Effects of exercise training on airway closure in asthmatics

2012 ◽  
Vol 113 (5) ◽  
pp. 714-718 ◽  
Author(s):  
Nicola Scichilone ◽  
Giuseppe Morici ◽  
Daniele Zangla ◽  
Rita Arrigo ◽  
Irene Cardillo ◽  
...  

We previously reported that responsiveness to methacholine (Mch) in the absence of deep inspiration (DI) decreased in healthy subjects after a short course of exercise training. We assessed whether a similar beneficial effect of exercise on airway responsiveness could occur in asthmatics. Nine patients (male/female: 3/6; mean age ± SD: 24 ± 2 yr) with mild untreated asthma [forced expiratory volume in 1 s (FEV1): 100 ± 7.4% pred; FEV1/vital capacity (VC): 90 ± 6.5%] underwent a series of single-dose Mch bronchoprovocations in the absence of DI in the course of a 10-wk training rowing program (6 h/wk of submaximal and maximal exercise), at baseline ( week 0), and at week 5 and 10. The single-dose Mch was established as the dose able to induce ≥15% reduction in inspiratory vital capacity (IVC) and was administered to each subject at every challenge occasion. Five asthmatics (male/female: 1/4; mean age ± SD: 26 ± 3 yr) with similar baseline lung function (FEV1: 102 ± 7.0% predicted; FEV1/VC: 83 ± 6.0%; P = 0.57 and P = 0.06, respectively) not participating in the exercise training program served as controls. In the trained group, the Mch-induced reduction in IVC from baseline was 22 ± 10% at week 0, 13 ± 11% at week 5 ( P = 0.03), and 11 ± 8% at week 10 ( P = 0.028). The Mch-induced reduction in FEV1 did not change with exercise ( P = 0.69). The reduction in responsiveness induced by exercise was of the same magnitude of that previously obtained in healthy subjects (50% with respect to pretraining). Conversely, Mch-induced reduction in IVC in controls remained unchanged after 10 wk (%reduction IVC at baseline: 21 ± 20%; after 10 wk: 29 ± 14%; P = 0.28). This study indicates that a short course of physical training is capable of reducing airway responsiveness in mild asthmatics.

1981 ◽  
Vol 51 (4) ◽  
pp. 858-863 ◽  
Author(s):  
D. L. Stokes ◽  
N. R. MacIntyre ◽  
J. A. Nadel

To study the effects of exercise on pulmonary diffusing capacity, we measured the lungs' diffusing capacity for carbon monoxide (DLCO) during exhalation from 30 to 45% exhaled vital capacity in eight healthy subjects at rest and during exercise while both sitting and supine. We found that DLCO at these lung volumes in resting subjects was 26.3 +/- 3.2% (mean +/- SE) higher in the supine than in the sitting position (P less than 0.001). We also found that, in both positions, DLCO at these lung volumes increased significantly (P less than 0.001) with increasing exercise and approached similar values at maximal exercise. The pattern of increase in DLCO with an increase in oxygen consumption in both positions was curvilinear in that the rate of increase in DLCO during mild exercise was greater than the rate of increase in DLCO during heavy exercise (P = 0.02). Furthermore, in the supine position during exercise, it appeared that DLCO reached a physiological maximum.


2002 ◽  
Vol 93 (4) ◽  
pp. 1384-1390 ◽  
Author(s):  
Emanuele Crimi ◽  
Riccardo Pellegrino ◽  
Manlio Milanese ◽  
Vito Brusasco

Deep breaths taken before inhalation of methacholine attenuate the decrease in forced expiratory volume in 1 s and forced vital capacity in healthy but not in asthmatic subjects. We investigated whether this difference also exists by using measurements not preceded by full inflation, i.e., airway conductance, functional residual capacity, as well as flow and residual volume from partial forced expiration. We found that five deep breaths preceding a single dose of methacholine 1) transiently attenuated the decrements in forced expiratory volume in 1 s and forced vital capacity in healthy ( n = 8) but not in mild asthmatic ( n = 10) subjects and 2) increased the areas under the curve of changes in parameters not preceded by a full inflation over 40 min, during which further deep breaths were prohibited, without significant difference between healthy ( n = 6) and mild asthmatic ( n = 16) subjects. In conclusion, a series of deep breaths preceding methacholine inhalation significantly enhances bronchoconstrictor response similarly in mild asthmatic and healthy subjects but facilitates bronchodilatation on further full inflation in the latter.


2000 ◽  
Vol 89 (2) ◽  
pp. 711-720 ◽  
Author(s):  
Trisevgeni Kapsali ◽  
Solbert Permutt ◽  
Beth Laube ◽  
Nicola Scichilone ◽  
Alkis Togias

In the absence of deep inspirations, healthy individuals develop bronchoconstriction with methacholine inhalation. One hypothesis is that deep inspiration results in bronchodilation. In this study, we tested an alternative hypothesis, that deep inspiration acts as a bronchoprotector. Single-dose methacholine bronchoprovocations were performed after 20 min of deep breath inhibition, in nine healthy subjects and in eight asthmatics, to establish the dose that reduces forced expiratory volume in 1 s by >15%. The provocation was repeated with two and five deep inspirations preceding methacholine. Additional studies were carried out to assess optimization and reproducibility of the protocol and to rule out the possibility that bronchoprotection may result from changes in airway geometry or from differential spasmogen deposition. In healthy subjects, five deep inspirations conferred 85% bronchoprotection. The bronchoprotective effect was reproducible and was not attributable to increased airway caliber or to differential deposition of methacholine. Deep inspirations did not protect the bronchi of asthmatics. We demonstrated that bronchoprotection is a potent physiologic function of lung inflation and established its absence, even in mild asthma. This observation deepens our understanding of airway dysfunction in asthma.


2021 ◽  
Vol 80 (1) ◽  
pp. 83-92
Author(s):  
Alain Boussana ◽  
Olivier Galy ◽  
Daniel Le Gallais ◽  
Olivier Hue

Abstract The Olympic distance triathlon includes maximal exercise bouts with transitions between the activities. This study investigated the effect of an Olympic distance triathlon (1.5-km swim, 40-km bike, 10-km run) on pulmonary diffusion capacity (DLCO). In nine male triathletes (age: 24 ± 4.7 years), we measured DLCO and calculated the DLCO to alveolar volume ratio (DLCO/VA) and performed spirometry testing before a triathlon (pre-T), 2 hours after the race (post-T), and the day following the race (post-T-24 h). DLCO was measured using the 9-s breath-holding method. We found that (1) DLCO decreased significantly between pre- and post-T values (38.52 ± 5.44 vs. 35.92 ± 6.63 ml∙min-1∙mmHg-1) (p < 0.01) and returned to baseline at post-T-24 h (38.52 ± 5.44 vs. 37.24 ± 6.76 ml∙min-1∙mmHg-1, p > 0.05); (2) DLCO/VA was similar at the pre-, post- and post-T-24 h DLCO comparisons; and (3) forced expiratory volume in the first second (FEV1) and mean forced expiratory flow during the middle half of vital capacity (FEF25-75%) significantly decreased between pre- and post-T and between pre- and post-T-24-h (p < 0.02). In conclusion, a significant reduction in DLCO and DLCO/VA 2 hours after the triathlon suggests the presence of pulmonary interstitial oedema. Both values returned to baseline 24 hours after the race, which reflects possible mild and transient pulmonary oedema with minimal physiological significance.


1990 ◽  
Vol 68 (4) ◽  
pp. 1528-1533 ◽  
Author(s):  
J. Regnard ◽  
P. Baudrillard ◽  
B. Salah ◽  
A. T. Dinh Xuan ◽  
L. Cabanes ◽  
...  

We studied changes in lung volumes and in bronchial response to methacholine chloride (MC) challenge when antishock trousers (AST) were inflated at venous occlusion pressure in healthy subjects in the standing posture, a maneuver known to shift blood toward lung vessels. On inflation of bladders isolated to lower limbs, lung volumes did not change but bronchial response to MC increased, as evidenced by a greater fall in the forced expiratory volume in 1 s (FEV1) at the highest dose of MC used compared with control without AST inflation (delta FEV1 = 0.94 +/- 0.40 vs. 0.66 +/- 0.46 liter, P less than 0.001). Full inflation of AST, i.e., lower limb and abdominal bladder inflated, significantly reduced vital capacity (P less than 0.001), functional residual capacity (P less than 0.01), and FEV1 (P less than 0.01) and enhanced the bronchial response to MC challenge compared with partial AST inflation (delta FEV1 = 1.28 +/- 0.47 liter, P less than 0.05). Because there was no significant reduction of lung volumes on partial AST inflation, the enhanced bronchial response to MC cannot be explained solely by changes in base-line lung volumes. An alternative explanation might be a congestion and/or edema of the airway wall on AST inflation. Therefore, to investigate further the mechanism of the increased bronchial response to MC, we pretreated the subjects with the inhaled alpha 1-adrenergic agonist methoxamine, which has both direct bronchoconstrictor and bronchial vasoconstrictor effects.(ABSTRACT TRUNCATED AT 250 WORDS)


1990 ◽  
Vol 68 (2) ◽  
pp. 586-593 ◽  
Author(s):  
E. E. Wolfel ◽  
W. R. Hiatt ◽  
H. L. Brammell ◽  
V. Travis ◽  
L. D. Horwitz

Exercise training has been shown to decrease plasma norepinephrine (NE) and epinephrine (EPI) levels during absolute levels of submaximal exercise, which may reflect alterations in sympathetic tone as a result of training. To determine if beta-adrenergic blockade altered these changes in the plasma concentration of catecholamines with exercise conditioning, we studied the effects of beta-adrenergic blockade on NE and EPI at rest and during exercise in 24 healthy, male subjects after a 6-wk exercise training program. The subjects were randomized to placebo (P), atenolol 50 mg twice daily (A), and nadolol 40 mg twice daily (N). There were no changes in resting NE and EPI compared with pretraining values in any subject group. During the same absolute level of submaximal exercise NE decreased in P and A but was unchanged in N, whereas EPI decreased only in P. At maximal exercise all three groups developed significant increases in NE after training that paralleled increases in systolic blood pressure. EPI at maximal exercise increased after training with N but was unchanged with P or A. These training-induced changes in plasma catecholamine levels were masked or blunted when the A and N groups were studied while still on medication after training. Thus beta-adrenergic blockade has important effects on adaptations of the sympathetic nervous system to training, especially during submaximal exercise.


2011 ◽  
Vol 110 (5) ◽  
pp. 1400-1405 ◽  
Author(s):  
David G. Chapman ◽  
Norbert Berend ◽  
Gregory G. King ◽  
Cheryl M. Salome

The mechanisms by which deep inspiration (DI) avoidance increases airway responsiveness in healthy subjects are not known. DI avoidance does not alter respiratory mechanics directly; however, computational modeling has predicted that DI avoidance would increase baseline ventilation heterogeneity. The aim was to determine if DI avoidance increased baseline ventilation heterogeneity and whether this correlated with the increase in airway responsiveness. Twelve healthy subjects had ventilation heterogeneity measured by multiple-breath nitrogen washout (MBNW) before and after 20 min of DI avoidance. This was followed by another 20-min period of DI avoidance before the inhalation of a single methacholine dose. The protocol was repeated on a separate day with the addition of five DIs at the end of each of the two periods of DI avoidance. Baseline ventilation heterogeneity in convection-dependent and diffusion-convection-dependent airways was calculated from MBNW. The response to methacholine was measured by the percent fall in forced expiratory volume in 1 s/forced vital capacity (FVC) (airway narrowing) and percent fall in FVC (airway closure). DI avoidance increased baseline diffusion-convection-dependent airways ( P = 0.02) but did not affect convection-dependent airways ( P = 0.9). DI avoidance increased both airway closure ( P = 0.002) and airway narrowing ( P = 0.02) during bronchial challenge. The increase in diffusion-convection-dependent airways due to DI avoidance did not correlate with the increase in either airway narrowing ( rs = 0.14) or airway closure ( rs = 0.12). These findings suggest that DI avoidance increases diffusion-convection-dependent ventilation heterogeneity that is not associated with the increase in airway responsiveness. We speculate that DI avoidance reduces surfactant release, which increases peripheral ventilation heterogeneity and also predisposes to peripheral airway closure.


2012 ◽  
Vol 113 (1) ◽  
pp. 25-30 ◽  
Author(s):  
David G. Chapman ◽  
Norbert Berend ◽  
Karla R. Horlyck ◽  
Gregory G. King ◽  
Cheryl M. Salome

Baseline ventilation heterogeneity is associated with airway hyperresponsiveness (AHR) in asthma; however, it is unknown whether increased baseline ventilation heterogeneity leads to AHR or both are independent effects of similar disease pathophysiology. Reducing functional residual capacity (FRC) in healthy subjects increases baseline ventilation heterogeneity and airway responsiveness, but the relationship between the two is unclear. The aim was to determine whether an increase in baseline ventilation heterogeneity due to a reduction in FRC correlated with the increase in response to methacholine. In 13 healthy male subjects, ventilation heterogeneity was measured by multiple-breath N2 washout before a cumulative high-dose (0.79–200 μmol) methacholine challenge. On a separate day, the protocol was performed with chest wall strapping (CWS) to reduce FRC. Indexes of ventilation heterogeneity in the convection-dependent (Scond) and diffusion-convection-dependent (Sacin) airways were calculated from the multiple-breath N2 washout. CWS decreased FRC by 15.6 ± 2.7% ( P < 0.0001). CWS increased the percent fall in forced expiratory volume in 1 s during bronchial challenge ( P = 0.006), and the magnitude of this effect was independently determined by the effect of CWS on Sacin and FRC ( radj2 = 0.55, P = 0.02). This suggests that changes in baseline ventilation heterogeneity in healthy subjects are sufficient to increase airway responsiveness, independent of the presence of disease pathology.


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