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

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.

1959 ◽  
Vol 14 (4) ◽  
pp. 499-506 ◽  
Author(s):  
K. Tokuyasu ◽  
A. Coblentz ◽  
H. R. Bierman

Estimation of pulmonary ventilation was attempted by measuring the elimination of nitrogen and helium with the mass spectrometer. Exhalatory concentrations of nitrogen and helium were continuously recorded in each of 12 normal subjects and 10 patients with pulmonary enphysema or space-occupying pulmonary lesions. Uniform values for both slow and rapid uneven ventilation were found in all normal subjects but always less than in emphysematous states. Ratios of effective tidal volume (Vt) and alveolar ventilation volume (f·Vt) to functional residual capacity P = Vt/Vr and Q = f·Vt/Vr were one half or less than those in the normal subject. Smaller values of uneven ventilation were found for helium than nitrogen. Data computed by the theory of 'periodic' ventilation gave greater values for uneven ventilation (Q) and more accurately represented the physiologic conditions than derived by ‘continuous’ ventilation. Submitted on August 7, 1958


1961 ◽  
Vol 16 (1) ◽  
pp. 27-29 ◽  
Author(s):  
Francisco Moreno ◽  
Harold A. Lyons

The changes produced by body posture on total lung capacity and its subdivisions have been reported for all positions except the prone position. Twenty normal subjects, twelve males and eight females, had determinations of total lung capacity in the three body positions, sitting, supine and prone. Tidal volume, minute ventilation and O2 consumption were also measured. The changes found on assumption of the supine position from the sitting position were similar to those previously reported. For the prone position, a smaller inspiratory capacity and a larger expiratory reserve volume were found. The mean values were changed, respectively, –8% and +37%. Associated with these changes was a significant increase of the functional residual capacity by 636 ml. Ventilation did not change significantly from that found during sitting, unlike the findings associated with the supine position, in which position the tidal volume was decreased. Respiratory frequency remained the same for all positions. Submitted on April 5, 1960


1996 ◽  
Vol 80 (4) ◽  
pp. 1270-1278 ◽  
Author(s):  
P. Sliwinski ◽  
S. Yan ◽  
A. P. Gauthier ◽  
P. T. Macklem

We evaluated the effect of global inspiratory muscle fatigue (GF) on respiratory muscle control during exercise at 30, 60, and 90% of maximal power output in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. Esophageal and gastric pressures, anteroposterior displacement of the rib cage and abdomen, breathing pattern, and perceived breathlessness were measured. Induction of GF had no effect on the ventilatory parameters during mild and moderate exercise. It altered, however, ventilatory response to heavy exercise by increasing breathing frequency and minute ventilation, with minor changes in tidal volume. This was accompanied by an increase in perceived breathlessness. GF significantly increased both the tonic and phasic activities of abdominal muscles that allowed 1) the diaphragm to maintain its function while developing less pressure, 2) the same tidal volume with lesser shortening of the rib cage inspiratory muscles, and 3) relaxation of the abdominal muscles to contribute to lung inflation. The increased work performed by the abdominal muscles may, however, lead to a reduction in their strength. GF may impair exercise performance in some healthy subjects that is probably not related to excessive breathlessness or other ventilatory factors. We conclude that the respiratory system is remarkably adaptable in maintaining ventilation during exercise even with impaired inspiratory muscle contractility.


1965 ◽  
Vol 20 (6) ◽  
pp. 1194-1198 ◽  
Author(s):  
S. T. Chiang ◽  
Neal H. Steigbigel ◽  
Harold A. Lyons

Trans-pulmonary pressure, respiratory flow, and tidal volume of seven normal subjects were measured at rest and during treadmill exercise on the level at a speed of 1.5 mph. Pulmonary compliance remained unchanged during exercise. Nonelastic resistance showed an insignificant increase (0.9—1.4 cm H2O per liter per sec). Examination of other parameters which may affect compliance were made. Functional residual capacity decreased 120—200 ml during exercise, tidal volume doubled, and respiratory frequency increased 43.5%, yet none of these factors affected the lung compliance. The phenomenon of “second wind” was experienced by four of the subjects, and nothing was observed to explain its occurrence during exercise. exercise second wind; change in functional residual capacity during exercise; effect of functional residual capacity on compliance; effect of tidal volume on compliance during exercise; effect of respiratory frequency on compliance Submitted on January 15, 1965


1986 ◽  
Vol 61 (1) ◽  
pp. 16-24 ◽  
Author(s):  
P. W. Collett ◽  
L. A. Engel

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.


1991 ◽  
Vol 70 (5) ◽  
pp. 2173-2180 ◽  
Author(s):  
D. A. Mulvey ◽  
N. G. Koulouris ◽  
M. W. Elliott ◽  
C. M. Laroche ◽  
J. Moxham ◽  
...  

We have investigated whether the capacity of the inspiratory muscles to generate pressure and flow during a ventilatory load is related to changes in inspiratory muscle relaxation rate. Five highly motivated normal subjects performed voluntary maximal isocapnic ventilation (MIV) for 2 min. Minute ventilation and esophageal, gastric, and transdiaphragmatic pressures were measured breath by breath. We observed that ventilation, peak inspiratory and expiratory pressures, and inspiratory flow rate declined from the start of the run to reach a plateau at 60 s that was sustained for the remainder of the exercise. In a subsequent series of studies, MIV was performed for variable durations between 15 and 120 s. The normalized maximum relaxation rate of unoccluded inspiratory sniffs (sniff MRR, %pressure loss/10 ms) was determined immediately on stopping MIV. Sniff MRR slowed as the duration of MIV increased and paralleled the decline in inspiratory pressure and ventilation observed during the 2-min exercise. No further slowing in MRR occurred when ventilation became sustainable. We conclude that, during MIV, the progressive loss of ventilation and capacity to generate pressure is associated with the early onset and progression of a peripheral fatiguing process within the inspiratory muscles.


1979 ◽  
Vol 46 (5) ◽  
pp. 867-871 ◽  
Author(s):  
A. Vinegar ◽  
E. E. Sinnett ◽  
D. E. Leith

Awake mice (22.6--32.6 g) were anesthetized intravenously during head-out body plethysmography. One minute after pentobarbital sodium anesthesia, tidal volume had fallen from 0.28 +/- 0.04 to 0.14 +/- 0.02 ml and frequency from 181 +/- 20 to 142 +/- 8. Functional residual capacity (FRC) decreased by 0.10 +/- 0.02 ml. Expiratory flow-volume curves were linear, highly repeatable, and submaximal over substantial portions of expiration in awake and anesthetized mice; and expiration was interrupted at substantial flows that abruptly fell to and crossed zero as inspiration interrupted relaxed expiration. FRC is maintained at a higher level in awake mice due to a higher tidal volume and frequency coupled with expiratory braking (persistent inspiratory muscle activity or increased glottal resistance). In anesthetized mice, the absence of braking, coupled with reductions in tidal volume and frequency and a prolonged expiratory period, leads to FRCs that approach relaxation volume (Vr). An equation in derived to express the difference between FRC and Vr in terms of the portion of tidal volume expired without braking, the slope of the linear portion of the expiratory flow-volume curve expressed as V/V, the time fraction of one respiratory cycle spent in unbraked expiration, and respiratory frequency.


1988 ◽  
Vol 64 (6) ◽  
pp. 2482-2489 ◽  
Author(s):  
P. Leblanc ◽  
E. Summers ◽  
M. D. Inman ◽  
N. L. Jones ◽  
E. J. Campbell ◽  
...  

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.


1963 ◽  
Vol 18 (3) ◽  
pp. 519-522 ◽  
Author(s):  
M. C. Hart ◽  
M. M. Orzalesi ◽  
C. D. Cook

The respiratory anatomic dead space has been measured by the single breath nitrogen washout method of Fowler in 73 normal subjects ranging from 4 to 42 years of age. The volume of the anatomic dead space correlated closely with height (Vd (ml) = 7.585 x Ht (cm)2.363 x 10-4·ɣ = .917), but also with body weight, surface area, and functional residual capacity. When compared on the basis of any of these parameters there was no significant difference between the anatomic dead space values for males and females. Comparisons with available data for newborn infants suggest that the value of the anatomic dead space has a relatively constant relation to height from birth to adulthood. Dead space appears to increase more rapidly than weight, surface area, and functional residual capacity during, at least, the early period of somatic growth. Note: (With the Technical Assistance of J. H. Shaw) Submitted on October 25, 1962


1999 ◽  
Vol 87 (4) ◽  
pp. 1491-1495 ◽  
Author(s):  
Joseph R. Rodarte ◽  
Gassan Noredin ◽  
Charles Miller ◽  
Vito Brusasco ◽  
Riccardo Pellegrino ◽  
...  

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.


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