Effects of Varied Vocal Intensity on Ventilation and Energy Expenditure in Women and Men

1998 ◽  
Vol 41 (2) ◽  
pp. 239-248 ◽  
Author(s):  
Bridget A. Russell ◽  
Frank J. Cerny ◽  
Elaine T. Stathopoulos
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Energy Expenditure ◽  
Minute Ventilation ◽  
Face Mask ◽  
Carbon Dioxide Production ◽  
Quiet Breathing ◽  
Energy Expenditures ◽  
Ventilatory Responses ◽  
End Tidal

This study was completed to determine how ventilatory responses change by means of speech reading at three different sound pressure levels (SPL) as compared to quiet breathing prior to each task. The energy required to alter SPL was also studied and compared to energy expenditures during a quiet breathing condition. Twenty-four adults (12 women, 12 men) were studied while reading a standard passage at low, comfortable, and high SPLs for 7 minutes with quiet breathing periods between each task to achieve respiratory steady state and serve as a control to which the reading tasks were compared. The last 2 minutes of exhaled air for all speaking and quiet breathing tasks were collected using a Hans Rudolph mouth breathing face mask. A Sensor Medics V max 29 TM series diagnostic instrument system measured all ventilatory responses and energy expenditures. Volume and timing alterations in ventilation were characterized by measuring tidal volume (V T ), inspiratory time (T I ), inspiratory flow rate (V T /T I ), and expiratory time (T E ). Average ventilation, energy expenditure, and adequacy of ventilation were measured using minute ventilation (V W E ), oxygen consumption V W O 2 ), carbon dioxide production (V W CO 2 ), and partial pressure of end-tidal carbon dioxide (end-tidal PET CO2 ). Results indicated volume, timing, ventilation, and energy expenditure values remained closest to quiet breathing values for the comfortable SPL. Volume, ventilation, and energy expenditure were significantly greater for the high SPL and lower for the low SPL, compared to the baseline steady state, indicating that the low SPL causes a ventilatory deficit that was found to be paid back at the end of the speech task during the quiet breathing period. These results demonstrate that an individual's comfortable SPL is the least energyrequiring way to speech breathe. As SPL rises above or below comfortable SPL, speech breathing requires more energy.

Measurement of ‘Basal’ and Total Metabolism in Hereditarily Obese-Hyperglycemic Mice

1958 ◽  
Vol 193 (3) ◽  
pp. 495-498 ◽  
Author(s):  
Ruth McClintock ◽  
Nathan Lifson
Keyword(s):  
Carbon Dioxide ◽  
Oxygen Consumption ◽  
Energy Expenditure ◽  
Voluntary Movement ◽  
Carbon Dioxide Production ◽  
Open Circuit ◽  
Energy Output ◽  
Obese Mice ◽  
Energy Expenditures ◽  
Isotope Method

Measurements of oxygen consumption and carbon dioxide production were made by the Haldane open circuit method on hereditarily obese mice and littermate controls, and the energy expenditures were estimated. Studies were made on mice for short periods under ‘basal’ conditions, and for periods of approximately a day with the mice fasted and confined, fasted and relatively unconfined, and fed and unconfined. The total energy expenditures of fed and unconfined obese mice were found to be higher than those of nonobese littermate controls by virtue of a) increased ‘basal metabolism’, b) greater energy expenditure associated with feeding, and possibly c) larger energy output for activity despite reduced voluntary movement. The values obtained for total metabolism confirm those previously determined by an isotope method for measuring CO2 output.

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.

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.

Effects of changes in level and pattern of breathing on the sensation of dyspnea

1990 ◽  
Vol 69 (4) ◽  
pp. 1290-1295 ◽  
Author(s):  
T. Chonan ◽  
M. B. Mulholland ◽  
M. D. Altose ◽  
N. S. Cherniack
Keyword(s):  
Steady State ◽  
Spontaneous Breathing ◽  
Minute Ventilation ◽  
Constant Level ◽  
Normal Male ◽  
Respiratory Effort ◽  
Breathing Frequency ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Male Subjects

Breathing during hypercapnia is determined by reflex mechanisms but may also be influenced by respiratory sensations. The present study examined the effects of voluntary changes in level and pattern of breathing on the sensation of dyspnea at a constant level of chemical drive. Studies were carried out in 15 normal male subjects during steady-state hypercapnia at an end-tidal PCO2 of 50 Torr. The intensity of dyspnea was rated on a Borg category scale. In one experiment (n = 8), the level of ventilation was increased or decreased from the spontaneously adopted level (Vspont). In another experiment (n = 9), the minute ventilation was maintained at the level spontaneously adopted at PCO2 of 50 Torr and breathing frequency was increased or decreased from the spontaneously adopted level (fspont) with reciprocal changes in tidal volume. The intensity of dyspnea (expressed as percentage of the spontaneous breathing level) correlated with ventilation (% Vspont) negatively at levels below Vspont (r = -0.70, P less than 0.001) and positively above Vspont (r = 0.80, P less than 0.001). At a constant level of ventilation, the intensity of dyspnea correlated with breathing frequency (% fspont) negatively at levels below fspont (r = -0.69, P less than 0.001) and positively at levels above fspont (r = 0.75, P less than 0.001). These results indicate that dyspnea intensifies when the level or pattern of breathing is voluntarily changed from the spontaneously adopted level. This is consistent with the possibility that ventilatory responses to changes in chemical drive may be regulated in part to minimize the sensations of respiratory effort and discomfort.

Dynamic and steady-state respiratory responses to bicycle exercise

1977 ◽  
Vol 42 (6) ◽  
pp. 959-967 ◽  
Author(s):  
D. H. Pearce ◽  
H. T. Milhorn
Keyword(s):  
Carbon Dioxide ◽  
Minute Ventilation ◽  
Work Load ◽  
Normal Male ◽  
Clear Cut ◽  
Ventilatory Responses ◽  
Delay Times ◽  
End Tidal ◽  
Repeated Runs ◽  
Respiratory Responses

The transient respiratory responses of 10 normal male volunteers to step changes in work load from 0 to 300, 600, and 800 kpm/min were determined by breath-by-breath analysis for tidal volume, minute ventilation, respiratory frequency, end-tidal oxygen and carbon dioxide tensins, oxygen uptake, carbon dioxide elimination, respiratory exchange ratio, and heart rate. Ten experiments were averaged on a 5-s interval basis. Quantitative measures of the dynamics (delay times, half-times, times to peaks, times to plateaus, and plateau amplitudes) are presented. These parameters generally vary with work load and reflect the speed of response of various components of the system. Rapid ventilatory responses were seen at the initiation and termination of exercise; however, they required up to 32.5 s for full development. Repeated runs on three subjects at 600 kpm/min indicate that the experiments are grossly repeatable. The data, at the initiation of exercise, are consistent with the concept of cardiodynamic hyperpnea while the results are not as clear-cut at the termination of exercise.

scholarly journals Minute ventilation/carbon dioxide production in chronic heart failure

2021 ◽  
Vol 30 (159) ◽  
pp. 200141
Author(s):  
Piergiuseppe Agostoni ◽  
Susanna Sciomer ◽  
Pietro Palermo ◽  
Mauro Contini ◽  
Beatrice Pezzuto ◽  
...  
Keyword(s):  
Heart Failure ◽  
Carbon Dioxide ◽  
Chronic Heart Failure ◽  
Dead Space ◽  
Minute Ventilation ◽  
Carbon Dioxide Production ◽  
Absolute Number ◽  
Prognostic Scores ◽  
And Gender ◽  
End Tidal

In chronic heart failure, minute ventilation (V′E) for a given carbon dioxide production (V′CO2) might be abnormally high during exercise due to increased dead space ventilation, lung stiffness, chemo- and metaboreflex sensitivity, early metabolic acidosis and abnormal pulmonary haemodynamics. The V′Eversus V′CO2 relationship, analysed either as ratio or as slope, enables us to evaluate the causes and entity of the V′E/perfusion mismatch. Moreover, the V′E axis intercept, i.e. when V′CO2 is extrapolated to 0, embeds information on exercise-induced dead space changes, while the analysis of end-tidal and arterial CO2 pressures provides knowledge about reflex activities. The V′Eversus V′CO2 relationship has a relevant prognostic power either alone or, better, when included within prognostic scores. The V′Eversus V′CO2 slope is reported as an absolute number with a recognised cut-off prognostic value of 35, except for specific diseases such as hypertrophic cardiomyopathy and idiopathic cardiomyopathy, where a lower cut-off has been suggested. However, nowadays, it is more appropriate to report V′Eversus V′CO2 slope as percentage of the predicted value, due to age and gender interferences. Relevant attention is needed in V′Eversus V′CO2 analysis in the presence of heart failure comorbidities. Finally, V′Eversus V′CO2 abnormalities are relevant targets for treatment in heart failure.

Mixed-effects Modeling of the Intrinsic Ventilatory Depressant Potency of Propofol in the Non-steady State

2004 ◽  
Vol 100 (2) ◽  
pp. 240-250 ◽  
Author(s):  
Thomas Bouillon ◽  
Joergen Bruhn ◽  
Lucian Radu-Radulescu ◽  
Corina Andresen ◽  
Carol Cohane ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Time Course ◽  
Minute Ventilation ◽  
Carbon Dioxide Production ◽  
Response Model ◽  
Indirect Response Model ◽  
Indirect Response ◽  
Arterial Blood ◽  
Ventilatory Depression

Background Despite the ubiquitous use of propofol for anesthesia and conscious sedation and numerous publications about its effect, a pharmacodynamic model for propofol-induced ventilatory depression in the non-steady state has not been described. To investigate propofol-induced ventilatory depression in the clinically important range (at and below the metabolic hyperbola while carbon dioxide is accumulating because of drug-induced ventilatory depression), the authors applied indirect effect modeling to Paco2 data at a fraction of inspired carbon dioxide of 0 during and after administration of propofol. Methods Ten volunteers underwent determination of their carbon dioxide responsiveness by a rebreathing design. The parameters of a power function were fitted to the end-expiratory carbon dioxide and minute ventilation data. The volunteers then received propofol in a stepwise ascending pattern with use of a target-controlled infusion pump until significant ventilatory depression occurred (end-tidal pressure of carbon dioxide > 65 mmHg and/or imminent apnea). Thereafter, the concentration was reduced to 1 microg/ml. Propofol pharmacokinetics and the Paco2 were determined from frequent arterial blood samples. An indirect response model with Bayesian estimates of the pharmacokinetics and carbon dioxide responsiveness in the absence of drug was used to describe the Paco2 time course. Because propofol reduces oxygen requirements and carbon dioxide production, a correction factor for propofol-induced decreasing of carbon dioxide production was included. Results The following pharmacodynamic parameters were found to describe the time course of hypercapnia after administration of propofol (population mean and interindividual variability expressed as coefficients of variation): F (gain of the carbon dioxide response), 4.37 +/- 36.7%; ke0, CO2, 0.95 min-1 +/- 59.8%; baseline Paco2, 40.9 mmHg +/- 12.8%; baseline minute ventilation, 6.45 l/min +/- 36.3%; kel, CO2, 0.11 min-1 +/- 34.2%; C50,propofol, 1.33 microg/ml +/- 49.6%; gamma, 1.68 +/- 21.3%. Conclusion Propofol at common clinical concentrations is a potent ventilatory depressant. An indirect response model accurately described the magnitude and time course of propofol-induced ventilatory depression. The indirect response model can be used to optimize propofol administration to reduce the risk of significant ventilatory depression.

Nitric Oxide Synthase Inhibitors Alter Ventilation in Isoflurane Anesthetized Rats 

1998 ◽  
Vol 88 (5) ◽  
pp. 1240-1248 ◽  
Author(s):  
Gaurav M. Patel ◽  
Damian J. Horstman ◽  
Milton J. Adams ◽  
George F. Rich
Keyword(s):  
Nitric Oxide ◽  
Carbon Dioxide ◽  
Minute Ventilation ◽  
Respiratory Rhythm ◽  
Anesthetic Depth ◽  
Ventilatory Responses ◽  
Nos Inhibitors ◽  
Carbon Dioxide Levels ◽  
End Tidal ◽  
Oxide Synthase

Background Nitric oxide (NO) is present in medullary structures and can modulate respiratory rhythm. The authors determined if spontaneous ventilation at rest and in response to increased carbon dioxide is altered by selective neuronal NO synthase (NOS; 7-nitro-indazole, 7-NI) or nonselective (neuronal plus endothelial) NOS (NG-L-arginine methyl ester [L-NAME] and NG-monomethyl L-arginine [L-NMMA]) inhibitors in rats anesthetized with isoflurane. Methods Fifty-four rats received either L-NAME or L-NMMA (1, 10, and 30 mg/kg) or 7-NI (20, 80, and 400 mg/kg) and were compared with time controls (isoflurane = 1.4%), with isoflurane concentrations (1.6%, 1.8%, and 2%) increased consistent with the increased anesthetic depth caused by NOS inhibitors, or with L-arginine (300 mg/kg). Tidal volume (VT), respiratory frequency (f), minute ventilation (VE), and ventilatory responses to increasing carbon dioxide were determined. Results L-NAME and L-NMMA decreased resting VT and VE, whereas 7-NI had no effect. Increasing concentrations of isoflurane decreased resting f, VT, and VE. L-NAME and L-NMMA decreased VT and VE, whereas 7-NI had no effect at 8%, 9%, and 10% end-tidal carbon dioxide (ETCO2). Increasing concentrations of isoflurane decreased f, VT, and VE at 8%, 9%, and 10% ETCO2. The slope of VE versus ETCO2 was decreased by isoflurane but was unaffected by L-NAME, L-NMMA, or 7-NI. L-arginine alone had no effect on ventilation. Conclusions Nonselective NOS inhibitors decreased VT and VE at rest and at increased carbon dioxide levels but did not alter the slope of the carbon dioxide response. Selective neuronal NOS inhibition had no effect, suggesting that endothelial NOS may be the isoform responsible for altering ventilation. Finally, the cause of the decreased ventilation is not a result of the enhanced anesthetic depth caused by NOS inhibitors.

Effects of airway anesthesia on ventilatory responses to graded dead spaces and CO2

1988 ◽  
Vol 64 (5) ◽  
pp. 1885-1892 ◽  
Author(s):  
C. Shindoh ◽  
W. Hida ◽  
Y. Kikuchi ◽  
T. Chonan ◽  
H. Inoue ◽  
...  
Keyword(s):  
Steady State ◽  
Dead Space ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Co2 Response ◽  
Co2 Gas ◽  
Ventilatory Responses ◽  
Before And After ◽  
End Tidal ◽  
And Control

Ventilatory response to graded external dead space (0.5, 1.0, 2.0, and 2.5 liters) with hyperoxia and CO2 steady-state inhalation (3, 5, 7, and 8% CO2 in O2) was studied before and after 4% lidocaine aerosol inhalation in nine healthy males. The mean ventilatory response (delta VE/delta PETCO2, where VE is minute ventilation and PETCO2 is end-tidal PCO2) to graded dead space before airway anesthesia was 10.2 +/- 4.6 (SD) l.min-1.Torr-1, which was significantly greater than the steady-state CO2 response (1.4 +/- 0.6 l.min-1.Torr-1, P less than 0.001). Dead-space loading produced greater oscillation in airway PCO2 than did CO2 gas loading. After airway anesthesia, ventilatory response to graded dead space decreased significantly, to 2.1 +/- 0.6 l.min-1.Torr-1 (P less than 0.01) but was still greater than that to CO2. The response to CO2 did not significantly differ (1.3 +/- 0.5 l.min-1.Torr-1). Tidal volume, mean inspiratory flow, respiratory frequency, inspiratory time, and expiratory time during dead-space breathing were also depressed after airway anesthesia, particularly during large dead-space loading. On the other hand, during CO2 inhalation, these respiratory variables did not significantly differ before and after airway anesthesia. These results suggest that in conscious humans vagal airway receptors play a role in the ventilatory response to graded dead space and control of the breathing pattern during dead-space loading by detecting the oscillation in airway PCO2. These receptors do not appear to contribute to the ventilatory response to inhaled CO2.

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