Impairment on Cardiopulmonary Function after Marathon: Role of Exhaled Nitric Oxide

Abstract

Background. The endurance exercise is capable of inducing skeletal muscle, heart, and respiratory fatigue, evidenced by morphofunctional cardiac changes, release of myocardial injury biomarkers, and reduction of maximal voluntary ventilation and oxygen consumption (VO2) at peak exercise. Purpose. The aim of this study was to investigate whether marathoners present cardiac fatigue after marathon and whether it correlates with pulmonary levels of exhaled nitric oxide (eNO) and pulmonary inflammation. Methods. 31 male marathoners, age 39±9 years, were evaluated by cardiopulmonary exercise test three weeks before and between three and 15 days after a marathon; eNO analysis and spirometry were evaluated before, immediately after, and 24 and 72 hours after the marathon, and sputum cellularity and cytokine level were assessed before and after the marathon. Results. Marathon induced an increase in the percentage of macrophages, neutrophils (from 0.65% to 4.28% and 6.79% to 14.11%, respectively), and epithelial cells and a decrease in cytokines in induced sputum, followed by an increase in eNO concentration (20±11 to 35±19 ppb), which presented a significant reduction 24 and 72 hours after marathon (9±12 e 12±9 ppb, p<0.05). We observed a decrease in the spirometry parameters in all time points assessed after the marathon (p<0.05) as well as in cardiopulmonary capacity, evidenced by a reduction in VO2 and ventilation peaks (57±6 to 55±6 mL·min-1·Kg-1 and 134±19 to 132±18 Lpm, respectively, p<0.05). Finally, we observed a negative correlation between the decrease in forced expiratory volume and decrease in eNO 24 and 72 hours after marathon (r=−0.4, p=0.05). Conclusion. Reduction in eNO bioavailability after marathon prevents the reduction in cardiopulmonary capacity induced by acute inflammatory pattern after marathon.

Association of Daily Dietary Intake and Inflammation Induced by Marathon Race

“…Prolonged exercise is a physiological stress which promotes hyperinflammation following anti-inflammatory compensatory response characterized by the increase on inflammatory mediators such as IL-6, IL-8, IL-ra, IL-10, and C-reactive protein (CRP) [1–5]. The exacerbated inflammation contributes to transient immunosuppression, as well as hematological and cardiopulmonary changes, and muscle and renal damage induced by exercise [6, 7].…”

Functional Analysis of Airway Remodeling is Related with Fibrotic Mediators in Asthmatic Children

“…NO can be measured noninvasively in the exhaled air by chemiluminescence, by using bench [16] or portable [12] NO detecting devices. In fact, increased levels of NO have been associated not only with several aspects of asthma [6,7,8,9], but also with exercise-induced bronchoconstriction, which is a highly prevalent characteristic of asthmatic patients [16,17]. In the present study, it was found that asthmatic children presented high levels of exhaled NO, ranging among 25-30 ppb, which clearly indicates an inflammatory process of the airways.…”

Functional Analysis of Airway Remodeling is Related with Fibrotic Mediators in Asthmatic Children

“…Beside Th2 mediators and growth factors, nitric oxide (NO), has also been linked to asthma development, severity and exacerbations [6,7,8,9].NO is aninstable gas, considered a highly reactive nitrogen specie, which present a very short half-life.NO can be measured noninvasively in the exhaled air by chemiluminescence, by using bench [16]or portable [12]NO detecting devices.In fact, increased levels of NO have been associated not only with several aspects of asthma [6,7,8,9], but also with exercise-induced bronchoconstriction, which is a highly prevalent characteristic of asthmatic patients [16,17]. In the present study, it was found that asthmatic children presented high levels of exhaled NO, ranging among 25-30ppb, which clearly indicates an inflammatory process of the airways.…”