Dynamic and steady-state respiratory responses to bicycle exercise

1977 ◽  
Vol 42 (6) ◽  
pp. 959-967 ◽  
Author(s):  
D. H. Pearce ◽  
H. T. Milhorn

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.

1978 ◽  
Vol 44 (1) ◽  
pp. 97-103 ◽  
Author(s):  
R. Casaburi ◽  
B. J. Whipp ◽  
K. Wasserman ◽  
S. N. Koyal

To investigate factors controlling ventilation under conditions where the applied work load remains constant, but where hypothesized proprioceptive influences would be expected to vary, five subjects exercised at a constant work rate of 50 W on a cycle ergometer at pedaling rates which varied sinusoidally between 40 and 80 rpm. Each subject exercised continuously for 30 min at each of five sinusoidal periods. Minute ventilation (VE), carbon dioxide output (VCO2), oxygen uptake (VO2), and heart rate were computed breath-by-breath and amplitude and phase relations were extracted. We observed small fluctuations in VCO2 and VO2 engendered by varying metabolic requirements of moving the legs at varying rates. VE fluctuations were closely in phase with VCO2 and the amplitudes of the fluctuations were highly significantly correlated (r = 0.83, P less than 0.001); consequently end-tidal carbon dioxide tension fluctuations were small. Variation of pedaling rate, therefore, did not produce a ventilatory response independent of the effect of VCO2. The ventilatory responses to these forcings are inconsistent with an appreciable role for neurally mediated influences from the exercising limbs and provide further evidence that the exercise hyperpnea is linked to CO2 flow to the central circulation.


2004 ◽  
Vol 97 (5) ◽  
pp. 1673-1680 ◽  
Author(s):  
Chris Morelli ◽  
M. Safwan Badr ◽  
Jason H. Mateika

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.


1977 ◽  
Vol 42 (6) ◽  
pp. 968-975 ◽  
Author(s):  
D. H. Pearce ◽  
H. T. Milhorn ◽  
G. H. Holloman ◽  
W. J. Reynolds

A computer-based system for the determination of tidal volume, respiratory frequency, minute ventilation, oxygen transfer, carbon dioxide transfer, respiratory exchange ratio, end-tidal oxygen, end-tidal carbon dioxide, and heart rate is presented. These variables are first determined on a breath-by-breath basis from data (expired carbon dioxide and oxygen fractions, airflow, and ECG) prerecorded on an FM magnetic type system. The breath-by-breath data are then averaged for each experimental run in 5-s increments. The 5-s increment data from a group of subjects can then be averaged and the SEM determined at prescribed periods of time. For the study of individual respiratory transient we found the 5-s increment data to be more useful than the breath-by-breath data because it has a lesser degree of fluctuation. The system is especially adapted to careful observation of the responses within the first few seconds of a change in work load. Appropriate computer programs are discussed. The results of several experiments are compared with data from other sources and found to be in good agreement.


1990 ◽  
Vol 69 (4) ◽  
pp. 1290-1295 ◽  
Author(s):  
T. Chonan ◽  
M. B. Mulholland ◽  
M. D. Altose ◽  
N. S. Cherniack

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.


1998 ◽  
Vol 41 (2) ◽  
pp. 239-248 ◽  
Author(s):  
Bridget A. Russell ◽  
Frank J. Cerny ◽  
Elaine T. Stathopoulos

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.


1998 ◽  
Vol 88 (5) ◽  
pp. 1240-1248 ◽  
Author(s):  
Gaurav M. Patel ◽  
Damian J. Horstman ◽  
Milton J. Adams ◽  
George F. Rich

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.


1998 ◽  
Vol 89 (3) ◽  
pp. 642-647. ◽  
Author(s):  
H. Daniel Babenco ◽  
Robert T. Blouin ◽  
Pattilyn F. Conard ◽  
Jeffrey B. Gross

Background Diphenhydramine is used as an antipruritic and antiemetic in patients receiving opioids. Whether it might exacerbate opioid-induced ventilatory depression has not been determined. Methods The ventilatory response to carbon dioxide during hyperoxia and the ventilatory response to hypoxia during hypercapnia (end-tidal pressure of carbon dioxide [PETCO2] is approximately equal to 54 mmHg) were determined in eight healthy volunteers. Ventilatory responses to carbon dioxide and hypoxia were calculated at baseline and during an alfentanil infusion (estimated blood levels approximately equal to 10 ng/ml) before and after diphenhydramine 0.7 mg/kg. Results The slope of the ventilatory response to carbon dioxide decreased from 1.08+/-0.38 to 0.79+/-0.36 l x min(-1) x mmHg(-1) (x +/- SD, P < 0.05) during alfentanil infusion; after diphenhydramine, the slope increased to 1.17+/-0.28 l x min(-1) x mmHg(-1) (P < 0.05). The minute ventilation (VE) at PETCO2 approximately equal to 46 mmHg (VE46) decreased from 12.1+/-3.7 to 9.7+/-3.6 l/min (P < 0.05) and the VE at 54 mmHg (VE54) decreased from 21.3+/-4.8 to 16.6+/-4.7 l/min during alfentanil (P < 0.05). After diphenhydramine, (VE46 did not change significantly, remaining lower than baseline at 9.9+/-2.9 l/min (P < 0.05), whereas VE54 increased significantly to 20.5+/-3.0 l/min. During hypoxia, VE at SpO2 = 90% (VE90) decreased from 30.5+/-9.7 to 23.1+/-6.9 l/min during alfentanil (P < 0.05). After diphenhydramine, the increase in VE90 to 27.2+/-9.2 l/min was not significant (P = 0.06). Conclusions Diphenhydramine counteracts the alfentanil-induced decrease in the slope of the ventilatory response to carbon dioxide. However, at PETCO2 = 46 mmHg, it does not significantly alter the alfentanil-induced shift in the carbon dioxide response curve. In addition, diphenhydramine does not exacerbate the opioid-induced depression of the hypoxic ventilatory response during moderate hypercarbia.


PEDIATRICS ◽  
1995 ◽  
Vol 95 (6) ◽  
pp. 864-867
Author(s):  
Janet G. Wingkun ◽  
Janet S. Knisely ◽  
Sidney H. Schnoll ◽  
Gary R. Gutcher

Objective. To determine whether there is a demonstrable abnormality in control of breathing in infants of substance-abusing mothers during the first few days of life. Methods. We enrolled 12 drug-free control infants and 12 infants of substance abusing mothers (ISAMs). These infants experienced otherwise uncomplicated term pregnancies and deliveries. The infants were assigned to a group based on the results of maternal histories and maternal and infant urine toxicology screens. Studies were performed during quiet sleep during the first few days of life. We measured heart rate, oxygen saturations via a pulse oximeter, end-tidal carbon dioxide (ET-CO2) level, respiratory rate, tidal volume, and airflow. The chemoreceptor response was assessed by measuring minute ventilation and the ET-CO2 level after 5 minutes of breathing either room air or 4% carbon dioxide. Results. The gestational ages by obstetrical dating and examination of the infants were not different, although birth weights and birth lengths were lower in the group of ISAMs. Other demographic data were not different, and there were no differences in the infants' median ages at the time of study or in maternal use of tobacco and alcohol. The two groups had comparable baseline (room air) ET-CO2 levels, respiratory rates, tidal volumes, and minute ventilation. When compared with the group of ISAMs, the drug-free group had markedly increased tidal volume and minute ventilation on exposure to 4% carbon dioxide. These increases accounted for the difference in sensitivity to carbon dioxide, calculated as the change in minute ventilation per unit change in ET-CO2 (milliliters per kg/min per mm Hg). The sensitivity to carbon dioxide of control infants was 48.66 ± 7.14 (mean ± SE), whereas that of ISAMs was 16.28 ± 3.14. Conclusions. These data suggest that ISAMs are relatively insensitive to challenge by carbon dioxide during the first few days of life. We speculate that this reflects an impairment of the chemoreceptor response.


1980 ◽  
Vol 48 (6) ◽  
pp. 1083-1091 ◽  
Author(s):  
R. Casaburi ◽  
R. W. Stremel ◽  
B. J. Whipp ◽  
W. L. Beaver ◽  
K. Wasserman

The effects of hyperoxia on ventilatory and gas exchange dynamics were studied utilizing sinusoidal work rate forcings. Five subjects exercised on 14 occasions on a cycle ergometer for 30 min with a sinusoidally varying work load. Tests were performed at seven frequencies of work load during air or 100% O2 inspiration. From the breath-by-breath responses to these tests, dynamic characteristics were analyzed by extracting the mean level, amplitude of oscillation, and phase lag for each six variables with digital computer techniques. Calculation of the time constant (tau) of the ventilatory responses demonstrated that ventilatory kinetics were slower during hyperoxia than during normoxia (P less than 0.025; avg 1.56 and 1.13 min, respectively). Further, for identical work rate fluctuations, end-tidal CO2 tension fluctuations were increased by hyperpoxia. Ventilation during hyperoxia is slower to respond to variations in the level of metabolically produced CO2, presumably because hyperoxia attenuates carotid body output; the arterial CO2 tension is consequently less tightly regulated.


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