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PubMed1993

The tidal volume response to incremental exercise in COPD.

Patients with severe COPD often exhibit a ventilatory limit to exercise. This is associated with a shallow breathing pattern when compared with normal control subjects. It is unclear, however, what factors affect differences in breathing patterns within this patient population. To further investigate the tidal volume (VT) response to exercise in severe COPD, nine patients were recruited to undergo a maximal incremental exercise test. Pulmonary function tests, collection of expired gases, and continuous pulse oximetry were performed. As a group, the results were as follows (mean +/- SD): The FEV1 was 31 +/- 7 percent of predicted, the FRC was 143 +/- 18 percent of predicted, and the DCO was 47 +/- 15 percent of predicted. Exercise testing showed an oxygen consumption at peak exercise of only 44 +/- 9 percent predicted, a dyspnea index of 101 +/- 19 percent predicted, a heart rate at peak exercise of 75 +/- 12 percent predicted, a tidal volume at peak exercise (PKVT) of 1.23 +/- .35, a respiratory rate at peak exercise (PKfb) of 26 +/- 6, and an oxygen saturation at peak exercise (PKO2sat) of 96 +/- 4 percent. An anaerobic threshold (AT) occurred in seven of the nine patients at a mean of 31 +/- 8 percent predicted maximal oxygen consumption. Regression analysis showed the PKVT to be inversely correlated with the FEV1 (r = -0.76; p = 0.01) and the PKfb (r = -0.85; p = 0.003), while positively correlating with the FRC (r = +0.80; p = 0.01) and the PKO2sat (r = +0.69; p = 0.04). Additionally, there was a trend for the PKVT to be inversely related with the AT (r = -0.72; p = 0.06). In COPD, the more severe the obstruction and hyperinflation, the larger the VT response to exercise. This may serve to avoid a deleterious increase in autoPEEP by promoting a lengthening of the expiratory time. Furthermore, given the association of an earlier AT and a higher PKO2sat with a larger PKVT, this would suggest that such a response may minimize the effects of dead space and/or autoPEEP on O2 delivery (early AT).

Anaerobic Threshold↗

PubMed1993

Tidal volume measurements in newborns using respiratory inductive plethysmography.

Respiratory inductive plethysmography (RIP) is a well-accepted noninvasive technology for monitoring breathing patterns in adults. Prior attempts to calibrate this device in babies have been fraught with technical difficulties, thereby limiting applications in this population. Recently, a new method, qualitative diagnostic calibration (QDC), has been shown to provide accurate calibration of tidal volume in adults. The QDC method is based upon principles of the isovolume maneuver and carried out during natural breathing without specialized respiratory maneuvers or postural changes. We calibrated RIP with QDC in the supine posture and compared tidal volume (VT) measured with RIP to VT by a face mask-pneumotachograph (PNT) in 21 healthy full-term newborns in supine and prone postures. Eleven of the babies were calibrated during active sleep and 10 in quiet sleep. The mean VT in the supine and prone postures were 19 and 25 ml, respectively. In the supine and prone postures, weighted mean difference between RIP (VT) and PNT (VT) and 95% confidence intervals were -0.05 ml (-0.27, 0.18) and -0.32 ml (-0.08, 0.55), respectively. There was no difference in the accuracy of RIP relative to PNT calibrated during active sleep when thoracoabdominal incoordination was present or quiet sleep when it was not in either the supine or the prone postures. Therefore, in full-term infants, RIP calibrated with QDC solely in the supine posture provides clinically acceptable measurements of VT in both supine and prone postures.

Analysis of Variance↗

PubMed1997

Heart rate change as a function of age, tidal volume and body position when breathing using voluntary cardiorespiratory synchronization.

Voluntary cardiorespiratory synchronization (VCRS), where inspiration and expiration follows a fixed number of heart beats, was used to investigate heart rate change (HRC) in 16 subjects (grouped as 20-30 and 46-57 years of age) as a function of age, body position, and respiratory tidal volumes of 500 and 1000 ml. In phase I, the subjects, following a tone, inspired for two heart beats and expired for three beats. In phase II, the older group's breathing pattern was 2/2, 2/3, 3/3, 4/4, 5/5, and 6/6 inspiratory and expiratory heart beats, respectively, per respiratory cycle. Comparing the younger and older groups, we found a statistically significant (p < 0.05) decrease in HRC for beat 1, 2, and 4 of the respiratory cycle in the supine position, and also for beat 2 in the sitting position, but no significant change with tidal volume. The ratio of the younger to older group's beat 2 HRC was 2.54 sitting and 3.54 supine. Increasing the number of beats per respiratory cycle from four to 12 resulted in the HRC growing from 1.8 to 7.5 beats over the respiratory cycle, showing the importance of respiratory rate in measuring HRC. VCRS can easily observe the influence of each phase of the respiratory cycle on the HRC and show the unique phase dependent changes that occur.

Adult↗

PubMed2004

Increased tidal volume variability in children is a better marker of opioid-induced respiratory depression than decreased respiratory rate.

OBJECTIVE: During opioid administration, decreasing respiratory rate is typically used as a predictor of respiratory depression. Prior to opioid-induced apnea, progressively irregular breathing patterns have been noticed. We hypothesize that opioid administration to children will increase tidal volume variability (TV(var)) and that this will be a better predictor of respiratory depression than a decrease in respiratory rate. METHODS: We recruited 32 children aged 2-8 years scheduled to undergo surgery. During spontaneous ventilation, flow rates and respiratory rates were continuously recorded, while remifentanil was infused at stepwise increasing doses each lasting 10 min. The infusion was continued until the patient showed signs of respiratory depression. Flow data from each dose was used to calculate tidal volumes, from which TV(var) was calculated. The respiratory rate and TV(var) during the last (D(last)), second to last (D-2), and third to last (D-3), administered doses were compared to those during baseline (fourth to last dose). We chose a threshold of TV(var) increase and compared it to a decrease in respiratory rate below 10 breaths per min as predictors of respiratory depression. RESULTS: Compared to baseline, the TV(var) increased by 336% and 668% during D(-2) and D(last), respectively, whereas respiratory rate decreased by 14.3%, 31.7%, and 55.5% during D(-3), D(-2), and D(last), respectively. A threshold increase in TV(var) of 150% over baseline correctly predicted respiratory depression in 41% of patients, compared to a drop in respiratory rate correctly predicting 22% of patients. CONCLUSIONS: TV(var) increases as children approach opioid-induced respiratory depression. This is a more useful predictor of respiratory depression than a fall in respiratory rate because the TV(var) increase is 10 times the drop in respiratory rate. A TV(var) increase also correctly predicts respiratory depression twice as often as decreased respiratory rate and is independent of age-related alterations in physiologic respiratory rates.

Analgesics, Opioid↗

PubMed2003

End-tidal CO2 as a function of tidal volume in mechanically ventilated infants.

OBJECTIVE: To test the hypothesis that end-tidal CO(2) (PETCO(2)) varies with tidal volume (Vt) in preterm infants. DESIGN: Intervention study, nonrandomized trial. SETTING: Neonatal ICU, regional referral center. SUBJECTS: 29 preterm infants 790 to 2135 g in weight requiring mechanical ventilation studied on 73 occasions. INTERVENTION: Measurement of PETCO(2) during variations of Vt. MEASUREMENT: Statistical correlation of PETCO(2) to Vt. RESULT: PETCO(2) is minimal when Vt is either too low or too high. CONCLUSION: Vt, through its effect on dead space/Vt (Vd/Vt) ratios and arterial-alveolar CO(2) differences, has a significant effect on PETCO(2). Observation of PETCO(2) across a range of Vt can be used to select an appropriate Vt for preterm infants requiring mechanical ventilation.

Birth Weight↗

PubMed1975

Effects of changes of frequency and tidal volume of controlled ventilation: measurements at constant arterial Pco2 in dogs.

Seven Alsatian dogs were anaesthetized with thiopentone, paralysed with pancuronium, and ventilated with 1% halothane in a mixture of air and oxygen in such a way as to maintain Paco2 at 40 mm Hg and Pao2 at 150 mm Hg. From various respiratory and circulatory measurementts the following variables were determined: physiologicaldeadspace, cardiac output, venous admixture, respiratory compliance and resistance, and oxygen and carbondioxide exchcnage. After a controlseries of measurements at a ventilator frequency of was doubled to 50/min and adjustments to tidal volume and inspired oxygen concentration made to maintain constancy of blood gas tensions. The same procedure was followed again at 25/min, l/min and finally at 25/min. At each frequency the I:E ratio was kept at 1/2, the shape of the inspiratory flow waveform was kept constant (a rapid increase followed by a steady decline to zero) and expiration was passive to atmosphere. Mean results showed that physiological deadspace changed relatively little with frequency so that the deadspace:tidal volume ratio increased significantly on changing to 50/min (by 24%) and decreased significantly on changing to 6/min (by 46%). Changes of cardiac output and venous admixture were either not significant or on the borderline of significance and the 95% confidence limits of these changes were within +14%, --12% for cardiac outpur and within plus or minus1.4% of cardiac output for venous admixture. Tt is concluded that, provided Paco2 and Pa02 and mean air way pressure are kept constant, the frequency of ventilation is not important, even over a wide range of values.

Airway Resistance↗

PubMed1990

Adverse effects of large tidal volume and low PEEP in canine acid aspiration.

When normal lungs are ventilated with large tidal volumes (VT) and end-inspired pressures (Pei), surfactant is depleted and pulmonary edema develops. Both effects are diminished by positive end-expiratory pressure (PEEP). We reasoned that ventilatory with large VT-low PEEP would similarly increase edema following acute lung injury. To test this hypothesis, we ventilated dogs 1 h after hydrochloric acid (HCl) induced pulmonary edema with a large VT (30 ml/kg) and low PEEP (3 cm H2O) (large VT-low PEEP) and compared their results with dogs ventilated with a smaller VT (15 ml/kg) and 12 cm H2O PEEP (small VT-high PEEP). The small VT was the smallest that maintained eucapnia in our preparation; the large VT was chosen to match Pei and end-inspired lung volume. Pulmonary capillary wedge transmural pressure (Ppwtm) was kept at 8 mm Hg in both groups. Five hours after injury, the median lung wet weight to body weight ratio (WW/BW) was 25 g/kg higher in the large VT-low PEEP group than in the small VT-high PEEP group (p less than 0.05). Venous admixture (Qva/Qt) was similarly greater in the large VT-low PEEP group (49.8 versus 23.5%) (p less than 0.05). We conclude that small VT-high PEEP is a better mode of ventilating acute lung injury than large VT-low PEEP because edema accumulation is less and venous admixture is less. These advantages did not result from differences in Pei, end-inspiratory lung volume, or preload (Ppwtm).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2003

Exhaled breath condensate nitrite and its relation to tidal volume in acute lung injury.

STUDY OBJECTIVE: Mechanical ventilation may damage the lung. Low tidal volume (VT) is protective, but VT is scaled to body weight (BW) and may be high in functionally small ARDS lungs. We hypothesized that exhaled breath condensate (EBC) nitrite (NO(2)(-)) concentration may increase with lung distension. DESIGN: Prospective, noncontrolled study. SETTING: University hospital and medical ICU. PATIENTS: Thirty-five ICU patients requiring mechanical ventilation (severe pneumonia, n = 31; exacerbated COPD, n = 4). Patients were scored according to American and European Consensus Conference on ARDS criteria (AECC) [no lung injury, n = 7; acute lung injury, n = 13; ARDS, n = 15], as well as the Murray lung injury severity score (LISS) [score 0, n = 3; score 0.1 to 2.5, n = 19; score > 2.5, n = 13]. INTERVENTIONS: EBC was collected and analyzed for NO(2)(-), interleukin (IL)-6, and IL-8. Serum was analyzed for IL-6, IL-8, and procalcitonin. RESULTS: and measurements: EBC NO(2)(-) correlated well with VT (milliliters per kilogram of BW; r = 0.79, p < 0.0001) and expiratory minute volume (r = 0.60, p < 0.0001) but not with other ventilatory parameters or parameters of pulmonary (EBC IL-6, EBC IL-8) or systemic (serum IL-6, IL-8, and procalcitonin) inflammation. The ratio of EBC NO(2)(-) and the size of the VT correlated directly with lung injury (AECC, r = 0.66, p < 0.0001; LISS, r = 0.84, p < 0.0001). CONCLUSION: EBC NO(2)(-) increased linearly with VT. The ratio of EBC NO(2)(-) to VT is assumed to reflect NO(2)(-) release at a given VT. An increase in this ratio indicates an inappropriate increase of NO(2)(-) production most likely due to mechanical stress of the remaining open lung units in injured lungs. We conclude that the EBC NO(2)(-)/VT ratio may help to identify situations of critical mechanical stress.

Acute Disease↗

PubMed1994

Automatic selection of tidal volume, respiratory frequency and minute ventilation in intubated ICU patients as start up procedure for closed-loop controlled ventilation.

OBJECTIVE: Before a patient can be connected to a mechanical ventilator, the controls of the apparatus need to be set up appropriately. Today, this is done by the intensive care professional. With the advent of closed loop controlled mechanical ventilation, methods will be needed to select appropriate start up settings automatically. The objective of our study was to test such a computerized method which could eventually be used as a start-up procedure (first 5-10 minutes of ventilation) for closed-loop controlled ventilation. DESIGN: Prospective Study. SETTINGS: ICU's in two adult and one children's hospital. PATIENTS: 25 critically ill adult patients (age > or = 15 y) and 17 critically ill children selected at random were studied. INTERVENTIONS: To stimulate 'initial connection', the patients were disconnected from their ventilator and transiently connected to a modified Hamilton AMADEUS ventilator for maximally one minute. During that time they were ventilated with a fixed and standardized breath pattern (Test Breaths) based on pressure controlled synchronized intermittent mandatory ventilation (PCSIMV). MEASUREMENTS AND MAIN RESULTS: Measurements of airway flow, airway pressure and instantaneous CO2 concentration using a mainstream CO2 analyzer were made at the mouth during application of the Test-Breaths. Test-Breaths were analyzed in terms of tidal volume, expiratory time constant and series dead space. Using this data an initial ventilation pattern consisting of respiratory frequency and tidal volume was calculated. This ventilation pattern was compared to the one measured prior to the onset of the study using a two-tailed paired t-test. Additionally, it was compared to a conventional method for setting up ventilators. The computer-proposed ventilation pattern did not differ significantly from the actual pattern (p > 0.05), while the conventional method did. However the scatter was large and in 6 cases deviations in the minute ventilation of more than 50% were observed. CONCLUSIONS: The analysis of standardized Test Breaths allows automatic determination of an initial ventilation pattern for intubated ICU patients. While this pattern does not seem to be superior to the one chosen by the conventional method, it is derived fully automatically and without need for manual patient data entry such as weight or height. This makes the method potentially useful as a start up procedure for closed-loop controlled ventilation.

Adolescent↗

PubMedDate not supplied

Whole-body plethysmography, does it measure tidal volume of small animals?

A whole-body plethysmograph was used for mice. The increase in pressure caused by each inhalation was equivalent to the increase that could be calculated to result from heating and humidification of the inhaled air. However, comprehending that a drop in temperature and humidity would cause an abrupt pressure decline during exhalation was difficult. Pressure changes in the plethysmograph were also studied with an artificial chest, modeling the respiratory mechanics, but without the "inhaled" air being heated or humidified. The "chest" consisted of a metal bellows oscillated by a stepper motor 25 to 175 times per minute. Hereby air (0.05 to 0.20 mL) moved in and out of the bellows. The air passed through a polyethylene tube, the length of which was proportional to "airway resistance" and varied from 5 to 35 cm. It was found that the pressure oscillation was affected not only by "tidal volume" of the mechanical chest but also by "respiratory rate" and by "airway resistance." We concur with previous investigators that the plethysmograph pressure reflects alveolar pressure and that fluctuations cannot be explained by changes in temperature and humidity. Accordingly, tidal volume can only be qualitatively and not quantitatively assessed.

Animals↗

PubMed1992

Lung and chest wall impedances in the dog: effects of frequency and tidal volume.

Dependences of the mechanical properties of the respiratory system on frequency (f) and tidal volume (VT) in the normal ranges of breathing are not clear. We measured, simultaneously and in vivo, resistance and elastance of the total respiratory system (Rrs and Ers), lungs (RL and EL), and chest wall (Rcw and Ecw) of five healthy anesthetized paralyzed dogs during sinusoidal volume oscillations at the trachea (50-300 ml, 0.2-2 Hz) delivered at a constant mean lung volume. Each dog showed the same f and VT dependences. The Ers and Ecw increased with increasing f to 1 Hz and decreased with increasing VT up to 200 ml. Although EL increased slightly with increasing f, it was independent of VT. The Rcw decreased from 0.2 to 2 Hz at all VT and decreased with increasing VT. Although the RL decreased from 0.2 to 0.6 Hz and was independent of VT, at higher f RL tended to increase with increasing f and VT (i.e., as peak flow increased). Finally, the f and VT dependences of Rrs were similar to those of Rcw below 0.6 Hz but mirrored RL at higher f. These data capture the competing influences of airflow nonlinearities vs. tissue nonlinearities on f and VT dependence of the lung, chest wall, and total respiratory system. More specifically, we conclude that 1) VT dependences in Ers and Rrs below 0.6 Hz are due to nonlinearities in chest wall properties, 2) above 0.6 Hz, the flow dependence of airways resistance dominates RL and Rrs, and 3) lung tissue behavior is linear in the normal range of breathing.

Airway Resistance↗

PubMed1983

A respiratory function jacket for measuring tidal volume and changes in FRC.

We describe a simple application of a mercury-in-rubber strain gauge in a jacket used to measure tidal volume in paralyzed, mechanically ventilated rabbits. The jacket produces a record with a straight base line. Shifts of this base line can be used to assess changes in functional residual capacity (FRC).

Animals↗

PubMed1990

[The tidal volume, arterial blood gas and functional residual capacity changes during negative extra-thoracic pressure ventilation and positive airway pressure ventilation].

Eight patients, of ASA physical status I or II soon after total knee replacement under general anesthesia, were studied to compare negative extra-thoracic pressure ventilation (NETPV) with positive airway pressure ventilation (PAPV). The measured parameters during the two ventilatory modes were tidal volume, arterial blood gas and functional residual capacity change (delta FRC). Tidal volume obtained during NETPV was 60 to 80% of that during PAPV at the same absolute values of peak pressure. delta FRC obtained during NETPV was 30 to 40% of that during PAPV at the same absolute values of end-expiratory pressure. A decrease in the esophageal pressure was 4 to 11cmH2O at an end-expiratory negative extra-thoracic pressure of -10 to -20 cmH2O. When the patients were ventilated with the same values of minute ventilation on NETPV and PAPV, there was no significant difference in blood gas values. These findings suggest that efficiency of NETPV is less than that of PAPV at the same absolute working pressure but pulmonary gas exchange of NETPV is almost equal to that of PAPV at the same minute ventilation in the normal lung.

Aged↗

PubMed2001

Influence of tidal volume on alveolar recruitment. Respective role of PEEP and a recruitment maneuver.

Both reduction in tidal volume (VT) and alveolar recruitment may be important to limit ventilator-associated lung injury during mechanical ventilation of patients with the acute respiratory distress syndrome (ARDS). The aim of this study was to assess the risk of alveolar derecruitment associated with VT reduction from 10 to 6 ml/kg. Whether this VT-related derecruitment could be reversed, either by a recruitment maneuver or by an increase in positive end-expiratory pressure (PEEP) level, was also investigated. Fifteen patients with ARDS were successively ventilated using conventional VT (CVT = 10 +/- 1 ml/kg) and low VT (LVT = 6 +/- 1 ml/ kg); total PEEP (PEEPtot) was individually set at the lower inflection point (Plip) of the pressure-volume curve (PEEPtot = 11 +/- 4 cm H(2)O). Pressure-volume curves were recorded from zero PEEP (ZEEP) and from PEEP, and recruited volume (Vrec) was calculated as the volume difference between the two curves for a given pressure. Despite a similar PEEPtot, Vrec was significantly lower with LVT than with CVT, indicating low VT-induced alveolar derecruitment. Reduction in VT was associated with a reduced Sa(O(2)). In 10 patients, Vrec was also measured before and after a recruitment maneuver (two sustained inflations at 45 cm H(2)O), and after an increase in PEEP (by 4 cm H(2)O). Low VT-induced derecruitment was reversed by a recruitment maneuver and by increasing PEEP. We conclude that a reduction in VT could be responsible for alveolar derecruitment, which may be transiently reversed by a reexpansion maneuver or prevented by a PEEP increase above Plip.

Adult↗

PubMed1990

Measurement of tidal volume using a pneumotachometer during high-frequency oscillation.

To assess the accuracy of a pneumotachometer (PN) for tidal volume (VT) measurements during high-frequency oscillation (HFO), we determined simultaneously VT using a PN and a full body plethysmograph (PL) in 12 rabbits. HFO was delivered with an oscillator at a frequency of 10 Hz, mean airway pressure of 8 cm H2O, and inspiratory time of 50%. Pressure amplitude (delta P) was varied as follows: 40, 60, 80, 20, 100, 40 cm H2O. Finally, in ten rabbits a spacer equal in deadspace (VD) to that of the PN (15 ml) was left in-line for 5 min. Blood gases were obtained before and after the spacer was added. We found that VT-PN correlates well with VT-PL (r = .92), although the difference between VT-PN and VT-PL is greater at large VT. Significant respiratory acidosis developed with the spacer in-line. PN may be used to trend VT during HFO but PN must not be left in-line, as increased VD seriously affects ventilation.

Animals↗

PubMed1992

Effect of tidal volume on gas exchange and oxygen transport in the adult respiratory distress syndrome.

The effect of tidal volume (VT) on gas exchange and oxygen delivery (DO2) was studied in nine patients with adult respiratory distress syndrome (ARDS) and in 10 postoperative open-heart surgery patients (CABG). During controlled mechanical ventilation, VT was initially 10 to 12 ml/kg, followed by an increase and reduction of 25% (1.25 VT and 0.75 VT, respectively). In both groups of patients, dead space (VD) correlated strongly with VT (p < 0.001), while the VD/VT ratio was independent of VT. PaO2 tended to increase in CABG patients and decrease in ARDS patients at 1.25 VT. Arterial oxygen saturation (SaO2) did not change at 1.25 VT but decreased at 0.75 VT (p < 0.001) in the ARDS group. Venous admixture (QS/QT) decreased with 1.25 VT and increased with 0.75 VT (p < 0.001). A relatively larger increase in cardiac output compensated for the increased QS/QT and the reduced SaO2, resulting in significantly higher DO2 with 0.75 VT (p < 0.01). A lower VT resulted in improved balance between pulmonary gas exchange and whole body oxygen supply.

Blood Gas Analysis↗

PubMed2002

Effects of body posture and tidal volume on inter- and intraregional ventilation distribution in healthy men.

The influences of body posture and tidal volume (VT) on inter- and intraregional ventilation inhomogeneity were assessed by normalized phase III slope (Sn(III)) analysis of multiple-breath washout recordings of SF(6) and He in 11 healthy men. Washouts with target VT of 750, 1,000, and 1,250 ml were performed standing and supine. A linear-fit method was used to establish the contributions of convection-dependent (interregional) (cdi) and diffusion-convection interaction-dependent (intraregional) inhomogeneity (dcdi). Overall inhomogeneity was defined as the sum of cdi and dcdi. The difference in first-breath Sn(III) for SF(6) vs. He, the (SF(6) - He)Sn(III), served as an index of intra-acinar inhomogeneity. Multiple-regression analysis revealed greater cdi supine vs. standing (P < 0.001) but no significant effects of posture on dcdi or overall inhomogeneity. Larger VT were associated with greater cdi (P < 0.001), particularly when supine, but reduced dcdi (P < 0.001), overall inhomogeneity (P < 0.001), and (SF(6) - He)Sn(III) (P = 0.031). In conclusion, during resting breathing overall and intraregional ventilation inhomogeneities remain unchanged when the supine posture is assumed and improve with larger VT, but supine posture and larger breaths result in greater interregional inhomogeneities.

Adolescent↗

PubMed1987

Beta-blockade reduces tidal volume during heavy exercise in trained and untrained men.

The effects of beta-blockade on tidal volume (VT), breath cycle timing, and respiratory drive were evaluated in 14 endurance-trained [maximum O2 uptake (VO2max) approximately 65 ml X kg-1 X min-1] and 14 untrained (VO2max approximately 50 ml X kg-1 X min-1) male subjects at 45, 60, and 75% of unblocked VO2max and at VO2max. Propranolol (PROP, 80 mg twice daily), atenolol (ATEN, 100 mg once a day) and placebo (PLAC) were administered in a randomized double-blind design. In both subject groups both drugs attenuated the increases in VT associated with increasing work rate. CO2 production (VCO2) was not changed by either drug during submaximal exercise but was reduced in both subject groups by both drugs during maximal exercise. The relationship between minute ventilation (VE) and VCO2 was unaltered by either drug in both subject groups due to increases in breathing frequency. In trained subjects VT was reduced during maximal exercise from 2.58 l/breath on PLAC to 2.21 l/breath on PROP and to 2.44 l/breath on ATEN. In untrained subjects VT at maximal exercise was reduced from 2.30 l/breath on PLAC to 1.99 on PROP and 2.12 on ATEN. These observations indicate that 1) since VE vs. VCO2 was not altered by beta-adrenergic blockade, the changes in VT and f did not result from a general blunting of the ventilatory response to exercise during beta-adrenergic blockade; and 2) blockade of beta 1- and beta 2-receptors with PROP caused larger reductions in VT compared with blockade of beta 1-receptors only (ATEN), suggesting that beta 2-mediated bronchodilation plays a role in the VT response to heavy exercise.

Adrenergic beta-Antagonists↗