Alveolar Pco2 oscillations and ventilation at sea level and at high altitude

2008 ◽  
Vol 104 (2) ◽  
pp. 404-415 ◽  
Author(s):  
D. J. Collier ◽  
A. H. Nickol ◽  
J. S. Milledge ◽  
H. J. A. van Ruiten ◽  
C. J. Collier ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Respiratory Control ◽  
Cycle Ergometer ◽  
Feedback Signal ◽  
Ventilatory Responses ◽  
Base Camp ◽  
Ventilatory Drive ◽  
The Face ◽  
End Tidal

This study examines the potential for a ventilatory drive, independent of mean Pco2, but depending instead on changes in Pco2 that occur during the respiratory cycle. This responsiveness is referred to here as “dynamic ventilatory sensitivity.” The normal, spontaneous, respiratory oscillations in alveolar Pco2 have been modified with inspiratory pulses approximating alveolar Pco2 concentrations, both at sea level and at high altitude (5,000 m, 16,400 ft.). All tests were conducted with subjects exercising on a cycle ergometer at 60 W. The pulses last about half the inspiratory duration and are timed to arrive in the alveoli during early or late inspiration. Differences in ventilation, which then occur in the face of similar end-tidal Pco2 values, are taken to result from dynamic ventilatory sensitivity. Highly significant ventilatory responses (early pulse response greater than late) occurred in hypoxia and normoxia at sea level and after more than 4 days at 5,000 m. The response at high altitude was eliminated by normalizing Po2 and was reduced or eliminated with acetazolamide. No response was present soon after arrival (<4 days) at base camp, 5,000 m, on either of two high-altitude expeditions (BMEME, 1994, and Kanchenjunga, 1998). The largest responses at 5,000 m were obtained in subjects returning from very high altitude (7,100–8,848 m). The present study confirms and extends previous investigations that suggest that alveolar Pco2 oscillations provide a feedback signal for respiratory control, independent of changes in mean Pco2, suggesting that natural Pco2 oscillations drive breathing in exercise.

Effects of a 1-yr stay at altitude on ventilation, metabolism, and work capacity

1992 ◽  
Vol 73 (5) ◽  
pp. 1749-1755 ◽  
Author(s):  
T. V. Serebrovskaya ◽  
A. A. Ivashkevich
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Ventilatory Response ◽  
Second Phase ◽  
Separate Analysis ◽  
Group Iii ◽  
Group I ◽  
Ventilatory Drive ◽  
Group Ii ◽  
End Tidal

The hypoxic and hypercapnic ventilatory drive, gas exchange, blood lactate and pyruvate concentrations, acid-base balance, and physical working capacity were determined in three groups of healthy males: 17 residents examined at sea level (group I), 24 sea-level natives residing at 1,680-m altitude for 1 yr and examined there (group II), and 17 sea-level natives residing at 3,650-m altitude for 1 yr and examined there (group III). The piecewise linear approximation technique was used to study the ventilatory response curves, which allowed a separate analysis of slopes during the first phase of slow increase in ventilation and the second phase of sharp increase. The hypoxic ventilatory response for both isocapnic and poikilocapnic conditions was greater in group II and even greater in group III. The first signs of consciousness distortion in sea-level residents appeared at an end-tidal O2 pressure level (4.09 +/- 0.56 kPa) higher than that of temporary residents of middle (3.05 +/- 0.12) and high altitude (2.90 +/- 0.07). The hypercapnic response was also increased, although to a lesser degree. Subjects with the highest hypoxic respiratory sensitivity at high altitude demonstrated greater O2 consumption at rest, greater ventilatory response to exercise, higher physical capacity, and a less pronounced anaerobic glycolytic flux but a lower tolerance to extreme hypoxia. That is, end-tidal O2 pressure that caused a distortion of the consciousness was higher in these subjects than in those with lower hypoxic sensitivity. Two extreme types of adaptation strategy can be distinguished: active, with marked reactions of “struggle for oxygen,” and passive, with reduced O2 metabolism, as well as several intermediate types.(ABSTRACT TRUNCATED AT 250 WORDS)

Selected Contribution: Acute and sustained ventilatory responses to hypoxia in high-altitude natives living at sea level

2003 ◽  
Vol 94 (3) ◽  
pp. 1255-1262 ◽  
Author(s):  
Alfredo Gamboa ◽  
Fabiola León-Velarde ◽  
Maria Rivera-Ch ◽  
Jose-Antonio Palacios ◽  
Timothy R. Pragnell ◽  
...  
Keyword(s):  
Confidence Interval ◽  
High Altitude ◽  
Sea Level ◽  
Hypoxic Exposure ◽  
Ventilatory Responses ◽  
High Altitude Natives ◽  
Ventilatory Depression ◽  
End Tidal ◽  
Sustained Hypoxia

High-altitude (HA) natives have blunted ventilatory responses to hypoxia (HVR), but studies differ as to whether this blunting is lost when HA natives migrate to live at sea level (SL), possibly because HVR has been assessed with different durations of hypoxic exposure (acute vs. sustained). To investigate this, 50 HA natives (>3,500 m, for >20 yr) now resident at SL were compared with 50 SL natives as controls. Isocapnic HVR was assessed by using two protocols: protocol 1, progressive stepwise induction of hypoxia over 5–6 min; and protocol 2, sustained (20-min) hypoxia (end-tidal Po 2 = 50 Torr). Acute HVR was assessed from both protocols, and sustained HVR from protocol 2. For HA natives, acute HVR was 79% [95% confidence interval (CI): 52–106%, P = not significant] of SL controls for protocol 1 and 74% (95% CI: 52–96%, P < 0.05) for protocol 2. By contrast, sustained HVR after 20-min hypoxia was only 30% (95% CI: −7–67%, P < 0.001) of SL control values. The persistent blunting of HVR of HA natives resident at SL is substantially less to acute than to sustained hypoxia, when hypoxic ventilatory depression can develop.

scholarly journals Changes in respiratory control in humans induced by 8 h of hyperoxia

2000 ◽  
Vol 89 (2) ◽  
pp. 655-662 ◽  
Author(s):  
Xiaohui Ren ◽  
Marzieh Fatemian ◽  
Peter A. Robbins
Keyword(s):  
Sea Level ◽  
Respiratory Control ◽  
Control Ventilation ◽  
Initial Increase ◽  
Air Breathing ◽  
Ventilatory Responses ◽  
End Tidal

In humans, 8 h of isocapnic hypoxia causes a progressive rise in ventilation associated with increases in the acute ventilatory responses to hypoxia (AHVR) and hypercapnia (AHCVR). To determine whether 8 h of hyperoxia causes the converse of these effects, three 8-h protocols were compared in 14 subjects: 1) poikilocapnic hyperoxia, with end-tidal Po 2 (Pet O2 ) = 300 Torr and end-tidal Pco 2(Pet CO2 ) uncontrolled; 2) isocapnic hyperoxia, with Pet O2 = 300 Torr and Pet CO2 maintained at the subject's normal air-breathing level; and 3) control. Ventilation was measured hourly. AHVR and AHCVR were determined before and 0.5 h after each exposure. During isocapnic hyperoxia, after an initial increase, ventilation progressively declined ( P< 0.01, ANOVA). After exposure to hyperoxia, 1) AHVR declined ( P < 0.05); 2) ventilation at fixed Pet CO2 decreased ( P< 0.05); and 3) air-breathing Pet CO2 increased ( P < 0.05); but 4) no significant changes in AHCVR or intercept were demonstrated. In conclusion, 8 h of hyperoxia have some effects opposite to those found with 8 h of hypoxia, indicating that there may be some “acclimatization to hypoxia” at normal sea-level values of Po 2.

Energy expenditure during load carriage at high altitude

1981 ◽  
Vol 51 (1) ◽  
pp. 14-18 ◽  
Author(s):  
A. Cymerman ◽  
K. B. Pandolf ◽  
A. J. Young ◽  
J. T. Maher
Keyword(s):  
Energy Expenditure ◽  
High Altitude ◽  
Sea Level ◽  
Prediction Equation ◽  
Cycle Ergometer ◽  
Load Carriage ◽  
Metabolic Rates ◽  
Specific Exercise ◽  
Upper Limit ◽  
Predicted Values

To determine the applicability of a prediction equation for energy expenditure during load carriage at high altitude that was previously validated at sea level, oxygen uptake (Vo2) was determined in five young men at 4,300 m while they walked with backpack loads of 0, 15, and 30 kg at treadmill grades of 0,8, and 16% at 1.12 m.s-1 for 10 min. Mean +/- SE maximal Vo2, determined on the cycle ergometer, was 42.2 +/- 2.3 at sea level and 35.6 +/- 1.7 ml.kg-1 .min-1 at altitude. There were no significant differences in daily Vo2 at any specific exercise intensity on days 1, 5, and 9 of exposure, nor were there any differences in endurance times at the two most difficult exercise intensities. Endurance times for 15- and 30-kg loads at 16% grade were 7.3 and 4.2 min, respectively. Measured energy expenditure was compared with that predicted by the formula of Pandolf et al. (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 43: 577–581, 1977) and found to be significantly different. The differences could be attributed to measurements at metabolic rates exceeding 730 W or 2.1 1.min-1 Vo2. These data indicate that the prediction equation can be used at altitude for exercise intensities not exceeding this upper limit. The observed deviations from predicted values at the high exercise intensities could possibly be attributed to the occurrence of appreciable oxygen deficits and the inability to achieve steady-state conditions.

Alteration by hyperoxia of ventilatory dynamics during sinusoidal work

1980 ◽  
Vol 48 (6) ◽  
pp. 1083-1091 ◽  
Author(s):  
R. Casaburi ◽  
R. W. Stremel ◽  
B. J. Whipp ◽  
W. L. Beaver ◽  
K. Wasserman
Keyword(s):  
Gas Exchange ◽  
Work Load ◽  
Cycle Ergometer ◽  
Work Rate ◽  
Phase Lag ◽  
Ventilatory Responses ◽  
Load Tests ◽  
The Mean ◽  
End Tidal ◽  
End Tidal Co2

The effects of hyperoxia on ventilatory and gas exchange dynamics were studied utilizing sinusoidal work rate forcings. Five subjects exercised on 14 occasions on a cycle ergometer for 30 min with a sinusoidally varying work load. Tests were performed at seven frequencies of work load during air or 100% O2 inspiration. From the breath-by-breath responses to these tests, dynamic characteristics were analyzed by extracting the mean level, amplitude of oscillation, and phase lag for each six variables with digital computer techniques. Calculation of the time constant (tau) of the ventilatory responses demonstrated that ventilatory kinetics were slower during hyperoxia than during normoxia (P less than 0.025; avg 1.56 and 1.13 min, respectively). Further, for identical work rate fluctuations, end-tidal CO2 tension fluctuations were increased by hyperpoxia. Ventilation during hyperoxia is slower to respond to variations in the level of metabolically produced CO2, presumably because hyperoxia attenuates carotid body output; the arterial CO2 tension is consequently less tightly regulated.

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 Adenosine receptor-dependent signaling is not obligatory for normobaric and hypobaric hypoxia-induced cerebral vasodilation in humans

2017 ◽  
Vol 122 (4) ◽  
pp. 795-808 ◽  
Author(s):  
Ryan L. Hoiland ◽  
Anthony R. Bain ◽  
Michael M. Tymko ◽  
Mathew G. Rieger ◽  
Connor A. Howe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Sea Level ◽  
Adenosine Receptor ◽  
Hypobaric Hypoxia ◽  
End Tidal ◽  
Double Blinded

Hypoxia increases cerebral blood flow (CBF) with the underlying signaling processes potentially including adenosine. A randomized, double-blinded, and placebo-controlled design, was implemented to determine if adenosine receptor antagonism (theophylline, 3.75 mg/Kg) would reduce the CBF response to normobaric and hypobaric hypoxia. In 12 participants the partial pressures of end-tidal oxygen ([Formula: see text]) and carbon dioxide ([Formula: see text]), ventilation (pneumotachography), blood pressure (finger photoplethysmography), heart rate (electrocardiogram), CBF (duplex ultrasound), and intracranial blood velocities (transcranial Doppler ultrasound) were measured during 5-min stages of isocapnic hypoxia at sea level (98, 90, 80, and 70% [Formula: see text]). Ventilation, [Formula: see text] and [Formula: see text], blood pressure, heart rate, and CBF were also measured upon exposure (128 ± 31 min following arrival) to high altitude (3,800 m) and 6 h following theophylline administration. At sea level, although the CBF response to hypoxia was unaltered pre- and postplacebo, it was reduced following theophylline ( P < 0.01), a finding explained by a lower [Formula: see text] ( P < 0.01). Upon mathematical correction for [Formula: see text], the CBF response to hypoxia was unaltered following theophylline. Cerebrovascular reactivity to hypoxia (i.e., response slope) was not different between trials, irrespective of [Formula: see text]. At high altitude, theophylline ( n = 6) had no effect on CBF compared with placebo ( n = 6) when end-tidal gases were comparable ( P > 0.05). We conclude that adenosine receptor-dependent signaling is not obligatory for cerebral hypoxic vasodilation in humans. NEW & NOTEWORTHY The signaling pathways that regulate human cerebral blood flow in hypoxia remain poorly understood. Using a randomized, double-blinded, and placebo-controlled study design, we determined that adenosine receptor-dependent signaling is not obligatory for the regulation of human cerebral blood flow at sea level; these findings also extend to high altitude.

Augmented hypoxic ventilatory response in men at altitude

1992 ◽  
Vol 73 (1) ◽  
pp. 101-107 ◽  
Author(s):  
M. Sato ◽  
J. W. Severinghaus ◽  
F. L. Powell ◽  
F. D. Xu ◽  
M. J. Spellman
Keyword(s):  
Sea Level ◽  
Ventilatory Response ◽  
Hypoxic Ventilatory Response ◽  
Co2 Response ◽  
Altitude Exposure ◽  
Arterial Ph ◽  
Ventilatory Drive ◽  
Normal Males ◽  
End Tidal ◽  
Arterial O2 Saturation

To test the hypothesis that the hypoxic ventilatory response (HVR) of an individual is a constant unaffected by acclimatization, isocapnic 5-min step HVR, as delta VI/delta SaO2 (l.min-1.%-1, where VI is inspired ventilation and SaO2 is arterial O2 saturation), was tested in six normal males at sea level (SL), after 1–5 days at 3,810-m altitude (AL1-3), and three times over 1 wk after altitude exposure (PAL1-3). Equal medullary central ventilatory drive was sought at both altitudes by testing HVR after greater than 15 min of hyperoxia to eliminate possible ambient hypoxic ventilatory depression (HVD), choosing for isocapnia a P′CO2 (end tidal) elevated sufficiently to drive hyperoxic VI to 140 ml.kg-1.min-1. Mean P′CO2 was 45.4 +/- 1.7 Torr at SL and 33.3 +/- 1.8 Torr on AL3, compared with the respective resting control end-tidal PCO2 of 42.3 +/- 2.0 and 30.8 +/- 2.6 Torr. SL HVR of 0.91 +/- 0.38 was unchanged on AL1 (30 +/- 18 h) at 1.04 +/- 0.37 but rose (P less than 0.05) to 1.27 +/- 0.57 on AL2 (3.2 +/- 0.8 days) and 1.46 +/- 0.59 on AL3 (4.8 +/- 0.4 days) and remained high on PAL1 at 1.44 +/- 0.54 and PAL2 at 1.37 +/- 0.78 but not on PAL3 (days 4–7). HVR was independent of test SaO2 (range 60–90%). Hyperoxic HCVR (CO2 response) was increased on AL3 and PAL1. Arterial pH at congruent to 65% SaO2 was 7.378 +/- 0.019 at SL, 7.44 +/- 0.018 on AL2, and 7.412 +/- 0.023 on AL3.(ABSTRACT TRUNCATED AT 250 WORDS)

Alveolar P CO 2 and P O 2 of high-altitude natives living at sea level

1996 ◽  
Vol 81 (4) ◽  
pp. 1605-1609 ◽  
Author(s):  
Fabiola León-Velarde ◽  
Manuel Vargas ◽  
Carlos Monge-C. ◽  
Robert W. Torrance ◽  
Peter A. Robbins
Keyword(s):  
Confidence Interval ◽  
High Altitude ◽  
Sea Level ◽  
Average Difference ◽  
Control Subjects ◽  
High Altitude Natives ◽  
End Tidal

León-Velarde, Fabiola, Manuel Vargas, Carlos Monge-C., Robert W. Torrance, and Peter A. Robbins. Alveolar[Formula: see text] and[Formula: see text] of high-altitude natives living at sea level. J. Appl. Physiol. 81(4): 1605–1609, 1996.—This study was designed to determine whether subjects born at high altitude (HA; 2,000 m or above) who subsequently move to near sea level (SL) develop end-tidal [Formula: see text]([Formula: see text]) and[Formula: see text]([Formula: see text]) values that equal those of SL natives living near SL. A total of 108 male HA natives living near SL were identified by survey of a district in Lima, Peru, and a further 108 male SL natives from the same district were identified as control subjects. Of these subjects, satisfactory data for inclusion in the study were obtained from 93 HA and 82 SL subjects. Mean [Formula: see text] and[Formula: see text] values were 37.7 ± 2.5 (SD) and 104.7 ± 3.2 Torr, respectively, in HA subjects and 37.7 ± 2.2 and 104.8 ± 3.0 Torr, respectively, in SL subjects. The average difference between SL natives and HA natives for[Formula: see text] was 0.07 Torr (−0.64 to 0.78; 95% confidence interval) and for[Formula: see text] was 0.05 Torr (−0.89 to 0.99, 95% confidence interval). The average age and weight of the SL and HA subjects did not differ, but the HA subjects were shorter and tended to have larger vital capacities, consistent with their origin at HA. We conclude that the[Formula: see text] and[Formula: see text] near SL of SL natives and HA natives do not differ.

scholarly journals UBC-Nepal expedition: markedly lower cerebral blood flow in high-altitude Sherpa children compared with children residing at sea level

2017 ◽  
Vol 123 (4) ◽  
pp. 1003-1010 ◽  
Author(s):  
Daniela Flück ◽  
Laura E. Morris ◽  
Shailesh Niroula ◽  
Christine M. Tallon ◽  
Kami T. Sherpa ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Saturation ◽  
High Altitude ◽  
Sea Level ◽  
Vessel Diameter ◽  
Cerebral Hemodynamic ◽  
Hemodynamic Pattern ◽  
End Tidal

Developmental cerebral hemodynamic adaptations to chronic high-altitude exposure, such as in the Sherpa population, are largely unknown. To examine hemodynamic adaptations in the developing human brain, we assessed common carotid (CCA), internal carotid (ICA), and vertebral artery (VA) flow and middle cerebral artery (MCA) velocity in 25 (9.6 ± 1.0 yr old, 129 ± 9 cm, 27 ± 8 kg, 14 girls) Sherpa children (3,800 m, Nepal) and 25 (9.9 ± 0.7 yr old, 143 ± 7 cm, 34 ± 6 kg, 14 girls) age-matched sea level children (344 m, Canada) during supine rest. Resting gas exchange, blood pressure, oxygen saturation and heart rate were assessed. Despite comparable age, height and weight were lower (both P < 0.01) in Sherpa compared with sea level children. Mean arterial pressure, heart rate, and ventilation were similar, whereas oxygen saturation (95 ± 2 vs. 99 ± 1%, P < 0.01) and end-tidal Pco2 (24 ± 3 vs. 36 ± 3 Torr, P < 0.01) were lower in Sherpa children. Global cerebral blood flow was ∼30% lower in Sherpa compared with sea level children. This was reflected in a lower ICA flow (283 ± 108 vs. 333 ± 56 ml/min, P = 0.05), VA flow (78 ± 26 vs. 118 ± 35 ml/min, P < 0.05), and MCA velocity (72 ± 14 vs. 88 ± 14 cm/s, P < 0.01). CCA flow was similar between Sherpa and sea level children (425 ± 92 vs. 441 ± 81 ml/min, P = 0.52). Scaling flow and oxygen uptake for differences in vessel diameter and body size, respectively, led to the same findings. A lower cerebral blood flow in Sherpa children may reflect specific cerebral hemodynamic adaptations to chronic hypoxia. NEW & NOTEWORTHY Cerebral blood flow is lower in Sherpa children compared with children residing at sea level; this may reflect a cerebral hemodynamic pattern, potentially due to adaptation to a hypoxic environment.

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