Influence of lung volume on oxygen cost of resistive breathing

1986 ◽  
Vol 61 (1) ◽  
pp. 16-24 ◽  
Author(s):  
P. W. Collett ◽  
L. A. Engel
Keyword(s):  
Lung Volume ◽  
Work Of Breathing ◽  
Respiratory Muscles ◽  
Normal Subjects ◽  
Constant Load ◽  
Inspiratory Muscle ◽  
Mechanical Coupling ◽  
Inspiratory Muscles ◽  
Inspiratory Resistance ◽  
Residual Capacity

We examined the relationship between the O2 cost of breathing (VO2 resp) and lung volume at constant load, ventilation, work rate, and pressure-time product in five trained normal subjects breathing through an inspiratory resistance at functional residual capacity (FRC) and when lung volume (VL) was increased to 37 +/- 2% (mean +/- SE) of inspiratory capacity (high VL). High VL was maintained using continuous positive airway pressure of 9 +/- 2 cmH2O and with the subjects coached to relax during expiration to minimize respiratory muscle activity. Six paired runs were performed in each subject at constant tidal volume (0.62 +/- 0.2 liters), frequency (23 +/- 1 breaths/min), inspiratory flow rate (0.45 +/- 0.1 l/s), and inspiratory muscle pressure (45 +/- 2% of maximum static pressure at FRC). VO2 resp increased from 109 +/- 15 ml/min at FRC by 41 +/- 11% at high VL (P less than 0.05). Thus the efficiency of breathing at high VL (3.9 +/- 0.2%) was less than that at FRC (5.2 +/- 0.3%, P less than 0.01). The decrease in inspiratory muscle efficiency at high VL may be due to changes in mechanical coupling, in the pattern of recruitment of the respiratory muscles, or in the intrinsic properties of the inspiratory muscles at shorter length. When the work of breathing at high VL was normalized for the decrease in maximum inspiratory muscle pressure with VL, efficiency at high VL (5.2 +/- 0.3%) did not differ from that at FRC (P less than 0.7), suggesting that the fall in efficiency may have been related to the fall in inspiratory muscle strength. During acute hyperinflation the decreased efficiency contributes to the increased O2 cost of breathing and may contribute to the diminished inspiratory muscle endurance.

Inspiratory muscles during exercise: a problem of supply and demand

1988 ◽  
Vol 64 (6) ◽  
pp. 2482-2489 ◽  
Author(s):  
P. Leblanc ◽  
E. Summers ◽  
M. D. Inman ◽  
N. L. Jones ◽  
E. J. Campbell ◽  
...  
Keyword(s):  
Lung Volume ◽  
Static Pressure ◽  
Total Lung Capacity ◽  
Supply And Demand ◽  
Normal Subjects ◽  
Esophageal Pressure ◽  
Maximum Exercise ◽  
Lung Capacity ◽  
Inspiratory Muscles ◽  
Residual Capacity

The capacity of inspiratory muscles to generate esophageal pressure at several lung volumes from functional residual capacity (FRC) to total lung capacity (TLC) and several flow rates from zero to maximal flow was measured in five normal subjects. Static capacity was 126 +/- 14.6 cmH2O at FRC, remained unchanged between 30 and 55% TLC, and decreased to 40 +/- 6.8 cmH2O at TLC. Dynamic capacity declined by a further 5.0 +/- 0.35% from the static pressure at any given lung volume for every liter per second increase in inspiratory flow. The subjects underwent progressive incremental exercise to maximum power and achieved 1,800 +/- 45 kpm/min and maximum O2 uptake of 3,518 +/- 222 ml/min. During exercise peak esophageal pressure increased from 9.4 +/- 1.81 to 38.2 +/- 5.70 cmH2O and end-inspiratory esophageal pressure increased from 7.8 +/- 0.52 to 22.5 +/- 2.03 cmH2O from rest to maximum exercise. Because the estimated capacity available to meet these demands is critically dependent on end-inspiratory lung volume, the changes in lung volume during exercise were measured in three of the subjects using He dilution. End-expiratory volume was 52.3 +/- 2.42% TLC at rest and 38.5 +/- 0.79% TLC at maximum exercise.

Respiratory movements of the vocal cords

1983 ◽  
Vol 54 (5) ◽  
pp. 1269-1276 ◽  
Author(s):  
T. Brancatisano ◽  
P. W. Collett ◽  
L. A. Engel
Keyword(s):  
Lung Volume ◽  
Respiratory Control ◽  
Respiratory Muscles ◽  
Normal Subjects ◽  
Tight Coupling ◽  
Tidal Breathing ◽  
Vocal Cords ◽  
Residual Capacity ◽  
The Relationship ◽  
Respiratory Movements

We examined the movements of the vocal cords during tidal breathing, panting, and large changes in lung volume in 12 normal subjects. The glottis was observed with a fiber-optic bronchoscope, and the glottic image was recorded together with flow, volume, and a time marker onto videotape. Phasic respiratory swings in glottic width (dg) and glottic area (Ag) were reproducible in all subjects but differed substantially between subjects. In the group as a whole dg and Ag increased during inspiration to 10.1 +/- 5.6 mm and 126 +/- 8 mm2 (mean +/- SE), respectively, whereas during expiration the lowest values were 5.7 +/- 0.5 mm and 70 +/- 7 mm2, respectively. These extreme dimensions corresponded closely to the midtidal volume points in the respiratory cycle. Glottic width during vital capacity (VC) expirations was nearly 30% greater at a flow of 1.2 l/s than at 0.5 l/s, but the relationship between dg and lung volume differed between subjects. When swings in dg were minimized by panting, there was no difference in dg between functional residual capacity (FRC) and a volume corresponding to midinspiratory capacity. However, tidal breathing at this lung volume was associated with a 20% decrease in dg compared with breathing at FRC. Our observations indicate a tight coupling between the pattern of glottic movement and the respiratory volume cycle. The results suggest that during voluntary respiratory maneuvers both intrinsic laryngeal and respiratory muscles are recruited, participating as effector organs in ventilatory and respiratory control.

Ventilatory compensation for changes in functional residual capacity during sleep

1987 ◽  
Vol 62 (3) ◽  
pp. 1299-1306 ◽  
Author(s):  
R. L. Begle ◽  
J. B. Skatrud ◽  
J. A. Dempsey
Keyword(s):  
Tidal Volume ◽  
Functional Residual Capacity ◽  
Minute Ventilation ◽  
Muscle Length ◽  
Normal Subjects ◽  
Conscious State ◽  
Inspiratory Muscle ◽  
Compensatory Response ◽  
Inspiratory Muscles ◽  
Residual Capacity

The role of conscious factors in the ventilatory compensation for shortened inspiratory muscle length and the potency of this compensatory response were studied in five normal subjects during non-rapid-eye-movement sleep. To shorten inspiratory muscles, functional residual capacity (FRC) was increased and maintained for 2–3 min at a constant level (range of increase 160–1,880 ml) by creating negative pressure within a tank respirator in which the subjects slept. Minute ventilation was maintained in all subjects over the entire range of increased FRC (mean change +/- SE = -3 +/- 1%) through preservation of tidal volume (-2 +/- 2%) despite slightly decreased breathing frequency (-6 +/- 2%). The decrease in frequency (-13 +/- 2%) was due to a prolongation in expiratory time. Inspiratory time shortened (-10 +/- 1%). Mean inspiratory flow increased 15 +/- 3% coincident with an increase in the slope of the moving time average of the integrated surface diaphragmatic electromyogram (67 +/- 21%). End-tidal CO2 did not rise. In two subjects, control tidal volume was increased 35–50% with CO2 breathing. This augmented tidal volume was still preserved when FRC was increased. We concluded that the compensatory response to inspiratory muscle shortening did not require factors associated with the conscious state. In addition, the potency of this response was demonstrated by preservation of tidal volume despite extreme shortening of the inspiratory muscles and increase in control tidal volumes caused by CO2 breathing. Finally, the timing changes we observed may be due to reflexes following shortening of inspiratory muscle length, increase in abdominal muscle length, or cardiovascular changes.

Oxygen cost of breathing during fatiguing inspiratory resistive loads

1989 ◽  
Vol 66 (5) ◽  
pp. 2045-2055 ◽  
Author(s):  
F. D. McCool ◽  
G. E. Tzelepis ◽  
D. E. Leith ◽  
F. G. Hoppin
Keyword(s):  
Lung Volume ◽  
Normal Subjects ◽  
Esophageal Pressure ◽  
Inspiratory Flow ◽  
Energy Utilization ◽  
Whole Body ◽  
Inspiratory Flow Rate ◽  
Inspiratory Muscles ◽  
Inspiratory Resistance ◽  
Resistive Loads

When a subject breathes against an inspiratory resistance, the inspiratory pressure, the inspiratory flow, and the lung volume at which the breathing task takes place all interact to determine the length of time the task can be sustained (Tlim). We hypothesized that the mechanism actually limiting tasks in which these parameters were varied involved the rate of energy utilization by the inspiratory muscles. To test this hypothesis, we studied four experienced normal subjects during fatiguing breathing tasks performed over a range of pressures and flows and at two different lung volumes. We assessed energy utilization by measuring the increment in the rate of whole body O2 consumption due to the breathing task (VO2 resp). Power and mean esophageal pressure correlated with Tlim but depended also on lung volume and inspiratory flow rate. In contrast, VO2 resp closely correlated with Tlim, and this relationship was not systematically altered by inspiratory flow or lung volume. The shape of the VO2 resp vs. Tlim curve was approximately hyperbolic, with high rates of VO2 resp associated with short endurance times and lower rates of VO2 resp approaching an asymptotic value at high Tlim. These findings are consistent with a mechanism whereby a critical rate of energy utilization determines the endurance of the inspiratory pump, and that rate varies with pressure, flow, and lung volume.

Role of Impaired Inspiratory Muscle Function in Limiting the Ventilatory Response to Carbon Dioxide in Chronic Airflow Obstruction

1983 ◽  
Vol 64 (5) ◽  
pp. 487-495 ◽  
Author(s):  
H. R. Gribbin ◽  
I. T. Gardiner ◽  
G. J. Heinz ◽  
G. J. Gibson ◽  
N. B. Pride
Keyword(s):  
Muscle Activation ◽  
Ventilatory Response ◽  
Work Of Breathing ◽  
Airflow Obstruction ◽  
Normal Subjects ◽  
Inspiratory Muscle ◽  
Pleural Pressure ◽  
Pulmonary Mechanics ◽  
Respiratory Drive ◽  
Inspiratory Muscles

1. Twenty patients with severe chronic airflow obstruction (CAFO), four of whom were hypercapnic, had greatly reduced ventilatory responses to rebreathing CO2 under hyperoxic conditions, compared with the responses in normal subjects. 2. Mouth occlusion pressure (P0.1) responses to CO2 were also reduced in the patients compared with those of normal subjects but the reduction was less severe than in the ventilatory response. 3. in ten patients with CAFO minimum pleural pressure during tidal breathing [Ppl min. (dynamic)] at a Pco2 of 8.0 kPa was only slightly less negative than in the normal subjects (−16.2 cm water vs −23.4 cm water). 4. During rebreathing end-expiratory volume (EEV) fell progressively in the normal subjects (mean fall = 800 ml); in the patients there was a progressive rise in EEV (mean rise = 390 ml). 5. When Ppl min. (dynamic) was compared with minimum static pleural pressures at the same lung volume the patients were generating a much higher proportion of their available static pressure (47.0%) than the normal subjects (26.4%) at a Pco2 of 8.0 kPa, suggesting that despite the slightly less negative Ppl min. (dynamic), inspiratory muscle activation was greater in the patients than in normal subjects. Similar conclusions were reached from an analysis of the inspiratory work of breathing. 6. We conclude that hyperinflation, by impairing the capacity of the inspiratory muscles to lower pleural pressure, reduces the ventilatory response to CO2 and adds to the effects of abnormalities in pulmonary mechanics so that measurements of absolute pleural pressure or work of breathing underestimate inspiratory muscle activation in patients with severe CAFO. 7. Hyperinflation and severe airflow obstruction also reduce the change in P0.1 for a given degree of inspiratory muscle activation. 8. Our results suggest that, despite the impaired pressure and ventilatory response to rebreathing CO2 in the patients, their central respiratory drive was greater than that of the normal subjects.

Effects of compressibility of alveolar gas on dynamics and work of breathing

1964 ◽  
Vol 19 (1) ◽  
pp. 83-91 ◽  
Author(s):  
M. J. Jaeger ◽  
A. B. Otis
Keyword(s):  
Tidal Volume ◽  
Airway Resistance ◽  
Dynamic Pressure ◽  
Work Of Breathing ◽  
Respiratory Muscles ◽  
Normal Subjects ◽  
Work Related ◽  
Negative Work ◽  
Inspiratory Muscles ◽  
Intraesophageal Pressure

Alveolar gas is compressed and expanded during every breathing cycle. The volume displacement measured at the mouth Vt (tidal volume) is therefore smaller than the volume displacement of the lung V't that may be measured with a body plethysmograph. Experimental data found in normal subjects and in patients with obstructive emphysema confirm the theoretical prediction that the ratio Vt/V't decreases with increasing airway resistance, breathing frequency, and lung volume. The effect was found to be very small in normal subjects breathing at different breathing rates; however, in patients with obstructive emphysema it may be appreciable, presumably because of the high airway resistance and the elevated functional residual capacity. With increasing altitude the effect is expected to be more pronounced. The mechanical work performed in compressing and expanding alveolar gas is not included in the conventional pressure-volume diagram, when intraesophageal pressure is plotted against the volume displacement measured at the mouth. This work may be determined, however, by recording the volume displacement of the lung simultaneously with tidal volume and intraesophageal pressure. Work related to compressibility is insignificant in most circumstances. In patients with obstructive emphysema, however, it becomes appreciable during hyperpnea. The compressibility of alveolar gas was also found to increase the negative work performed by respiratory muscles. volume displacement of the lung (V't); Vt/V't in obstructive emphysema; dynamic pressure-volume diagram; mechanical model - respiratory dynamics; ventilation; negative work of inspiratory muscles; ventilation and breathing work at high altitudes; mechanics of breathing Submitted on June 21, 1963

Tonic inspiratory muscle activity as a cause of hyperinflation in histamine-induced asthma

1980 ◽  
Vol 49 (5) ◽  
pp. 869-874 ◽  
Author(s):  
N. Muller ◽  
A. C. Bryan ◽  
N. Zamel
Keyword(s):  
Lung Volume ◽  
Muscle Activity ◽  
Normal Subjects ◽  
Inspiratory Muscle ◽  
Intercostal Muscle ◽  
Tonic Activity ◽  
Surface Electrodes ◽  
Inspiratory Muscles ◽  
Thoracic Gas Volume ◽  
Gas Volume

We studied the change in tonic activity of the inspiratory muscles during acute hyperinflation. Hyperinflation was provoked in two asthmatic and three normal subjects by progressively doubling doses of histamine. Changes in lung volume were determined with magnetometers and with a body plethysmograph. Intercostal muscle activity was recorded with surface electrodes and diaphragmatic activity with esophageal electrodes. Tonic activity was defined as electrical activity in the electromyogram present at end expiration. After histamine the maximal observed increase in plethysmographic thoracic gas volume in the five subjects was 29.8 +/- 6.4% of control (mean +/- SE). Hyperinflation was accompanied by a significant increase in tonic activity of the intercostal muscles (P < 0.01) and the diaphragm (P < 0.01). There was a significant correlation between the increase in thoracic gas volume and the increase in tonic intercostal (r = 0.82, P = 0.003) and diaphragmatic (r = 0.89, P = 0.003) activity. We conclude that histamine-induced hyperinflation is accompanied by persistent inspiratory muscle activity throughout expiration.

scholarly journals Lung elastic recoil during breathing at increased lung volume

1999 ◽  
Vol 87 (4) ◽  
pp. 1491-1495 ◽  
Author(s):  
Joseph R. Rodarte ◽  
Gassan Noredin ◽  
Charles Miller ◽  
Vito Brusasco ◽  
Riccardo Pellegrino ◽  
...  
Keyword(s):  
Stress Relaxation ◽  
Tidal Volume ◽  
Lung Volume ◽  
Normal Subjects ◽  
Dynamic Hyperinflation ◽  
Airway Closure ◽  
Elastic Recoil ◽  
Volume Increase ◽  
Before And After ◽  
Residual Capacity

During dynamic hyperinflation with induced bronchoconstriction, there is a reduction in lung elastic recoil at constant lung volume (R. Pellegrino, O. Wilson, G. Jenouri, and J. R. Rodarte. J. Appl. Physiol. 81: 964–975, 1996). In the present study, lung elastic recoil at control end inspiration was measured in normal subjects in a volume displacement plethysmograph before and after voluntary increases in mean lung volume, which were achieved by one tidal volume increase in functional residual capacity (FRC) with constant tidal volume and by doubling tidal volume with constant FRC. Lung elastic recoil at control end inspiration was significantly decreased by ∼10% within four breaths of increasing FRC. When tidal volume was doubled, the decrease in computed lung recoil at control end inspiration was not significant. Because voluntary increases of lung volume should not produce airway closure, we conclude that stress relaxation was responsible for the decrease in lung recoil.

Gravity effects on upper airway area and lung volumes during parabolic flight

1998 ◽  
Vol 84 (5) ◽  
pp. 1639-1645 ◽  
Author(s):  
Maurice Beaumont ◽  
Redouane Fodil ◽  
Daniel Isabey ◽  
Frédéric Lofaso ◽  
Dominique Touchard ◽  
...  
Keyword(s):  
Lung Volume ◽  
Parabolic Flight ◽  
Upper Airway ◽  
Normal Subjects ◽  
Lung Volumes ◽  
Acoustic Reflection ◽  
Volume Functional ◽  
Airway Caliber ◽  
Gravity Effects ◽  
Residual Capacity

We measured upper airway caliber and lung volumes in six normal subjects in the sitting and supine positions during 20-s periods in normogravity, hypergravity [1.8 + head-to-foot acceleration (Gz)], and microgravity (∼0 Gz) induced by parabolic flights. Airway caliber and lung volumes were inferred by the acoustic reflection method and inductance plethysmography, respectively. In subjects in the sitting position, an increase in gravity from 0 to 1.8 +Gz was associated with increases in the calibers of the retrobasitongue and palatopharyngeal regions (+20 and +30%, respectively) and with a concomitant 0.5-liter increase in end-expiratory lung volume (functional residual capacity, FRC). In subjects in the supine position, no changes in the areas of these regions were observed, despite significant decreases in FRC from microgravity to normogravity (−0.6 liter) and from microgravity to hypergravity (−0.5 liter). Laryngeal narrowing also occurred in both positions (about −15%) when gravity increased from 0 to 1.8 +Gz. We concluded that variation in lung volume is insufficient to explain all upper airway caliber variation but that direct gravity effects on tissues surrounding the upper airway should be taken into account.

Pressure-flow effects on endurance of inspiratory muscles

1986 ◽  
Vol 60 (1) ◽  
pp. 299-303 ◽  
Author(s):  
F. D. McCool ◽  
D. R. McCann ◽  
D. E. Leith ◽  
F. G. Hoppin
Keyword(s):  
Normal Subjects ◽  
Esophageal Pressure ◽  
Inspiratory Flow ◽  
Inspiratory Muscle ◽  
Negative Slope ◽  
Muscle Endurance ◽  
Inspiratory Muscles ◽  
Wide Range ◽  
Flow Effects ◽  
Forced Breathing

We examined the effects of varying inspiratory pressures and flows on inspiratory muscle endurance. Four normal subjects performed voluntary forced breathing with various assigned inspiratory tasks. Duty cycle, tidal volume, and mean lung volume were the same in all tasks. Mean esophageal pressure, analogous to a pressure-time integral (PTes), was varied over a wide range. In each task the subject maintained an assigned PTes while breathing on one of a range of inspiratory resistors, and this gave a range of inspiratory flows at any given PTes. Inspiratory muscle endurance for each task was assessed by the length of time the task could be maintained (Tlim). For a given resistor, Tlim increased as PTes decreased. At a given PTes, Tlim increased as the external resistance increased and therefore as mean inspiratory flow rate (VI) decreased. Furthermore, for a given Tlim, PTes and VI were linearly related with a negative slope. We conclude that inspiratory flow, probably because of its relationship to the velocity of muscle shortening, is an independent variable importantly influencing endurance of the inspiratory muscles.

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