Exercise can imply a considerable strain on the airways. In people with asthma, this can lead to the induction of exercise-induced asthma (EIA), with cough, wheezing and shortness of breath. In recent years, the term “exercise-induced bronchoconstriction” (EIB) has been commonly used; EIB is defined as a measured reduction in FEV ⩾10% occurring after a standardised exercise test, accompanied by comparable symptoms.1 Both phenomena are based on bronchial hyper-reactivity of the airways. The key stimulus for the occurrence of EIA/EIB is not the exercise itself, but rather the coinciding hyperventilation.2 3 With a prevalence of 12–15% in the entire population4 and 23–50% amongst performance and elite athletes,5 6 EIA is one of the most common disorders encountered in clinical sports medicine.

In order to diagnose the presence of an EIA/EIB, a number of pulmonary test procedures are used, including inhalation tests (using pharmacologically active substances such as histamine or mannitol), eucapnic voluntary hyperventilation (EVH) and exercise provocation tests. In the latter, EIB symptoms are induced by a controlled ergometric load, and the extent of the pulmonary impairment is measured by spirometrically recording respiratory parameters. However, studies have shown that the presence of an EIB remains undiagnosed in 5–15% of people.7 Apart from the frequent lack of association between the exercise situation and clear asthma symptoms, the main reason underlying these false-negative findings might be an inadequate standardisation of exercise protocols. Large discrepancies in exercise prescriptions can be found in the literature.5 8 9 10 11 12 13 Recommendations for the required exercise period vary from 4 to 20 minutes. Highly inconsistent information is also provided regarding the required exercise load, varying from 80 to 90% of the maximum heart rate (HR_max) and from 50 to 80% of the maximum oxygen uptake (VO_2max). The American Thoracic Society (ATS) guidelines8 recommend an exercise intensity of 80–90% of HR_max, determined by the formula: HR  = 220– age, for a period of 4 minutes. As there is a high individual variance in the HR_max,14 applying an age-derived HR formula entails a high risk of misjudging the optimum exercise intensity. Early recognition of possible EIB, which is very important for successful treatment, is then sometimes extremely complicated or often even impossible. Therefore, the usefulness of the aforementioned recommendations for bronchial exercise testing in sports science have to be called into question.

The objective of the present study was to investigate whether the ATS standard protocol for exercise challenge testing (ECT) is precise enough to specify sufficient exercise intensity for inducing EIB.

METHODS

Ethics approval was not required for the study. All participants gave informed consent.

Subjects

An ECT was carried out under laboratory conditions on 100 clinically healthy students of various types of sports at the University of Bielefeld. The students (62 men, 38 women; mean age 23.9 (SD3.1) years; height 177.9 (8.6) cm, weight 71.1 (10.7) kg; body mass index (BMI) 20.9 (2.4), forced expiratory volume in 1 second (FEV₁) 99.4 (12.8)%) had been clinically assessed as non-asthmatic, and were considered to be athletically fit because of their field of study and personal details.

Design

Before starting the study, anthropometric data (age, sex, height and weight) was taken as a basis for determining the individual reference values of the lung-function parameters. In accordance with ATS guidelines, the treadmill (Ergo ELG 2; Woodway, Weil am Rhein, Germany) exercise was started at a low speed, progressively increasing during the first 2–3 minutes of exercise until the target HR was reached. This target HR, derived from the formula HR = (220−age)×0.85, had to be maintained for 4 minutes. During these 6–8 minutes of exercise on the treadmill, HR was continuously monitored using an HR meter (F1; Polar, Kempele, Finland). Before and after exercise, blood pressure was measured (Riva Rocci sphygmomanometer; Bosch and Sohn, Jungingen, Germany) to exclude any possible cardiovascular anomalies. Using body plethysmography (Bodyscope-S, Ganshorn Medizin Electronic, Niederlauer, Germany), FEV₁, peak expiratory flow (PEF) and maximum expiratory flow at 50% vital capacity (MEF₅₀) were measured before and 10 minutes after exercise. To record the metabolic response to exercise as well as the exercise intensity, blood samples were taken before and immediately after the treadmill ergometry from the hyperaemic ear lobe and blood gas analysis (BGA) (ABL 50; Radiometer A/S, Copenhagen, Denmark) and measurement of blood lactate concentration after exercise (Super GL analyser; Dr. Müller Gerätebau GmbH, Freitel, Germany) were carried out.

Statistical analysis

Statistical analyses were performed using SPSS V.14.0 for Windows software. Data are given as mean (SD). For testing differences, the Student t tests for dependent and independent random samples were used. The Shapiro–Wilks test was used to check for a normal distribution. The level of statistical significance was set at p<0.05 and p<0.01 was considered highly significant.15

RESULTS

Mean post-exercise lactate concentration of the entire statistical sample was 5.9 (SD 2.64) mmol/l (figure 1). Lactate concentrations of < 4 mmol/l were measured in 30% of subjects, 26% had lactate values of 4–6 mmol/l and 44% had lactate levels >6 mmol/l.

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Figure 1

Distribution of lactate values after exercise (mean 5.9 (SD 2.6) mmol/l; n = 100).

In order to determine a possible influence of exercise intensity on pulmonary-function parameters, subjects were divided according to their lactate values into a high-lactate (>6 mmol/l) group and a low-lactate (<6 mmol/l) group (figure 2). The results showed a highly significant difference in FEV₁ (p<0.01). For the high-lactate group, a highly significant (p<0.01) decrease in FEV₁ (mean −4.4 (SD 1.5)%) was found, and there was also an increase in the low-lactate group (mean 0.56 (SD 0.6)%).

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Figure 2

Change in FEV₁ depending on anaerobic lactate metabolism (mean (SD); n = 100). FEV₁, forced expiratory volume in 1 second.

Assuming a decline in FEV₁ of ⩾10% after exercise as an indicator for bronchial obstruction, 5% of subjects showed a positive finding (FEV₁ after exercise −10% to −47%). None of these subjects had previously been diagnosed as having asthma. The metabolic parameters of these subjects showed post-exercise lactate values of 6.48 to 11.7 mmol/l and post-exercise pH values of 7.204 to 7.259, respectively, representing predominantly anaerobic lactate metabolism. No subject with a post-exercise lactate level <6.48 mmol/l showed a pathological bronchial obstruction.

DISCUSSION

The objective of the present study was to investigate whether the ATS standard protocol for ECT8 is precise enough to ensure sufficient exercise intensity for inducing EIB. An exercise load of 80–90% of the HR_max is recommended in the ATS guidelines for implementing ECT-induced bronchial provocation in order to induce hyperventilation and detect EIB. Hence, from a sports-science viewpoint, a load predominantly realised by anaerobic lactate metabolism is required, because only these loads lead to increased lactate accumulation and proton (hydrogen ion) surplus. The result is a raised buffering activity with simultaneous excitation of the respiratory centre inducing compensatory increase in ventilation.

The results of our study show that the required exercise load could not be ensured for all subjects when determining exercise intensity by the ATS formula (figure 1). According to the literature, there is a high individual variation not only in HR_max14 but also the heart rate at the transition from mainly aerobic to mainly anaerobic metabolism.16 17 18 19 20 The formula-based determination of the target HR, therefore, induced different relative workloads for our subjects. In some, the protocol caused an aerobic workload, whereas in others anaerobic lactate metabolism was induced, as indicated by the highly variable post-exercise lactate (figure 1) and pH values. The reference lactate-based method in determining the transition from mainly aerobic to anaerobic metabolism is the maximum lactate steady state, defined as the highest work rate that can be maintained over time without continual blood lactate accumulation.21 According to the literature,20 21 22 23 this transition in running occurs at a mean lactate concentration of 4–5 (SD 0.5–1) mmol/l. An energetic load of >6 mmol/l, therefore, can be assumed to be predominantly anaerobic. Only in 44 of our 100 subjects was a lactate concentration of >6 mmol/l measured after exercise, thus, in 56 subjects exercise intensity determined by the heart rate formula could not be ensured as sufficient to induce an exercise-induced obstruction. This result was supported by a differentiated consideration of the lung-function parameters depending on the workload (figure 2). The results show that bronchial obstruction only occurred in the five subjects showing with post-exercise lactate values >6.48 mmol/l, indicating anaerobic lactate metabolism. These five subjects had a decrease in FEV₁ of ≥10%, classifying them as having EIA.1 10 24 25

Furthermore, the prevalence of a positive EIB finding in this study was 5%, which is below the rate of 12–15% reported in the literature.4 One reason for this could be the fact that for technical reasons only one post-exercise lung- function measurement could be made; usually, lung function is measured immediately after exercise and then repeatedly at short intervals (eg, 3, 6, 10 and 15 minutes) to detect the maximum post-exercise bronchoconstriction.1 Therefore it cannot be excluded that in some subjects the maximum reduction in lung function could have been missed.

However, a more likely reason for the low prevalence is that a pre-existing EIB condition remained undisclosed in some of the 56 subjects because of the insufficient exercise intensity. This is supported by a study by Carlsen et al on 20 children with asthma.10 In that study, more people with EIA were identified, and far higher reductions in FEV₁ were found after a bronchial provocation test with an exercise intensity of 95% HR_max than with 85% HR_max. The HR_max in that study was also derived by the formula HR = 220−age. In 1987 Noviski et al26 also found that exercising at high intensity provoked significantly more severe EIB than exercising at low intensity, and they stated that the severity of EIB response is determined by the intensity. Randolph stressed the importance of documentation and compliance to specific diagnostic criteria such as the duration, mode and intensity of exercise for obtaining reliable study results.27

CONCLUSION

The sensitivity of ECT using an exercise control derived from a heart-rate formula must be cast into doubt by our results. From a sports-science viewpoint, determination of the individual aerobic capacity should be achieved before ECT in order to ensure optimum control of exercise intensity for bronchial exercise provocation. One objective of further study should be to acquire appropriate control parameters for ECT to develop a practical and highly sensitive provocation protocol.