESON, D. R. JONES, and W. K. MILSOM. "An Examination of Central Chemosensitivity in an Air-Breathing Fish (Amia Calva)." Journal of Experimental Biology 155, no. 1 (January 1, 1991): 165–74. http://dx.doi.org/10.1242/jeb.155.1.165.
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The role of central chemosensitivity in the control of ventilation in fishes was investigated directly by perfusing a mock extradural fluid (EDF) through the cranial space in the medullary region of conscious air-breathing fish, Amia calva. Perfusions with Sudan Black dye showed that the mock EDF communicated with the cerebrospinal fluid (CSF) and entered the cerebral ventricles. Altering the PO2, PCO2 and/or pH of the mock EDF had no effect on gill- or air-breathing rates, heart rate or blood pressure during exposure to normoxic water. Aquatic hypoxia, however, stimulated gill ventilation and elevated blood pressure, but did not affect heart rate; altering the gas tensions and/or pH of mock EDF still had no effect on recorded variables. Sodium cyanide (NaCN) added to the mock EDF caused struggling at concentrations above 500 μgml−1, but did not uniformly stimulate ventilation. These results suggest that central chemoreceptors, which mediate cardiovascular or ventilatory reflexes, are absent in Amia.
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Curtis, Andrew N., Michael L. Walsh, and Matthew D. White. "Influence of passive hyperthermia on human ventilation during rest and isocapnic hypoxia." Applied Physiology, Nutrition, and Metabolism 32, no. 4 (August 2007): 721–32. http://dx.doi.org/10.1139/h07-035.
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The purpose of this study was to examine the potential interaction of core temperature and isocapnic hypoxia on human ventilation and heart rate (HR). In 2 resting head-out water-immersion trials, 8 males first breathed air and then 12% O2 in N2 while the end-tidal partial pressure of carbon dioxide was kept 0.98 (0.66) mmHg (mean (SD)) above normothermic resting levels. The first immersion trial was with a normothermic esophageal temperature (Tes) of ~36.7 °C, and for the second trial, 1 h later, water temperature was increased to give a hyperthermic Tes of ~38.2 °C. Isocapnic hypoxia increased normothermic ventilation by 4 L·min–1 (p = 0.01) from 10.12 (1.07) to 14.20 (3.21) L·min–1, and hyperthermic ventiliation by 7 L·min–1 (p = 0.002) from 13.58 (2.58) to 20.79 (3.73) L·min–1. Ventilation increases during hyperthermia were mediated by breathing frequency and, during isocapnic hypoxia, by tidal volume. Unexpectedly, there was an absence of any hypoxic ventilatory decline that could be attributed to a hydrostatic effect of immersion. Isocapnic hypoxia increased the HR by similar amounts of ~10 and ~11 beats·min–1 in normothermia and hyperthermia, respectively. In conclusion, it appears that hyperthermia increases human ventilatory but not heart rate responses to isocapnic hypoxia.
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Kinsman, Tahnee A., Allan G. Hahn, Christopher J. Gore, Bradley R. Wilsmore, David T. Martin, and Chin-Moi Chow. "Respiratory events and periodic breathing in cyclists sleeping at 2,650-m simulated altitude." Journal of Applied Physiology 92, no. 5 (May 1, 2002): 2114–18. http://dx.doi.org/10.1152/japplphysiol.00737.2001.
Full textAbstract:
We examined the initial effect of sleeping at a simulated moderate altitude of 2,650 m on the frequency of apneas and hypopneas, as well as on the heart rate and blood oxygen saturation from pulse oximetry (SpO2 ) during rapid eye movement (REM) and non-rapid eye movement (NREM) sleep of 17 trained cyclists. Pulse oximetry revealed that sleeping at simulated altitude significantly increased heart rate (3 ± 1 beats/min; means ± SE) and decreased SpO2 (−6 ± 1%) compared with baseline data collected near sea level. In response to simulated altitude, 15 of the 17 subjects increased the combined frequency of apneas plus hypopneas from baseline levels. On exposure to simulated altitude, the increase in apnea was significant from baseline for both sleep states (2.0 ± 1.3 events/h for REM, 9.9 ± 6.2 events/h for NREM), but the difference between the two states was not significantly different. Hypopnea frequency was significantly elevated from baseline to simulated altitude exposure in both sleep states, and under hypoxic conditions it was greater in REM than in NREM sleep (7.9 ± 1.8 vs. 4.2 ± 1.3 events/h, respectively). Periodic breathing episodes during sleep were identified in four subjects, making this the first study to show periodic breathing in healthy adults at a level of hypoxia equivalent to 2,650-m altitude. These results indicate that simulated moderate hypoxia of a level typically chosen by coaches and elite athletes for simulated altitude programs can cause substantial respiratory events during sleep.
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van den Aardweg, J. G., and J. M. Karemaker. "Repetitive apneas induce periodic hypertension in normal subjects through hypoxia." Journal of Applied Physiology 72, no. 3 (March 1, 1992): 821–27. http://dx.doi.org/10.1152/jappl.1992.72.3.821.
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Periodic increases in blood pressure (BP) can occur in the sleep apnea syndrome (SAS) during recurrent apneas. To investigate the mechanisms causing this periodic hypertension, we simulated SAS by imposing a matching breathing pattern on seven healthy awake male volunteers. Continuous finger arterial BP, electrocardiogram, arterial O2 saturation (SaO2), end-tidal CO2, and tidal volume were measured. The role of hypoxia was studied by comparing apneas during depletion of O2 in the spirometer with those during 100% O2 breathing. In all subjects, BP periodically reached values greater than 150/95 mmHg in the hypoxic series. During the hyperoxic apnea series, however, BP remained stable. End-apneic mean BP was shown to be inversely correlated to SaO2 in six subjects in the SaO2 range from 60 to 100%. Although the hypoxic BP pattern closely mimicked that in SAS, the heart rate pattern in four of our subjects remained distinct from that in patients. Atropine could not prevent large BP swings in the hypoxic series. We conclude that SaO2 is a major determinant of periodic hypertension in recurrent apneas. Its effect probably results from chemoreflex modulation of peripheral resistance.
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Huang, J., C. Suguihara, D. Hehre, J. Lin, and E. Bancalari. "Effects of GABA receptor blockage on the respiratory response to hypoxia in sedated newborn piglets." Journal of Applied Physiology 77, no. 2 (August 1, 1994): 1006–10. http://dx.doi.org/10.1152/jappl.1994.77.2.1006.
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Brain gamma-aminobutyric acid (GABA) levels increase during hypoxia, which may modulate the ventilatory response to hypoxia. To test the possibility that the depressed neonatal ventilatory response to hypoxia may be related to increased central nervous system GABA activity, 26 sedated spontaneously breathing newborn piglets (age 5 +/- 1 day, wt 1.7 +/- 0.4 kg) were studied. Minute ventilation (VE), oxygen consumption, heart rate, arterial blood pressure, and arterial blood gases were measured in room air and after 1, 5, and 10 min of hypoxia (inspired O2 fraction 0.10) before drug intervention. Immediately after these measurements, an infusion of saline or the GABA alpha-receptor blocker (bicuculline, 0.3 mg/kg iv) or beta-receptor blocker (CGP-35348, 100–300 mg/kg iv) was administered while animals were hypoxic. All measurements were repeated at 1, 5, and 10 min after initiation of the drug infusion. Basal VE was similar among groups. During hypoxia, VE increased significantly in the animals that received either a GABA alpha- or beta-receptor blocker but not in those receiving saline. Changes in arterial Po2, oxygen consumption, heart rate, and arterial blood pressure were similar among groups before and after saline or GABA antagonist infusion. These results suggest that the decrease in ventilation during the biphasic ventilatory response to hypoxia in the neonatal piglet is in part mediated through the depressant effect of GABA on the central nervous system.
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Barrett, Karlene T., Shabih U. Hasan, Morris H. Scantlebury, and Richard J. A. Wilson. "Impaired neonatal cardiorespiratory responses to hypoxia in mice lacking PAC1 or VPAC2 receptors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 316, no. 5 (May 1, 2019): R594—R606. http://dx.doi.org/10.1152/ajpregu.00250.2018.
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The stress peptide pituitary adenylate cyclase activating polypeptide (PACAP) and its specific receptor PACAP type 1 receptor (PAC1) have been implicated in sudden infant death syndrome (SIDS). PACAP is also critical to the neonatal cardiorespiratory response to homeostatic stressors identified in SIDS, including hypoxia. However, which of PACAP’s three receptors, PAC1, vasoactive intestinal peptide receptor type 1 (VPAC1), and/or vasoactive intestinal peptide receptor type 2 (VPAC2), are involved is unknown. In this study, we hypothesized that PAC1, but not VPAC2, is involved in mediating the cardiorespiratory response to hypoxia during neonatal development. To test this hypothesis, head-out plethysmography and surface ECG electrodes were used to assess the cardiorespiratory variables of unanesthetized postnatal day 4 PAC1 and VPAC2-knockout (KO) and wild-type (WT) mice in response to a 10% hypoxic challenge. Our results demonstrate that compared with WT pups, the early and late hypoxic rate of expired CO2 (V̇co2), V̇co2 and ventilatory responses were blunted in PAC1-KO neonates, and during the posthypoxic period, minute ventilation (V̇e), V̇co2 and heart rate were increased, while the increase in apneas normally associated with the posthypoxic period was reduced. Consistent with impaired cardiorespiratory control in these animals, the V̇e/V̇co2 slope was reduced in PAC1-KO pups, suggesting that breathing was inappropriately matched to metabolism. In contrast, VPAC2-KO pups exhibited elevated heart rate variability during hypoxia compared with WT littermates, but the effects of the VPAC2-KO genotype on breathing were minimal. These findings suggest that PAC1 plays the principal role in mediating the cardiorespiratory effects of PACAP in response to hypoxic stress during neonatal development and that defective PACAP signaling via PAC1 may contribute to the pathogenesis of SIDS.
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Burggren, Warren W., Gil Martinez Bautista, Susana Camarillo Coop, Gabriel Márquez Couturier, Salomón Páramo Delgadillo, Rafael Martínez García, and Carlos Alfonso Alvarez González. "Developmental cardiorespiratory physiology of the air-breathing tropical gar, Atractosteus tropicus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 311, no. 4 (October 1, 2016): R689—R701. http://dx.doi.org/10.1152/ajpregu.00022.2016.
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The physiological transition to aerial breathing in larval air-breathing fishes is poorly understood. We investigated gill ventilation frequency ( fG), heart rate ( fH), and air breathing frequency ( fAB) as a function of development, activity, hypoxia, and temperature in embryos/larvae from day (D) 2.5 to D30 posthatch of the tropical gar, Atractosteus tropicus, an obligate air breather. Gill ventilation at 28°C began at approximately D2, peaking at ∼75 beats/min on D5, before declining to ∼55 beats/min at D30. Heart beat began ∼36–48 h postfertilization and ∼1 day before hatching. fH peaked between D3 and D10 at ∼140 beats/min, remaining at this level through D30. Air breathing started very early at D2.5 to D3.5 at 1–2 breaths/h, increasing to ∼30 breaths/h at D15 and D30. Forced activity at all stages resulted in a rapid but brief increase in both fG and fH, (but not fAB), indicating that even in these early larval stages, reflex control existed over both ventilation and circulation prior to its increasing importance in older fishes. Acute progressive hypoxia increased fG in D2.5–D10 larvae, but decreased fG in older larvae (≥D15), possibly to prevent branchial O2 loss into surrounding water. Temperature sensitivity of fG and fH measured at 20°C, 25°C, 28°C and 38°C was largely independent of development, with a Q10 between 20°C and 38°C of ∼2.4 and ∼1.5 for fG and fH, respectively. The rapid onset of air breathing, coupled with both respiratory and cardiovascular reflexes as early as D2.5, indicates that larval A. tropicus develops “in the fast lane.”
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Greenberg, Harly E., Anthony Sica, Deirdre Batson, and Steven M. Scharf. "Chronic intermittent hypoxia increases sympathetic responsiveness to hypoxia and hypercapnia." Journal of Applied Physiology 86, no. 1 (January 1, 1999): 298–305. http://dx.doi.org/10.1152/jappl.1999.86.1.298.
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We sought to determine whether chronic exposure to intermittent hypoxia (CIH) increases sympathetic responsiveness to subsequent chemoreflex stimulation. Sprague-Dawley rats were exposed to 30 days of CIH: exposure chamber %O2 [fractional concentration of chamber O2([Formula: see text])] nadir 6.5–7% with return to 21% each minute for 8 h/day during the diurnal sleep period (Exp group). Sham controls (SC group) were similarly handled but kept at 21%[Formula: see text] and compared with unhandled controls (UC group). Rats were then anesthetized with urethan, and preganglionic cervical sympathetic activity (CSA), diaphragm electromyogram, arterial pressure, and electrocardiogram were recorded while the rats were spontaneously breathing 100% O2, room air, 10% O2, 12% CO2, and 10% O2-12% CO2. CSA and heart rate were also recorded during phenylephrine infusion to assess baroreceptor function. Mean arterial pressure was significantly greater in Exp than in SC and UC rats during all conditions ( P < 0.05). A vasopressor response to 10% O2-12% CO2 was observed only in Exp rats. CSA was greater in Exp than in SC and UC rats during 10% O2, 12% CO2, and 10% O2-12% CO2 but not during room-air exposure. A significant increase in CSA compared with room air was noted during 10% O2, 12% CO2, and 10% O2-12% CO2 in Exp but not in SC or UC rats. No differences in baroreceptor function were observed among groups. We conclude that CIH leads to increased sympathetic responsiveness to chemoreflex stimulation.
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Saldívar, Enrique, Pedro Cabrales, Amy G. Tsai, and Marcos Intaglietta. "Microcirculatory changes during chronic adaptation to hypoxia." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 5 (November 2003): H2064—H2071. http://dx.doi.org/10.1152/ajpheart.00349.2003.
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Microcirculatory changes in the window chamber preparation in Syrian golden hamsters, secondary to chronic hypoxia adaptation, are presented herein. Adaptation was attained by keeping animals in a 10% oxygen environment for 1 wk and 5% the following week. The following groups were studied: group 1, adapted to chronic hypoxia and kept in a 5% oxygen environment throughout the experiment; group 2, adapted to chronic hypoxia and kept in a 21% oxygen environment 24 h before and during the experiment; and group 3, control. Adaptation caused venule enlargement and hematocrit increase (68.6 ± 2.44 in group 1, 70 ± 2.66 in group 2, and 43.27 ± 2.30 in group 3; P < 0.05). Whereas heart rate decreased in adapted animals, blood pressure remained constant. Group 1 presented alkalosis, hypocapnia, and hypoxemia. The adapted groups had decreased blood flow velocity in arterioles and veins. We found no difference in microvasculature oxygen tension between groups 2 and 3; however, the number of capillaries with flow was markedly reduced in group 1 but significantly increased in group 2. Our findings suggest that, as an adaptation to hypoxia, erythropoiesis may prove beneficial by increasing blood viscosity and shear stress, leading to vasodilatation, in addition to the increase in oxygen-carrying capacity. Calculations show that oxygen extraction in the tissue of the window chamber model was significantly lowered in adapted animals breathing 5% oxygen, but was unchanged from the control when breathing 21% oxygen, even though blood hemoglobin content was increased from 14.5 ± 0.07 g/dl at control to 21.04 ± 1.24 g/dl in the adapted animals ( P < 0.05).
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Leung, Richard S. T., John S. Floras, and T. Douglas Bradley. "Respiratory modulation of the autonomic nervous system during Cheyne–Stokes respirationThis paper is one of a selection of papers published in this Special Issue, entitled Young Investigator's Forum." Canadian Journal of Physiology and Pharmacology 84, no. 1 (January 2006): 61–66. http://dx.doi.org/10.1139/y05-145.
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Cheyne–Stokes respiration (CSR) is associated with increased mortality among patients with heart failure. However, the specific link between CSR and mortality remains unclear. One possibility is that CSR results in excitation of the sympathetic nervous system. This review relates evidence that CSR exerts acute effects on the autonomic nervous system during sleep, and thereby influences a number of cardiovascular phenomena, including heart rate, blood pressure, atrioventricular conduction, and ventricular ectopy. In patients in sinus rhythm, heart rate and blood pressure oscillate during CSR in association with respiratory oscillations, such that both peak heart rate and blood pressure occur during the hyperpneic phase. Inhalation of CO2 abolishes both CSR and the associated oscillations in heart rate and blood pressure. In contrast, O2 inhalation sufficient to eliminate hypoxic dips has no significant effect on CSR, heart rate, or blood pressure. In patients with atrial fibrillation, ventricular rate oscillates in association with CSR despite the absence of within-breath respiratory arrhythmia. The comparison of RR intervals between the apneic and hyperpneic phases of CSR indicates that this breathing disorder exerts its effect on ventricular rate by inducing cyclical changes in atrioventricular node conduction properties. In patients with frequent ventricular premature beats (VPBs), VPBs occur more frequently during the hyperpneic phase than the apneic phase of CSR. VPB frequency is also higher during periods of CSR than during periods of regular breathing, with or without correction of hypoxia. In summary, CSR exerts multiple effects on the cardiovascular system that are likely manifestations of respiratory modulation of autonomic activity. It is speculated that the rhythmic oscillations in autonomic tone brought about by CSR may ultimately contribute to the sympatho-excitation and increased mortality long observed in patients with heart failure and CSR.
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Curran, Aidan K., Joshua R. Rodman, Peter R. Eastwood, Kathleen S. Henderson, Jerome A. Dempsey, and Curtis A. Smith. "Ventilatory responses to specific CNS hypoxia in sleeping dogs." Journal of Applied Physiology 88, no. 5 (May 1, 2000): 1840–52. http://dx.doi.org/10.1152/jappl.2000.88.5.1840.
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Our study was concerned with the effect of brain hypoxia on cardiorespiratory control in the sleeping dog. Eleven unanesthetized dogs were studied; seven were prepared for vascular isolation and extracorporeal perfusion of the carotid body to assess the effects of systemic [and, therefore, central nervous system (CNS)] hypoxia (arterial [Formula: see text] = 52, 45, and 38 Torr) in the presence of a normocapnic, normoxic, and normohydric carotid body during non-rapid eye movement sleep. A lack of ventilatory response to systemic boluses of sodium cyanide during carotid body perfusion demonstrated isolation of the perfused carotid body and lack of other significant peripheral chemosensitivity. Four additional dogs were carotid body denervated and exposed to whole body hypoxia for comparison. In the sleeping dog with an intact and perfused carotid body exposed to specific CNS hypoxia, we found the following. 1) CNS hypoxia for 5–25 min resulted in modest but significant hyperventilation and hypocapnia (minute ventilation increased 29 ± 7% at arterial [Formula: see text] = 38 Torr); carotid body-denervated dogs showed no ventilatory response to hypoxia. 2) The hyperventilation was caused by increased breathing frequency. 3) The hyperventilatory response developed rapidly (<30 s). 4) Most dogs maintained hyperventilation for up to 25 min of hypoxic exposure. 5) There were no significant changes in blood pressure or heart rate. We conclude that specific CNS hypoxia, in the presence of an intact carotid body maintained normoxic and normocapnic, does not depress and usually stimulates breathing during non-rapid eye movement sleep. The rapidity of the response suggests a chemoreflex meditated by hypoxia-sensitive respiratory-related neurons in the CNS.
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Horstick, Georg, Oliver Berg, Axel Heimann, Harald Darius, Hans Anton Lehr, Sucharit Bhakdi, Oliver Kempski, and Jürgen Meyer. "Surgical procedure affects physiological parameters in rat myocardial ischemia: need for mechanical ventilation." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 2 (February 1, 1999): H472—H479. http://dx.doi.org/10.1152/ajpheart.1999.276.2.h472.
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Several surgical approaches are being used to induce myocardial ischemia in rats. The present study investigated two different operative procedures in spontaneously breathing and mechanically ventilated rats under sham conditions. A snare around the left coronary artery (LCA) was achieved without occlusion. Left lateral thoracotomy was performed in spontaneously breathing and mechanically ventilated rats (tidal volume 8 ml/kg) with a respiratory rate of 90 strokes/min at different levels of O2 supplementation (room air and 30, 40, and 90% O2). All animals were observed for 60 min after thoracotomy. Rats operated with exteriorization of the heart through left lateral thoracotomy while breathing spontaneously developed severe hypoxia and hypercapnia despite an intrathoracic operation time of <1 min. Arterial O2 content decreased from 18.7 ± 0.5 to 3.3 ± 0.9 vol%. Lactate increased from 1.2 ± 0.1 to 5.2 ± 0.3 mmol/l. Significant signs of ischemia were seen in the electrocardiogram up to 60 min. Mechanically ventilated animals exhibited a spectrum ranging from hypoxia (room air) to hyperoxia (90% O2). In order not to jeopardize findings in experimental myocardial ischemia-reperfusion injury models, stable physiological parameters can be achieved in mechanically ventilated rats at an O2application of 30–40% at 90 strokes/min.
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Hammond, M. D., G. E. Gale, K. S. Kapitan, A. Ries, and P. D. Wagner. "Pulmonary gas exchange in humans during normobaric hypoxic exercise." Journal of Applied Physiology 61, no. 5 (November 1, 1986): 1749–57. http://dx.doi.org/10.1152/jappl.1986.61.5.1749.
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Previous studies (J. Appl. Physiol. 58: 978–988 and 989–995, 1985) have shown both worsening ventilation-perfusion (VA/Q) relationships and the development of diffusion limitation during heavy exercise at sea level and during hypobaric hypoxia in a chamber [fractional inspired O2 concentration (FIO2) = 0.21, minimum barometric pressure (PB) = 429 Torr, inspired O2 partial pressure (PIO2) = 80 Torr]. We used the multiple inert gas elimination technique to compare gas exchange during exercise under normobaric hypoxia (FIO2 = 0.11, PB = 760 Torr, PIO2 = 80 Torr) with earlier hypobaric measurements. Mixed expired and arterial respiratory and inert gas tensions, cardiac output, heart rate (HR), minute ventilation, respiratory rate (RR), and blood temperature were recorded at rest and during steady-state exercise in 10 normal subjects in the following order: rest, air; rest, 11% O2; light exercise (75 W), 11% O2; intermediate exercise (150 W), 11% O2; heavy exercise (greater than 200 W), 11% O2; heavy exercise, 100% O2 and then air; and rest 20 minutes postexercise, air. VA/Q inequality increased significantly during hypoxic exercise [mean log standard deviation of perfusion (logSDQ) = 0.42 +/- 0.03 (rest) and 0.67 +/- 0.09 (at 2.3 l/min O2 consumption), P less than 0.01]. VA/Q inequality was improved by relief of hypoxia (logSDQ = 0.51 +/- 0.04 and 0.48 +/- 0.02 for 100% O2 and air breathing, respectively). Diffusion limitation for O2 was evident at all exercise levels while breathing 11% O2.(ABSTRACT TRUNCATED AT 250 WORDS)