Cardiovascular and ventilatory response to isocapnic hypoxia at sea level and at 5,050 m

1996 ◽  
Vol 80 (5) ◽  
pp. 1724-1730 ◽  
Author(s):  
G. Insalaco ◽  
S. Romano ◽  
A. Salvaggio ◽  
A. Braghiroli ◽  
P. Lanfranchi ◽  
...  
Keyword(s):  
Oxygen Saturation ◽  
Sea Level ◽  
Minute Ventilation ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Ventilatory Responses ◽  
Hypoxic Conditions ◽  
Progressive Hypoxia ◽  
End Tidal ◽  
End Tidal Co2

To assess the effect of chronic hypoxic conditions on ventilatory, heart rate (HR), and blood pressure (BP) responses to acute progressive isocapnic hypoxia, we studied five healthy Caucasian subjects (3 men and 2 women). Each subject performed one rebreathing test at sea level (SL) and two tests at the Pyramid laboratory at Lobuche, Nepal, at the altitude of 5,050 m, 1 day after arrival (HA1) and after 24 days of sojourn (HA2). The effects of progressive isocapnic hypoxia were tested by using a standard rebreathing technique. BP, electrocardiogram, arterial oxygen saturation, airflow and end-tidal CO2 and O2 were recorded. For each subject, the relationships between arterial oxygen saturation and HR, systolic BP and minute ventilation (VE), respectively, were evaluated. At HA1, the majority of subjects showed a significant increase in VE and BP response and a decrease in HR response to progressive isocapnic hypoxia as compared to SL. At HA2, VE and BP responses further increased, whereas the HR response remained similar to that observed at HA1. A significant relationship between hypoxic ventilatory responses and both systolic and diastolic BP responses to progressive hypoxia was found. No significant correlation was found between hypoxic ventilatory and HR responses.

Heart rate response to isocapnic hypoxia in conscious man

1978 ◽  
Vol 234 (2) ◽  
pp. H129-H132 ◽  
Author(s):  
A. S. Slutsky ◽  
A. S. Rebuck
Keyword(s):  
Heart Rate ◽  
Oxygen Saturation ◽  
Heart Rate Response ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Ventilatory Responses ◽  
Progressive Hypoxia ◽  
The Subject ◽  
End Tidal ◽  
Mixed Venous

We studied the effect of acute progressive hypoxia on heart rate in conscious healthy subjects. The PCO2 was held constant (+/- 1.5 mmHg) midway between the resting end-tidal and mixed-venous levels. Hypoxia was induced by having the subject rebreathe from a small bag so that the PO2 fell at a rate related to the subject's oxygen consumption. Arterial oxygen saturation (Sao2) was measured continuously during the procedure with an ear oximeter. We found that heart rate (HR) was best fitted to an inverse linear relation to arterial oxygen saturation and a power relation to PO2. The range of deltaHR/deltaSao2 was 0.62-1.46 beats/min per 1% fall in Sao2 (mean +/- SE = 0.98 +/- 0.06). There was no relationship between heart rate and ventilatory responses to hypoxia.

scholarly journals Erythropoiesis in women during 11 days at 4,300 m is not affected by menstrual cycle phase

2001 ◽  
Vol 91 (6) ◽  
pp. 2579-2586 ◽  
Author(s):  
John T. Reeves ◽  
Stacy Zamudio ◽  
Thomas E. Dahms ◽  
Ingrid Asmus ◽  
Barry Braun ◽  
...  
Keyword(s):  
Menstrual Cycle ◽  
Oxygen Saturation ◽  
Cell Volume ◽  
Sea Level ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Cycle Phase ◽  
Red Cell ◽  
Menstrual Cycle Phase ◽  
Red Cell Volume

Because the ovarian steroid hormones, progesterone and estrogen, have higher blood levels in the luteal (L) than in the follicular (F) phase of the menstrual cycle, and because of their known effects on ventilation and hematopoiesis, we hypothesized that less hypoxemia and less erythropoiesis would occur in the L than the F phase of the cycle after arrival at altitude. We examined erythropoiesis with menstrual cycle phase in 16 women (age 22.6 ± 0.6 yr). At sea level, 11 of 16 women were studied during both menstrual cycle phases, and, where comparison within women was available, cycle phase did not alter erythropoietin ( n= 5), reticulocyte count ( n = 10), and red cell volume ( n = 9). When all 16 women were taken for 11 days to 4,300-m altitude (barometric pressure = 462 mmHg), paired comparisons within women showed no differences in ovarian hormone concentrations at sea level vs. altitude on menstrual cycle day 3 or 10 for either the F ( n = 11) or the L ( n = 5) phase groups. Arterial oxygen saturation did not differ between the F and L groups at altitude. There were no differences by cycle phase on day 11 at 4,300 m for erythropoietin [22.9 ± 4.7 (L) vs. 18.8 ± 3.4 mU/ml (F)], percent reticulocytes [1.9 ± 0.1 (L) vs. 2.1 ± 0.3% (F)], hemoglobin [13.5 ± 0.3 (L) vs. 13.7 ± 0.3 g/100 ml (F)], percent hematocrit [40.6 ± 1.4 (L) vs. 40.7 ± 1.0% (F)], red cell volume [31.1 ± 3.6 (L) vs. 33.0 ± 1.6 ml/kg (F)], and blood ferritin [8.9 ± 1.7 (L) vs. 10.2 ± 0.9 μg/l (F)]. Blood level of erythropoietin was related ( r= 0.77) to arterial oxygen saturation but not to the levels of progesterone or estradiol. We conclude that erythropoiesis was not altered by menstrual cycle phase during the first days at 4,300-m altitude.

P6480Asymmetric dimethylarginine (ADMA) predicts altitude-associated hypoxic pulmonary arterial hypertension

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
R H Boeger ◽  
P Siques ◽  
J Brito ◽  
E Schwedhelm ◽  
E Pena ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Logistic Regression ◽  
Oxygen Saturation ◽  
High Altitude ◽  
Sea Level ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Arterial Blood ◽  
Pulmonary Arterial

Abstract Prolonged exposure to altitude-associated chronic hypoxia (CH) may cause high altitude pulmonary hypertension (HAPH). Chronic intermittent hypobaric hypoxia (CIH) occurs in individuals who commute between sea level and high altitude. CIH is associated with repetitive acute hypoxic acclimatization and conveys the long-term risk of HAPH. As nitric oxide (NO) is an important regulator of systemic and pulmonary vascular tone and asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NO synthesis that increases in hypoxia, we aimed to investigate whether ADMA predicts the incidence of HAPH among Chilean frontiers personnel exposed to six months of CIH. We performed a prospective study of 123 healthy male subjects who were subjected to CIH (5 days at appr. 3,550 m, followed by 2 days at sea level) for six months. ADMA, SDMA, L-arginine, arterial oxygen saturation, systemic arterial blood pressure, and haematocrit were measured at baseline and at months 1, 4, and 6 at high altitude. Acclimatization to high altitude was determined using the Lake Louise Score and the presence of acute mountain sickness (AMS). Echocardiography was performed after six months of CIH in a subgroup of 43 individuals with either good (n=23) or poor (n=20) aclimatization to altitude, respectively. Logistic regression was used to assess the association of biomarkers with HAPH. 100 study participants aged 18.3±1.3 years with complete data sets were included in the final analysis. Arterial oxygen saturation decreased upon the first ascent to altitude and plateaued at about 90% during the further course of the study. Haematocrit increased to about 47% after one month and remained stable thereafter. ADMA continuously increased and SDMA decreased during the study course, whilst L-arginine levels showed no distinct pattern. The incidence of AMS and the Lake Louise Score were high after the first ascent (53 and 3.1±2.4, respectively) and at one month of CIH (47 and 3.0±2.6, respectively), but decreased to 20 and 1.4±2.0 at month 6, respectively (both p<0.001 for trend). In echocardiography, 18 participants (42%) showed a mean pulmonary arterial pressure (mPAP) greater than 25 mm Hg (mean ± SD, 30.4±3.9 mm Hg), out of which 9 (21%) were classified as HAPH (mPAP ≥30 mm Hg; mean ± SD, 33.9±2.2 mm Hg). Baseline ADMA, but not SDMA, was significantly associated with mPAP at month 6 in univariate logistic regression analysis (R = 0.413; p=0.007). In ROC analysis, a cut-off for baseline ADMA of 0.665 μmol/l was determined as the optimal cut-off level to predict HAPH (mPAP >30 mm Hg) with a sensitivity of 100% and a specificity of 63.6%. ADMA concentration increases during long-term CIH. It is an independent predictive biomarker for the incidence of HAPH. SDMA concentration decreases during CIH and shows no association with HAPH. Our data support a role of impaired NO-mediated pulmonary vasodilation in the pathogenesis of high altitude pulmonary hypertension. Acknowledgement/Funding CONICYT/FONDEF/FONIS Sa 09I20007; FIC Tarapaca BIP 30477541-0; BMBF grant 01DN17046 (DECIPHER); Georg & Jürgen Rickertsen Foundation, Hamburg

Sea-level PCO2 relates to ventilatory acclimatization at 4,300 m

1993 ◽  
Vol 75 (3) ◽  
pp. 1117-1122 ◽  
Author(s):  
J. T. Reeves ◽  
R. E. McCullough ◽  
L. G. Moore ◽  
A. Cymerman ◽  
J. V. Weil
Keyword(s):  
Sea Level ◽  
Ventilatory Response ◽  
Arterial Oxygen Saturation ◽  
Barometric Pressure ◽  
Interindividual Variation ◽  
Arterial Oxygen ◽  
Hypoxic Ventilatory Response ◽  
Wide Range ◽  
Time Required ◽  
End Tidal

There is considerable variation among individuals in the extent of, and the time required for, ventilatory acclimatization to altitude. Factors related to this variation are unclear. The present study tested whether interindividual variation in preascent ventilation or magnitude of hypoxic ventilatory response related to ventilatory acclimatization to altitude. Measurements in 37 healthy resting male subjects at sea level indicated a wide range (34–48 Torr) of end-tidal PCO2 values. When these subjects were taken to Pikes Peak, CO (4,300 m, barometric pressure 462 mmHg), the end-tidal PCO2 values measured on arrival and repeatedly over 19 days were correlated with the sea-level end-tidal PCO2. At 4,300 m, subjects with high end-tidal PCO2 had low values of arterial oxygen saturation (SaO2). Also, sea-level end-tidal PCO2 related to SaO2 after 19 days at 4,300 m. Twenty-six of the subjects had measurements of isocapnic hypoxic ventilatory response (HVR) at sea level. The end-tidal PCO2 values on arrival and after 19 days residence at 4,300 m were inversely related to the sea-level HVR values. Thus both the PCO2 and the HVR as measured at sea level related to the extent of subsequent ventilatory acclimatization (decrease in end-tidal PCO2) and the level of oxygenation at altitude. The finding in our cohort of subjects that sea-level end-tidal PCO2 was inversely related to HVR raised the possibility that among individuals the magnitude of the hypoxic drive to breathe influenced the amount of ventilation at all altitudes, including sea level.

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.

Low chemoresponsiveness and inadequate hyperventilation contribute to exercise-induced hypoxemia

1995 ◽  
Vol 79 (2) ◽  
pp. 575-580 ◽  
Author(s):  
C. A. Harms ◽  
J. M. Stager
Keyword(s):  
Oxygen Consumption ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Arterial Oxygen Saturation ◽  
Maximal Oxygen Consumption ◽  
Co2 Production ◽  
Arterial Oxygen ◽  
Ventilatory Parameters ◽  
Exercise Induced ◽  
End Tidal

Is inadequate hyperventilation a cause of the exercise-induced hypoxemia observed in some athletes during intense exercise? If so, is this related to low chemoresponsiveness? To test the hypothesis that exercise-induced hypoxemia, inadequate hyperventilation, and chemoresponsiveness are related, 36 nonsmoking healthy men were divided into hypoxemic (Hyp; n = 13) or normoxemic (Nor; n = 15) groups based on arterial oxygen saturation (SaO2; Hyp < or = 90%, Nor > 92%) observed during maximum O2 uptake (VO2max). Men with intermediate SaO2 values (n = 8) were only included in correlation analysis. Ventilatory parameters were collected at rest, during a treadmill maximal oxygen consumption (VO2max) test, and during a 5-min run at 90% VO2max. Chemoresponsiveness at rest was assessed via hypoxic ventilatory response (HVR) and hypercapnic ventilatory response (HCVR). VO2max was not significantly different between Nor and Hyp. SaO2 was 93.8 +/- 0.9% (Nor) and 87.7 +/- 2.0% (Hyp) at VO2max. End-tidal PO2 and the ratio of minute ventilation to oxygen consumption (VE/VO2) were lower while PETCO2 was higher for Hyp (P < or = 0.01). End-tidal PO2, end-tidal PCO2, and VE/VO2 correlated (P < or = 0.05) to SaO2 (r = 0.84, r = -0.70, r = 0.72, respectively), suggesting that differences in oxygenation were due to differences in ventilation. HVR and HCVR were significantly lower for Hyp. HVR was related to VE/VO2 (r = 0.43), and HCVR was related to the ratio of VE to CO2 production at VO2max (r = 0.61)

Effect of Almitrine on Hypoxic Ventilatory Drive Measured by Transient and Progressive Isocapnic Hypoxia in Normal Men

1989 ◽  
Vol 77 (4) ◽  
pp. 431-437 ◽  
Author(s):  
M. A. A. Airlie ◽  
D. C. Flenley ◽  
P. M. Warren
Keyword(s):  
Oxygen Saturation ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Controlled Study ◽  
Peripheral Chemoreceptor ◽  
Ventilatory Drive ◽  
The Difference ◽  
Normal Men

1. In a double-blind placebo-controlled study, we have investigated the effect of the peripheral chemoreceptor stimulant drug almitrine bismesylate on hypoxic ventilatory drive (expressed as the slope of the minute ventilation/arterial oxygen saturation relationship in litres min−1 %−1) as measured by both progressive isocapnic hypoxia at rest and transient hypoxia (three breaths of 100% N2) during moderate exercise, in seven normal men, to determine if the ventilatory response to the transient hypoxic stimulus is a more specific measure of peripheral chemoreceptor sensitivity to hypoxia. 2. Hypoxic ventilatory drive measured using progressive isocapnic hypoxia ranged from −0.13 to −2.65 litres min−1 % −1 after placebo and from − 0.20 to − 6.48 litres min−1 %−1 after almitrine. The response was greater after almitrine in six of the seven subjects, and the difference was significant for the whole group (P < 0.05). 3. Hypoxic ventilatory drive measured using transient hypoxia ranged from −0.19 to −1.59 litres min−1 %−1 after placebo and from −0.09 to −1.62 litres min−1 %−1 after almitrine. The response was not consistently greater after almitrine, and the difference was not significant for the group. 4. Difficulties in accurately quantifying a brief rise in minute ventilation after transient hypoxia, particularly in subjects with a low hypoxic ventilatory drive, may have masked small changes in the slope of the minute ventilation/arterial oxygen saturation relationship with this method. However, the significant increase in the response to progressive isocapnic hypoxia after almitrine suggests that the failure to demonstrate an effect using transient hypoxic stimuli was not solely due to between-day variation in hypoxic ventilatory drive or the small numbers of subjects studied. 5. We conclude that, although transient hypoxia avoids any central depression of ventilation that might result from the prolonged hypoxia used in the conventional steady state or progressive isocapnic methods (thereby leading to underestimation of the hypoxic ventilatory drive), the ventilatory response to such transient stimuli is also affected by factors other than peripheral chemoreceptor activity.

Effect of hyperoxia and hypoxia on exercise-induced breathlessness in normal subjects

1988 ◽  
Vol 74 (5) ◽  
pp. 531-537 ◽  
Author(s):  
N. Chronos ◽  
L. Adams ◽  
A. Guz
Keyword(s):  
Oxygen Saturation ◽  
Oxygen Concentration ◽  
Time Course ◽  
Minute Ventilation ◽  
Arterial Oxygen Saturation ◽  
Normal Subjects ◽  
Secondary Response ◽  
Arterial Oxygen ◽  
Air Breathing ◽  
Inspired Oxygen

1. The subjective changes accompanying alterations in inspired oxygen concentration during heavy exercise have been investigated single blind, in normal subjects. 2. In particular, the intensity of the sensation of breathlessness was quantified using a visual analogue scale and changes were compared with those in objective ventilatory measures. 3. Eleven subjects performed three steady-state workload exercise tests on different days and 100% O2, 15% O2 or air were randomly administered for a fixed interval during each test. 4. Compared with air breathing, all subjects felt less breathless during 100% O2 breathing, and ten of them felt more breathless when inspiring 15% O2; these changes were reversed on return to air breathing. 5. During and after 100% O2, the time course of changes in breathlessness was similar to those for ear arterial oxygen saturation and minute ventilation such that it could be a secondary response to either. However, during and after inspiration of 15% O2, changes in breathlessness occurred relatively more quickly than those in ventilation, more closely reflecting changes in oxygen saturation; this suggests that hypoxia, per se, could contribute to the genesis of this sensation. 6. Individual variability in breathlessness responses to exercise and changes in inspired oxygen concentration did not correlate with objective ventilatory changes; neither were changes in breathlessness in the group particularly associated with changes in respiratory frequency or tidal volume.

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