Search

Purpose: Estimate influences of standard physical exercise on lactic acid concentration and acid-base equilibrium in patients with mild and moderate bronchial asthma compared with healthy trained persons and do not ones., Material and Methods: In 47 asthmatic patients and 20 healthy persons: 1) bronchial reactivity was investigated; 2) at rest and 1, 5 and 10 min after 8 min exercise (PWC85%max, bicycle ergometer): FEV1, lactic acid concentration (LAC), pH, pO2, pCO2 and HCO3 (in capillary blood) were investigated. Among asthmatic patients: 1) 21 experienced exercise-induced asthma (EIA), 2) 20 reacted to histamine in concentration of 0.125 mg/ml/3', 3) 6 reacted to histamine in concentration of 0.25 mg/ml/3'. In healthy persons, without EIA and reaction to histamine, were: 12 who did not train, and 8 athletes., Results: After exercise LAC increased in all groups (p<0.05); the increase was significantly higher in patients and persons who did not train, then athletes, and did not normalised, in opposite to athletes, however in persons who did not train was significantly lower then in asthmatics. pH and pCO2 did not change significantly in all examined persons, but HCO3 decreased significantly in patients with bronchial hyperactivity and in persons who did not train. Significant increase of pO2 appeared only in healthy persons., Conclusion: Physical effort caused significant greater metabolic changes in asthmatic patients then in healthy persons, especially athletes

We investigated whether the level of plasma adenosine (ADO) changed during exercise and whether this could be related to exercise-induced bronchoconstriction. Baseline levels of ADO did not differ, but exercise resulted in higher ADO in patients with asthma than in healthy subjects (86 +/- 35 vs 59 +/- 16 nmol/L; P <.001). In patients with asthma, the increase in ADO was related to decreases in FEV(1) (r (2) = 0.475; P <.05) and SaO(2) (r (2) = 0.693; P <.05). These data suggest that adenosine might be involved in the development of exercise-induced bronchoconstriction.

As many as 71 bronchial asthma (BA) patients and 12 patients suffering from chronic asthmatic bronchitis were examined in the stage of subsiding exacerbation. Before and 10 minutes after exercise measurements were made of the blood content of histamine (H), PGF2 alpha and PGE, adrenaline (A) and noradrenaline (NA), hydroperoxides (HP), and of the general and non-protein thiol groups. The initial level of H, PGF2 alpha, HP, A and NA was so much higher than the control value and the degree of its increase after exercise was so much more significant the more pronounced bronchospasm of effort (BE). The content of PGE after exercise rose to an approximately equal measure both in patients and in healthy subjects thereby pointing out to the relationship between the PGE increment and muscular work itself. The low level of thiol group in BA patients' blood determined by the pathological process was noticeably reduced after exercise, paralleled by an increase in the content of HP. Thus, muscular work in BA patients demonstrates high responsiveness of the systems that produce bronchoconstricting substances. It is likely that BE and its degree in BA patients may be predicted more significantly on the basis of the blood content of H, PGF2 alpha and HP rather than on the basis of the clinical and functional parameters.

The content of acetylcholine, histamine and the total amount of catecholamines were measured in blood of 33 patients with bronchial asthma, in 6 patients with preasthma and in 10 practically normal subjects before and after the use of graded exercise (bicycle ergometry). Subgroups of the patients with asthma of effort were singled out. In such patients, exercises resulted in a significant rise of histamine (p less than 0.05) or acetylcholine level (p less than 0.05). Histaminemia was mostly accompanied by an immediate obstructive response of the bronchi to exercise in the distal parts. In patients with a high acetylcholine content, obstruction of the large bronchi was mainly observed, with a slightly delayed response to exercise.

Eight asthmatic patients and two normal subjects performed two identical exercise tests 140 minutes apart (first test preceded by inhalation of saline and the second by terbutaline sulphate). A ninth asthmatic patient exercised twice after placebo 40 minutes apart. Arterial plasma levels of histamine and cyclic AMP, expiratory flow rates and volumes were measured at rest and during and after exercise. After the first test the mean +/- SEM fall in PEFR was 45.2 +/- 2.6%. In five asthmatics there was an increase in plasma histamine (mean +/- SEM 14.8 +/- 3.3 pmol ml-1) coinciding with exercise-induced asthma (EIA). Histamine levels returned to pre-exercise values within 30 minutes. After terbutaline these five patients had histamine levels greater than those observed before, during, or after the first test. This effect may have been the result of changes in pulmonary microcirculation. After the second test the levels decreased indicating no further release of histamine in response to exercise. No EIA occurred in these patients after terbutaline. The other patients and the two normal subjects had little or no change in histamine throughout the study. The one patient in whom exercise was repeated after placebo demonstrated less histamine release and less EIA after the second test.

Arterial plasma histamine concentrations were measured after exercise in 10 subjects with extrinsic atopic asthma, 10 who were non-atopic and non-asthmatic and seven who were atopic but non-asthmatic, by a single isotope radioenzymatic assay. Significantly higher plasma histamine concentrations were found in the asthmatic subjects before exercise than in the non-atopic controls (p less than 0.05). The mean histamine concentration rose after exercise in all groups but the increased levels were not significantly different from pre-exercise values. Similarly, mean circulating basophil counts increased in all groups after exercise, and a highly significant correlation was found between basophil counts and whole blood histamine concentrations (p less than 0.001). In vitro studies showed that there was a significant correlation between the number of basophils added to plasma samples and the concentrations of histamine subsequently detected. Although the mean concentrations of plasma histamine and whole blood histamine and number of basophils in the atopic control group were intermediate between those found in the atopic asthmatic and non-atopic controls, none of the differences was significant. Venous plasma histamine concentrations after exercise were measured in a further five subjects with extrinsic atopic asthma and five non-atopic, non-asthmatic subjects before and after exercise with the more sensitive and specific double isotope radioenzymatic assay. Concentrations of plasma histamine measured by this assay were about one tenth of those measured by the single isotope radioenzymatic assay. Although a small rise in mean plasma histamine concentration occurred in both groups after exercise there was no significant difference in these levels either between or within the groups. We find no evidence from these studies on measurement of peripheral blood histamine to support the hypothesis that mast cell mediator release is implicated in the pathogenesis of exercise induced asthma.

The effect of exercise on isoprenaline-induced cyclic adenosine monophosphate (cAMP) production was studied in peripheral-blood lymphocytes obtained from ten patients with atopic asthma, seven subjects who were atopic but did not have asthma and eight non-atopic, non-asthmatic control subjects. The asthma in the atopic subjects was mild only requiring intermittent treatment with inhaled beta adrenoceptor agonists, none of which were taken in the 48 hr prior to the study. Exercise consisted of a standardized 6-min run on a treadmill sufficient to raise the subject's pulse rate to greater than 160 bpm and respiratory function was measured before and at 5, 10, 15, 20, 30 and 60 min after the test. Blood samples were taken 5 min before and at 10 and 60 min after exercise, lymphocytes were separated by density gradient centrifugation and cAMP measured by a competitive radioimmunoassay. Exercise led to a significant decrease (27%) in the forced expiratory volume in 1 sec (FEV1) in the ten atopic asthmatic subjects but no change (less than 3%) in the non-atopic and atopic non-asthmatics. There was no significant difference in the unstimulated cAMP levels before exercise in the three groups, but stimulation with isoprenaline caused a significantly greater rise in cAMP in the non-atopic, non-asthmatic subjects when compared to both the atopic asthmatics and the atopic subjects without asthma. Exercise led to a significant elevation of cAMP in all three groups of subjects, but the same differences between the groups remained.(ABSTRACT TRUNCATED AT 250 WORDS)

1. Venous plasma histamine was measured by a specific and sensitive radioenzymatic assay in seven male extrinsic asthmatic and six age-matched non-atopic non-asthmatic male subjects during exercise and voluntary isocapnic hyperventilation. 2. There was no change in peak expiratory flow in normal subjects with exercise or hyperventilation, but asthmatic subjects showed a 29.4 +/- SEM 5.8% fall after exercise and a 29.0 +/- 5.4% fall after matched hyperventilation. 3. Plasma histamine was significantly higher (P less than 0.05) in asthmatic (6.2 +/- 0.95 nmol/l) than that in normal subjects (3.4 +/- 0.61 mol/l) and showed a significant (P less than 0.01) rise (to 14.4 +/- 1.83 nmol/l) during exercise in asthmatic, but not in normal subjects. This suggests that discharge of mast-cell mediators may occur during exercise in asthmatic subjects who develop exercise-induced asthma. 4. With hyperventilation there was no change in plasma histamine in either asthmatic or normal subjects, but this does not exclude the possibility that mediators may be released locally in the airways.

A failure of the usual increase in plasma adrenaline and noradrenaline concentrations during submaximal exercise has been suggested as a contributory cause of exercise induced asthma. Six normal subjects and six asthmatic patients underwent a standard graded maximal exercise test. Measurements of oxygen consumption, minute ventilation, exercise time, blood lactate concentration, and heart rate indicated that the two groups achieved similarly high work loads during exercise. Mean FEV1 fell by 20% in asthmatic patients after exercise. Basal plasma adrenaline concentrations (nmol/l) increased in normal subjects from 0.05 to 2.7 and in asthmatic patients from 0.12 to 1.6 at peak exercise. Noradrenaline concentrations (nmol/l) increased in normal subjects from 2.0 to 14.3 and in asthmatic patients from 1.9 to 13.7 at peak exercise. The increases in adrenaline and noradrenaline in the asthmatic patients did not differ significantly from the increases in normal subjects. Thus a reduced sympathoadrenal response to exercise seems unlikely to be an important mechanism in the pathogenesis of exercise induced asthma.

Serum potassium concentrations were measured before, during, and after exercise in 32 patients with asthma (12 with exercise induced asthma), and in seven normal subjects. The changes in serum potassium in response to exercise did not differ significantly in the two groups or between those with and without exercise induced asthma. The potassium response to exercise is unlikely to be relevant to the mechanism underlying exercise induced bronchoconstriction.

1. Arterial plasma histamine concentrations, forced expiratory volume in 1.0 s (FEV1.0) and peak expiratory flow rate were determined in nine patients with exercise-induced asthma and in five control subjects before and after 8 min of cycle-ergometer exercise. 2. In the controls neither FEV1.0 nor peak expiratory flow rate fell by more than 5% in any individual during the 30 min postexercise period. The asthmatic patients all experienced a fall in FEV1.0 or peak expiratory flow rate, or both, of 15% or more in the period 5-20 min after completion of the exercise. 3. There was no difference between the control subjects and the asthmatic patients in the plasma histamine response to exercise. In both groups there was an insignificant rise of about 40% during exercise, although the initial levels were higher in the asthmatic patients. 4. The mean plasma histamine peak of the asthmatic patients preceded the mean maximal fall of FEV1.0 and peak expiratory flow rate by approximately 15 min. However, no positive correlation was found between rise in, or peak, plasma histamine levels and decrease in lung function. 5. Three non-atopic asthmatic patients had a significantly higher mean plasma histamine concentration during exercise than had the atopic subjects. 6. A strong positive correlation in asthmatic patients, and asthmatic and control subjects together was found between age and mean postexercise plasma histamine concentrations. 7. The results do not support a direct role for histamine in the production of exercise-induced asthma.