Exhaled nitric oxide during exercise: site of release and modulation by ventilation and blood flow

Abstract

To define the site of release and factors modulating exhaled nitric oxide (NO) during exercise in humans, we measured exhaled NO output during exercise, during exercise after balloon occlusion of the nasopharynx (to exclude nasal NO), and at rest with isocapneic hyperventilation or dobutamine infusion. Exhaled NO output increased from rest to exercise (57 +/- 10 to 171 +/- 30 nl.min-1.m-2; P < 0.003; n = 8). Exclusion of nasal NO reduced exhaled NO at rest and during exercise. Calculated nasal contribution at rest (53 +/- 5%) decreased during exercise (29 +/- 6%; P < 0.05), whereas nonnasal contribution increased (47 +/- 5 to 71 +/- 6%; P < 0.05). Isocapneic hyperventilation at rest increased exhaled NO output (51 +/- 8 to 94 +/- 22 nl.min-1.m-2; P = 0.05). Dobutamine infusion did not increase exhaled NO output. We conclude that nasal exhaled NO decreases (and nonnasal exhaled NO increases) with exercise. We also conclude that, under the conditions of this study, increased exhaled NO output during exercise is more closely related to increased ventilation than to increased blood flow.

Bronchial obstruction and exhaled nitric oxide response during exercise in cold air

“…The mechanism that causes a rise in V 'NO during exercise is not clear. The close relationship observed between V 'NO and variables related to metabolism magnitude strongly suggests that the origin of exhaled NO is linked to structures that are dependent on functions that become involved progressively as metabolism increases [15,17,18]. Thus, both haemodynamic alteration and hyperventilation have been suggested as being important stimuli for NO-production during exercise [15,18,19].…”

“…The close relationship observed between V 'NO and variables related to metabolism magnitude strongly suggests that the origin of exhaled NO is linked to structures that are dependent on functions that become involved progressively as metabolism increases [15,17,18]. Thus, both haemodynamic alteration and hyperventilation have been suggested as being important stimuli for NO-production during exercise [15,18,19]. Moreover, it has been suggested recently that exercise does not necessarily increase V 'NO but only shifts the elimination of a proportion of the V 'NO from the blood to the airways, less NO diffusing into the blood and more being removed by ventilation [20].…”

“…NO may be detected in the air exhaled by humans and the amount of NO exhaled over time (V 'NO) may be measured accurately and continuously [15][16][17][18]. Although the NO detected at the mouth is the difference between what is produced in the respiratory system and what is transformed or eliminated continuously by other endogenous pathways, V 'NO is generally assumed to reflect the NO produced by cells within the respiratory tract.…”

“…Moreover, NO mediates the nonadrenergic, noncholinergic neural inhibitory responses which represent the only neural bronchodilator mechanism in human airways [12,13]. In addition, NO may contribute to acute inflammation and host defence in the lung [14].NO may be detected in the air exhaled by humans and the amount of NO exhaled over time (V 'NO) may be measured accurately and continuously [15][16][17][18]. Although the NO detected at the mouth is the difference between what is produced in the respiratory system and what is transformed or eliminated continuously by other endogenous pathways, V 'NO is generally assumed to reflect the NO produced by cells within the respiratory tract.…”

Bronchoalveolar lavage, sputum and exhaled clinically relevant inflammatory markers: values in healthy adults

“…They include sex and sexual hormones, body weight and age, circadian changes of respiratory function in health and disease, caffeine and alcohol, meals rich in nitrate, genetic background for some enzymes, upper respiratory tract infection, exercise, drugs (including inhibitors of NO synthases) and of course smoking [46,[54][55][56][57][58][59][60][61][62][63][64][65][66][67][68][69][70][71][72][73]. Moreover, FeNO levels in healthy subjects are influenced by atopy, i.e.…”