Alterations in respiratory control during 8 h of isocapnic and poikilocapnic hypoxia in humans

1995 ◽  
Vol 78 (3) ◽  
pp. 1098-1107 ◽  
Author(s):  
L. S. Howard ◽  
P. A. Robbins
Keyword(s):  
Analysis Of Variance ◽  
Ventilatory Response ◽  
Acute Hypoxia ◽  
Respiratory Control ◽  
Companion Paper ◽  
Tidal Forcing ◽  
Nasal Catheter ◽  
The Subject ◽  
Per Se ◽  
End Tidal

In the preceding companion paper (L. S. G. E. Howard and P.A. Robbins, J. Appl. Physiol. 78: 1092–1097, 1995), we showed that ventilation rises during 8 h of isocapnic hypoxia. In the present study we report the changes that occur in the ventilatory response to acute hypoxia (AHVR) over 8 h of both isocapnic and poikilocapnic hypoxia. Ten subjects completed the study. Each was seated inside a chamber in which the inspired gas could be controlled so as to maintain the desired end-tidal gases (sampled via nasal catheter) constant. Three 8-h protocols were compared: 1) isocapnic hypoxia, at an end-tidal PO2 of 55 Torr with the end-tidal PCO2 held at the subject's resting value; 2) poikilocapnic hypoxia, at the same end-tidal PO2; and 3) control, where the inspired gas was air. AHVR was measured before and at 20 min and 4 and 8 h after the start of the experiment. A sequence of hypoxic square waves and sawtooth inputs was imposed by an end-tidal forcing system, with the subject breathing through a mouthpiece. End-tidal PCO2 was held constant at 1–1.5 Torr above resting. Values for hypoxic sensitivity (Gp; 1.min-1.%-1) and hypoxia-independent ventilation (Vc; l/min) were calculated for each test of AHVR. Both Gp and Vc increased significantly during both hypoxic exposures in relation to control (P < 0.001, analysis of variance). Over the 8-h period, increases in Gp were 87% in isocapnic hypoxia and 44% in poikilocapnic hypoxia, and increases in Vc were 89% in isocapnic hypoxia and 84% in poikilocapnic hypoxia. There were no significant differences between the isocapnic and poikilocapnic exposures. We conclude that Gp and Vc rise mainly as result of hypoxia per se and not the associated alkalosis.

Ventilatory response to 8 h of isocapnic and poikilocapnic hypoxia in humans

1995 ◽  
Vol 78 (3) ◽  
pp. 1092-1097 ◽  
Author(s):  
L. S. Howard ◽  
P. A. Robbins
Keyword(s):  
Analysis Of Variance ◽  
Ventilatory Response ◽  
Progressive Increase ◽  
Nasal Catheter ◽  
Partial Pressures ◽  
End Tidal ◽  
Almost All ◽  
And Control

Almost all studies of the effects of prolonged hypoxia on ventilation (VE) in humans have been performed with the end-tidal PCO2 (PETCO2) left uncontrolled. The purpose of this study was to compare the effects of 8 h of hypoxia with PETCO2 held constant with 8 h of hypoxia with PETCO2 left uncontrolled. Ten subjects completed the study. Each was seated inside a chamber in which the inspired gas could be controlled so as to maintain the desired partial pressures of end-tidal gases (sampled via nasal catheter) constant (see L.S.G.E. Howard et al. J. Appl. Physiol. 78:1088–1091, 1995.). Three 8-h protocols were employed: 1) isocapnic hypoxia, at an end-tidal PO2 of 55 Torr with PETCO2 held at the subject's resting value; 2) poikilocapnic hypoxia, at the same end-tidal PO2; and 3) control, where the inspired gas was air. VE was measured (over 3 min) at 0 and 20 min and at hourly intervals between 1.5 and 7.5 h. There was a rise in VE during isocapnic hypoxia [from an initial VE of 16.2 +/- 1.3 (SE) l/min to a final VE of 24.8 +/- 1.6 l/min], which was significant compared with poikilocapnic hypoxia and control values (P < 0.001, analysis of variance). There was no significant progressive rise in VE during poikilocapnic hypoxia compared with control values. These results show that isocapnic hypoxia produces a progressive increase in VE when sustained over an 8-h period. The onset of this response is faster than has been noted in studies of the progressive rise in VE associated with the poikilocapnic hypoxia of altitude.

Respiratory control in humans after 8 h of lowered arterial Po 2, hemodilution, or carboxyhemoglobinemia

2001 ◽  
Vol 90 (4) ◽  
pp. 1189-1195 ◽  
Author(s):  
Xiaohui Ren ◽  
Keith L. Dorrington ◽  
Peter A. Robbins
Keyword(s):  
Oxygen Content ◽  
Ventilatory Response ◽  
Acute Hypoxia ◽  
Venous Blood ◽  
Respiratory Control ◽  
Progressive Increase ◽  
Arterial Oxygen ◽  
Hypoxic Ventilatory Response ◽  
Arterial Oxygen Content ◽  
End Tidal

In humans exposed to 8 h of isocapnic hypoxia, there is a progressive increase in ventilation that is associated with an increase in the ventilatory sensitivity to acute hypoxia. To determine the relative roles of lowered arterial Po 2 and oxygen content in generating these changes, the acute hypoxic ventilatory response was determined in 11 subjects after four 8-h exposures: 1) protocol IH (isocapnic hypoxia), in which end-tidal Po 2 was held at 55 Torr and end-tidal Pco 2 was maintained at the preexposure value; 2) protocol PB (phlebotomy), in which 500 ml of venous blood were withdrawn; 3) protocol CO, in which carboxyhemoglobin was maintained at 10% by controlled carbon monoxide inhalation; and 4) protocol C as a control. Both hypoxic sensitivity and ventilation in the absence of hypoxia increased significantly after protocol IH ( P < 0.001 and P < 0.005, respectively, ANOVA) but not after the other three protocols. This indicates that it is the reduction in arterial Po 2 that is primarily important in generating the increase in the acute hypoxic ventilatory response in prolonged hypoxia. The associated reduction in arterial oxygen content is unlikely to play an important role.

Changes in respiratory control during and after 48 h of isocapnic and poikilocapnic hypoxia in humans

1998 ◽  
Vol 85 (6) ◽  
pp. 2125-2134 ◽  
Author(s):  
John G. Tansley ◽  
Marzieh Fatemian ◽  
Luke S. G. E. Howard ◽  
Marc J. Poulin ◽  
Peter A. Robbins
Keyword(s):  
Ventilatory Response ◽  
Respiratory Control ◽  
Hypoxic Ventilatory Response ◽  
Text Response ◽  
Per Se ◽  
Significant Change ◽  
End Tidal ◽  
Hypocapnic Alkalosis

Ventilatory acclimatization to hypoxia is associated with an increase in ventilation under conditions of acute hyperoxia (V˙e hyperoxia) and an increase in acute hypoxic ventilatory response (AHVR). This study compares 48-h exposures to isocapnic hypoxia ( protocol I) with 48-h exposures to poikilocapnic hypoxia ( protocol P) in 10 subjects to assess the importance of hypocapnic alkalosis in generating the changes observed in ventilatory acclimatization to hypoxia. During both hypoxic exposures, end-tidal [Formula: see text] was maintained at 60 Torr, with end-tidal [Formula: see text] held at the subject’s prehypoxic level ( protocol I) or uncontrolled ( protocol P).V˙e hyperoxiaand AHVR were assessed regularly throughout the exposures.V˙e hyperoxia( P < 0.001, ANOVA) and AHVR ( P < 0.001) increased during the hypoxic exposures, with no significant differences between protocols I and P. The increase inV˙e hyperoxiawas associated with an increase in slope of the ventilation-end-tidal [Formula: see text] response ( P < 0.001) with no significant change in intercept. These results suggest that changes in respiratory control early in ventilatory acclimatization to hypoxia result from the effects of hypoxia per se and not the alkalosis normally accompanying hypoxia.

Living high-training low increases hypoxic ventilatory response of well-trained endurance athletes

2002 ◽  
Vol 93 (4) ◽  
pp. 1498-1505 ◽  
Author(s):  
Nathan E. Townsend ◽  
Christopher J. Gore ◽  
Allan G. Hahn ◽  
Michael J. McKenna ◽  
Robert J. Aughey ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Control ◽  
Endurance Athletes ◽  
Hypoxic Exposure ◽  
Dependent Manner ◽  
Hypoxic Ventilatory Response ◽  
Ambient Conditions ◽  
Altitude Exposure ◽  
End Tidal

This study determined whether “living high-training low” (LHTL)-simulated altitude exposure increased the hypoxic ventilatory response (HVR) in well-trained endurance athletes. Thirty-three cyclists/triathletes were divided into three groups: 20 consecutive nights of hypoxic exposure (LHTLc, n = 12), 20 nights of intermittent hypoxic exposure (four 5-night blocks of hypoxia, each interspersed with 2 nights of normoxia, LHTLi, n = 10), or control (Con, n = 11). LHTLc and LHTLi slept 8–10 h/day overnight in normobaric hypoxia (∼2,650 m); Con slept under ambient conditions (600 m). Resting, isocapnic HVR (ΔV˙e/ΔSpO2 , whereV˙e is minute ventilation and SpO2 is blood O2 saturation) was measured in normoxia before hypoxia (Pre), after 1, 3, 10, and 15 nights of exposure (N1, N3, N10, and N15, respectively), and 2 nights after the exposure night 20 (Post). Before each HVR test, end-tidal Pco 2(Pet CO2 ) and V˙e were measured during room air breathing at rest. HVR (l · min−1 · %−1) was higher ( P < 0.05) in LHTLc than in Con at N1 (0.56 ± 0.32 vs. 0.28 ± 0.16), N3 (0.69 ± 0.30 vs. 0.36 ± 0.24), N10 (0.79 ± 0.36 vs. 0.34 ± 0.14), N15 (1.00 ± 0.38 vs. 0.36 ± 0.23), and Post (0.79 ± 0.37 vs. 0.36 ± 0.26). HVR at N15 was higher ( P < 0.05) in LHTLi (0.67 ± 0.33) than in Con and in LHTLc than in LHTLi. Pet CO2 was depressed in LHTLc and LHTLi compared with Con at all points after hypoxia ( P < 0.05). No significant differences were observed for V˙e at any point. We conclude that LHTL increases HVR in endurance athletes in a time-dependent manner and decreases Pet CO2 in normoxia, without change inV˙e. Thus endurance athletes sleeping in mild hypoxia may experience changes to the respiratory control system.

A fast gas-mixing system for breath-to-breath respiratory control studies

1982 ◽  
Vol 52 (5) ◽  
pp. 1358-1362 ◽  
Author(s):  
P. A. Robbins ◽  
G. D. Swanson ◽  
A. J. Micco ◽  
W. P. Schubert
Keyword(s):  
High Voltage ◽  
Special Form ◽  
Low Voltage ◽  
Respiratory Control ◽  
Gas Mixing ◽  
Tidal Forcing ◽  
Mixing Chamber ◽  
Computer Controlled ◽  
End Tidal ◽  
Gas Fractions

A computer-controlled gas-mixing system that manipulates inspired CO2 and O2 on a breath-to-breath basis has been developed. The system uses pairs of solenoid valves, one pair for each gas. These valves can either be fully shut when a low voltage is applied, or fully open when a high voltage is applied. The valves cycle open and shut every 1/12 s. A circuit converts signals from the computer, which dictates the flows of the gases, into a special form for driving the valve pairs. These signals determine the percentage of time within the 1/12-s cycle each valve spends in a open state and the percentage of time it spends shut, which, in effect, set the average flows of the various gases to the mixing chamber. The delay for response of the system to commanded CO2 or O2 changes is less than 200 ms. The system has application for the manipulation of inspired gas fractions so as to achieve desired end-tidal forcing functions.

Cardiorespiratory and cerebrovascular responses to acute poikilocapnic hypoxia following intermittent and continuous exposure to hypoxia in humans

2007 ◽  
Vol 102 (5) ◽  
pp. 1953-1961 ◽  
Author(s):  
Philip N. Ainslie ◽  
Alice Barach ◽  
Kevin J. Cummings ◽  
Carissa Murrell ◽  
Mike Hamlin ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Intermittent Hypoxia ◽  
Cerebral Perfusion ◽  
Ventilatory Response ◽  
Acute Hypoxia ◽  
Group Differences ◽  
Continuous Exposure ◽  
Artery Blood Flow ◽  
End Tidal

We tested the hypothesis that intermittent hypoxia (IH) and/or continuous hypoxia (CH) would enhance the ventilatory response to acute hypoxia (HVR), thereby altering blood pressure (BP) and cerebral perfusion. Seven healthy volunteers were randomly selected to complete 10–12 days of IH (5-min hypoxia to 5-min normoxia repeated for 90 min) before ascending to mild CH (1,560 m) for 12 days. Seven other volunteers did not receive any IH before ascending to CH for the same 12 days. Before the IH and CH, following 12 days of CH and 12–13 days post-CH exposure, all subjects underwent a 20-min acute exposure to poikilocapnic hypoxia (inspired fraction of O2, 0.12) in which ventilation, end-tidal gases, arterial O2 saturation, BP, and middle cerebral artery blood flow velocity (MCAV) were measured continuously. Following the IH and CH exposures, the peak HVR was elevated and was related to the increase in BP ( r = 0.66 to r = 0.88, respectively; P < 0.05) and to a reciprocal decrease in MCAV ( r = 0.73 to r = 0.80 vs. preexposures; P < 0.05) during the hypoxic test. Following both IH and CH exposures, HVR, BP, and MCAV sensitivity to hypoxia were elevated compared with preexposure, with no between-group differences following the IH and/or CH conditions, or persistent effects following 12 days of sea level exposure. Our findings indicate that IH and/or mild CH can equally enhance the HVR, which, by either direct or indirect mechanisms, facilitates alterations in BP and MCAV.

Control of breathing in Sherpas at low and high altitude

1980 ◽  
Vol 49 (3) ◽  
pp. 374-379 ◽  
Author(s):  
P. H. Hackett ◽  
J. T. Reeves ◽  
C. D. Reeves ◽  
R. F. Grover ◽  
D. Rennie
Keyword(s):  
High Altitude ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Arterial Oxygen Saturation ◽  
Carbon Dioxide Tension ◽  
Arterial Oxygen ◽  
Hypoxic Ventilatory Response ◽  
Oxygen Administration ◽  
End Tidal

Sherpas are well known for their physical performance at extreme altitudes, yet they are reported to have blunted ventilatory responses to acute hypoxia and relative hypoventilation in chronic hypoxia. To examine this paradox, we studied ventilatory control in Sherpas in comparison to that in Westerners at both low and high altitude. At low altitude, 25 Sherpas had higher minute ventilation, higher respiratory frequency, and lower end-tidal carbon dioxide tension than 25 Westerners. The hypoxic ventilatory response of Sherpas was found to be similar to that in Westerners, even though long altitude exposure had blunted the responses of some Sherpas. At high altitude, Sherpas again had higher minute ventilation and a tendency toward higher arterial oxygen saturation than Westerners. Oxygen administration increased ventilation further in Sherpas but decreased ventilation in Westerners. We conclude that Sherpas differ from other high-altitude natives; their hypoxic ventilatory response is not blunted, and they exhibit relative hyperventilation.

Variable inhibition by falling CO2 of hypoxic ventilatory response in humans

1984 ◽  
Vol 56 (1) ◽  
pp. 207-210 ◽  
Author(s):  
L. G. Moore ◽  
S. Y. Huang ◽  
R. E. McCullough ◽  
J. B. Sampson ◽  
J. T. Maher ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Acute Hypoxia ◽  
Hypoxic Ventilatory Response ◽  
Co2 Response ◽  
Low Co2 ◽  
Two Factors ◽  
Variable Extent ◽  
The Difference ◽  
End Tidal ◽  
Ventilatory Response To Co2

Acute hypoxia stimulates an increase in ventilation but the resulting hypocapnia limits the magnitude of the increase. Thus the hypoxic ventilatory response is usually measured during isocapnia, but this may not reflect events at high altitude. We hypothesized that the degree of inhibition by hypocapnia might depend on individual ventilatory response to CO2 and thus vary between persons. To test this hypothesis we compared the isocapnic hypoxic ventilatory response (end-tidal PCO2 maintained by CO2 addition) with the response in which CO2 was not added and the end-tidal PCO2 fell to a variable extent (poikilocapnic hypoxia). In 14 healthy persons we found that the poikilocapnic hypoxic ventilatory response was determined by two factors: sensitivity to isocapnic hypoxia acting to increase ventilation and sensitivity to CO2 acting to decrease the hypoxic ventilatory response. The ventilatory response to poikilocapnic hypoxia correlated with but was generally less than the isocapnic hypoxic response. The magnitude of the difference between them related to the hypercapnic response. Further, the results suggested that the CO2 response in the high CO2 range related to ventilatory events in the low CO2 range. Thus the magnitude of ventilatory inhibition by hypocapnia may depend on individual ventilatory responsiveness to CO2.

The process of cardiorespiratory autoresuscitation in intact newborn rats

2001 ◽  
Vol 79 (12) ◽  
pp. 1036-1043 ◽  
Author(s):  
Chikako Saiki ◽  
Mizuho Ikeda ◽  
Toshimi Nishikawa ◽  
Takeshi Tanimoto ◽  
Shinki Yoshida ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Acute Hypoxia ◽  
Recovery Period ◽  
Respiratory Control ◽  
Sudden Infant Death ◽  
Recovery Phase ◽  
Sudden Infant ◽  
Hypoxic Ventilatory Response ◽  
Newborn Rats ◽  
Heart Arrhythmia

To examine the process of spontaneous autoresuscitation and the recovery of the hypoxic ventilatory response (HVR) after prolonged anoxia, we monitored respiratory frequency (f, by body plethysmography) and heart rate (HR, by ECG) in intact newborn rats (n = 12, day 2–4) before, during, and after 100% N2 exposure. The rat before anoxia showed signs of HVR: f changes at acute hypoxia (10% O2) and hyperoxia (100% O2). During anoxia, the spontaneous respiratory movement "gasping" appeared for 21 min (mean). At O2 restoration (with 100% O2), gasping stopped and no respiratory flow was detected for 1 min. One rat failed to autoresuscitate and had heart arrhythmia during the transient apnea, but 11 rats recovered respiration after the HR acceleration. Despite the successful autoresuscitation, the rats did not show HVR at 10 min into the recovery period and the recovery of HVR required more than 30 min. The results indicate that O2 inhalation is useful to trigger autoresuscitation even when the rat has already been in a state of profound hypoxic depression, but the rat becomes transiently insensitive to HVR after autoresuscitation. We estimate that reform of the respiratory control system in newborn rats is not yet firmly established to track HVR early in the recovery phase after prolonged anoxia.Key words: anoxia, hypoxic ventilatory response, cardiopulmonary resuscitation (CPR), sudden infant death (SID).

Sign in / Sign up

Export Citation Format

Share Document