scholarly journals Breathing during exercise in subjects with mild-to-moderate airflow obstruction: effects of physical training

1999 ◽  
Vol 87 (5) ◽  
pp. 1697-1704 ◽  
Author(s):  
Riccardo Pellegrino ◽  
Carlo Villosio ◽  
Ugo Milanese ◽  
Giuseppe Garelli ◽  
Joseph R. Rodarte ◽  
...  

In this study we explored the effects of physical training on the response of the respiratory system to exercise. Eight subjects with irreversible mild-to-moderate airflow obstruction [forced expiratory volume in 1 s of 85 ± 14 (SD) % of predicted and ratio of forced expiratory volume in 1 s to forced vital capacity of 68 ± 5%] and six normal subjects with similar anthropometric characteristics underwent a 2-mo physical training period on a cycle ergometer three times a week for 31 min at an intensity of ∼80% of maximum heart rate. At this work intensity, tidal expiratory flow exceeded maximal flow at control functional residual capacity [FRC; expiratory flow limitation (EFL)] in the obstructed but not in the normal subjects. An incremental maximum exercise test was performed on a cycle ergometer before and after training. Training improved exercise capacity in all subjects, as documented by a significant increase in maximum work rate in both groups ( P < 0.001). In the obstructed subjects at the same level of ventilation at high workloads, FRC was greater after than before training, and this was associated with an increase in breathing frequency and a tendency to decrease tidal volume. In contrast, in the normal subjects at the same level of ventilation at high workloads, FRC was lower after than before training, so that tidal volume increased and breathing frequency decreased. These findings suggest that adaptation to breathing under EFL conditions does not occur during exercise in humans, in that obstructed subjects tend to increase FRC during exercise after experiencing EFL during a 2-mo strenuous physical training period.

1976 ◽  
Vol 41 (3) ◽  
pp. 341-347 ◽  
Author(s):  
L. J. Bynum ◽  
J. E. Wilson ◽  
A. K. Pierce

Distribution of ventilation (V) and perfusion (Q) was studied with 133Xe in eight supine, normal subjects comparing spontaneous breathing (SB) and intermittent positive-pressure breathing (IPPB). Tidal volume, inspiratory flow, and breathing frequency measured during SB were closely matched during automatically triggered IPPB. V and Q in the lung bases (adjacent to the diaphragm) were decreased relative to other regions during SB and further diminished by IPPB at similar volumes. During IPPB, basilar V and Q improvedwhen tidal volume was increased; however; spontaneous hyperinflation resulted in significantly higher basilar V and Q than large tidal volumes delivered by IPPB. Thus, changes in lung volumes and gas exchange in the supine posture are attributable to impaired V and Q in the bases but not in dependent (posterior) regions. IPPB further reduces basilar V and Q, possibly due to loss of interdependence resulting from diminished respiratory muscle contraction. These findings may explain atelectasis during prolonged IPPB in supine patients. Although large tidal volumes improve basilar V during IPPB, spontaneous deep breaths are more effective and may prevent atelectasis better than IPPB at similar tidal volumes.


2017 ◽  
Vol 49 (3) ◽  
pp. 1602055 ◽  
Author(s):  
James A. Stockley ◽  
Asem M. Ismail ◽  
Siân M. Hughes ◽  
Ross Edgar ◽  
Robert A. Stockley ◽  
...  

Pathological studies suggest that loss of small airways precedes airflow obstruction and emphysema in chronic obstructive pulmonary disease (COPD). Not all α1-antitrypsin deficiency (AATD) patients develop COPD, and measures of small airways function might be able to detect those at risk.Maximal mid-expiratory flow (MMEF), forced expiratory volume in 1 s (FEV1), ratio of FEV1/forced vital capacity (FVC), health status, presence of emphysema (computed tomography (CT) densitometry) and subsequent decline in FEV1 were assessed in 196 AATD patients.FEV1/FVC, FEV1 % predicted and lung densitometry related to MMEF % pred (r2=0.778, p<0.0001; r2=0.787, p<0.0001; r2=0.594, p<0.0001, respectively) in a curvilinear fashion. Patients could be divided into those with normal FEV1/FVC and MMEF (group 1), normal FEV1/FVC and reduced MMEF (group 2) and those with spirometrically defined COPD (group 3). Patients in group 2 had worse health status than group 1 (median total St George's Respiratory Questionnaire (SGRQ) 23.15 (interquartile range (IQR) 7.09–39.63) versus 9.67 (IQR 1.83–22.35); p=0.006) and had a greater subsequent decline in FEV1 (median change in FEV1 −1.09% pred per year (IQR −1.91–0.04% pred per year) versus −0.04% pred per year (IQR −0.67–0.03% pred per year); p=0.007).A reduction in MMEF is an early feature of lung disease in AATD and is associated with impaired health status and a faster decline in FEV1.


2019 ◽  
Vol 127 (1) ◽  
pp. 31-39 ◽  
Author(s):  
E. T. Geier ◽  
R. J. Theilmann ◽  
G. K. Prisk ◽  
R. C. Sá

Some subjects with asthma have ventilation defects that are resistant to bronchodilator therapy, and it is thought that these resistant defects may be due to ongoing inflammation or chronic airway remodeling. However, it is unclear whether regional obstruction due to bronchospasm alone persists after bronchodilator therapy. To investigate this, six young, healthy subjects, in whom inflammation and remodeling were assumed to be absent, were bronchoconstricted with a PC20 [the concentration of methacholine that elicits a 20% drop in forced expiratory volume in 1 s (FEV1)] dose of methacholine and subsequently bronchodilated with a standard dose of albuterol on three separate occasions. Specific ventilation imaging, a proton MRI technique, was used to spatially map specific ventilation across 80% of each subject’s right lung in each condition. The ratio between regional specific ventilation at baseline and after intervention was used to classify areas that had constricted. After albuterol rescue from methacholine bronchoconstriction, 12% (SD 9) of the lung was classified as constricted. Of the 12% of lung units that were classified as constricted after albuterol, approximately half [7% (SD 7)] had constricted after methacholine and failed to recover, whereas half [6% (SD 4)] had remained open after methacholine but became constricted after albuterol. The incomplete regional recovery was not reflected in the subjects’ FEV1 measurements, which did not decrease from baseline ( P = 0.97), nor was it detectable as an increase in specific ventilation heterogeneity ( P = 0.78). NEW & NOTEWORTHY In normal subjects bronchoconstricted with methacholine and subsequently treated with albuterol, not all regions of the healthy lung returned to their prebronchoconstricted specific ventilation after albuterol, despite full recovery of integrative lung indexes (forced expiratory volume in 1 s and specific ventilation heterogeneity). The regions that remained bronchoconstricted following albuterol were those with the highest specific ventilation at baseline, which suggests that they may have received the highest methacholine dose.


Author(s):  
William J.M. Kinnear ◽  
James H. Hull

This chapter describes how the amount of air going in and out of the lungs increases on exercise. The predicted value for minute ventilation (VE) is calculated for each subject from their own forced expiratory volume in one second (FEV1), rather than taken from published tables. Normally, ventilation does not limit exercise and VE does not reach 80% of the predicted value. If VE at peak exercise is more than 80% of predicted, it is likely there is something wrong with the lungs. VE increases by a combination of a larger tidal volume and an increase in breathing frequency. The pattern of increase is normally gradual. An erratic pattern suggests dysfunctional breathing.


1993 ◽  
Vol 84 (2) ◽  
pp. 159-167 ◽  
Author(s):  
Rachel C. Wilson ◽  
W. L. G. Oldfield ◽  
P. W. Jones

1. The effect of residence at altitude on the perception of breathlessness after return to sea level was examined in normal subjects. Breathlessness (Borg scale), minute ventilation, respiratory frequency, tidal volume, ‘oxygen pulse’ (oxygen consumption/heart rate) and the ventilatory equivalent for oxygen (minute ventilation/oxygen consumption) were measured at exercise (cycle-ergometer) during 5 months of training before 4 weeks at 4000 m and during the 6 month period after return to sea level. 2. There was no change in the subjects' pattern of breathing (respiratory frequency and tidal volume) or ‘oxygen pulse’ after the period at altitude (P = 0.0001). The ventilatory equivalent for oxygen was increased at all work rates after the period at altitude (P = 0.02). This ratio was slightly lower after 6 weeks and had returned to normal by 6 months (P = 0.4). 3. During training there was no change in breathlessness score (P = 0.6). On return to sea level, breathlessness score relative to ventilation was reduced (P = 0.0001). This was maintained for at least 6 weeks, but not as long as 6 months. 4. This study has demonstrated that, in normal subjects, the otherwise stable and reproducible relationship between breathlessness and ventilation may be disrupted for several weeks by factors other than lung disease. 5. The mechanism responsible for this is not clear, but the observations are consistent with the hypothesis that prior experience of breathlessness may condition subsequent estimates of breathlessness.


1987 ◽  
Vol 63 (5) ◽  
pp. 1822-1828 ◽  
Author(s):  
T. Chonan ◽  
M. B. Mulholland ◽  
N. S. Cherniack ◽  
M. D. Altose

The study evaluated the interrelationships between the extent of thoracic movements and respiratory chemical drive in shaping the intensity of the sensation of dyspnea. Normal subjects rated their sensations of dyspnea as PCO2 increased during free rebreathing and during rebreathing while ventilation was voluntarily maintained at a constant base-line level. Another trial evaluated the effects on the intensity of dyspnea, of voluntary reduction in the level of ventilation while PCO2 was held constant. During rebreathing, there was a power function relationship between changes in PCO2 and the intensity of dyspnea. At a given PCO2, constraining tidal volume and breathing frequency to the prerebreathing base-line level resulted in an increase in dyspnea. The fractional differences in the intensity of dyspnea between free and constrained rebreathing were independent of PCO2. However, the absolute difference in the intensity of dyspnea between free and constrained rebreathing enlarged with increasing hypercapnia. At PCO2 of 50 Torr, this difference correlated significantly with the increase in both minute ventilation (r = 0.675) and tidal volume (r = 0.757) above the base line during free rebreathing. Similarly, during steady-state hypercapnia at 50 Torr PCO2, the intensity of dyspnea increased progressively as ventilation was voluntarily reduced from the spontaneously adopted free-breathing level. These results indicate that dyspnea increases with the level of respiratory chemical drive but that the intensity of the sensation is further accentuated when ventilation is constrained below that demanded by the level of chemical drive. This may be explained by a loss of inhibitory feedback from lung or chest wall mechanoreceptors acting on brain stem and/or cortical centers.


2004 ◽  
Vol 96 (5) ◽  
pp. 1651-1657 ◽  
Author(s):  
S. K. Kjærgaard ◽  
O. F. Pedersen ◽  
M. R. Miller ◽  
T. R. Rasmussen ◽  
J. C. Hansen ◽  
...  

Sixteen healthy nonsmoking subjects (7 women), 21-49 yr old, were exposed in a climate chamber to either clean air or 300 parts/billion ozone on 4 days for 5 h each day. Before each exposure, the subjects had been pretreated with either oxidants (fish oil) or antioxidants (multivitamins). The study design was double-blind crossover with randomized allocation to the exposure regime. Full and partial flow-volume curves were recorded in the morning and before and during a histamine provocation at the end of the day. Nasal cavity volume and inflammatory markers in nasal lavage fluid were also measured. Compared with air, ozone exposure decreased peak expiratory flow, forced expiratory volume in 1 s, and forced vital capacity (FVC), with no significant effect from the pretreatment regimens. Ozone decreased the ratio of maximal to partial flow at 40% FVC by 0.08 ± 0.03 (mean ± SE, analysis of variance: P = 0.018) and at 30% FVC by 0.10 ± 0.05 ( P = 0.070). Ozone exposure did not significantly increase bronchial responsiveness, but, after treatment with fish oil, partial flows decreased more than after vitamins during the histamine test, without changing the maximal-to-partial flow ratio. The decreased effect of a deep inhalation after ozone exposure can be explained by changes in airway hysteresis relative to parenchymal hysteresis, due either to ozone-induced airway inflammation or to less deep inspiration after ozone, not significantly influenced by multivitamins or fish oil.


1993 ◽  
Vol 74 (5) ◽  
pp. 2552-2558 ◽  
Author(s):  
R. Pellegrino ◽  
V. Brusasco ◽  
J. R. Rodarte ◽  
T. G. Babb

To investigate the impact of expiratory flow limitation (FL) on breathing pattern and end-expiratory lung volume (EELV), we imposed a small expiratory threshold load for a few breaths during exercise in nine volunteers (29–62 yr): six were healthy and three had mild-to-moderate airflow obstruction (67–71% predicted forced expiratory volume in 1 s). Six subjects showed evidence of FL, i.e., tidal expiratory flow impinging on maximal forced expiratory flow, at one or more exercise levels. Whenever an expiratory threshold load was imposed, mean expiratory flow decreased (P < 0.02) in association with an increased expiratory time (TE; P < 0.05). When the load was imposed during non-FL conditions, TE increased less than expiratory flow decreased and EELV tended to increase. In contrast, during FL, with the load, TE increased more than expiratory flow decreased, subjects did not achieve maximal expiratory flow until a lower volume, and EELV decreased (P < 0.001). Under both FL and no-FL conditions, unloading reversed the changes associated with loading. These data indicate that the increase in EELV during exercise is linked to the occurrence of FL. We suggest that compression of airways downstream from the flow-limiting segment may elicit a reflex mechanism that influences breathing pattern by terminating expiration prematurely, thus increasing EELV.


1989 ◽  
Vol 67 (1) ◽  
pp. 264-269 ◽  
Author(s):  
S. E. Szal ◽  
R. B. Schoene

Rowing is a unique exercise for humans, and the imposed biomechanical motion may alter both respiratory mechanics and timing. To investigate the ventilatory patterns of competitive rowers while rowing, we studied the pulmonary function of eight members of the University of Washington Women's Crew and one former member of the 1984 Women's Olympic Rowing Team on a rowing ergometer. Ventilatory performance of the oarswomen was compared both with their performance to exhaustion on a cycle ergometer and with the ventilatory response of six untrained controls on a rowing and a cycle ergometer. We found rowing elicited a higher ventilatory response in both the oarswomen and controls in submaximal and maximal work loads (P less than 0.001). Both oarswomen and controls had higher maximal breathing frequencies when rowing compared with cycling [rowers, 54.7 +/- 1.9 vs 49.8 +/- 0.09 (SE) breaths/min, P less than 0.05; and controls, 53.6 +/- 2.5 vs. 49.2 +/- 4.7, P less than 0.05] and lower maximal tidal volumes (rowers, 1.94 +/- 0.12 vs. 2.21 +/- 0.09 liters, P less than 0.01; controls, 1.59 +/- 0.09 vs. 1.68 +/- 0.19, difference not significant). Both oarswomen and controls were more hypocapnic while rowing compared with cycling (rowers, P less than 0.001; controls, P less than 0.02), although oarswomen were less hypocapnic while rowing than nonrowers (P less than 0.03). These results indicate that rowing causes hyperventilation with a higher breathing frequency and lower tidal volume. This alteration of pattern is possibly secondary to a change in mechanics, which possibly arises from the generation of high exercise ventilation in a variable seated position.


1985 ◽  
Vol 59 (2) ◽  
pp. 515-520 ◽  
Author(s):  
G. C. Smaldone ◽  
M. S. Messina

We studied deposition of radioactive monodisperse 1.5-micron aerosol in humans following inhalation during quiet breathing. Two groups were studied: normal, defined by tidal loops below the maximum expiratory flow-volume (MEFV) envelope [forced expiratory volume at 1 s at percent of forced vital capacity (FEV1%) 62–78]; and flow-limited, with tidal loops superimposed on MEFV relationship (FEV1% 21–57) and flow-limiting segments (FLS) known to exist in central airways. During simultaneous imaging with a gamma camera, fraction of inhaled aerosol deposited in the lung (DF) was determined by right-angle light scattering. With regions of interest defined by an equilibrium image of 133Xe, regional deposition was normalized for area and lung thickness and expressed as a central-to-peripheral (C/P) ratio. Deposition was uniform throughout the lung in normal subjects [C/P 1.02 +/- 0.07 (SD), n = 6]. In flow-limited group, central deposition predominated (C/P 1.98 +/- 0.64, n = 6, P less than 0.05). Tidal volume and inspiratory flow, forces thought to influence deposition during inspiration, were not different between groups. Spontaneous cough occurred in five flow-limited subjects during aerosol inhalation, with further increase in central deposition when compared with quiet breathing (C/P 1.85 +/- 0.60 to 2.69 +/- 0.600, P less than 0.01). During cough, tidal volume (ml) was reduced significantly (576 +/- 151 to 364 +/- 117, P less than 0.01) with no change in inspiratory flow (l/s) (1.37 +/- 0.23 to 1.38 +/- 0.40, P = NS). DF, however, was unaffected by cough (0.34 +/- 0.13 to 0.61 +/- 0.12, P = NS).


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