Effects of inhaled bronchodilators and corticosteroids on exercise induced arterial hypoxaemia in trained male athletes

Abstract

Objectives: To determine the effect of prophylactic treatment with an inhaled bronchodilator and antiinflammatory on arterial saturation (SaO 2 ) in trained non-asthmatic male athletes with exercise induced arterial hypoxaemia (EIAH). Methods: Nine male athletes (mean (SD) age 26.3 (6.7) years, height 182.6 (7.9) cm, weight 79.3 (10.5) kg, VO 2 MAX 62.3 (6.3) ml/kg/min, SaO 2 MIN 92.5 (1.1)%) with no history of asthma were tested in two experimental conditions. A combination of a therapeutic dose of salbutamol and fluticasone or an inert placebo was administered in a randomised crossover design for seven days before maximal cycling exercise. Oxygen consumption (VO 2 ), ventilation (VE), heart rate (HR), power output, and SaO 2 were monitored during the exercise tests. Results: There were no significant differences between the drug (D) and placebo (P) conditions for minimal SaO 2 (D = 93.6 (1.4), P = 93.0 (1.1)%; p = 0.93) VO 2 MAX (D = 61.5 (7.2), P = 61.9 (6.3) ml/kg/min; p = 0.91), peak power (D = 444.4 (48.3), P = 449.4 (43.9) W; p = 0.90), peak VE (D = 147.8 (19.1), P = 149.2 (15.5) litres/min; p = 0.82), or peak heart rate (D = 182.3 (10.0), P = 180.8 (5.5) beats/ min; p = 0.76). Conclusions: A therapeutic dose of salbutamol and fluticasone did not attenuate EIAH during maximal cycling in a group of trained male non-asthmatic athletes.H istorically, 50% of highly trained male athletes 1 and a greater number of female athletes 2 develop exercise induced arterial hypoxaemia (EIAH) during maximal exercise. These athletes, unable to maintain arterial oxygen saturation (SaO 2 ), show decreases in indicators of endurance performance 3 and a reduced maximal aerobic capacity. 4 These observations have fuelled research over the last two decades to investigate the possible mechanisms, which include intrapulmonary shunting of blood, relative alveolar hypoventilation, ventilation perfusion inequality, and pulmonary diffusion limitations. 5 These mechanisms have attracted a great deal of attention but the underlying causes of EIAH have yet to be completely understood. 5It has been documented that athletes unable to maintain SaO 2 show hindered physical performance in terms of decreased maximal aerobic capacity 4 and physical working capacity. 3In this study, the response to asthma inhaler medication was examined in normal subjects assumed to be nonasthmatic. Subjects with asthma have increased inflammation of the lung, and compromised ventilation secondary to bronchoconstriction is common. The standard of care for these patients is the administration of inhaled corticosteroids and bronchodilators. These drugs are effective in reversing airway obstruction and reducing lung inflammation, which allows asthmatics to perform sport and physical activity similar to normal, healthy people.Strenuous exercise, in asthmatic and non-asthmatic athletes, initiates an acute inflammatory response with leucocytosis, neutrophil activation, and release of inflammatory mediators and acute phase proteins. 6 Mediators of airway or vascular t...

Nedocromil sodium and diphenhydramine HCl ameliorate exercise‐induced arterial hypoxemia in highly trained athletes

“…If the onset of EIAH is mediated by the presence of an inflammatory response and a sub‐clinical, transient pulmonary edema, then individuals lacking abnormally high Q̇ C ’s––and subsequently lacking abnormally high PAP’s––would not be afflicted in the same manner as those who do. This inference garners additional support from the higher arterial oxyhemoglobin saturation values observed in Wetter (Wetter et al, 2002 ) and Hodges (Hodges et al, 2005 ) studies, which were approximately 92% S a O 2 at max exercise in the placebo condition. This is in comparison to the present subjects’ desaturation in the placebo condition to 90% S a O 2 at max, with two individuals reaching nearly 85% S a O 2 .…”

“…They concluded that “airway inflammation is of insufficient magnitude to cause impairments in gas exchange” as the administered drugs did not alleviate EIAH, nor were increased inflammatory markers observed in post‐exercise sputum (Wetter et al, 2002 ). Additionally, Hodges et al ( 2005 ) found that dosing twice daily over 7 days with a cocktail of 400 µg of salbutamol (selective short acting β 2 ‐adrenergic antagonist bronchodilator) and 500 µg of fluticasone (an anti‐inflammatory corticosteroid) did not significantly affect S a O 2 compared to placebo in nine male cyclists. However, male subjects in the Wetter (Wetter et al, 2002 ) and Hodges (Hodges et al, 2005 ) studies had average V̇O 2max values of <62 ml·kg −1 ·min −1 , whereas our subjects had an average V̇O 2max of nearly 75 ml·kg −1 ·min −1 , with no subjects below 70 ml·kg −1 ·min −1 .…”

“…Additionally, Hodges et al ( 2005 ) found that dosing twice daily over 7 days with a cocktail of 400 µg of salbutamol (selective short acting β 2 ‐adrenergic antagonist bronchodilator) and 500 µg of fluticasone (an anti‐inflammatory corticosteroid) did not significantly affect S a O 2 compared to placebo in nine male cyclists. However, male subjects in the Wetter (Wetter et al, 2002 ) and Hodges (Hodges et al, 2005 ) studies had average V̇O 2max values of <62 ml·kg −1 ·min −1 , whereas our subjects had an average V̇O 2max of nearly 75 ml·kg −1 ·min −1 , with no subjects below 70 ml·kg −1 ·min −1 . If the onset of EIAH is mediated by the presence of an inflammatory response and a sub‐clinical, transient pulmonary edema, then individuals lacking abnormally high Q̇ C ’s––and subsequently lacking abnormally high PAP’s––would not be afflicted in the same manner as those who do.…”

Respiratory disorders in endurance athletes &ndash; how much do they really have to endure?

“…107 According to the IOC Consensus Statement on Asthma in Elite Athletes (January 2008), inhaled corticosteroids are considered as the most effective drugs for long term control of asthma and prevention of EIB. 108 , 109 …”