Influence of body size and gender on control of ventilation

1986 ◽  
Vol 60 (6) ◽  
pp. 1894-1899 ◽  
Author(s):  
M. L. Aitken ◽  
J. L. Franklin ◽  
D. J. Pierson ◽  
R. B. Schoene
Keyword(s):  
Metabolic Rate ◽  
Vital Capacity ◽  
Shape Parameter ◽  
Statistical Significance ◽  
Co2 Production ◽  
Control Of Ventilation ◽  
Ventilatory Responses ◽  
And Gender ◽  
Mouth Occlusion Pressure ◽  
End Tidal

Hypoxic (HVR) and hypercapnic (HCVR) ventilatory responses are influenced by both metabolic activity and hormonal factors. By studying 67 subjects of both sexes, including those at the extremes of stature, we examined the influence of gender, CO2 production (VCO2), O2 consumption (VO2), body surface area (BSA), and vital capacity (VC) on resting ventilation (VE), HVR, and HCVR. We measured resting VE, VO2, and VCO2 and then performed isocapnic progressive hypoxic and hypercapnic ventilatory responses. The effect of stature was reflected in higher VE and metabolic rate (both P less than 0.001) in tall men compared with short men that was ablated by correction for BSA. Perhaps because their heights vary less than those of the men, tall women were not statistically distinguishable from short women in any of these measured parameters. Tall men tended to have greater hypoxic chemosensitivity than short men but this was not significantly different (P = 0.07). Gender affected the control of ventilation in a number of ways. Men had higher VE (P less than 0.05) and metabolic rate (P less than 0.001) than women. Even after correction for BSA men still had higher metabolic rates. Women had higher VE/VCO2 than men (P less than 0.05) and lower resting end-tidal Pco2 (PETCO2) values (P less than 0.05). Both A, the shape parameter of the hyperbolic HVR curve, and HVR determined from mouth occlusion pressure (AP) were greater in women than in men, although only AP reached statistical significance. However, corrections of A for BSA (P less than 0.05), VCO2 (P less than 0.01), and VC (P less than 0.001) amplified these differences.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of caffeine on ventilatory responses to hypercapnia, hypoxia, and exercise in humans

1990 ◽  
Vol 68 (1) ◽  
pp. 322-328 ◽  
Author(s):  
A. D. D'Urzo ◽  
R. Jhirad ◽  
H. Jenne ◽  
M. A. Avendano ◽  
I. Rubinstein ◽  
...  
Keyword(s):  
Metabolic Rate ◽  
Tidal Volume ◽  
Anaerobic Threshold ◽  
Co2 Production ◽  
Moderate Exercise ◽  
Double Blind ◽  
Ventilatory Responses ◽  
Physiological Variables ◽  
End Tidal ◽  
Exercise In Humans

The effect of oral caffeine on resting ventilation (VE), ventilatory responsiveness to progressive hyperoxic hypercapnia (HCVR), isocapnic hypoxia (HVR), and moderate exercise (EVR) below the anaerobic threshold (AT) was examined in seven healthy adults. Ventilatory responses were measured under three conditions: control (C) and after ingestion of either 650 mg caffeine (CF) or placebo (P) in a double-blind randomized manner. None of the physiological variables of interest differed significantly for C and P conditions (P greater than 0.05). Caffeine levels during HCVR, HVR, and EVR were 69.5 +/- 11.8, 67.8 +/- 10.8, and 67.8 +/- 10.9 (SD) mumol/l, respectively (P greater than 0.05). Metabolic rate at rest and during exercise was significantly elevated during CF compared with P. An increase in VE from 7.4 +/- 2.5 (P) to 10.5 +/- 2.1 l/min (CF) (P less than 0.05) was associated with a decrease in end-tidal PCO2 from 39.1 +/- 2.7 (P) to 35.1 +/- 1.3 Torr (CF) (P less than 0.05). Caffeine increased the HCVR, HVR, and EVR slopes (mean increase: 28 +/- 8, 135 +/- 28, 14 +/- 5%, respectively) compared with P; P less than 0.05 for each response. Increases in resting ventilation, HCVR, and HVR slopes were associated with increases in tidal volume (VT), whereas the increase in EVR slope was accompanied by increases in both VT and respiratory frequency. Our results indicate that caffeine increases VE and chemosensitivity to CO2 inhalation, hypoxia, and CO2 production during exercise below the AT.

Developmental pattern of hypercapnic and hypoxic ventilatory responses from childhood to adulthood

1994 ◽  
Vol 76 (1) ◽  
pp. 314-320 ◽  
Author(s):  
C. L. Marcus ◽  
W. B. Glomb ◽  
D. J. Basinski ◽  
S. L. Davidson ◽  
T. G. Keens
Keyword(s):  
Heart Rate ◽  
Body Weight ◽  
Body Size ◽  
Respiratory Rate ◽  
Body Surface ◽  
Vital Capacity ◽  
Developmental Pattern ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Arterial O2 Saturation

The developmental pattern of ventilatory responses, through childhood and puberty into adulthood, is not known. Therefore we studied hypercapnic (HCVR) and hypoxic ventilatory responses (HOVR) in 59 subjects (29 males and 30 females) 4–49 yr of age, of whom 35 were children ( < 18 yr old). There was a significant correlation between HCVR and weight (r = 0.33, P < 0.02), vital capacity (r = 0.30, P < 0.05), and body surface area (r = 0.30, P < 0.05) but not height (r = 0.22, NS). There was no correlation between HOVR and any of the correcting factors. To account for disparities in body size, volume-related results were scaled for body weight. The HCVR corrected for weight (HCVR/WT) decreased with age (r = -0.57, P < 0.001). HCVR/WT was significantly higher in children than in adults (0.056 +/- 0.024 vs. 0.032 +/- 0.015 l.kg-1 x min-1. Torr end-tidal PCO2-1, P < 0.001). The (tidal volume/inspiratory duration)/weight, respiratory rate, and heart rate responses to hypercapnia were increased in the children, and the CO2 threshold was lower (36 +/- 5 vs. 40 +/- 6 Torr, P < 0.05). Similarly, the HOVR corrected for weight (HOVR/WT) decreased with age (r = 0.34, P < 0.05), and HOVR/WT was significantly higher in children than in adults (-0.035 +/- 0.017 vs. -0.024 +/- 0.016 l.kg-1 x min-1.% arterial O2 saturation-1, P < 0.02). The respiratory rate and heart rate responses to hypoxia were increased in the children. We conclude that rebreathing HCVR and HOVR are higher during childhood than during adulthood.

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.

Somatostatin inhibits the ventilatory response to hypoxia in humans

1986 ◽  
Vol 60 (3) ◽  
pp. 997-1002 ◽  
Author(s):  
D. L. Maxwell ◽  
P. Chahal ◽  
K. B. Nolop ◽  
J. M. Hughes
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Open Circuit ◽  
Co2 Production ◽  
Adult Males ◽  
Hypoxic Response ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Hypercapnic Response ◽  
Ventilatory Response To Hypoxia

The effects of a 90-min infusion of somatostatin (1 mg/h) on ventilation and the ventilatory responses to hypoxia and hypercapnia were studied in six normal adult males. Minute ventilation (VE) was measured with inductance plethysmography, arterial 02 saturation (SaO2) was measured with ear oximetry, and arterial PCO2 (Paco2) was estimated with a transcutaneous CO2 electrode. The steady-state ventilatory response to hypoxia (delta VE/delta SaO2) was measured in subjects breathing 10.5% O2 in an open circuit while isocapnia was maintained by the addition of CO2. The hypercapnic response (delta VE/delta PaCO2) was measured in subjects breathing first 5% and then 7.5% CO2 (in 52–55% O2). Somatostatin greatly attenuated the hypoxic response (control mean -790 ml x min-1.%SaO2 -1, somatostatin mean -120 ml x min-1.%SaO2 -1; P less than 0.01), caused a small fall in resting ventilation (mean % fall - 11%), but did not affect the hypercapnic response. In three of the subjects progressive ventilatory responses (using rebreathing techniques, dry gas meter, and end-tidal Pco2 analysis) and overall metabolism were measured. Somatostatin caused similar changes (mean fall in hypoxic response -73%; no change in hypercapnic response) and did not alter overall O2 consumption nor CO2 production. These results show an hitherto-unsuspected inhibitory potential of this neuropeptide on the control of breathing; the sparing of the hypercapnic response is suggestive of an action on the carotid body but does not exclude a central effect.

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 &lt; 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 &lt; 0.01). The central and peripheral carbon dioxide sensitivities decreased by about 30% (P &lt; 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.

Maturational differences in step vs. ramp hypoxic and hypercapnic ventilatory responses

1994 ◽  
Vol 76 (5) ◽  
pp. 1968-1975 ◽  
Author(s):  
D. Gozal ◽  
R. Arens ◽  
K. J. Omlin ◽  
C. L. Marcus ◽  
T. G. Keens
Keyword(s):  
Vital Capacity ◽  
Stimulus Presentation ◽  
Peripheral Chemoreceptors ◽  
Prepubertal Children ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Step Responses

The influence of the speed of stimulus presentation on hypoxic and hypercapnic ventilatory responses (step vs. ramp) is not known. Furthermore, it is unclear whether children and adults respond similarly. We tested ramp ventilatory responses to hypercapnia and hypoxia with use of rebreathing in 8 prepubertal children and 11 adults. We tested step ventilatory responses to hypercapnia with single vital capacity breaths of 15% CO2 in O2 and to hypoxia with five tidal breaths of 100% N2. For children, slopes of step hypercapnic ventilatory responses were always greater than those of ramp responses (0.85 +/- 0.07 vs. 0.71 +/- 0.07 l.min-1.Torr end-tidal PCO2-1; P < 0.0005). Conversely, for adults, step responses were always less than ramp responses (0.88 +/- 0.19 vs. 2.10 +/- 0.29 l.min-1.Torr end-tidal PCO2-1; P < 0.0007). Similarly, for children, the slopes of step hypoxic ventilatory responses were always greater than those of ramp responses (-0.71 +/- 0.09 vs. -0.45 +/- 0.04 l.min-1.Torr O2 saturation-1; P < 0.02), and for adults, step responses were always less than ramp responses (-0.68 +/- 0.14 vs. -1.85 +/- 0.46 l.min-1.Torr O2 saturation-1; P < 0.04). We conclude that ventilatory responses vary depending on step vs. ramp presentation of hypercapnia or hypoxia and that the ratio of these responses is reversed in children compared with adults. We speculate that the responsiveness of peripheral chemoreceptors is increased in children compared with adults and that it may play a role in the mechanisms leading to increased ventilatory responses observed during childhood.

Combined effects of female hormones and metabolic rate on ventilatory drives in women

1989 ◽  
Vol 66 (2) ◽  
pp. 808-813 ◽  
Author(s):  
J. G. Regensteiner ◽  
W. D. Woodard ◽  
D. D. Hagerman ◽  
J. V. Weil ◽  
C. K. Pickett ◽  
...  
Keyword(s):  
Metabolic Rate ◽  
Ventilatory Response ◽  
Full Term ◽  
Term Pregnancy ◽  
Ventilatory Responses ◽  
Female Hormones ◽  
Conjugated Equine Estrogens ◽  
End Tidal ◽  
Equine Estrogens ◽  
Estrogen Administration

Increased resting ventilation (VE) and hypoxic and hypercapnic ventilatory responses occur during pregnancy in association with elevations in female hormones and metabolic rate. To determine whether increases in progestin, estrogen, and metabolic rate produced a rise in VE and hypoxic ventilatory response (HVR) similar in magnitude to that observed at full-term pregnancy, we studied 12 postmenopausal women after 1 wk of treatment with placebo, progestin (20 mg tid medroxyprogesterone acetate), estrogen (1.25 mg bid conjugated equine estrogens), and combined progestin and estrogen. Progestin alone or with estrogen raised VE at rest and decreased end-tidal PCO2 (PETCO2) by 3.9 +/- 0.8 and 3.3 +/- 0.6 Torr, respectively (both P less than 0.05), accounting for approximately one-fourth of the rise in VE and three-fourths of the PETCO2 reduction seen at full-term pregnancy. The addition of mild exercise sufficient to raise metabolic rate by 33–36% produced the remaining three-fourths of the rise in VE but no further decline in PETCO2. Combined progestin and estrogen raised HVR and hypercapnic ventilatory response more consistently than progestin alone and could account for one-half of the increase in HVR seen at full-term pregnancy. Mild exercise alone did not raise HVR, but when exercise was combined with progestin and estrogen administration, HVR rose by amounts equal to that seen at full-term pregnancy. We concluded that female hormones together with mild elevation in metabolic rate were likely responsible for the pregnancy-associated increases in VE and HVR.

Increased HVR in pregnancy: relationship to hormonal and metabolic changes

1987 ◽  
Vol 62 (1) ◽  
pp. 158-163 ◽  
Author(s):  
L. G. Moore ◽  
R. E. McCullough ◽  
J. V. Weil
Keyword(s):  
Metabolic Rate ◽  
Shape Parameter ◽  
Ventilatory Response ◽  
Co2 Production ◽  
Hormonal Changes ◽  
Hypoxic Ventilatory Response ◽  
Additional Increase ◽  
Arterial Ph ◽  
Partial Pressure Of Co2 ◽  
Low Altitude

In prior studies at high altitude, we have found that pregnancy increases maternal hypoxic ventilatory response (HVR) but the factors responsible are unknown. Changes in metabolic rate and hormones that occur during pregnancy have previously been shown to influence HVR. We therefore sought to determine the contribution of metabolic rate and hormonal changes to the pregnancy-associated rise in HVR. Pregnancy increased HVR in each of 20 normal, low-altitude (1,600 m) residents. As measured by the shape parameter A, HVR at week 36 was 237 +/- 26 (SE) or twofold higher than the 124 +/- 13 value measured 3 mo postpartum (P less than 0.01) despite the presence of the potentially depressant effects of hypocapnia [change in alveolar partial pressure of CO2 (delta PACO2) = -4 +/- 1 mmHg] and alkalosis [change in arterial pH (delta pHa) = 0.02 +/- 0.01 U] during pregnancy. Sixty percent of the increase in HVR values had occurred by week 20 of gestation at which time O2 consumption (VO2) and CO2 production (VCO2) were unchanged relative to values measured postpartum. The remaining 40% rise in HVR paralleled increases in VO2 and VCO2, and further elevation in VO2 and VCO2 with moderate exercise produced an additional increase in HVR. Serum estradiol and progesterone levels increased with pregnancy, but levels did not correlate with HVR. The women reporting the greatest symptoms of dyspnea had higher HVR A values at week 36 than the least dyspneic women (285 +/- 28 vs. 178 +/- 34, respectively, P less than 0.05). We concluded that factors intrinsic to pregnancy in combination with increased metabolic rate raised HVR twofold with pregnancy and may have contributed to the often-reported symptoms of dyspnea in pregnant women.

Role of endogenous female hormones in hypoxic chemosensitivity

1997 ◽  
Vol 83 (5) ◽  
pp. 1706-1710 ◽  
Author(s):  
Koichiro Tatsumi ◽  
Cheryl K. Pickett ◽  
Christopher R. Jacoby ◽  
John V. Weil ◽  
Lorna G. Moore
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Shape Parameter ◽  
Ovarian Hormones ◽  
Serum Progesterone ◽  
Ventilatory Responses ◽  
Female Hormones ◽  
Before And After ◽  
End Tidal

Tatsumi, Koichiro, Cheryl K. Pickett, Christopher R. Jacoby, John V. Weil, and Lorna G. Moore. Role of endogenous female hormones in hypoxic chemosensitivity. J. Appl. Physiol. 83(5): 1706–1710, 1997.—Effective alveolar ventilation and hypoxic ventilatory response (HVR) are higher in females than in males and after endogenous or exogenous elevation of progesterone and estrogen. The contribution of normal physiological levels of ovarian hormones to resting ventilation and ventilatory control and whether their site(s) of action is central and/or peripheral are unclear. Accordingly, we examined resting ventilation, HVR, and hypercapnic ventilatory responses (HCVR) before and 3 wk after ovariectomy in five female cats. We also compared carotid sinus nerve (CSN) and central nervous system translation responses to hypoxia in 6 ovariectomized and 24 intact female animals. Ovariectomy decreased serum progesterone but did not change resting ventilation, end-tidal[Formula: see text], or HCVR (all P = NS). Ovariectomy reduced the HVR shape parameter A in the awake (38.9 ± 5.5 and 21.2 ± 3.0 before and after ovariectomy, respectively, P < 0.05) and anesthetized conditions. The CSN response to hypoxia was lower in ovariectomized than in intact animals (shape parameter A = 22.6 ± 2.5 and 54.3 ± 3.5 in ovariectomized and intact animals, respectively, P < 0.05), but central nervous system translation of CSN activity into ventilation was similar in ovariectomized and intact animals. We concluded that ovariectomy decreased ventilatory and CSN responsiveness to hypoxia, suggesting that the presence of physiological levels of ovarian hormones influences hypoxic chemosensitivity by acting primarily at peripheral sites.

Influences of gender and sex hormones on hypoxic ventilatory response in cats

1991 ◽  
Vol 71 (5) ◽  
pp. 1746-1751 ◽  
Author(s):  
K. Tatsumi ◽  
B. Hannhart ◽  
C. K. Pickett ◽  
J. V. Weil ◽  
L. G. Moore
Keyword(s):  
Gender Differences ◽  
Body Weight ◽  
Sex Hormones ◽  
Shape Parameter ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Co2 Production ◽  
Potential Contribution ◽  
Hypoxic Ventilatory Response ◽  
End Tidal

Hypoxic ventilatory response (HVR) is known to be increased by female as well as male sex hormones, but whether there are differences in HVR between men and women remains unclear. To determine whether gender differences exist in HVR, we undertook systematic comparisons of resting ventilation and HVR in awake male and female cats. Furthermore to explore the potential contribution of sex hormones to gender differences observed, we compared neutered and intact cats of both sexes. Resting ventilation differed among the four groups, but differences disappeared with correction for body weight. Intact females had a lower end-tidal PCO2 than intact male cats (females: 31.6 +/- 0.4 Torr vs. males: 33.6 +/- 0.4 Torr, P less than 0.05), indicating an increased alveolar ventilation per unit CO2 production. HVR expressed as the shape parameter A was similar among the four groups of animals. However, baseline (hyperoxic; end-tidal PO2 greater than 200 Torr) minute ventilation [VI(PO2 greater than 200)] differed among the groups. Therefore we normalized HVR by dividing the shape parameter A by VI(PO2 greater than 200) to compare the relative hypoxic chemosensitivity among the various groups of animals. In addition, we further normalized HVR for body weight, because body size influences ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

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