Background ventilatory stimulus as a determinant of load compensation

1989 ◽  
Vol 66 (3) ◽  
pp. 1352-1358 ◽  
Author(s):  
H. E. Greenberg ◽  
D. M. Rapoport ◽  
P. J. Gloeggler ◽  
R. M. Goldring
Keyword(s):  
Interindividual Variability ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Co2 Production ◽  
Control Mechanisms ◽  
Co2 Response ◽  
Co2 Partial Pressure ◽  
Load Compensation ◽  
Resistive Loading

Compensation for inspiratory flow-resistive loading was compared during progressive hypercapnia and incremental exercise to determine the effect of changing the background ventilatory stimulus and to assess the influence of the interindividual variability of the unloaded CO2 response on evaluation of load compensation in normal subjects. During progressive hypercapnia, ventilatory response was incompletely defended with loading (mean unloaded delta VE/delta PCO2 = 3.02 +/- 2.29, loaded = 1.60 +/- 0.67 1.min-1.Torr-1 CO2, where VE is minute ventilation and PCO2 is CO2 partial pressure; P less than 0.01). Furthermore the degree of defense of ventilation with loading was inversely correlated with the magnitude of the unloaded CO2 response. During exercise, loading produced no depression in ventilatory response (mean delta VE/delta VCO2 unloaded = 20.5 +/- 1.9, loaded = 19.2 +/- 2.5 l.min-1.l-1.min-1 CO2 where VCO is CO2 production; P = NS), and no relationship was demonstrated between degree of defense of the exercise ventilatory response and the unloaded CO2 response. Differences in load compensation during CO2 rebreathing and exercise suggest the presence of independent ventilatory control mechanisms in these states. The type of background ventilatory stimulus should therefore be considered in load compensation assessment.

Sexual influence on the control of breathing

1983 ◽  
Vol 54 (4) ◽  
pp. 874-879 ◽  
Author(s):  
D. P. White ◽  
N. J. Douglas ◽  
C. K. Pickett ◽  
J. V. Weil ◽  
C. W. Zwillich
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Premenopausal Women ◽  
Co2 Production ◽  
Menstrual Phase ◽  
Co2 Partial Pressure ◽  
Ventilatory Responses ◽  
Chemical Stimuli ◽  
Low Levels ◽  
Normal Women

Previous investigation has demonstrated that progesterone, a hormone found in premenopausal women, is a ventilatory stimulant. However, fragmentary data suggest that normal women may have lower ventilatory responses to chemical stimuli than men, in whom progesterone is found at low levels. As male-female differences have not been carefully studied, we undertook a systematic comparison of resting ventilation and ventilatory responses to chemical stimuli in men and women. Resting ventilation was found to correlate closely with CO2 production in all subjects (r = 0.71, P less than 0.001), but women tended to have a greater minute ventilation per milliliter of CO2 produced (P less than 0.05) and consequently a lower CO2 partial pressure (PCO2) (men 35.1 +/- 0.5 Torr, women 33.2 +/- 0.5 Torr; P less than 0.02). Women were also found to have lower tidal volumes, even when corrected from body surface area (BSA), and greater respiratory frequency than comparable males. The hypoxic ventilatory response (HVR) quantitated by the shape parameter A was significantly greater in men [167 +/- 22 (SE)] than in women (109 +/- 13; P less than 0.05). In men this hypoxic response was found to correlate closely with O2 consumption (r = 0.75, P less than 0.001) but with no measure of size or metabolic rate in women. The hypercapnic ventilatory response, expressed as the slope of ventilation vs. PCO2, was also greater in men (2.30 +/- 0.23) than in women (1.58 +/- 0.19, P less than 0.05). Finally women tended to have higher ventilatory responses in the luteal than in the follicular menstrual phase, but this was significant only for HVR (P less than 0.05). Women, with relatively higher resting ventilation, have lower responses to hypoxia and hypercapnia.

Control of ventilation in elite synchronized swimmers

1987 ◽  
Vol 63 (3) ◽  
pp. 1019-1024 ◽  
Author(s):  
R. L. Bjurstrom ◽  
R. B. Schoene
Keyword(s):  
Heart Rate ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Mean Value ◽  
Heart Rate Change ◽  
Breath Holding ◽  
Breath Hold ◽  
Lung Volumes ◽  
Co2 Partial Pressure ◽  
Control Of Ventilation

Synchronized swimmers perform strenuous underwater exercise during prolonged breath holds. To investigate the role of the control of ventilation and lung volumes in these athletes, we studied the 10 members of the National Synchronized Swim Team including an olympic gold medalist and 10 age-matched controls. We evaluated static pulmonary function, hypoxic and hypercapnic ventilatory drives, and normoxic and hyperoxic breath holding. Synchronized swimmers had an increased total lung capacity and vital capacity compared with controls (P less than 0.005). The hypoxic ventilatory response (expressed as the hyperbolic shape parameter A) was lower in the synchronized swimmers than controls with a mean value of 29.2 +/- 2.6 (SE) and 65.6 +/- 7.1, respectively (P less than 0.001). The hypercapnic ventilatory response [expressed as S, minute ventilation (1/min)/alveolar CO2 partial pressure (Torr)] was no different between synchronized swimmers and controls. Breath-hold duration during normoxia was greater in the synchronized swimmers, with a mean value of 108.6 +/- 4.8 (SE) vs. 68.03 +/- 8.1 s in the controls (P less than 0.001). No difference was seen in hyperoxic breath-hold times between groups. During breath holding synchronized swimmers demonstrated marked apneic bradycardia expressed as either absolute or heart rate change from basal heart rate as opposed to the controls, in whom heart rate increased during breath holds. Therefore the results show that elite synchronized swimmers have increased lung volumes, blunted hypoxic ventilatory responses, and a marked apneic bradycardia that may provide physiological characteristics that offer a competitive advantage for championship performance.(ABSTRACT TRUNCATED AT 250 WORDS)

Augmentation of CO2 drives by chlormadinone acetate, a synthetic progesterone

1984 ◽  
Vol 56 (6) ◽  
pp. 1627-1632 ◽  
Author(s):  
H. Kimura ◽  
F. Hayashi ◽  
A. Yoshida ◽  
S. Watanabe ◽  
I. Hashizume ◽  
...  
Keyword(s):  
Minute Ventilation ◽  
Inspiratory Flow ◽  
Pressure Response ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Physiological Basis ◽  
Load Compensation ◽  
Chlormadinone Acetate ◽  
Arterial Blood ◽  
Resistive Loading

We studied 10 male subjects who were administered chlormadinone acetate (CMA), a potent synthetic progesterone, to clarify the physiological basis of its respiratory effects. Arterial blood gas tension, resting ventilation, and respiratory drive assessed by ventilatory and occlusion pressure response to CO2 with and without inspiratory flow-resistive loading were measured before and 4 wk after CMA administration. In all subjects, arterial PCO2 decreased significantly by 5.7 +/- 0.6 (SE) Torr with an increase in minute ventilation by 1.8 +/- 0.6 l X min-1, whereas no significant changes were seen in O2 uptake. During unloaded conditions, both slopes of occlusion pressure and ventilatory response to CO2 increased, being statistically significant in the former but showing nonsignificant trends in the latter. Furthermore, inspiratory flow-resistive loading (16 cmH2O X l(-1) X s) increased both slopes more markedly after CMA. The magnitudes of load compensation, assessed by the ratio of loaded to unloaded slope of the occlusion pressure response curve, were increased significantly. We concluded CMA is a potent respiratory stimulant that increases the CO2 chemosensitivity and neuromechanical drives in the load-compensation mechanism.

Ventilatory response to transient hyperoxia in head injury hyperventilation

1980 ◽  
Vol 49 (1) ◽  
pp. 52-58 ◽  
Author(s):  
A. G. Leitch ◽  
J. E. McLennan ◽  
S. Balkenhol ◽  
R. L. McLaurin ◽  
R. G. Loudon
Keyword(s):  
Head Injury ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Control ◽  
Normal Subjects ◽  
Respiratory Alkalosis ◽  
Cerebral Injury ◽  
Peripheral Chemoreceptor ◽  
Male Patients ◽  
Almost All

We have measured breath-by-breath instantaneous minute ventilation (VIinst) before, during, and after the administration of 10 breaths of 100% oxygen to seven male patients with head injury hyperventilation. The patients were hypoxemic (PaO2 61.2 ± 6.3) and hypocapnic (PaCO2 26.6 ± 5.9) with a respiratory alkalosis (pH 7.53 ± 0.06) while breathing air. Following the oxygen VIinst fell on the average by 40 ± 12.7% from 16.06 ± 3.75 1.min-1 to a minimum of 9.73 ± 3.20 1.min-1 at 20.4 ± 2.9 s after the first breath of oxygen. In the majority of our hyperventilating patients, almost all of the resting hyperventilation could be abolished transiently by 100% oxygen. This fall in ventilation represents the peripheral chemoreceptor contribution to resting ventilation and is increased in the head injury patients in comparison with normal subjects breathing air or hypoxic gas mixtures, altitude-acclimatized subjects and patients who are hypoxic because of chronic bronchitis or interstitial lung disease. We suggest that the increased reflex hypoxic drive to ventilation found in our patients is secondary to their cerebral injury, resulting in a reduction of descending cortical inhibitory influences on the medullary respiratory control centers.

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.

Metabolic rate and breathing during sleep

1985 ◽  
Vol 59 (2) ◽  
pp. 384-391 ◽  
Author(s):  
D. P. White ◽  
J. V. Weil ◽  
C. W. Zwillich
Keyword(s):  
Metabolic Rate ◽  
Eye Movement ◽  
Sleep Stage ◽  
Minute Ventilation ◽  
Respiratory Control ◽  
Normal Subjects ◽  
Co2 Production ◽  
Sleep Stages ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep

Recent investigation suggests that both ventilation (VE) and the chemical sensitivity of the respiratory control system correlate closely with measures of metabolic rate [O2 consumption (VO2) and CO2 production (VCO2)]. However, these associations have not been carefully investigated during sleep, and what little information is available suggests a deterioration of the relationships. As a result we measured VE, ventilatory pattern, VO2, and VCO2 during sleep in 21 normal subjects (11 males and 10 females) between the ages of 21 and 77 yr. When compared with values for awake subjects, expired ventilation decreased 8.2 +/- 2.3% (SE) during sleep and was associated with a 8.5 +/- 1.6% decrement in VO2 and a 12.3 +/- 1.7% reduction in VCO2, all P less than 0.01. The decrease in ventilation was a product primarily of a significant decrease in tidal volume with little change in frequency. None of these findings were dependent on sleep stage with results in rapid-eye-movement (REM) and non-rapid-eye-movement sleep being similar. Through all sleep stages ventilation remained tightly correlated with VO2 and VCO2 both within a given individual and between subjects. Although respiratory rhythmicity was somewhat variable during REM sleep, minute ventilation continued to correlate with VO2 and VCO2. None of the parameters described above were influenced by age or gender, with male and female subjects demonstrating similar findings. Ten of the subjects demonstrated at least occasional apneas. These individuals, however, were not found to differ from those without apnea in any other measure of ventilation or metabolic rate.

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.

scholarly journals Respiratory load compensation and perception during 10‐breath sustained inspiratory resistive loading in normal subjects

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Matthew Paul Davenport ◽  
Justin Feinstein ◽  
Sahib Khalsa ◽  
Andreas Leupoldt ◽  
Paul Wesley Davenport
Keyword(s):  
Normal Subjects ◽  
Load Compensation ◽  
Resistive Loading

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.

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.

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