(Chest. 2003;124:1602-1605.)
© 2003
American College of Chest Physicians
Extrathoracic Obstruction and Hypoxemia Occurring During Exercise in a Competitive Female Cyclist*
Hans Haverkamp, MS;
Jordan Miller, MS;
Joshua Rodman, PhD;
Lee Romer, PhD;
David Pegelow, BS;
Marcus Santana, MD and
Jerome Dempsey, PhD
* From the Department of Population Health Sciences, John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin-Madison, Madison, WI.
Correspondence to: Hans C. Haverkamp, MS, 504 N Walnut St, Madison, WI 53726; e-mail: hchaverkamp{at}students.wisc.edu
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Abstract
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A 22-year-old competitive female cyclist complained of cough, chest tightness, and wheeze during high-intensity exercise that had previously been diagnosed as exercise-induced bronchospasm (EIB). A loud stridor, a sensation of her "throat closing," and severe dyspnea developed during maximal cycling exercise with concomitant reductions in both inspiratory and expiratory flow rates. A decrease of 25 L/min (26%) in minute ventilation and arterial hypoxemia (PaO2 decrease, 93 to 76.5 mm Hg) resulted from this obstruction. Spontaneous tidal flow-volume loops (FVLs) during exercise exhibited a sawtooth pattern during inspiration, and substantial drops in flow rates after the stridor developed. However, maximal FVLs were unchanged from baseline following exercise, indicating that the obstruction was not EIB. We suggest that the continuous measurement of spontaneous breath-by-breath tidal FVLs may be a useful diagnostic tool for the identification of exercise-induced extrathoracic obstruction. Additionally, extrathoracic obstruction should be considered as an uncommon but potential cause of inadequate ventilation and arterial hypoxemia during exercise.
Key Words: exercise-induced arterial hypoxemia • exercise-induced bronchospasm • stridor • upper airway dysfunction
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Introduction
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Airway resistance during exercise is normally maintained at or below resting levels because the intrathoracic airways undergo bronchodilation1
and the abductor muscles of the upper airway provide maximum glottal aperture during both inspiration and expiration.2
Several reports3
4
have documented the presence of an extrathoracic obstruction following the termination of an exercise bout that previously had been misdiagnosed as exercise-induced bronchospasm (EIB). Indeed, EIB is known to occur after exercise cessation, although a small amount of bronchospasm has been shown to develop during the exercise period.5
In this case report, spontaneous tidal flow-volume loops (FVLs) and arterial blood gas levels during exercise are reported for a female cyclist who developed an apparent extrathoracic obstruction that had been misdiagnosed as EIB.
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Case Report
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A 22-year-old competitive female cyclist attended the laboratory in association with an asthma study. Her major complaints were wheeze, severe dyspnea, and cough during heavy exercise. She had been diagnosed with asthma, EIB, and allergic rhinitis, and was atopic to several common allergens, as indicated by the results of skin prick testing. An induced sputum analysis revealed a high macrophage count with no airway eosinophilia or neutrophilia. At the time of study, the patient was using a nasal corticosteroid spray (fluticasone propionate; GlaxoSmithKline; Research Triangle Park, NC), a combination bronchodilator/corticosteroid inhalation powder (Advair Diskus; GlaxoSmithKline) daily, and a fast-acting ß-agonist when she felt it necessary. Her baseline FEV1/FVC ratio was 78% and was unchanged following administration of a fast-acting bronchodilator, suggesting the presence of a mild, but fixed, obstruction. The shape of the inspiratory and expiratory limbs of the maximal volitional flow-volume envelope performed at rest were normal (ie, smooth with no truncation of flow-rates).
Cycling exercise was performed on a magnetically braked cycle ergometer after a catheter was placed in the radial artery for the collection of arterial blood. After a brief warmup (3 min each at 50% and 75% of peak oxygen uptake [
O2]), the patient began exercising at a fixed workload that previously had been determined to elicit a O2 of approximately 90% peak O2, and exercise was performed until exhaustion (total time, 13 min). Thirty minutes later, and after another brief warmup (3 min at 90% O2 peak), exercise was recommenced at her previously determined maximal workload (ie, 100% peak O2) and was performed to exhaustion (total time, 1.25 min). Pulmonary function tests were performed at 5, 10, and 20 min after both exercise bouts.
Spontaneous tidal exercise FVLs obtained during exercise at 50%, 75%, and 90% of peak O2 are shown in Figure 1
, left, A, and during maximal exercise in Figure 1
, right, B. The inspiratory limbs exhibited a sawtooth pattern, which became more pronounced as intensity increased (Fig 1
, left, A). During maximal exercise (Fig 1
, right, B), a loud stridor and severe dyspnea appeared at the same time that both inspiratory and expiratory flow rates were clearly reduced when compared with those values obtained only 30 s earlier at the initiation of the maximal workload. A breath-by-breath analysis of breathing mechanics during the maximal workload (Fig 2
) revealed sudden and significant decreases in peak inspiratory and expiratory flows, breathing frequency, and minute ventilation at the same time the symptoms appeared. A significant CO2 retention and moderate arterial hypoxemia occurred immediately following the onset of symptoms (Table 1
). On exercise termination, the dyspnea and stridor disappeared almost immediately. As summarized in Table 2
, expiratory flow rates at both high lung volumes (ie, FEV1) and lower lung volumes (midexpiratory range of forced expiratory flow) were not different from baseline values at all time points postexercise.
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Figure 1. Tidal exercise FVLs obtained during exercise at 50%, 75%, and 90% of O2 peak (left, A), and during maximal exercise before and after the development of an extrathoracic obstruction (right, B). FVLs were created by taking the average of 10 tidal breaths. Note the significant drop in both inspiratory and expiratory flows during maximal exercise after the appearance of symptoms, and the sawtooth pattern in the inspiratory flows even at submaximal exercise.
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Figure 2. Breath-by-breath analysis of breathing frequency (fb), tidal volume (VT), minute ventilation (E), peak inspiratory flow (Insp flow) and expiratory flow (Exp flow), and partial pressures of end-tidal O2 (PETO2) and CO2 (PETCO2) during the entire period of exercise at the maximal workload. Breath 1 represents the first breath of the maximal workload, and breath 43 represents the final breath of the workload. The vertical line indicates the breath at which symptoms appeared. The subject was able to exercise for a total of 75 s, even though the stridor appeared at 37 s into the workload. Also note the initial increase in breathing frequency and the concomitant decrease in tidal volume at the onset of the workload as the subject adjusted to the increased work rate.
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Discussion
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The major finding in this case was a significant restriction of inspiratory and expiratory tidal flow rates during maximal intensity exercise due to an apparent extrathoracic upper airway obstruction, causing extreme dyspnea, alveolar hypoventilation, and arterial hypoxemia in an otherwise healthy endurance athlete. Our findings support those of previous investigations that prolapse of supraglottic structures into the airway3
4
or paradoxical inward movement of the true or false vocal cords6
during exercise can be misdiagnosed and treated as EIB.
An important finding in this study was that by using tidal FVLs the increase in pulmonary resistance was shown to appear during exercise while the subject was maintaining power output. Previously, maximal volitional FVLs have been used to document extrathoracic obstruction after subjects had stopped exercising.3
6
The first signs of obstruction appeared during submaximal exercise, at which time the inspiratory limb of the tidal FVL exhibited a sawtooth pattern, and then more obviously with a sudden reduction in flow rate on the inspiratory and expiratory limb of the tidal FVL during maximal exercise, coincident with the onset of loud stridor and severe dyspnea. In contrast to these changes during exercise, maximum volitional FVLs obtained at 5, 10, and 20 min during the recovery period showed no abnormalities. This is important in light of the fact that a reduction in postexercise maximal FVLs is the "gold standard" for the diagnosis of EIB. Thus, we think that our data support the use of continuous breath-by-breath measurement of tidal FVLs during exercise as a useful diagnostic tool for the identification of exercise-induced upper airway dysfunction. These breath-by-breath measurements also have been shown to be valuable in identifying the onset and progression of expiratory flow limitation, and its effects on dynamic hyperinflation and dyspnea during exercise in healthy individuals and in patients with COPD and chronic heart failure.7
8
9
Our findings also demonstrate for the first time that CO2 retention and arterial hypoxemia occur commensurate with the onset of an increased upper airway resistance during heavy exercise. Exercise-induced arterial hypoxemia (EIAH) has been observed in a subpopulation of otherwise healthy, habitually active endurance athletes. It normally occurs immediately at the onset of heavy exercise and persists throughout the exercise session. EIAH is attributed primarily to a widened alveolar-to-arterial PO2 difference in combination with a limited hyperventilatory response, which is due, at least in part, to expiratory flow limitation.10
This case report suggests that upper airway dysfunction also should be considered as a potential cause of ventilatory constraint contributing to EIAH.
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Table 2. Pulmonary Function Measured at Baseline, 5 min, 10 min, and 20 min after the 90% and 100% Peak O2 Exercise Bouts *
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Acknowledgements
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We thank Dr. Nizar Jarjour for access to the patient’s medical records.
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Footnotes
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This research was supported by the National Heart, Lung, and Blood Institute and by a grant from the Department of Veterans Affairs/Department of Defense.
Abbreviations: EIAH = exercise-induced arterial hypoxemia; EIB = exercise-induced bronchospasm; FVL = flow-volume loop; O2 = oxygen uptake
Received for publication December 11, 2002.
Accepted for publication April 3, 2003.
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References
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- Bittleman, D, Smith, R, Weiler, J Abnormal movement of the arytenoid region during exercise presenting as exercise-induced asthma in an adolescent athlete. Chest 1994;106,615-616[Abstract/Free Full Text]
- Bjornsdottir, U, Gudmundsson, K, Hjartarson, H, et al Exercise-induced laryngochalasia: an imitator of exercise-induced bronchospasm. Ann Allergy Asthma Immunol 2000;85,387-391[Medline]
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- McFadden, E, Zawadski, K Vocal cord dysfunction masquerading as exercise-induced asthma, a physiologic cause for "choking" during athletic activities. Am J Respir Crit Care Med 1996;153,942-947[Abstract]
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Abstract
Introduction
