
Impairment on Cardiopulmonary Function after Marathon: Role of Exhaled Nitric Oxide
Author(s) -
Ana Sierra,
Manoel Carneiro OliveiraJunior,
Francine Maria de Almeida,
Marino Benetti,
Rodrigo Oliveira,
Soraia Nogueira Felix,
Isabella Santos de Genaro,
Beatriz Mangueira Saraiva Romanholo,
Nabil Ghorayeb,
Maria Augusta P. D. Kiss,
Maria Fernanda Cury-Boaventura,
João Bosco Pesquero,
Rodolfo Paula Vieira
Publication year - 2019
Publication title -
oxidative medicine and cellular longevity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.494
H-Index - 93
eISSN - 1942-0900
pISSN - 1942-0994
DOI - 10.1155/2019/5134360
Subject(s) - exhaled nitric oxide , spirometry , medicine , ventilation (architecture) , nitric oxide , cardiology , respiratory minute volume , respiratory system , sputum , vo2 max , anesthesia , heart rate , asthma , pathology , blood pressure , tuberculosis , mechanical engineering , engineering
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 (VO 2 ) 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 VO 2 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.