Effect of resistive loading on ventilatory response to hypoxia

1975 ◽  
Vol 38 (6) ◽  
pp. 965-968 ◽  
Author(s):  
A. S. Rebuck ◽  
E. F. Juniper
Keyword(s):  
Response Curve ◽  
Mechanical Load ◽  
Ventilatory Response ◽  
Arterial Oxygen Saturation ◽  
Normal Subjects ◽  
Arterial Oxygen ◽  
Resistive Load ◽  
O2 Concentration ◽  
Resistive Loading ◽  
Ventilatory Response To Hypoxia

Ventilatory responses to hypoxia, with and without an inspiratory resistive load, were measured in eight normal subjects, using a rebreathing technique. During the studies, the end-tidal P-CO2 was kept constant at mixed venous level (Pv-CO2) by drawing expired gas through a variable CO2-absorbing bypass. The initial bag O2 concentration was 24% and rebreathing was continued until the O2 concentration in the bag fell to 6% or the subject's arterial oxygen saturation (Sa-O2), monitored continuously by ear oximetry, fell to 70%. Studies with and without the load were performed in a formally randomized order for each subject. Linear regressions for rise in ventilation against fall in Sa-O2 were calculated. The range of unloaded responses was 0.78–3.59 1/min per 1% fall in Sa-O2 and loaded responses 0.37–1.68 1/min per 1% fall in Sa-O2. In each subject, the slope of the response curve during loading fell by an almost constant fraction of the unloaded response, such that the ratio of loaded to unloaded slope in all subjects ranged from 0.41 to 0.48. However, the extrapolated intercept of the response curve on the Sa-O2 axis did not alter significantly indicating that the P-CO2 did not alter between experiments. These results suggest that the change in ventilatory response to hypoxia during inspiratory resistive loading is related to the mechanical load applied, with the loaded slope being directly proportional to the unloaded one.

scholarly journals Importance of Testosterone on Adaptation at High Altitude

2018 ◽  
Vol 2 (4) ◽  
pp. 689-697 ◽  
Author(s):  
Gustavo Gonzales
Keyword(s):  
Androgen Receptor ◽  
High Altitude ◽  
Ventilatory Response ◽  
Arterial Oxygen Saturation ◽  
Serum Testosterone ◽  
Arterial Oxygen ◽  
High Altitudes ◽  
Chronic Mountain Sickness ◽  
Mountain Sickness ◽  
Ventilatory Response To Hypoxia

Adaptation or natural acclimatization results from the interaction between genetic variations and acclimatization resulting in individuals with ability to live and reproduce without problems at high altitudes. Testosterone is a hormone that increases erythropoiesis and inhibits ventilation. It could therefore, be associated to the adaptation to high altitudes. Excessive erythrocytosis, which in turn will develop chronic mountain sickness is caused by low arterial oxygen saturation and ventilatory inefficiency and blunted ventilatory response to hypoxia. Testosterone is elevated in natives at high altitude with excessive erythrocytosis (>21 g /dl hemoglobin in men and >19 g/dl in women). Natives from the Peruvian central Andes with chronic mountain sickness express gene SENP1 that enhances the activity of the androgen receptor. Results of the current investigations suggest that increase in serum testosterone and hemoglobin is not adequate for adaptation to high altitude.

The Ventilatory Response to Hypoxia during Exercise in Cyanotic Congenital Heart Disease

1973 ◽  
Vol 45 (1) ◽  
pp. 99-105 ◽  
Author(s):  
M. R. H. Taylor
Keyword(s):  
Congenital Heart Disease ◽  
Heart Disease ◽  
Congenital Heart ◽  
Ventilatory Response ◽  
Arterial Oxygen Saturation ◽  
Haemoglobin Concentration ◽  
Cyanotic Congenital Heart Disease ◽  
Arterial Oxygen ◽  
Normal Adults ◽  
Ventilatory Response To Hypoxia

1. In contrast to the diminished ventilatory response to hypoxia which has been found at rest in cyanotic congenital heart disease, hyperventilation was noted on exercise in children who were cyanosed. 2. Sixteen children had low arterial oxygen saturations on exercise and thirteen of these hyperventilated by an amount similar to that reported in normal adults breathing hypoxic gas mixtures. 3. The three children who had little ventilatory response in relation to the increase of hypoxia during exercise all had a triad of long-standing cyanosis starting early in life, high haemoglobin concentration and low arterial oxygen saturation at rest in air.

Hypoxic Arousal Responses in Normal Infants

PEDIATRICS ◽  
1992 ◽  
Vol 89 (5) ◽  
pp. 860-864 ◽  
Author(s):  
Sally L. Davidson Ward ◽  
Daisy B. Bautista ◽  
Thomas C. Keens
Keyword(s):  
Ventilatory Response ◽  
Arterial Oxygen Saturation ◽  
Periodic Breathing ◽  
High Risk Group ◽  
Arterial Oxygen ◽  
Sudden Infant ◽  
Hypoxic Ventilatory Response ◽  
Quiet Sleep ◽  
Term Infants ◽  
Increased Risk

Failure to arouse in response to hypoxia has been described in infants at increased risk for sudden infant death syndrome (SIDS) and has been suggested as a possible mechanism for SIDS. However, most SIDS victims are not in a high-risk group before death. Thus, if a hypoxic arousal disorder is an important contributor to SIDS, normal infants might fail to arouse from sleep in response to hypoxia. To test this hypothesis, the authors studied hypoxic arousal responses in 18 healthy term infants younger than 7 months of age (age 12.1 ± 1.7 [SEM] weeks; 56% girls). Hypoxic arousal challenges were performed during quiet sleep by rapidly decreasing inspired oxygen tension (Pio2) to 80 mm Hg for 3 minutes or until arousal (eye opening, agitation, and crying) occurred. Tests were performed in duplicate when possible. Only 8 infants (44%) aroused in response to one or more hypoxic challenges; arousal occurred during 8 (32%) of 25 trials. There were no significant differences in lowest Pio2 or arterial oxygen saturation during hypoxia between those infants who aroused and those who failed to arouse. All 18 infants had a fall in their end-tidal carbon dioxide tension during hypoxia, suggesting that each had a hypoxic ventilatory response despite failure to arouse in the majority. Periodic breathing occurred following hypoxia in only 1 (13%) of the 8 trials that resulted in arousal, compared with 16 (94%) of 17 trials without arousal (P < .005). It is concluded that the majority of normal infants younger than 7 months of age fail to arouse from quiet sleep in response to hypoxia, despite the apparent presence of a hypoxic ventilatory response.

Effect of elastic loading on ventilatory response to hypoxia in conscious man

1975 ◽  
Vol 39 (4) ◽  
pp. 548-551 ◽  
Author(s):  
A. S. Rebuck ◽  
M. Betts ◽  
N. A. Saunders
Keyword(s):  
Ventilatory Response ◽  
Variable Speed ◽  
Ventilatory Responses ◽  
Elastic Load ◽  
Resistive Loading ◽  
Elastic Loading ◽  
Progressive Hypoxia ◽  
End Tidal ◽  
Linear Regressions ◽  
Ventilatory Response To Hypoxia

Ventilatory responses to isocapnic hypoxia, with and without an inspiratory elastic load (12.1 cmH2O/l), were measured in seven healthy subjects using a rebreathing technique. During each experiment, the end-tidal PCO2 was held constant using a variable-speed pump to draw gas from the rebreathing bag through a CO2 absorbing bypass. Studies with and without the load were performed in a formally randomized order for each subject. Linear regressions for rise in ventilation against fall in SaO2 were calculated. The range of unloaded responses was 0.74–1.38 1/min per 1% fall in SaO2 and loaded responses 0.71–1.56 1/min per 1% fall in SaO2. Elastic loading did not significantly alter the ventilatory response to progressive hypoxia (P greater than 0.2). In all subjects there was, however, a change in breathing pattern during loading, whereby increments in ventilation were attained by smaller tidal volumes and higher frequencies than in the control experiments. These results support the hypothesis previously proposed in our studies of resistive loading during progressive hypoxia, that a similar control pathway appears to be involved in response to the application of loads to breathing, whether ventilation is stimulated by hypoxia or hypercapnia.

Two patterns of daily hypoxic exposure and their effects on measures of chemosensitivity in humans

2007 ◽  
Vol 103 (6) ◽  
pp. 1973-1978 ◽  
Author(s):  
Michael S. Koehle ◽  
A. William Sheel ◽  
William K. Milsom ◽  
Donald C. McKenzie
Keyword(s):  
Oxygen Saturation ◽  
Intermittent Hypoxia ◽  
Ventilatory Response ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Hypoxic Exposure ◽  
Hypoxic Ventilatory Response ◽  
The Third ◽  
Long Duration ◽  
The Mean

The purpose of this study was to compare chemoresponses following two different intermittent hypoxia (IH) protocols in humans. Ten men underwent two 7-day courses of poikilocapnic IH. The long-duration IH (LDIH) protocol consisted of daily 60-min exposures to normobaric 12% O2. The short-duration IH (SDIH) protocol comprised twelve 5-min bouts of 12% O2, separated by 5-min bouts of room air, daily. Isocapnic hypoxic ventilatory response (HVR) was measured daily during the protocol and 1 and 7 days following. Hypercapnic ventilatory response (HCVR) and CO2 threshold and sensitivity (by the modified Read rebreathing technique) were measured on days 1, 8, and 14. Following 7 days of IH, the mean HVR was significantly increased from 0.47 ± 0.07 and 0.47 ± 0.08 to 0.70 ± 0.06 and 0.79 ± 0.06 l·min−1·%SaO2−1 (LDIH and SDIH, respectively), where %SaO2 is percent arterial oxygen saturation. The increase in HVR reached a plateau after the third day. One week post-IH, HVR values were unchanged from baseline. HCVR increased from 3.0 ± 0.4 to 4.0 ± 0.5 l·min−1·mmHg−1. In both the hyperoxic and hypoxic modified Read rebreathing tests, the slope of the CO2/ventilation plot was unchanged by either intervention, but the CO2/ventilation curve shifted to the left following IH. There were no correlations between the changes in response to hypoxia and hypercapnia. There were no significant differences between the two IH protocols for any measures, indicating that comparable changes in chemoreflex control occur with either protocol. These results also suggest that the two methods of measuring CO2 response are not completely concordant and that the changes in CO2 control do not correlate with the increase in the HVR.

Depression of hypoxic ventilatory response in humans by somatostatin

1988 ◽  
Vol 65 (3) ◽  
pp. 1050-1054 ◽  
Author(s):  
R. B. Filuk ◽  
D. J. Berezanski ◽  
N. R. Anthonisen
Keyword(s):  
Intravenous Infusion ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Small Decrease ◽  
Hypoxic Ventilatory Response ◽  
Arterial O2 Saturation ◽  
Ventilatory Response To Hypoxia

In nine normal subjects we measured the ventilatory response to isocapnic hypoxia with and without an intravenous infusion of 1 mg of somatostatin. Arterial O2 saturation was rapidly lowered to 80 +/- 2% in 2 min and maintained for 30 min. During control experiments, ventilation increased immediately (3-5 min) and then declined so that at 25 min of hypoxia ventilation was little above that in room air. Somatostatin was associated with a small decrease in ventilation while the subjects breathed room air. With hypoxia there was no immediate increase in ventilation for the group as a whole, although an increase was observed in one subject. With somatostatin, after 25 min of hypoxia, mean ventilation was lower than at any other time in the study; as hypoxia was discontinued ventilation increased slightly. Somatostatin causes profound depression of the ventilatory response to hypoxia by a mechanism that is not known but may be central. With somatostatin hypoxia of 25-min duration tends to depress ventilation.

Effect of ethanol and naloxone on control of ventilation and load perception

1983 ◽  
Vol 55 (3) ◽  
pp. 929-934 ◽  
Author(s):  
T. M. Michiels ◽  
R. W. Light ◽  
C. K. Mahutte
Keyword(s):  
Normal Subjects ◽  
Ethanol Ingestion ◽  
Resistive Load ◽  
Load Compensation ◽  
Ventilatory Responses ◽  
Resistive Loading ◽  
Resistive Loads ◽  
Mouth Occlusion Pressure ◽  
Load Perception ◽  
Respiratory Depressant

The respiratory depressant effects of ethanol and their potential reversibility by naloxone were studied in 10 normal subjects. Ventilatory and mouth occlusion pressure (P0.1) responses to hypercapnia and hypoxia without and with an inspiratory resistive load (13 cmH2O X 1(-1) X S) were measured. The resistive load detected with 50% probability (delta R50) and the exponent (n) in Stevens' psychophysical law for magnitude estimation of resistive loads were studied using standard psychophysical techniques. Each of these studies was performed before ethanol ingestion, after ethanol ingestion (1.5 ml/kg, by mouth), and then again after naloxone (0.8 mg iv). Ethanol increased delta R50 (P less than 0.05) and decreased n (P less than 0.05). Naloxone caused no further change in these parameters. The load compensation (Lc), defined as the ratio of loaded to unloaded response slopes, was not significantly changed after ethanol and naloxone. No correlation was found between the Lc and delta R50 or n. The ventilatory and P0.1 responses to hypercapnia and hypoxia with and without inspiratory resistive loading decreased after ethanol (P less than 0.05, hypercapnia; NS, hypoxia). After naloxone the hypercapnic ventilatory responses increased (P less than 0.05). This suggests that the respiratory depressant effects of ethanol may be mediated via endorphins.

Relationship between inspiratory drive and perceived inspiratory effort in normal man

1990 ◽  
Vol 78 (5) ◽  
pp. 493-496 ◽  
Author(s):  
J. E. Clague ◽  
J. Carter ◽  
M. G. Pearson ◽  
P. M. A. Calverley
Keyword(s):  
Ventilatory Response ◽  
Free Breathing ◽  
Normal Subjects ◽  
Inspiratory Effort ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Resistive Loading ◽  
Mouth Occlusion Pressure ◽  
The Individual ◽  
Induced Changes

1. To examine the relationship between the inspiratory effort sensation (IES) and respiratory drive as reflected by mouth occlusion pressure (P0.1) we have studied loaded and unloaded ventilatory responses to CO2 in 12 normal subjects. 2. The individual coefficient of variation of the effort sensation response to CO2 (IES/Pco2) between replicate studies was 21% and was similar to the variability of the ventilatory response (VE/Pco2) (18%) and the occlusion pressure response (P0.1/Pco2) (22%). 3. IES was well correlated with P0.1 (r >0.9) for both free-breathing and loaded runs. 4. Resistive loading reduced the ventilatory response to hypercapnia from 19.3 1 min−1 kPa−1 (sd 7.5) to 12.6 1 min−1 kPa−1 (sd 3.9) (P <0.01). IES and P0.1 responses increased with resistive loading from 2.28 (sd 0.9) to 3.15 (sd 1.1) units/kPa and 2.8 (sd 1.2) to 3.73 (sd 1.5) cmH2O/kPa, respectively (P <0.01). 5. Experimentally induced changes in Pco2 and respiratory impedance were accompanied by increases in IES and P0.1. We found no evidence that CO2 increased IES independently of its effect on respiratory drive.

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.

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