Maximal Oxygen Uptake, Lung Volume and Ventilatory Response to Carbon Dioxide and Hypoxia in a Pair of Identical Twin Athletes

1975 ◽  
Vol 48 (3) ◽  
pp. 235-238 ◽  
Author(s):  
A. G. Leitch ◽  
L. Clancy ◽  
D. C. Flenley
Keyword(s):  
Carbon Dioxide ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Major Part ◽  
Genetic Factors ◽  
Ventilatory Response ◽  
Identical Twin ◽  
Lung Volumes ◽  
Ventilatory Responses ◽  
High Degree

1. Maximal oxygen uptake (V̇o2 max.), lung volumes, and ventilatory responses to carbon dioxide and hypoxia have been measured in identical twin athletes, who were trained to a similar high degree. 2. The results confirm previous findings for V̇o2 max. and lung volumes in identical twins, and are in keeping with the suggestion that genetic factors play a major part in determining the ventilatory response to carbon dioxide and hypoxia.

Ventilatory responses to carbon dioxide at low and high levels of oxygen are elevated after episodic hypoxia in men compared with women

2004 ◽  
Vol 97 (5) ◽  
pp. 1673-1680 ◽  
Author(s):  
Chris Morelli ◽  
M. Safwan Badr ◽  
Jason H. Mateika
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
High Oxygen ◽  
Set Point ◽  
Ventilatory Responses ◽  
Episodic Hypoxia ◽  
Before And After ◽  
Oxygen Gas ◽  
End Tidal

We hypothesized that the acute ventilatory response to carbon dioxide in the presence of low and high levels of oxygen would increase to a greater extent in men compared with women after exposure to episodic hypoxia. Eleven healthy men and women of similar race, age, and body mass index completed a series of rebreathing trials before and after exposure to eight 4-min episodes of hypoxia. During the rebreathing trials, subjects initially hyperventilated to reduce the end-tidal partial pressure of carbon dioxide (PetCO2) below 25 Torr. Subjects then rebreathed from a bag containing a normocapnic (42 Torr), low (50 Torr), or high oxygen gas mixture (150 Torr). During the trials, PetCO2 increased while the selected level of oxygen was maintained. The point at which minute ventilation began to rise in a linear fashion as PetCO2 increased was considered to be the carbon dioxide set point. The ventilatory response below and above this point was determined. The results showed that the ventilatory response to carbon dioxide above the set point was increased in men compared with women before exposure to episodic hypoxia, independent of the oxygen level that was maintained during the rebreathing trials (50 Torr: men, 5.19 ± 0.82 vs. women, 4.70 ± 0.77 l·min−1·Torr−1; 150 Torr: men, 4.33 ± 1.15 vs. women, 3.21 ± 0.58 l·min−1·Torr−1). Moreover, relative to baseline measures, the ventilatory response to carbon dioxide in the presence of low and high oxygen levels increased to a greater extent in men compared with women after exposure to episodic hypoxia (50 Torr: men, 9.52 ± 1.40 vs. women, 5.97 ± 0.71 l·min−1·Torr−1; 150 Torr: men, 5.73 ± 0.81 vs. women, 3.83 ± 0.56 l·min−1·Torr−1). Thus we conclude that enhancement of the acute ventilatory response to carbon dioxide after episodic hypoxia is sex dependent.

The Ventilatory Effects of Doxapram in Normal Man

1983 ◽  
Vol 65 (1) ◽  
pp. 65-69 ◽  
Author(s):  
P. M. A. Calverley ◽  
R. H. Robson ◽  
P. K. Wraith ◽  
L. F. Prescott ◽  
D. C. Flenley
Keyword(s):  
Oxygen Uptake ◽  
Ventilatory Response ◽  
Co2 Production ◽  
Central Action ◽  
Ventilatory Responses ◽  
Ventilatory Effects ◽  
Normal Man ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Ventilatory Response To Co2

1. To determine the mode of action of doxapram in man we have measured ventilation, oxygen uptake, CO2 production, hypoxic and hypercapnic ventilatory responses in six healthy men before and during intravenous infusion to maintain a constant plasma level. 2. Doxapram changed neither resting oxygen uptake nor CO2 production but produced a substantial increase in resting ventilation at both levels of end-tidal CO2 studied. 3. Doxapram increased the ventilatory response to isocapnic hypoxia from − 0.8 ± 0.4 litre min−1 (%Sao2)−1 to −1.63 ± 0.9 litres min−1 (%Sao2)−1. This was similar to the increase in hypoxic sensitivity which resulted from raising the end-tidal CO2 by 0.5 kPa without adding doxapram. 4. The slope of the ventilatory response to rebreathing CO2 rose from 11.6 ± 5.3 litres min−1 kPa−1 to 20,4 ± 9.8 litres min−1 kPa−1 during doxapram infusion. 5. The marked increase in the ventilatory response to CO2 implies that doxapram has a central action, but the potentiation of the hypoxic drive also suggests that the drug acts on peripheral chemoreceptors, or upon their central connections, at therapeutic concentrations in normal unanaesthetized subjects.

Dynamics of the Ventilatory Response to Step Changes in End-Tidal PCO2 in Older Humans

1997 ◽  
Vol 22 (4) ◽  
pp. 368-383 ◽  
Author(s):  
Marc J. Poulin ◽  
David A. Cunningham ◽  
Donald H. Paterson
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Older Men ◽  
Young Group ◽  
Control Of Breathing ◽  
Ventilatory Responses ◽  
Key Words Ageing ◽  
Younger Men ◽  
End Tidal ◽  
Mild Hypoxia

The purpose of this study was to examine the ventilatory response to carbon dioxide (CO2) in young and older men. Six square-wave steps of end-tidal CO2 (PETCO2) were administered in euoxia (PETO2 = 100 torr), hyperoxia (PETO2 = 500 torr), and mild hypoxia (PETO2 = 60 torr) The peripheral and central chemoreflex loops were described by three parameters including a gain (gp and gc), time constant of the response(τp, τc), and a time delay (Tp, Tc), respectively. The young and older men showed similar characteristics for Tp and Tc, with Tp, being 3 to 5 s shorter than Tc. In hypoxia, the ventilatory responses of the old group were characterised by a significantly smaller gc and a smaller gp. In hypoxia, τc was significantly shortened from its euoxic value in the young group, but not in the old group. Thus, this study demonstrated that in older men, the ventilatory responses to CO2 in euoxia and hyperoxia are similar to younger men, while in hypoxia the ventilatory responses are characterised by smaller gain terms. Key words: ageing, hypercapnia, hypoxia, hyperoxia, control of breathing

Assessment of Responsiveness to Carbon Dioxide in Patients with Chronic Airways Obstruction by Rate of Isometric Inspiratory Pressure Development

1976 ◽  
Vol 50 (3) ◽  
pp. 199-205 ◽  
Author(s):  
A. W. Matthews ◽  
J. B. L. Howell
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Pressure Change ◽  
Significant Negative Correlation ◽  
Inspiratory Pressure ◽  
Normal Range ◽  
Ventilatory Responses ◽  
Airways Obstruction ◽  
Pressure Development ◽  
Mechanical Factors

1. Responsiveness to CO2 was measured in forty patients with chronic airways obstruction in terms of ventilation and rate of isometric inspiratory pressure change [(dP/dt)max.]. 2. The ventilatory response was below the normal range in eighteen out of twenty-two patients with normal arterial CO2 tensions and in all of eighteen patients with CO2 retention. 3. The (dP/dt)max. response was distributed throughout the normal range in all but one of the patients with normal arterial CO2 tension. In all the patients with CO2 retention the (dP/dt)max. response was either at or below the lower limit of the normal range. 4. Although the ventilatory responses correlated significantly with FEV1 there was no such correlation for the (dP/dt)max. responses. 5. The (dP/dt)max. response showed a significant negative correlation with Pa,co2. 6. It is believed that the (dP/dt)max. response to CO2 can be used to assess central CO2 responsiveness in subjects with airways obstruction independently of mechanical factors limiting their ventilation.

Influences of Morphine on the Ventilatory Response to Isocapnic Hypoxia 

1997 ◽  
Vol 86 (6) ◽  
pp. 1342-1349 ◽  
Author(s):  
Aad Berkenbosch ◽  
Luc J. Teppema ◽  
Cees N. Olievier ◽  
Albert Dahan
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Shape Parameter ◽  
Ventilatory Response ◽  
Depressant Effect ◽  
Ventilatory Responses ◽  
Before And After ◽  
End Tidal ◽  
Ventilatory Response To Hypoxia ◽  
Carbon Dioxide Sensitivity

Background The ventilatory response to hypoxia is composed of the stimulatory activity from peripheral chemoreceptors and a depressant effect from within the central nervous system. Morphine induces respiratory depression by affecting the peripheral and central carbon dioxide chemoreflex loops. There are only few reports on its effect on the hypoxic response. Thus the authors assessed the effect of morphine on the isocapnic ventilatory response to hypoxia in eight cats anesthetized with alpha-chloralose-urethan and on the ventilatory carbon dioxide sensitivities of the central and peripheral chemoreflex loops. Methods The steady-state ventilatory responses to six levels of end-tidal oxygen tension (PO2) ranging from 375 to 45 mmHg were measured at constant end-tidal carbon dioxide tension (P[ET]CO2, 41 mmHg) before and after intravenous administration of morphine hydrochloride (0.15 mg/kg). Each oxygen response was fitted to an exponential function characterized by the hypoxic sensitivity and a shape parameter. The hypercapnic ventilatory responses, determined before and after administration of morphine hydrochloride, were separated into a slow central and a fast peripheral component characterized by a carbon dioxide sensitivity and a single offset B (apneic threshold). Results At constant P(ET)CO2, morphine decreased ventilation during hyperoxia from 1,260 +/- 140 ml/min to 530 +/- 110 ml/ min (P < 0.01). The hypoxic sensitivity and shape parameter did not differ from control. The ventilatory response to carbon dioxide was displaced to higher P(ET)CO2 levels, and the apneic threshold increased by 6 mmHg (P < 0.01). The central and peripheral carbon dioxide sensitivities decreased by about 30% (P < 0.01). Their ratio (peripheral carbon dioxide sensitivity:central carbon dioxide sensitivity) did not differ for the treatments (control = 0.165 +/- 0.105; morphine = 0.161 +/- 0.084). Conclusions Morphine depresses ventilation at hyperoxia but does not depress the steady-state increase in ventilation due to hypoxia. The authors speculate that morphine reduces the central depressant effect of hypoxia and the peripheral carbon dioxide sensitivity at hyperoxia.

Ventilatory Responses During Submaximal Exercise in Children With Prader–Willi Syndrome

2018 ◽  
Vol 30 (3) ◽  
pp. 411-417 ◽  
Author(s):  
Adam M. Hyde ◽  
Robert G. McMurray ◽  
Frank A. Chavoya ◽  
Daniela A. Rubin
Keyword(s):  
Carbon Dioxide ◽  
Body Mass Index ◽  
Oxygen Uptake ◽  
Tidal Volume ◽  
Body Mass ◽  
Metabolic Cost ◽  
Prader Willi Syndrome ◽  
Breathing Frequency ◽  
Ventilatory Responses ◽  
Carbon Dioxide Output

Purpose: Prader–Willi syndrome (PWS) is a genetic neurobehavioral disorder presenting hypothalamic dysfunction and adiposity. At rest, PWS exhibits hypoventilation with hypercapnia. We characterized ventilatory responses in children with PWS during exercise. Methods: Participants were children aged 7–12 years with PWS (n = 8) and without PWS with normal weight (NW; n = 9, body mass index ≤ 85th percentile) or obesity (n = 9, body mass index ≥ 95th percentile). Participants completed three 5-minute ambulatory bouts at 3.2, 4.0, and 4.8 km/h. Oxygen uptake, carbon dioxide output, ventilation, breathing frequency, and tidal volume were recorded. Results: PWS had slightly higher oxygen uptake (L/min) at 3.2 km/h [0.65 (0.46–1.01) vs 0.49 (0.34–0.83)] and at 4.8 km/h [0.89 (0.62–1.20) vs 0.63 (0.45–0.97)] than NW. PWS had higher ventilation (L/min) at 3.2 km/h [16.2 (13.0–26.5) vs 11.5 (8.4–17.5)], at 4.0 km/h [16.4 (13.9–27.9) vs 12.7 (10.3–19.5)], and at 4.8 km/h [19.7 (17.4–31.8) vs 15.2 (9.5–21.6)] than NW. PWS had greater breathing frequency (breaths/min) at 3.2 km/h [38 (29–53) vs 29 (22–35)], at 4.0 km/h [39 (29–58) vs 29 (23–39)], and at 4.8 km/h [39 (33–58) vs 32 (23–42)], but similar tidal volume and ventilation/carbon dioxide output to NW. Conclusion: PWS did not show impaired ventilatory responses to exercise. Hyperventilation in PWS may relate to excessive neural stimulation and metabolic cost.

Influences of Subanesthetic Isoflurane on Ventilatory Control in Humans

1995 ◽  
Vol 83 (3) ◽  
pp. 478-490. ◽  
Author(s):  
Maarten van den Elsen ◽  
Albert Dahan ◽  
Jacob DeGoede ◽  
Aad Berkenbosch ◽  
Jack van Kleef
Keyword(s):  
Carbon Dioxide ◽  
Healthy Volunteers ◽  
Ventilatory Response ◽  
Carbon Dioxide Tension ◽  
Central Component ◽  
Ventilatory Control ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Peripheral Chemoreflex ◽  
Ventilatory Response To Hypoxia

Background The purpose of this study was to quantify in humans the effects of subanesthetic isoflurane on the ventilatory control system, in particular on the peripheral chemoreflex loop. Therefore we studied the dynamic ventilatory response to carbon dioxide, the effect of isoflurane wash-in upon sustained hypoxic steady-state ventilation, and the ventilatory response at the onset of 20 min of isocapnic hypoxia. Methods Study 1: Square-wave changes in end-tidal carbon dioxide tension (7.5-11.5 mmHg) were performed in eight healthy volunteers at 0 and 0.1 minimum alveolar concentration (MAC) isoflurane. Each hypercapnic response was separated into a fast, peripheral component and a slow, central component, characterized by a time constant, carbon dioxide sensitivity, time delay, and off-set (apneic threshold). Study 2: The ventilatory changes due to the wash-in of 0.1 MAC isoflurane, 15 min after the induction of isocapnic hypoxia, were studied in 11 healthy volunteers. Study 3: The ventilatory responses to a step decrease in end-tidal oxygen (end-tidal oxygen tension from 110 to 44 mmHg within 3-4 breaths; duration of hypoxia 20 min) were assessed in eight healthy volunteers at 0, 0.1, and 0.2 MAC isoflurane. Results Values are reported as means +/- SF. Study 1: The peripheral carbon dioxide sensitivities averaged 0.50 +/- 0.08 (control) and 0.28 +/- 0.05 l.min-1.mmHg-1 (isoflurane; P < 0.01). The central carbon dioxide sensitivities (control 1.20 +/- 0.12 vs. isoflurane 1.04 +/- 0.11 l.min-1.mmHg-1) and off-sets (control 36.0 +/- 0.1 mmHg vs. isoflurane 34.5 +/- 0.2 mmHg) did not differ between treatments. Study 2: Within 30 s of exposure to 0.1 MAC isoflurane, ventilation decreased significantly, from 17.7 +/- 1.6 (hypoxia, awake) to 15.0 +/- 1.5 l.min-1 (hypoxia, isoflurane). Study 3: At the initiation of hypoxia ventilation increased by 7.7 +/- 1.4 (control), 4.1 +/- 0.8 (0.1 MAC; P < 0.05 vs. control), and 2.8 +/- 0.6 (0.2 MAC; P < 0.05 vs. control) l.min-1. The subsequent ventilatory decrease averaged 4.9 +/- 0.8 (control), 3.4 +/- 0.5 (0.1 MAC; difference not statistically significant), and 2.0 +/- 0.4 (0.2 MAC; P < 0.05 vs. control) l.min-1. There was a good correlation between the acute hypoxic response and the hypoxic ventilatory decrease (r = 0.9; P < 0.001). Conclusions The results of all three studies indicate a selective and profound effect of subanesthetic isoflurane on the peripheral chemoreflex loop at the site of the peripheral chemoreceptors. We relate the reduction of the ventilatory decrease of sustained hypoxia to the decrease of the initial ventilatory response to hypoxia.

Fetal chemoreception: a developing story

1996 ◽  
Vol 8 (3) ◽  
pp. 471 ◽  
Author(s):  
DF Teitel
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Current Knowledge ◽  
Chemical Stimulus ◽  
Lung Inflation ◽  
Ventilatory Responses ◽  
Central Inhibition ◽  
Chemical Stimuli ◽  
The Difference ◽  
Efficient Uptake

The central and peripheral chemoreceptors are critical to the efficient uptake and delivery of oxygen and the removal of carbon dioxide after birth. However, the importance and activity of fetal chemoreception has been questioned, since oxygen uptake and carbon dioxide removal are not regulated in the lungs in the fetus. Early studies suggested that chemotransduction-the conversion of a chemical stimulus to cardiovascular and ventilatory responses via the integration of chemoreceptor stimulation, neural afferent activity and neurohormonal effector mechanisms-was immature in its individual components or their interaction. However, it now appears that the chemoreceptor cascade is structurally and functionally intact in the late-term fetus, and responds actively to normal and other chemical stimuli. The differences between fetal and postnatal chemotransduction appear to be primarily dependent on the central inhibition of the ventilatory response, the inhibitory area being localized to the lateral pons. It appears to be mediated in part by a placental factor which is removed at birth, allowing for the expression of the ventilatory response. The suppression of this response is also responsible for the difference in the heart rate response: the postnatal tachycardia is caused by the lung inflation reflex; when abolished, bradycardia is seen, just as in the fetus. Despite the suppression of the ventilatory component of chemoreception, the fetal carotid chemoreceptor is more important than the aortic, even though it has been considered to be more important to ventilatory than to cardiovascular stability. This review discusses current knowledge of the various components of the mature chemoreceptor cascade, and presents the fetal story within that framework.

Responses to Exercise in Normobaric Hypoxia: Comparison of Elite and Recreational Ski Mountaineers

2014 ◽  
Vol 9 (6) ◽  
pp. 978-984 ◽  
Author(s):  
Raphael Faiss ◽  
Claudia von Orelli ◽  
Olivier Dériaz ◽  
Grégoire P. Millet
Keyword(s):  
Heart Rate ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Hypobaric Hypoxia ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Normobaric Hypoxia ◽  
Hypoxic Ventilatory Response ◽  
Treadmill Test ◽  
National Team

Purpose:Hypoxia is known to reduce maximal oxygen uptake (VO2max) more in trained than in untrained subjects in several lowland sports. Ski mountaineering is practiced mainly at altitude, so elite ski mountaineers spend significantly longer training duration at altitude than their lower-level counterparts. Since acclimatization in hypobaric hypoxia is effective, the authors hypothesized that elite ski mountaineers would exhibit a VO2max decrement in hypoxia similar to that of recreational ski mountaineers.Methods:Eleven elite (E, Swiss national team) and 12 recreational (R) ski mountaineers completed an incremental treadmill test to exhaustion in normobaric hypoxia (H, 3000 m, FIO2 14.6% ± 0.1%) and in normoxia (N, 485 m, FIO2 20.9% ± 0.0%). Pulse oxygen saturation in blood (SpO2), VO2max, minute ventilation, and heart rate were recorded.Results:At rest, hypoxic ventilatory response was higher (P < .05) in E than in R (1.4 ± 1.9 vs 0.3 ± 0.6 L · min−1 · kg−1). At maximal intensity, SpO2 was significantly lower (P < .01) in E than in R, both in N (91.1% ± 3.3% vs 94.3% ± 2.3%) and in H (76.4% ± 5.4% vs 82.3% ± 3.5%). In both groups, SpO2 was lower (P < .01) in H. Between N and H, VO2max decreased to a greater extent (P < .05) in E than in R (–18% and –12%, P < .01). In E only, the VO2max decrement was significantly correlated with the SpO2 decrement (r = .74, P < .01) but also with VO2max measured in N (r = .64, P < .05).Conclusion:Despite a probable better acclimatization to altitude, VO2max was more reduced in E than in R ski mountaineers, confirming previous results observed in lowlander E athletes.

scholarly journals Ventilatory responses to acute hypoxia and hypercapnia in humans with a patent foramen ovale

2019 ◽  
Vol 126 (3) ◽  
pp. 730-738 ◽  
Author(s):  
James T. Davis ◽  
Lindsey M. Boulet ◽  
Alyssa M. Hardin ◽  
Alex J. Chang ◽  
Andrew T. Lovering ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
High Altitude ◽  
Patent Foramen Ovale ◽  
Ventilatory Response ◽  
Acute Hypoxia ◽  
Acute Exposure ◽  
Foramen Ovale ◽  
Hypoxic Ventilatory Response ◽  
Ventilatory Responses ◽  
Peripheral Chemoreflex

Subjects with a patent foramen ovale (PFO) have blunted ventilatory acclimatization to high altitude compared with subjects without PFO. The blunted response observed could be because of differences in central and/or peripheral respiratory chemoreflexes. We hypothesized that compared with subjects without a PFO (PFO−), subjects with a PFO (PFO+) would have blunted ventilatory responses to acute hypoxia and hypercapnia. Sixteen PFO+ subjects (9 female) and 15 PFO− subjects (8 female) completed four 20-min trials on the same day: 1) normoxic hypercapnia (NH), 2) hyperoxic hypercapnia (HH), 3) isocapnic hypoxia (IH), and 4) poikilocapnic hypoxia (PH). Hypercapnic trials were completed before the hypoxic trials, the order of the hypercapnic (NH & HH) and hypoxic (IH & PH) trials were randomized, and trials were separated by ≥40 min. During the NH trials but not the HH trials subjects who were PFO+ had a blunted hypercapnic ventilatory response compared with subjects who were PFO− (1.41 ± 0.46 l·min−1·mmHg−1 vs. 1.98 ± 0.71 l·min−1·mmHg−1, P = 0.02). There were no differences between the PFO+ and PFO− subjects with respect to the acute hypoxic ventilatory response during IH and PH trials. Hypoxic ventilatory depression was similar between subjects who were PFO+ and PFO− during IH. These data suggest that compared with subjects who were PFO−, subjects who were PFO+ have normal ventilatory chemosensitivity to acute hypoxia but blunted ventilatory chemosensitivity to carbon dioxide, possibly because of reduced carbon dioxide sensitivity of either the central and/or the peripheral chemoreceptors. NEW & NOTEWORTHY Patent foramen ovale (PFO) is found in ~25%–40% of the population. The presence of a PFO appears to be associated with blunted ventilatory responses during acute exposure to normoxic hypercapnia. The reason for this blunted ventilatory response during acute exposure to normoxic hypercapnia is unknown but may suggest differences in either central and/or peripheral chemoreflex contribution to hypercapnia.

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