Ventilatory adjustments during sustained mechanical loading in conscious humans

1983 ◽  
Vol 55 (4) ◽  
pp. 1211-1218 ◽  
Author(s):  
K. Axen ◽  
S. S. Haas ◽  
F. Haas ◽  
D. Gaudino ◽  
A. Haas

Ventilatory responses to inspiratory elastic and resistive loads of 67 men were analyzed. During the 1st, 5th, and 10th consecutively loaded breaths 1) individual responses ranged from a rapid-shallow to a slow-deep breathing pattern; 2) strong tidal volume (VT) defenders employed longer inspirations than did weak VT defenders; and 3) individual frequency responses were mediated by changes in inspiratory and/or expiratory timing. Thus the group response was qualitatively similar on the 1st, 5th, and 10th loaded breaths. Quantitatively, however, the group's mean minute ventilation increased throughout each episode owing to progressively larger tidal volumes coupled with equal breathing frequencies. During elastic loading this amplified VT defense was achieved by stronger inspirations with no systematic changes in timing, whereas during resistive loading it was achieved both by stronger and longer inspirations. Inspiring 5% CO2 induced a degree of hypercapnia exceeding that accompanying mechanical loading and yet elicited a comparatively modest enhancement of respiratory output. These findings suggest that in conscious humans 1) repeated mechanical loading activates neural load-compensating mechanisms; 2) the range of these neural adjustments varies with both load size and type; and 3) the stimulus to initiate this behavior is largely nonchemical.

1984 ◽  
Vol 56 (1) ◽  
pp. 175-181 ◽  
Author(s):  
K. Axen ◽  
F. Haas ◽  
D. Gaudino ◽  
S. S. Haas

First-breath ventilatory responses to graded inspiratory elastic and resistive loads were obtained from 80 women unfamiliar with respiratory experimentation. For each load 1) responses from different subjects ranged from a weak tidal volume defense coupled with an increased breathing frequency to a strong tidal volume defense coupled with a decreased frequency; 2) strong tidal volume defenders employed longer inspirations than did weak tidal volume defenders; and 3) individual respiratory frequency responses were mediated by changes in inspiratory and/or expiratory timing. Thus the group response was qualitatively the same as that reported for 80 men. Quantitatively, however, mean inspiratory airflow responses of women exceeded those of men by an amount attributable to women's higher intrinsic respiratory elastance. Tidal volume responses, on the other hand, did not differ significantly, suggesting that men and women produce different neural adjustments to loads. In support of this hypothesis, analysis of respiratory timing responses revealed that 1) men actively prolonged inspiration more than women during resistive loading; and 2) women actively shortened inspiration more than men during elastic loading. These findings indicate that the load-compensating behavior exhibited by men and women is similar but not identical.


1984 ◽  
Vol 56 (4) ◽  
pp. 1099-1103 ◽  
Author(s):  
K. Axen

Ventilatory responses to graded elastic and resistive loads from 20 quadriplegic men were analyzed. During the 1st, 5th, and 10th consecutively loaded inspirations 1) responses from different subjects ranged from a weak tidal volume defense coupled with an increased breathing frequency to a strong tidal volume defense coupled with a decreased frequency; 2) strong tidal volume defenders generally employed longer inspirations than did weak tidal volume defenders; and 3) individual respiratory frequencies were mediated by similar changes in inspiratory and/or expiratory timing. Thus the group response was qualitatively similar on the 1st, 5th, and 10th loaded breaths. Quantitatively, however, minute ventilation increased throughout each 10-breath episode due to progressively larger tidal volumes coupled with equal breathing frequencies. These larger tidal volumes were due to progressively stronger inspirations with no changes in timing during elastic loading, whereas they were due to both stronger and longer inspirations during resistive loading. These findings, which are qualitatively the same as those found in healthy subjects, indicate that sensory input from the mouth, lung, and diaphragm, and motor output to the diaphragm and accessory muscles are sufficient, by themselves, to mediate normal patterns of ventilatory adjustments during consecutively loaded breaths.


1987 ◽  
Vol 62 (4) ◽  
pp. 1647-1654 ◽  
Author(s):  
K. Axen ◽  
M. Bishop ◽  
F. Haas

First-breath ventilatory responses to graded elastic and resistive loads were obtained from 15 people with Duchenne muscular dystrophy (DMD), 5 people with facioscapulohumeral MD (FSH), 3 people with Becker MD, and 3 people with limb-girdle MD. For each load tidal volumes from different individuals ranged from relatively small to comparatively large values, indicating a correspondingly wide range of end-inspiratory efforts; strong tidal volume defenders generally employed longer inspirations and higher mean inspiratory airflows than did weak tidal volume defenders; and individual frequency responses were mediated by changes in inspiratory and/or expiratory timing. Thus the loaded breathing responses of people with MD are qualitatively the same as those of quadriplegic and able-bodied people. Quantitatively, however, the DMD group generated considerably larger tidal volumes than did the FSH group during both elastic and resistive loading. These larger tidal volumes were achieved by both longer inspirations (a neurally mediated phenomenon) and higher mean inspiratory airflows (a mechanically and/or neurally mediated phenomenon). These findings, which could not be attributed to differences in respiratory motor function, suggest that there are differences between the respiratory sensory and/or central functions in the Duchenne and facioscapulohumeral types of MD.


1988 ◽  
Vol 65 (2) ◽  
pp. 541-548 ◽  
Author(s):  
D. E. O'Donnell ◽  
R. Sanii ◽  
M. Younes

To determine whether upper airway mechanoreceptors partly subserve the ventilatory response to external mechanical loading in conscious humans, we studied 11 laryngectomized subjects. The oropharynx (OP) or tracheostomy was selectively loaded (in random order) by attaching the mouth or tracheal tube to a special pressure-generating apparatus, and steady-state ventilatory responses were recorded. Phasic negative pressure changes generated at the OP to simulate inspiratory resistive loading, expiratory resistive unloading, and elastic loading resulted in trivial prolongation of inspiratory duration by 12, 9, and 4%, respectively; other ventilatory variables were not significantly altered. Phasic positive pressure changes at the OP that simulated inspiratory resistive unloading and expiratory resistive loading had little effect on breathing pattern. When the above loads were applied via the tracheostomy, using pressures of similar magnitude, ventilatory responses were qualitatively similar and quantitatively not significantly different from those of normal healthy controls. The results suggest that the OP does not make an important contribution to ventilatory responses during external mechanical loading in conscious humans. Loading responses to conventional mechanical loads are preserved in the absence of afferent information from the upper airways.


1975 ◽  
Vol 39 (4) ◽  
pp. 548-551 ◽  
Author(s):  
A. S. Rebuck ◽  
M. Betts ◽  
N. A. Saunders

Ventilatory responses to isocapnic hypoxia, with and without an inspiratory elastic load (12.1 cmH2O/l), were measured in seven healthy subjects using a rebreathing technique. During each experiment, the end-tidal PCO2 was held constant using a variable-speed pump to draw gas from the rebreathing bag through a CO2 absorbing bypass. Studies with and without the load were performed in a formally randomized order for each subject. Linear regressions for rise in ventilation against fall in SaO2 were calculated. The range of unloaded responses was 0.74–1.38 1/min per 1% fall in SaO2 and loaded responses 0.71–1.56 1/min per 1% fall in SaO2. Elastic loading did not significantly alter the ventilatory response to progressive hypoxia (P greater than 0.2). In all subjects there was, however, a change in breathing pattern during loading, whereby increments in ventilation were attained by smaller tidal volumes and higher frequencies than in the control experiments. These results support the hypothesis previously proposed in our studies of resistive loading during progressive hypoxia, that a similar control pathway appears to be involved in response to the application of loads to breathing, whether ventilation is stimulated by hypoxia or hypercapnia.


1983 ◽  
Vol 55 (3) ◽  
pp. 929-934 ◽  
Author(s):  
T. M. Michiels ◽  
R. W. Light ◽  
C. K. Mahutte

The respiratory depressant effects of ethanol and their potential reversibility by naloxone were studied in 10 normal subjects. Ventilatory and mouth occlusion pressure (P0.1) responses to hypercapnia and hypoxia without and with an inspiratory resistive load (13 cmH2O X 1(-1) X S) were measured. The resistive load detected with 50% probability (delta R50) and the exponent (n) in Stevens' psychophysical law for magnitude estimation of resistive loads were studied using standard psychophysical techniques. Each of these studies was performed before ethanol ingestion, after ethanol ingestion (1.5 ml/kg, by mouth), and then again after naloxone (0.8 mg iv). Ethanol increased delta R50 (P less than 0.05) and decreased n (P less than 0.05). Naloxone caused no further change in these parameters. The load compensation (Lc), defined as the ratio of loaded to unloaded response slopes, was not significantly changed after ethanol and naloxone. No correlation was found between the Lc and delta R50 or n. The ventilatory and P0.1 responses to hypercapnia and hypoxia with and without inspiratory resistive loading decreased after ethanol (P less than 0.05, hypercapnia; NS, hypoxia). After naloxone the hypercapnic ventilatory responses increased (P less than 0.05). This suggests that the respiratory depressant effects of ethanol may be mediated via endorphins.


1981 ◽  
Vol 51 (2) ◽  
pp. 262-269 ◽  
Author(s):  
Y. Jammes ◽  
M. J. Mathiot ◽  
J. P. Roll ◽  
C. Prefaut ◽  
F. Berthelin ◽  
...  

In healthy humans, we studied the effect of high-frequency mechanical vibrations applied unilaterally to the tendon of the biceps or triceps brachialis on ventilation and the breathing pattern. This stimulus preferentially activates the muscle spindle afferents. Increase of respiratory frequency and changes in the ventilatory timing started at the first or second inspiration during tendon stimulation, and no adaptation occurred as long as the vibrations continued. The tidal volume and mean inspiratory flow rate were only enhanced in individuals having high-frequency breathing during eupnea. The changes in ventilatory variables were observed when the motor response to vibrations was tested under isometric or isotonic conditions. Various experimental procedures enabled us to induce a tonic reflex contraction in either the vibrated muscle or the antagonist of no reflex contraction in either group of muscles. In all cases the increase in minute ventilation was identical. These changes in breathing pattern was not associated with a significant decrease in alveolar CO2 pressure and did not seem to be responsible for important variations in respiratory gas exchanges. The response to high-frequency vibrations was also studied after ventilation was increased with added dead space. The magnitude of hyperventilation an the pattern of ventilatory response produced by tendon stimulation did not change with increased ventilation. In conclusion, the stimulation of muscle spindles in human induces changes in ventilation and pattern of breathing , and the occurrence of a reflex muscular contraction does not seem necessary in order to obtain such effects.


1985 ◽  
Vol 59 (1) ◽  
pp. 229-236 ◽  
Author(s):  
L. Y. Lee ◽  
R. F. Morton ◽  
D. T. Frazier

To determine whether the acute ventilatory responses to inhaled cigarette smoke are affected by a difference in nicotine level, control cigarettes (low-nicotine research cigarettes) were laced with nicotine to generate an increase of 330% (mean) in nicotine content with little or no change in the levels of other smoke constituents. Acute ventilatory responses to both control and nicotine-laced cigarettes were determined and compared in six awake chronic dogs. Spontaneous inhalation of nicotine-laced cigarette smoke (10% concn, 750 ml vol) via a tracheostomy tube caused distinct and consistent changes in breathing pattern on the first or second breath of inhaled smoke: an apnea in three dogs, an augmented inspiration in two dogs, and rapid shallow breathing in one dog. No significant change in breathing pattern was found immediately following inhalation of control cigarette smoke. Both types of cigarettes caused a delayed hyperpnea. However, the increase in minute ventilation induced by nicotine-laced cigarettes (from a base line of 2.8 to a peak of 25.7 l/min) was significantly greater than that by control cigarettes (from 2.9 to 5.5 l/min). Results of this study suggest that nicotine is responsible for the elicitation of both the immediate and delayed ventilatory responses to inhaled cigarette smoke generated under our experimental conditions.


1985 ◽  
Vol 59 (1) ◽  
pp. 34-38 ◽  
Author(s):  
A. D. D'Urzo ◽  
K. R. Chapman ◽  
A. S. Rebuck

Ventilatory responses to progressive exercise, with and without an inspiratory elastic load (14.0 cmH2O/l), were measured in eight healthy subjects. Mean values for unloaded ventilatory responses were 24.41 +/- 1.35 (SE) l/l CO2 and 22.17 +/- 1.07 l/l O2 and for loaded responses were 24.15 +/- 1.93 l/l CO2 and 20.41 +/- 1.66 l/l O2 (P greater than 0.10, loaded vs. unloaded). At levels of exercise up to 80% of maximum O2 consumption (VO2max), minute ventilation (VE) during inspiratory elastic loading was associated with smaller tidal volume (mean change = 0.74 +/- 0.06 ml; P less than 0.05) and higher breathing frequency (mean increase = 10.2 +/- 0.98 breaths/min; P less than 0.05). At levels of exercise greater than 80% of VO2max and at exhaustion, VE was decreased significantly by the elastic load (P less than 0.05). Increases in respiratory rate at these levels of exercise were inadequate to maintain VE at control levels. The reduction in VE at exhaustion was accompanied by significant decreases in O2 consumption and CO2 production. The changes in ventilatory pattern during extrinsic elastic loading support the notion that, in patients with fibrotic lung disease, mechanical factors may play a role in determining ventilatory pattern.


1995 ◽  
Vol 78 (2) ◽  
pp. 555-561 ◽  
Author(s):  
D. A. Sidney ◽  
C. S. Poon

To investigate how breathing is controlled during CO2 stimulation, steady-state ventilatory responses to rebreathing through a tube (DS) and inspiring a fixed PCO2 (INH) were compared in healthy human subjects. Tests were performed in hyperoxia with (IRL) and without (NL) an inspiratory resistive load (15 cmH2O.l–1.s at 1 l/s). The mean slope of the minute ventilation (VE)-end-tidal PCO2 relationship was significantly higher in DS-IRL than in INH-IRL [1.86 +/- 0.67 (SD) vs. 1.40 +/- 0.32 l.min-1.Torr-1, P < 0.01], and it was significantly different between INH-NL and INH-IRL (1.64 +/- 0.41 vs. 1.40 +/- 0.32 l.min-1.Torr-1, P < 0.05) but not between DS-NL and DS-IRL (1.85 +/- 0.72 vs. 1.86 +/- 0.67 l.min-1.Torr-1). The slope of the VE-tidal volume relationship was significantly lower in DS-NL than in INH-NL (19.6 +/- 3.8 vs. 21.2 +/- 5.1 min-1, P < 0.05), but other comparisons in breathing pattern between NL and IRL and between DS and INH failed to reach significance. We concluded that 1) alterations in alveolar PCO2 temporal profile by DS could induce changes in VE-end-tidal PCO2 sensitivity and ventilatory pattern, 2) these changes may be modified by increased mechanical impairment resulting from IRL, and 3) carotid chemoreceptor mediation is not necessary for the observed effects of DS.


Sign in / Sign up

Export Citation Format

Share Document