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1 Thoracic Diseases Research Unit, Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, Minnesota 55905; and 2 John Rankin Laboratory of Pulmonary Medicine, Departments of Preventive Medicine and Medicine, The University of Wisconsin, Madison, Wisconsin 53705
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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We compared pulmonary mechanics measured during
long-term exercise (LTX = 20 min) with long-term isocapnic
hyperventilation (LTIH = 20 min) in the same asthmatic individuals
(n = 6). Peak expiratory flow (PEF)
and forced expiratory volume in 1 s
(FEV1) decreased during LTX
(
19.7 and 22.0%, respectively) and during LTIH
(6.66 and 10.9%, respectively). In contrast, inspiratory pulmonary resistance
(RLI) was
elevated during LTX (57.6%) but not during LTIH (9.62%). As expected,
airway function deteriorated post-LTX and post-LTIH
(FEV1 = 30.2 and
21.2%;
RLI = 111.8 and 86.5%, respectively). We conclude that the degree of airway
obstruction observed during LTX is of a greater magnitude than that
observed during LTIH. Both modes of hyperpnea induced similar levels of airway obstruction in the posthyperpnea period. However, the greater airway obstruction during LTX suggests that a different process may be
responsible for the changes in airway function during and after the two
modes of hyperpnea. This finding raises questions about the equivalency
of LTIH and LTX in the study of airway function during exercise-induced asthma.
exercise-induced asthma; pulmonary resistance
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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IN EXERCISE-INDUCED ASTHMA (EIA) a transient airway obstruction occurs 5-15 min after the cessation of exercise (2, 6, 20, 31). Voluntary hyperventilation and exercise are often used interchangeably to induce airway obstruction in asthmatic subjects (16, 20). Two studies have shown that airway obstruction also develops during exercise of 20 min or longer duration (4, 32). On the other hand, airway obstruction does not seem to occur during isocapnic hyperventilation of <12-min duration (6, 16, 31). To date there has been no direct comparison of changes in airway function during exercise and hyperventilation in asthmatic subjects other than the limited study (3 asthmatic subjects) of Stirling and colleagues (31). In this study, a decrease in pulmonary resistance in asthmatic individuals was reported during both exercise and isocapnic hyperventilation of ~12-min duration.
To directly compare the changes in airway function during exercise and
voluntary hyperventilation, we measured pulmonary responses to both
modes of hyperpnea in the same asthmatic individuals while attempting
to match minute ventilation (
E). We
quantified events occurring during as well as after hyperpnea. We
hypothesized that similar changes in airway function (i.e., presence or
absence of airway obstruction) would occur during both types of hyperpnea.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Individuals (n = 6 men) with a
clinical history of EIA and a positive exercise challenge test,
indicated by a reduction in forced expiratory volume in 1 s
(FEV1) >10% of the baseline
value postexercise, were included. Subjects regularly used an inhaled 
2-adrenergic agonist and/or
oral theophylline. None of the participants utilized oral steroids or
inhaled corticosteroids in their medication regimen. Informed consent
was obtained from each individual before participation. This study was
approved by the Human Subjects Committee Review Board at the University
of Wisconsin-Madison.
Pulmonary function and the maximal exercise test. Vital capacity, FEV1, and inspiratory capacity were determined by using a Collins 13.5-liter water-sealed spirometer (Warren E. Collins, Braintree, MA). Functional residual capacity (FRC) was determined in a Collins body plethysmograph. Total lung capacity (TLC) was determined as the sum of FRC and inspiratory capacity. Pulmonary function tests were performed after antiasthmatic medications were withheld for at least 12 h.
Immediately after pulmonary function tests, a progressive exercise test was performed on a treadmill to determine each subject's exercise capacity. Each participant started by walking at 4.0 miles/h (mph) and 0% grade for 3 min as a warm-up. The speed was then increased to 6.0 mph. Every 3 min the speed of the treadmill was increased by 1 mph until the running cadence was satisfactory to the participant. (Note that 1 subject remained at a speed of 4.0 mph throughout his progressive exercise test, but his treadmill incline level was progressively increased.) From this point the treadmill was maintained at a constant speed, and grade was increased by 2% until a maximal volitional effort was achieved. Maximal oxygen consumption (O2 max) was
calculated by using open-circuit expired-gas analysis, as
previously described (26). Measurements of expired gas,
inspiratory capacity, end-expiratory lung volume (EELV), and
inspiratory and expiratory flow rate were made during the last minute
of each exercise stage.
Evaluation of pulmonary mechanics. The breathing circuit used to obtain spirometry, ventilation, and pulmonary mechanics data consisted of a Hans Rudolph two-way nonrebreathing valve (model 2700, Hans Rudolph, Kansas City, MO). Matched Hans Rudolph pneumotachographs (model 3813) were used to measure inspired and expired flows. End-tidal gases were sampled at the mouthpiece and analyzed by a Perkin-Elmer mass spectrometer (model 1100). Signals were relayed at 75 Hz through an analog-to-digital board (Scientific Solutions Labmaster PGH) to a personal computer, where data were kept in files for later analysis. Inspired and expired volumes were calculated by integration of the flow signals. A Validyne transducer (model MP 45-871 Validyne, Northridge, CA, ±300 cmH2O) connected to polyethylene tubing (PE-200) measured mouth pressure. Esophageal pressure (Pes) was measured with a 10-cm latex balloon, positioned 8-10 cm above the gastroesophageal junction, connected by polyethylene tubing (PE-200) to a Validyne transducer (model MP 45-871, ±200 cmH2O). Transpulmonary pressure (Ptp) was obtained by computer subtraction of mouth pressure from Pes. Inspiratory pulmonary resistance (RLI) was calculated at the volume corresponding to peak inspiratory flow (PIF). The resistive pressure was determined by subtraction of the elastic pressure drop caused by the volume at peak flow from the Pes at peak flow. The resistive pressure was then divided by PIF to determine inspiratory pulmonary resistance. In other words
![R<SC>l</SC>,i = [Ptp(PIF) − Ptp(EELV) − &ugr;V<SC>l</SC>/C<SC>l</SC>dyn]/PIF](/content/vol87/issue3/fulltext/1107/img001.gif)
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VL is volume above EELV at
PIF, and CLdyn is dynamic compliance for each breath (14). By using the mean flow-volume and
pressure-volume (F-V and P-V, respectively) loops plotted for each
individual at rest, during exercise, and during recovery, ventilatory
volume variables and ventilatory timing variables were measured to
obtain an estimation of the ventilatory work. This method is described
in detail by Otis (25). Flow and pressure signals were verified to be
in phase up to 12 Hz.
Esophageal temperature was measured as an index of body core
temperature. A nasopharyngeal temperature sensor (Mon-a-therm, size
9-Fr, Mallinckrodt Medical, St. Louis, MO) was inserted through the
nares into the esophagus. The position of the temperature probe was
30-35 cm from the nares. The temperature was read from a
Mon-a-therm digital display box (model 6500, Mallinckrodt Medical). This system gives a temperature reading that is updated every 4 s. The
temperature of the expired air was obtained with similar equipment by
using a probe placed at the expired port of the breathing valve. This
corresponded to a distance of 5-10 cm from the mouth.
EELV was measured by having individuals perform inspiratory capacity
maneuvers during each collection period. To verify that TLC was
attained during each inspiratory capacity maneuver, we confirmed that a
peak negative Pes similar to that obtained during the inspiratory
capacity maneuver at rest was attained. An index of the difficulty of
breathing or dyspnea was also obtained at each collection period by
having the subject select a number on the Borg rate scale of perceived
exertion (10-point category ratio) (21).
Long-term exercise (LTX) session.
Subjects were asked to return within 1 wk for LTX at 70%-85% of their
personal O2 max.
The duration of exercise was 20 min. To ensure that a maximal EIA
response would occur postexercise, the subjects withheld their
antiasthmatic medications for at least 12 h before each session.
Standard measurements of spirometry were obtained to evaluate the
status of lung volume and maximal expiratory flows before, during, and
after exercise. To obtain the F-V loops used to match ventilation in
the long-term isocapnic hyperventilation (LTIH) session, 10-20 F-V
tidal breaths immediately preceding the inspiratory capacity maneuvers
were averaged, thereby providing representative F-V and P-V loops. The
individual subject's average F-V loop or P-V loop was obtained by
dividing each tidal volume
(VT) into 1% increments. The
flow or pressure value for each increment was summed and divided by the
total number of averaged breaths to calculate a mean for each volume increment.
LTIH session.
The LTIH session was conducted within 2 wk of the LTX session. The
session involved 20 min with ventilation equal to or higher than the
exercise E obtained near the end of the
LTX session. Participants withheld their antiasthmatic medication for
at least 12 h before each session (the same as for the LTX session).
Measurements were made and analyzed as in the LTX session: breathing
circuit, Pes, Ptp, pulmonary resistance, work of breathing,
temperature, EELV, rate of perceived exertion, and spirometry. Subjects
were asked to match their averaged
Pes-VT loop obtained during LTX while matching respiratory rate by using a metronome. Their
real-time P-V loop was displayed on a storage oscilloscope
(Tektronix 5111A, Beaverton, OR) where the averaged
Pes-VT loop from the previous LTX session was displayed and superimposed on the screen. The subject
was instructed to match the superimposed loop. In addition, a
metronome signaled the desired breathing frequency (inspiration and expiration) and ratio of inspiratory time to total breath time
(TI/TT).
This arrangement allowed us to match
VT, frequency, TI/TT,
Pes excursion, and duration of LTIH. Before the start of LTIH, resting
levels of end-tidal PCO2
(PETCO2) were obtained; this
level was maintained during LTIH by adding CO2 to the inspired gas.
Data analysis. Statistical comparisons within and between the LTX or LTIH sessions were made by using repeated-measures ANOVA followed by paired t-tests. All data are shown as means ± SE unless otherwise noted. All statistical tests of significance were set at a P < 0.05 level.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Maximal exercise test session.
Subject characteristics are shown in Table
1. Baseline pulmonary function showed that
all subjects were within the normal range of predicted values for TLC,
vital capacity, and FRC (Table 2).
Two subjects had a reduced FEV1
(<80% predicted), and one of them had a lower than predicted
FEV1-to-FVC ratio,
indicating a mild airflow limitation. None of the subjects
had an increased FRC (gas trapping).
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LTX session.
During the LTX session all subjects showed changes during recovery
consistent with EIA, i.e., a fall in both
FEV1 and peak expiratory flow
(PEF) >10% of the preexercise value. The mean PEF fell 24.2% from
the baseline value of 8.7 l/s at rest.
FEV1 decreased by 30.2%, whereas
mean RLI
increased by 111.77%. All preexercise-to-postexercise comparisons were
significantly different (P < 0.05)
(Figs.
1-3).
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19.7 and 22.0%,
respectively (Figs. 1 and 2), whereas
RLI showed
a significant increase of 57.6% (Fig. 3).
Table 3 displays the ventilatory responses
during LTX and LTIH. E was relatively
constant, ranging from 74.0 to 86 l/min as
O2 consumption was maintained
between 73.0 and 80.0% of (mean = 76.0%) during LTX. The exercise
VT also remained fairly constant throughout exercise (2.2-2.5 liters), whereas breathing frequency increased from 31.0 breaths/min at minute
2 to 40 breaths/min at minutes
15 and 20. EELV
(expressed as %TLC) remained at its preexercise level of 44% (3.1 liters) early in exercise but by minute
20 had increased significantly to 57% of TLC (4.0 liters). EELV tended to be elevated postexercise when compared with
rest (54% of TLC, P = 0.06).
End-inspiratory lung volume (EILV) increased significantly from 78% of
TLC during early exercise to 89% of TLC at 20 min of exercise. The
work of breathing ranged from 181.0 J/min at 2 min to 349.0 J/min at
minute 20 (P = 0.02).
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LTIH session.
Changes in PEF, FEV1, and
RLI
pre-LTIH to post-LTIH were 18.5, 21.2, and 86.5%,
respectively, indicating similar levels of bronchospasm to those
obtained during LTX (Figs. 1-3).
6.67%) and
FEV1 (10.9%) decreased
significantly but that
RLI
(9.62%) remained unchanged during the later stages of LTIH.
Table 3 displays the ventilatory responses during LTIH. In contrast to
during exercise (during which E had a
tendency to slowly increase) subjects maintained constant target levels
of E during LTIH, ranging from 93.0 to
97.0 l/min. PETCO2 was
maintained at resting levels (4.6%-4.7%).
VT also remained constant
throughout LTIH (2.6-2.7 liters). Breathing frequency increased to
the constant value of 38.0 breaths/min at minute 2 and was constant throughout LTIH. EELV remained at
44% of TLC (3.1 liters) during minute
2 of mimicking, but by minute
20 reached a level to 50% of TLC (3.5 liters). EELV
was not increased post-LTIH when compared with rest. EILV increased
from 64.0% of TLC at rest to 83.0% of TLC during early LTIH and
increased further to 92.0% of TLC at 20 min of LTIH. The work of
breathing ranged from 307.0 J/min at minute
2 to 394.0 J/min at minute
20.
LTX session compared with LTIH session (Table 3). The percent changes in PEF, FEV1, and RLI at 4 min after hyperpnea compared with prehyperpnea were not significantly different between LTX and LTIH (Figs. 1-3). However, the percent changes between minutes 2 and 20 of hyperpnea were different between sessions, indicating that a more intense bronchospasm developed during LTX compared with LTIH.
E was higher at the initial stages of
LTIH, but, by minute 5 of both
challenges, this difference was no longer statistically significant
between sessions at comparative time points. This reflects the target
levels of ventilation presented to the subjects, who attempted to match
E obtained at later stages of LTX.
VT was similar at all time
points during LTIH compared with LTX. TI/TT
(0.46 ± 0.01 during both LTX and LTIH) and EELV were similar during
both sessions. Relative humidity (45 ± 3% for LTX vs. 45 ± 2%
for LTIH) and room temperature were also similar during both sessions.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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This study measured and directly compared pulmonary mechanics in the same asthmatic individuals during LTX and LTIH matched for ventilation. Previous studies that investigated pulmonary responses during isocapnic hyperventilation and exercise cannot be used to directly compare the two modes of challenge. Blackie and colleagues (6) measured FEV1 in five asthmatic subjects during 16 min of isocapnic hyperventilation and reported no change in FEV1. Although their results are consistent with our data obtained during the first 4 min of LTIH, they did not report data during exercise. Stirling et al. (31) measured pulmonary resistance in three asthmatic subjects during exercise and isocapnic hyperventilation, but their calculations of expiratory pulmonary resistance could have been significantly affected by dynamic compression of the airway. We expanded on both studies by directly measuring inspiratory resistance and spirometry throughout LTX and LTIH. RLI is an effort-independent parameter and is unaffected by dynamic compression of the airway (32). In addition, we conducted statistical analyses within and between both sessions for the full 20-min duration. Gilbert and colleagues (16) conducted a study utilizing the same asthmatic individuals during exercise and isocapnic hyperventilation of 6-min duration. However, they reported FEV1 values only prehyperpnea and posthyperpnea. No values during the exercise or hyperventilation were given.
Limitations.
During LTIH we attempted to replicate several key respiratory
parameters found during LTX: VT,
respiratory frequency, E, and Pes swings.
Our results indicate that an individual's breathing frequency,
PETCO2, EELV,
VT, and
TI/TT
were matched but that E values in the
early stages of exercise were not matched. Although
E tended to be higher throughout the LTIH
session, this difference was not statistically significant in later
stages of hyperpnea. Because it is known that the level of
E is associated with the severity of EIA
(2, 20), our higher absolute level of E
during LTIH should have produced a more severe airway obstruction. However, all indexes of airway obstruction showed comparable changes at
4 min post-LTX and 4 min post-LTIH. The difficulty in matching ventilatory parameters during LTX and LTIH has been reported in a study
by Aaron and colleagues (1) in which subjects tended to overbreathe
even though careful attempts were made to control E, respiratory rate,
VT, and EELV. Our results
followed a similar pattern. However, because we were interested in
instigating EIA during LTIH, having subjects exceed their target
ventilation assured us that the absence of airway obstruction was not
caused by insufficient ventilation. In addition, the nonrebreathing
diaphragms prevented blow-by gases from flowing across the expiration
port of the breathing valve during LTIH.
Potential mechanisms. Our results imply that different factors could have contributed to the maintenance of airway patency during LTIH compared with LTX. These potential factors include level of ventilation, breathing pattern, body core temperature, airway temperature, water content of expired air, cardiac output, plasma catecholamines, or locally released mediators.
The level of ventilation and water content of the expired air are thought to have the greatest influence on respiratory heat loss (20) because respiratory heat loss is thought to be directly related to the severity of airway obstruction in EIA (8). Our estimated mean respiratory heat loss (1.44 kcal/min) during LTIH was similar to that reported by Deal and colleagues (10), whose subjects experienced slightly greater bronchospasm compared with ours for the same respiratory heat loss. Because of higher total ventilation, respiratory heat loss was higher for LTIH compared with LTX in our subjects, which would lead us to expect more bronchoconstriction, not less. Similarly, because room air relative humidity was similar in the two trials, the airway global water losses should have been similar or greater during LTIH because of the higherE achieved.
An increased VT could be
associated with the bronchodilation observed during hyperpnea (6, 18,
19, 23, 31) caused by a reflex inhibition of bronchomotor tone via
slowly adapting pulmonary stretch receptors (19, 30) or direct
mechanical stretch of airway smooth muscle (14). Then tendency to
higher VT observed during LTIH
compared with LTX in our study may thus have inhibited airway
obstruction during LTIH until VT
returned to resting levels in the recovery period. This explanation and our data seem to fit well with the concept of lung inflation modulating airway smooth muscle contraction (15, 33). During LTX, EELV continued
to increase progressively above rest (>44% of TLC). The EILV
achieved was similar during LTX and LTIH (89 and 92% of TLC,
respectively); this EILV value was similar to those previously reported
for LTX (32). One consequence of breathing at such high lung volumes is
increasing the work of breathing. The mean total work of breathing that
our asthmatic subjects achieved during LTX and LTIH was higher compared
with the level of total ventilatory work achieved by normal subjects
(125 J/min) working at a higher %O2 max (85%) and
level of ventilation (120 l/min) (1).
One interpretation of our breathing pattern results is that, early in
LTX, airway patency is maintained (less airway obstruction) because of
a higher VT compared with
baseline. However, VT continued to progressively decrease (5 of 6 participants) during LTX
concomitantly with the appearance of airway obstruction. Maintaining
VT during LTIH could possibly
have prevented airway obstruction. In the recovery period
VT decreased (approaching
baseline values), and bronchoconstriction developed after both challenges.
Esophageal temperature has previously been utilized as an indirect
measure of the thermal changes taking place in the airway (9, 17, 27).
The upper esophageal probe utilized in the above-referenced studies was
positioned ~29-33 cm from the tip of the nares, similar to the
position of our temperature probe. At this position (retrotracheal),
temperature changes should reflect changes in tracheal mucosal
temperature. Because both esophageal and pulmonary tissue intervene
between the probe and the airways, the esophageal temperature was
probably higher than actual airway temperature and overestimated the
amount of warming observed during LTX. However, our observed esophageal
temperature strongly indicates a warming (Table
4). The time constant of the thermocouple
in contact with the airway mucosa is <100 ms once it has reached the
flat portion of the time constant curve. The time constant of the
thermocouple in air is <1 s for a 0.3°C temperature change on the
flat portion of the time constant curve. This indicates accurate
temperature measurements of changes up to 0.3°C at a breathing
frequency of 30 breaths/min (i.e., 0.15°C change at a breathing
frequency of 60 breaths/min). Body core temperature steadily increases
with exercise and reaches peak values at 15-20 min, depending on
the exercise intensity (27). Because asthmatic subjects are believed to
have hypertrophied bronchopulmonary vasculature (12) and hyperreactive
airways (5), an increase in body temperature may induce an increase in
airway mucosal blood flow. This increase in warm blood could cause
vascular edema and congestion and therefore produce airway obstruction
(8, 10, 20, 22, 28). Increases in esophageal temperature would reflect
thermal changes occurring in the esophageal mucosa, which receives
blood at body temperature much like the airway mucosa.
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O2 max for 36 min
in 6-min intervals. At the higher intensity (higher cardiac output),
airway obstruction decreased, whereas at the lower intensity (lower
cardiac output), airway obstruction increased, arguing against cardiac output playing a significant role in bronchodilation.
There are multiple chemical mediators that likely affect airway
function during exercise and cause the bronchoconstriction seen after
exercise in asthmatic subjects. Multiple studies have shown that
histamine (7, 11) and leukotrienes (13) (both of which are released by
mast cells) play a role in postexercise bronchoconstriction. During
exercise, it has been shown that release of vagal tone in normal
subjects may be responsible for improvement in airway function.
However, this has not been shown in asthmatic subjects. There is only
indirect evidence suggesting that bronchodilator mediators could play a
role in regulating airway tone during exercise. Epinephrine levels
increase during exercise (3), but studies in normal individuals suggest
that epinephrine has little influence on bronchomotor tone.
Furthermore, differences in epinephrine levels between LTX and LTIH
could not explain the present results because the bronchodilator
influence would most likely be less during LTIH, during which we
documented lower
RLI
compared with LTX. Other bronchodilator mediators include prostaglandin
E2, found in epithelial cells, and
nitric oxide, which can be generated by nonadrenergic noncholinergic
nerves (30), epithelial cells, or inflammatory cells of the airway.
There is no direct evidence that either nitric oxide or prostaglandins
play a role in controlling airway function during exercise, nor that
differences in the activity of mediators could explain the differences
in airway function between LTX and LTIH that we documented.
Conclusion. We measured ventilatory parameters during exercise and isocapnic hyperventilation in the same asthmatic individuals and found a difference in airway function between LTX and LTIH. Airway patency, reflected by a decrease or no change in pulmonary resistance, was maintained throughout LTIH. Conversely, a higher degree of airway obstruction was observed during the later stages of LTX, even though both modes of challenge produced similar degrees of airway obstruction in the posthyperpnic period. Events that occur during LTX and during LTIH need to be accounted for and analyzed in any theory attempting to explain EIA. A description of pulmonary mechanics and analysis of breathing pattern during exercise or hyperventilation can provide a better understanding of EIA pathophysiology. In view of the differences in airway function encountered during both bouts of hyperpnea, when mechanisms of EIA are being investigated, it is imperative that exercise be utilized as the specific mode of hyperpnea. Further investigation is needed on the role of exercise and isocapnic hyperventilation used interchangeably to induce and study airway obstruction in individuals with EIA.
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ACKNOWLEDGEMENTS |
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The authors thank Dr. Rolf D. Hubmayr for assistance and advice in the preparation of this manuscript. We also greatly appreciate the secretarial assistance of Lori L. Oeltjenbruns and the technical assistance of Catherine M. Swee.
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FOOTNOTES |
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This study was partially funded by National Heart, Lung, and Blood Institute Grants RO1-HL-52230 and HL-15469. M. A Babcock was a Parker B. Francis Fellow in Pulmonary Research at the John Rankin Laboratory of Pulmonary Medicine at the University of Wisconsin-Madison.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: O. E. Suman, Rm. 4-411 Alfred Bldg., Mayo Clinic and Foundation, 200 First St. SW, Rochester, MN 55905 (E-mail suman.oscar{at}mayo.edu).
Received 9 October 1998; accepted in final form 27 May 1999.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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1.
Aaron, E.,
B. Johnson,
C. Seow,
and
J. Dempsey.
Oxygen cost of exercise hyperpnea: measurement.
J. Appl. Physiol.
72:
1810-1817,
1992
2.
Andserson, S. D.
Issues in exercise-induced asthma.
J. Allergy Clin. Immunol.
76:
763-772,
1985[Medline].
3.
Barnes, P. J.,
M. J. Brown,
M. Silverman,
and
C. T. Dollery.
Circulating catecholamines in exercise and hyperventilation induced asthma.
Thorax
87:
435-440,
1981.
4.
Beck, K.,
K. Offord,
and
P. Scanlon.
Bronchoconstriction occurring during exercise in asthmatic subjects.
Am. J. Respir. Crit. Care Med.
149:
352-357,
1994[Abstract].
5.
Benson, M. K.
Bronchial hyperreactivity.
Br. J. Dis. Chest
69:
227-239,
1975[Medline].
6.
Blackie, S.,
C. Hilliam,
R. Village,
and
P. Paré.
The time course of bronchoconstriction in asthmatics during and after isocapnic hyperventilation.
Am. Rev. Respir. Dis.
142:
1133-1136,
1990[Medline].
7.
Clee, M. D.,
C. G. Ingram,
P. C. Reid,
and
A. S. Robertson.
The effect of astemizole on exercise-induced asthma.
Br. J. Dis. Chest
78:
180-183,
1984[Medline].
8.
Deal, E. C., Jr.,
E. R. McFadden, Jr.,
R. H. Ingram, Jr.,
and
J. J. Jaeger.
Hyperpnea and heat flux: initial reaction sequence in exercise-induced asthma.
J. Appl. Physiol.
46:
476-483,
1979
9.
Deal, E. C., Jr.,
E. R. McFadden, Jr.,
R. H. Ingram, Jr.,
and
J. J. Jaeger.
Esophageal temperature during exercise in asthmatic and nonasthmatic subjects.
J. Appl. Physiol.
46:
484-490,
1979
10.
Deal, E. C., Jr.,
E. R. McFadden, Jr.,
R. H. Ingram, Jr.,
R. H. Strauss,
and
J. J. Jaeger.
Role of respiratory heat exchange in production of exercise-induced asthma.
J. Appl. Physiol.
46:
467-475,
1979
11.
Dorward, A. J.,
and
K. R. Patel.
A comparison of ketotifen with clemastine, ipratropium bromide and sodium cromoglycate in exercise-induced asthma.
Clin. Allergy
12:
355-362,
1982[Medline].
12.
Dunnill, M. S.
The pathology of asthma, with special reference to changes in the bronchial mucosa.
J. Clin. Pathol.
13:
27-33,
1960.
13.
Finnerty, J. P.,
R. Wood-Baker,
H. Thomson,
and
S. T. Holgate.
Role of leukotrienes in exercise-induced asthma: inhibitory effect of ICI 204219, a potent leukotriene D4 receptor antagonist.
Am. Rev. Respir. Dis.
145:
746-749,
1992[Medline].
14.
Frank, N. R.,
J. Mead,
and
B. G. Ferris, Jr.
The mechanical behavior of the lungs in healthy elderly persons.
J. Clin. Invest.
36:
1680-1687,
1957.
15.
Fredberg, J. J.,
D. Inouye,
B. Miller,
M. Nathan,
S. Jafari,
S. H. Raboudi,
J. P. Butler,
and
S. A. Shore.
Airway smooth muscle, tidal stretches, and dynamically determined contractile states.
Am. J. Respir. Crit. Care Med.
156:
1752-1759,
1997
16.
Gilbert, I. A.,
J. M. Fouke,
and
E. R. McFadden, Jr.
Intra-airway thermodynamics during exercise and hyperventilation in asthmatics.
J. Appl. Physiol.
64:
2167-2174,
1988
17.
Jaeger, J. J.,
E. C. Deal, Jr.,
D. E. Roberts,
R. H. Ingram, Jr.,
and
E. R. McFadden, Jr.
Cold air inhalation and esophageal temperature in exercising humans.
Med. Sci. Sports Exerc.
12:
365-369,
1980[Medline].
18.
Johnson, B. D.,
P. D. Scanlon,
and
K. C. Beck.
Regulation of ventilatory capacity during exercise in asthmatics.
J. Appl. Physiol.
79:
892-901,
1995
19.
Karlsson, J. A.,
G. Sant'Ambrogio,
and
J. Widdicombe.
Afferent neural pathways in cough and reflex bronchoconstriction.
J. Appl. Physiol.
65:
1007-1023,
1988
20.
Mahler, D. A.
Exercise-induced asthma.
Med. Sci. Sports Exerc.
25:
554-561,
1993[Medline].
21.
Mahler, D.,
K. Faryniarz,
T. Lentine,
J. Ward,
E. Olmstead,
and
G. O'Connor.
Measurement of breathlessness during exercise in asthmatics.
Am. Rev. Respir. Dis.
144:
39-44,
1991[Medline].
22.
McFadden, E., Jr.
Respiratory thermal events and airway function.
Can. J. Sport Sci.
12:
63S-65S,
1987.
23.
Mitchell, G. S.,
and
E. H. Vidruk.
Neural and humoral factors in control of tracheal caliber.
J. Appl. Physiol.
59:
198-204,
1985
24.
Morris, A. H.,
R. E. Kanner,
R. O. Crapo,
and
R. M. Gardner.
Clinical Pulmonary Function Testing (2nd ed.). Salt Lake City, UT: Intermountain Thoracic Soc., 1984.
25.
Otis, A. B.
The work of breathing.
In: Handbook of Physiology. Respiration. Bethesda, MD: Am. Physiol. Soc., 1964, sect. 3, vol. I, chapt. 17, p. 463-476.
26.
Power, S.
Measurement of oxygen uptake in the non-steady state.
Aviat. Space Environ. Med.
58:
323-27,
1987[Medline].
27.
Saltin, B.,
and
L. Hermansen.
Esophageal, rectal, and muscle temperature during exercise.
J. Appl. Physiol.
21:
1757-1762,
1966
28.
Solway, J.
Airway heat and water fluxes and the tracheobronchial tree.
Eur. Respir. J.
3, Suppl. 12:
608S-617S,
1990.
29.
Solway, J.
Respiratory air conditioning and the bronchial circulation.
In: The Bronchial Circulation, edited by J. Butler. New York: Dekker, 1992, vol. 57, chapt. 9, p. 291-336. (Lung Health Biol. Ser.)
30.
Sorkness, R. L.,
W. J. Calhoun,
and
W. W. Busse.
Neural control of the airways and cholinergic mechanisms.
In: Bronchial Asthma: Mechanisms and Therapeutics (3rd ed.). Boston, MA: Little, Brown, 1993.
31.
Stirling, D. R.,
D. J. Cotton,
B. L. Graham,
W. C. Hodgson,
D. W. Cockroft,
and
J. A. Dosman.
Characteristics of airway tone during exercise in patients with asthma.
J. Appl. Physiol.
54:
934-942,
1983
32.
Suman, O.,
M. Babcock,
D. Pegelow,
N. Jarjour,
and
W. Reddan.
Airway obstruction during exercise in asthma.
Am. J. Respir. Crit. Care Med.
152:
24-31,
1995[Abstract].
33.
Younes, M.,
and
G. Kivinen.
Respiratory mechanics and breathing pattern during and following maximal exercise.
J. Appl. Physiol.
57:
1773-1782,
1984
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) and
long-term isocapnic hyperventilation (LTIH; 
) across time. Each
point represents mean ± SE as %change from baseline (preexercise
or prehyperventilation). All postchallenge measurements were taken 4 min postchallenge. * Statistically significant prechallenge vs.
postchallenge comparisons within mode of hyperpnea,
P < 0.05. ** Statistically
significant 2- vs. 20-min comparisons within mode of hyperpnea,
P < 0.05. ++ Statistically
significant 2- to 20-min %change comparison between sessions,
P < 0.05.
