Altitude acclimatization: influence on periodic breathing and chemoresponsiveness during sleep

1987 ◽  
Vol 63 (1) ◽  
pp. 401-412 ◽  
Author(s):  
D. P. White ◽  
K. Gleeson ◽  
C. K. Pickett ◽  
A. M. Rannels ◽  
A. Cymerman ◽  
...  
Keyword(s):  
Sea Level ◽  
Eye Movement ◽  
Ventilatory Response ◽  
Periodic Breathing ◽  
Rapid Eye Movement ◽  
Initial Exposure ◽  
Ventilatory Responses ◽  
Altitude Acclimatization ◽  
Hypercapnic Ventilatory Response ◽  
Arterial O2 Saturation

Although the influence of altitude acclimatization on respiration has been carefully studied, the associated changes in hypoxic and hypercapnic ventilatory responses are the subject of controversy with neither response being previously evaluated during sleep at altitude. Therefore, six healthy males were studied at sea level and on nights 1, 4, and 7 after arrival at altitude (14,110 ft). During wakefulness, ventilation and the ventilatory responses to hypoxia and hypercapnia were determined on each occasion. During both non-rapid-eye-movement and rapid-eye-movement sleep, ventilation, ventilatory pattern, and the hypercapnic ventilatory response (measured at ambient arterial O2 saturation) were determined. There were four primary observations from this study: 1) the hypoxic ventilatory response, although similar to sea level values on arrival at altitude, increased steadily with acclimatization up to 7 days; 2) the slope of the hypercapnic ventilatory response increased on initial exposure to a hypoxic environment (altitude) but did not increase further with acclimatization, although the position of this response shifted steadily to the left (lower PCO2 values); 3) the sleep-induced decrements in both ventilation and hypercapnic responsiveness at altitude were equivalent to those observed at sea level with similar acclimatization occurring during wakefulness and sleep; and 4) the quantity of periodic breathing during sleep at altitude was highly variable and tended to occur more frequently in individuals with higher ventilatory responses to both hypoxia and hypercapnia.

Time course of augmentation and depression of hypoxic ventilatory responses at altitude

1994 ◽  
Vol 77 (1) ◽  
pp. 313-316 ◽  
Author(s):  
M. Sato ◽  
J. W. Severinghaus ◽  
P. Bickler
Keyword(s):  
Pulse Oximetry ◽  
Sea Level ◽  
Time Course ◽  
Ventilatory Response ◽  
Barometric Pressure ◽  
Hypoxic Ventilatory Response ◽  
Set Point ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Arterial O2 Saturation

Hypoxic ventilatory response (HVR) and hypoxic ventilatory depression (HVD) were measured in six subjects before, during, and after 12 days at 3,810-m altitude (barometric pressure approximately 488 Torr) with and without 15 min of preoxygenation. HVR was tested by 5-min isocapnic steps to 75% arterial O2 saturation measured by pulse oximetry (Spo2) at an isocapnic PCO2 (P*CO2) chosen to set hyperoxic resting ventilation to 140 ml.kg-1.min-1. Hypercapnic ventilatory response (HCVR, 1.min-1.Torr-1) was tested at ambient and high SPO2 6–8 min after a 6- to 10-Torr step increase of end-tidal PCO2 (PETCO2) above P*CO2. HCVR was independent of preoxygenation and was not significantly increased at altitude (when corrected to delta logPCO2). Preoxygenated HVR rose from -1.13 +/- 0.23 (SE) l.min-1.%SPO2(-1) at sea level to -2.17 +/- 0.13 by altitude day 12, without reaching a plateau, and returned to control after return to sea level for 4 days. Ambient HVR was measured at P*CO2 by step reduction of SPO2 from its ambient value (86–91%) to approximately 75%. Ambient HVR slope was not significantly less, but ventilation at equal levels of SPO2 and PCO2 was lower by 13.3 +/- 2.4 l/min on day 2 (SPO2 = 86.2 +/- 2.3) and by 5.9 +/- 3.5 l/min on day 12 (SPO2 = 91.0 +/- 1.5; P < 0.05). This lower ventilation was estimated (from HCVR) to be equivalent to an elevation of the central chemoreceptor PCO2 set point of 9.2 +/- 2.1 Torr on day 2 and 4.5 +/- 1.3 on day 12.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Impact of interrupted leptin pathways on ventilatory control

2004 ◽  
Vol 96 (3) ◽  
pp. 991-998 ◽  
Author(s):  
Vsevolod Y. Polotsky ◽  
Marc C. Smaldone ◽  
Matthew T. Scharf ◽  
Jianguo Li ◽  
Clarke G. Tankersley ◽  
...  
Keyword(s):  
Eye Movement ◽  
Ventilatory Response ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Hypoxic Ventilatory Response ◽  
Wild Type ◽  
Hypercapnic Ventilatory Response ◽  
Leptin Deficiency ◽  
Significant Depression ◽  
Deficient Mice

Leptin deficiency in ob/ob mice produces marked depression of the hypercapnic ventilatory response, particularly during sleep. We now extend our previous findings to determine whether 1) leptin deficiency affects the hypoxic ventilatory response and 2) blockade of the downstream excitatory actions of leptin on melanocortin 4 receptors or inhibitory actions on neuropeptide Y (NPY) pathways has an impact on hypercapnic and hypoxic sensitivity. We have found that leptin-deficient ob/ob mice have the same hypoxic ventilatory response as weight-matched wild-type obese mice. There were no differences in the hypoxic sensitivity between agouti yellow mice and weight-matched controls, or NPY-deficient mice and wild-type littermates. Agouti yellow mice, with blocked melanocortin pathways, exhibited a significant depression of the hypercapnic sensitivity compared with weight-matched wild-type controls during non-rapid eye movement sleep (5.8 ± 0.7 vs. 8.9 ± 0.7 ml·min-1·%CO2-1, P < 0.01), but not during wakefulness. NPY-deficient transgenic mice exhibited a small increase in the hypercapnic ventilatory response compared with wild-type littermates, but this was only present during wakefulness. We conclude that interruption of leptin pathways does not affect hypoxic sensitivity during sleep and wakefulness but that melanocortin 4 blockade is associated with depressed hypercapnic sensitivity in non-rapid eye movement sleep.

scholarly journals Ventilatory responses to specific CNS hypoxia in sleeping dogs

2000 ◽  
Vol 88 (5) ◽  
pp. 1840-1852 ◽  
Author(s):  
Aidan K. Curran ◽  
Joshua R. Rodman ◽  
Peter R. Eastwood ◽  
Kathleen S. Henderson ◽  
Jerome A. Dempsey ◽  
...  
Keyword(s):  
Eye Movement ◽  
Carotid Body ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Whole Body ◽  
Hypoxic Exposure ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Cardiorespiratory Control ◽  
Ventilatory Responses

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.

Ventilatory response to hypercapnia during sleep and wakefulness in cats

1984 ◽  
Vol 56 (5) ◽  
pp. 1347-1354 ◽  
Author(s):  
A. Netick ◽  
W. J. Dugger ◽  
R. A. Symmons
Keyword(s):  
Eye Movement ◽  
Response Curve ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Ventilatory Responses ◽  
A Value ◽  
The Right ◽  
Hypercapnic Response

Eucapnic breathing and ventilatory responses to hypercapnia were studied in seven cats during sleep and wakefulness. No significant differences were found in minute ventilation (VE), alveolar ventilation (VA), or alveolar PCO2 (PACO2) between wakefulness (W) and non-rapid-eye-movement (NREM) sleep, but VA and VE were less during rapid-eye-movement (REM) sleep than W, and PACO2 declined during REM compared with NREM. To test the hypercapnic response, cats were required to rebreathe from a bag containing 6% CO2 and 94% O2 (to eliminate the hypoxic response). The response curve was displaced to the right during NREM and REM; the slope was reduced only during REM to a value about 75% of W and NREM. Eye movements, quantifying phasic REM, were only slightly correlated (negatively) with the deviation of ventilation from the response curve. The hypercapnic response was diminished, not eliminated, during REM, even during phasic REM. The reduced slope arose principally from the failure of the expiratory time to shorten with hypercapnia as during W and NREM. The cat's hypercapnic response compared with the dog's, measured by others with the same methodology, suggests that differences between species may be more crucial than methodology in explaining earlier contradictory results.

Ventilatory pattern after hypoxic stimulation during wakefulness and NREM sleep

1993 ◽  
Vol 75 (1) ◽  
pp. 397-404 ◽  
Author(s):  
K. Gleeson ◽  
L. W. Sweer
Keyword(s):  
Eye Movement ◽  
Ventilatory Response ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Identical Stimulus ◽  
Discharge Mechanism ◽  
Ventilatory Pattern ◽  
End Tidal ◽  
Arterial O2 Saturation ◽  
Stimulation Of

The ventilatory after-discharge mechanism (VAD) may stabilize ventilation (VE) after hyperventilation but has not been studied in detail in humans. Several studies conducted during wakefulness suggest that VAD is present, although none has been conducted during sleep, when disordered ventilation is most common. We conducted two experiments during wakefulness and non-rapid-eye-movement (NREM) sleep in 14 healthy young men to characterize the ventilatory response after termination of a 45- to 60-s 10–12% O2 hypoxic stimulus. Eight subjects had triplicate hypoxic trials terminated by 100% O2 during wakefulness and NREM sleep. Hypoxia caused a drop in arterial O2 saturation to 78.5 +/- 0.5%, an increase in VE of 4.4 +/- 0.6 l/min, and a decrease in end-tidal PCO2 of 4.4 +/- 0.4 Torr during wakefulness, with no significant differences during sleep. When the hypoxia was terminated with 100% O2, VE was variable within and between subjects during wakefulness. During sleep, all subjects developed hypopnea (VE < 67% baseline) with a mean decrease of 65.5 +/- 7.8% at the onset of hyperoxia (P < 0.05 compared with baseline VE). We hypothesized that this uniform decrease in VE might be due to the nonphysiological hyperoxia employed. We therefore studied six additional subjects, all during NREM sleep, with identical hypoxic stimulation of breathing terminated by 100% O2 or room air. We again found that termination of hypoxia with 100% O2 produced uniform hypoventilation. However, when the identical stimulus was terminated with room air, no hypoventilation occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

Occlusion pressure and ventilation during sleep in normal humans

1986 ◽  
Vol 61 (4) ◽  
pp. 1279-1287 ◽  
Author(s):  
D. P. White
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Nrem Sleep ◽  
Respiratory Drive ◽  
Rapid Eye Movement ◽  
System Sensitivity ◽  
Hypercapnic Ventilatory Response ◽  
Normal Humans

Previous investigation in normal humans has demonstrated reduced ventilation and ventilatory responses to chemical stimuli during sleep. Most have interpreted this to be a product of decreasing central nervous system sensitivity to the normal stimuli that maintain ventilation, whereas other factors such as increasing airflow resistance could also contribute to this reduction in respiration. To improve our understanding of these events, we measured ventilation and occlusion pressures (P0.1) during unstimulated ventilation and rebreathing-induced hypercapnia during wakefulness and non-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep. Eighteen subjects (10 males and 8 females) of whom seven were snorers (5 males and 2 females) were studied. Ventilation was reduced during both NREM and REM sleep (P less than 0.05), but this decrement in minute ventilation tended to be greater in snorers than nonsnorers. Unstimulated P0.1, on the other hand, was maintained or increased during sleep in all groups studied, with males and snorers showing the largest increase. The hypercapnic ventilatory response fell during both NREM and REM sleep and tended to be lower during REM than NREM sleep. However, the P0.1 response to hypercapnia during NREM sleep was well maintained at the waking level although the REM response was statistically reduced. These studies suggest that the mechanism of the reduction in ventilation and the hypercapnic ventilatory response seen during sleep, particularly NREM sleep, is likely to be multifactorial and not totally a product of decreasing central respiratory drive.

Reduction in Obstructive Breathing Events During Body Rocking: A Controlled Polygraphic Study in Preterm and Full-Term Infants

PEDIATRICS ◽  
1995 ◽  
Vol 96 (1) ◽  
pp. 64-68
Author(s):  
J. Groswasser ◽  
M. Sottiaux ◽  
E. Rebuffat ◽  
T. Simon ◽  
M. Vandeweyer ◽  
...  
Keyword(s):  
Eye Movement ◽  
Preterm Infants ◽  
Upper Airway ◽  
Periodic Breathing ◽  
Full Term ◽  
Rapid Eye Movement ◽  
Term Infants ◽  
Obstructive Sleep ◽  
Significant Difference ◽  
Obstructive Sleep Apneas

Objective. To investigate the effect of body rocking on infant respiratory behavior during sleep. Methods. Eighteen infants with documented obstructive sleep apneas were studied. There were eight premature infants with persistent bradycardias and 10 infants born full-term, admitted after an idiopathic apparent life-threatening event. No cause for the obstructive apneas was found. The infants were recorded with polygraphic techniques during two successive nights. They were randomly assigned to a rocking or a nonrocking mattress. The conditions were reversed the following night, in a crossover design. Results. In both groups of infants, no significant difference was seen between the two consecutive nights for most of the variables studied: total sleep time, the proportion of non-rapid-eye-movement and rapid-eye-movement sleep, the number of arousals, the number and maximal duration of central apneas, the frequency of periodic breathing, the level of oxygen saturation, and heart rate. During the nonrocking nights, all infants had repeated obstructive breathing events. In seven of the eight preterm infants and in nine of the 10 full-term subjects, body rocking was associated with a significant decrease in the frequency of obstructive events. During rocking, in the preterm infants the obstructions fell from a median of 2.5 to 1.8 episodes per hour (P = .034). In the full-term infants, rocking reduced the obstructive events from a median of 1.5 obstructions per hour to 0.7 (P = .005). No difference was seen for the duration of the obstructive episodes. Conclusion. In preterm and full-term infants prone to obstructive sleep apneas, gentle side-to-side body rocking is associated with a significant decrease in the frequency of upper-airway obstructions.

Hypocapnia and sustained hypoxia blunt ventilation on arrival at high altitude

1984 ◽  
Vol 56 (3) ◽  
pp. 602-606 ◽  
Author(s):  
S. Y. Huang ◽  
J. K. Alexander ◽  
R. F. Grover ◽  
J. T. Maher ◽  
R. E. McCullough ◽  
...  
Keyword(s):  
High Altitude ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Ventilatory Responses ◽  
Low Altitude ◽  
Arterial O2 Saturation ◽  
Sustained Hypoxia

Hypoxia at high altitude stimulates ventilation, but inhibitory influences in the first days after arrival limit the ventilatory response. Possible inhibitory influences include hypocapnia and depression of ventilation during sustained hypoxia. Our approach was to compare hypoxic ventilatory responses at low altitude with ventilation at high altitude. In 12 subjects we compared responses both to isocapnic hypoxia and poikilocapnic (no CO2 added) hypoxia during acute (less than 10 min) and sustained (30 min) hypoxia in Denver (1,600 m) with ventilations measured on each of 5 days on Pikes Peak (4,300 m). On Pikes Peak, day 1 ventilation [minute ventilation = 10.0 1/min, BTPS; arterial O2 saturation (Sao2) = 82%] was less than predicted by either acute isocapnic or poikilocapnic tests. However, sustained poikilocapnic hypoxia (Sao2 approximately = 82%) in Denver yielded ventilation similar to that on Pikes Peak on day 1. By Pikes Peak days 4 and 5, endtidal PCO2, pHa, and Sao2 approached plateaus, and ventilation (12.4 1/min, BTPS) on these days was as predicted by the acute isocapnic test. Thus the combination of hypocapnia and sustained hypoxia may have blunted the ventilatory increase on Pikes Peak day 1 but apparently not after 4 or 5 days of acclimatization.

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