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

A. Sierra,M. Oliveira-Júnior,F. Almeida,M. Benetti,Rodrigo A Oliveira,S. N. Felix,I. S. Genaro,B. Romanholo,N. Ghorayeb,M. Kiss,M. F. Cury-Boaventura,J. Pesquero,R. Vieira

Published 2019 in Oxidative Medicine and Cellular Longevity

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.

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