EIA is usually defined as a postexercise decrease in FEVi of 15 percent or a decrease in Sgaw of 35 percent compared with basal preexercise values. In the present study, all asthmatic patients had postexercise bronchoconstriction, but the severity of this reaction varied. When using a less sensitive parameter, such as FEVi, to evaluate bronchial tone, the postexercise measurements of the NEIA patients did not differ from those of the C group. With the more sensitive plethysmographic method of detecting airways obstruction, a significant increase in postexercise bronchial tone was found also in the NEIA group. Thus, the C group had no postexercise decrease of Sgaw, while the NEIA patients responded with a postexercise decrease of Sgaw which was about half as pronounced as that found in the EIA group. Hence, postexercise bronchoconstriction seems to be a general phenomenon in asthma and not restricted to the subgroup of asthmatic patients with clinical symptoms of EIA.
In this study there was no difference in the catecholamine response to orthostatic provocation or exercise when comparisons between asthmatic patients and healthy control subjects were made. The adrenaline levels in the EIA patients were similar to those of the C group after exercise. Thus, this degree of bronchoconstriction does not seem to be a potent stimulus for adrenaline secretion. Several earlier studies of sympathoadrenal activity in bronchial asthma have shown enhanced plasma nor-drenaline levels during exercise in patients with EIA compared with healthy control subjects and patients with NEIA. The conclusion of these studies has been that the exaggerated noradrenaline response causes bronchoconstriction by a-adrenoceptor stimulation. Two studies, however, found no difference in postexercise noradrenaline levels when comparing EIA patients with healthy control subjects, and one study found lower levels in EIA patients. The discrepancies in results and conclusions of these different studies may be related to differences in patient selection, treatment, analytical methodology, and standardization of experiments. What may be cause of asthma in children – you can learn in article “Imbalanced diet and inadequate exercise may underlie asthma in children“.
We have attempted to define our patients and control subjects and to standardize the exercise tests. The HPLC method used for determining plasma catecholamines in this study has a good sensitivity and selectivity and has been validated against radio-enzymatic methodology. In earlier studies patients have not always been very well defined, and in some studies there are signs of bronchoconstriction in the basal state. In most of these studies the plasma catecholamine concentrations have been analyzed by fluorometric methods. The exceptions are the studies of Reinhardt et al and Barnes et al, which employed radioenzymatic methods. Several of these earlier studies report high basal plasma catecholamine levels or small increases in plasma noradrenaline or both following exercise. Plasma adrenaline levels also increased little or not at all following exercise. Barnes et al found a clear-cut increase of plasma adrenaline in healthy control subjects following exercise, but no increase in asthmatic patients. There is thus a discrepancy with regard to the catecholamine reaction following exercise in our study and these previous studies, since we found low basal plasma catecholamine levels and clear-cut increases in both noradrenaline and adrenaline following exercise.
A limitation of the present and earlier studies of the catecholamine response to exercise is the possibility that sympathetic activity is unevenly distributed. There may be increases in sympathetic activity to the bronchial smooth muscle in EIA without a generalized increase in sympathetic activity, which would be reflected in elevated plasma catecholamine levels. However, our results lend no support to the above-mentioned claims of an exaggerated plasma noradrenaline response to exercise in EIA.
Prolonged treatment with -agonists may influence the results of studies on asthmatic patients, since it is well known that a continuous stimulation of the -adrenoceptor reduces its sensitivity to further stimuli. Thus, the sensitivity to endogenous -adrenoceptor agonists, especially the /fe-agonist adrenaline, may also be reduced. In earlier studies the medication was withdrawn 8 hours, 12 hours, or 72 hours before the exercise tests, or was not specified. In our study no treatment was allowed for at least one week before the test to preclude any possible effect of drug treatment on the results. It has been shown that the number of -adrenoceptor binding sites on lymphocytes is normalized seven days after the discontinuation of /fe-agonist treatment. Holgate et al have stated that seven to ten days is required for the normalization of fi-adrenoceptor sensitivity in the lungs of healthy volunteers following treatment with ^-adrenoceptor agonists. Furthermore, most of our patients had only symptomatic treatment before this medication-free week, and it is therefore very unlikely that drug treatment influenced the results of our study. The drawback of our nontreatment requirement, of course, is that only patients with mild asthma who could be without treatment for this period were studied Thus, our results may not apply to severe cases of asthma.
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One interesting finding was a negative correlation between postexercise bronchoconstriction and increases in plasma cAMP following exercise in the EIA group. A blunted plasma cAMP response to exercise in EIA patients has been reported by others. It is not known by which mechanism plasma cAMP is increased by exercise, but endogenously produced adrenaline may be important. Adrenaline is a potent stimulus for plasma cAMP increases in the dog and in man. The plasma cAMP elevating effect of adrenaline seems to be linked to 02-adrenoceptor stimulation. Correlations between increases in adrenaline and increases in cAMP have been shown after surgery and exercise (present results). Since the plasma adrenaline response of the EIA patients to exercise was not reduced, it is possible that their -adrenoceptor sensitivity is reduced. Preliminary results of studies of plasma cAMP responses to Isoprenaline and 02-adrenoceptor sensitivity of lymphocytes are consistent with this hypothesis. The 02-adrenoceptor sensitivity of bronchial smooth muscle, however, has not been studied in EIA patients.
The pathophysiology underlying EIA is not fully known. Recent studies have shown that the energy loss caused by humidification and warming of the inhaled air is correlated to the degree of postexercise bronchoconstriction in asthmatic patients. In the present study the ambient temperature and humidity was relatively stable on the occasions when the subjects were monitored. The Ve during exercise tended to be greatest in the EIA group and smallest in the NEIA group, although this difference was not statistically significant. Since the energy cost of humidifying and warming inhaled air is correlated with the magnitude of ventilation, it is possible that asthmatic patients without a history of EIA tend to maintain a lower Ve during exercise to minimize the energy loss from the airway mucosa. This hypothesis requires further investigation.
In conclusion, the results of the present study indicate that not only patients with symptoms of EIA but also other asthmatic patients obtain increases in bronchial tone following exercise. We found no evidence in favor of altered sympathoadrenal reactivity in EIA or NEIA. The possibility of a reduced 02-adrenoceptor sensitivity in EIA patients is subject to further investigation in our laboratory.
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