Effects of nitric oxide inhalation on pulmonary gas exchange during exercise in highly trained athletes

Durand,; Mucci,; Safont,; Prefaut,

doi:10.1046/j.1365-201x.1999.00480.x

Cited by 18 publications

(19 citation statements)

References 33 publications

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“…As VA/Q mismatching contributes to EIH [15,38,48], it is tempting to suggest that low NO levels may favour EIH development. This is in accordance with Durand et al [10], who showed that exogenous NO may modify EIH in athletes during the last phase of an incremental test in normoxic conditions. By contrast, Sheel et al [40] failed to find any effect of NO inhalation on gas exchange during normoxic and hypoxic maximal exercises in the same population.…”

Section: No In Athletes With Eihsupporting

confidence: 88%

“…During intense exercise, several previous studies have suggested that these athletes may experience VA/Q mismatch leading to pulmonary gas exchange impairment and hypoxaemia [38,48]. Durand et al [10] recently showed that inhaled NO may modify the drop in oxygen arterial partial pressure (PaO 2 ) suggesting that NO may be involved in EIH probably by modulating VA/Q homogeneity. Moreover, Duplain et al [9] recently pointed out that subjects with a low level of exhaled NO had higher pulmonary arterial pressure during exposure to hypoxia.…”

Section: Introductionmentioning

confidence: 98%

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Exhaled nitric oxide level during and after heavy exercise in athletes with exercise-induced hypoxaemia

Kippelen

Caillaud

Robert

et al. 2002

Pflügers Arch - Eur J Physiol

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Endogenous nitric oxide (NO) is an important mediator of vasodilatation, bronchodilatation and lung inflammation. We hypothesised that the exhaled NO level may be modified in some endurance-trained athletes during and after intense exercise. Nine athletes with exercise-induced hypoxaemia (EIH), 12 athletes without EIH and 10 untrained subjects exercised for 15 min at 90% maximal oxygen consumption (VO(2)max). Exhaled NO was measured during exercise, and after 1 h and 22 h of recovery. Exhaled NO concentration ( C(NO)) decreased significantly during exercise in all subjects and returned to basal values after 1 h of recovery with no further modification. Exhaled NO output (V(NO)) rose significantly during exercise, rapidly dropped down following exercise and was similar to resting values after 1 h and 22 h of recovery. The results also showed that C(NO) and V(NO) were significantly lower in the athletes with EIH in comparison with the untrained subjects (V(NO) was 5.32 +/- 0.77 nmol/min versus 3.61 +/- 0.72 nmol/min at rest, 18.52 +/- 1.50 nmol/min versus 15.00 +/- 2.06 nmol/min during heavy exercise, and 5.52 +/- 1.04 nmol/min versus 3.79 +/- 0.76 nmol/min after 22 h recovery, in untrained subjects and EIH athletes, respectively). These findings do not confirm the hypothesis of pulmonary inflammation associated with EIH. However, potential NO epithelial down-regulation may occur and contribute to the development of gas exchange abnormality in some endurance-trained athletes.

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Section: No In Athletes With Eihsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 98%

Exhaled nitric oxide level during and after heavy exercise in athletes with exercise-induced hypoxaemia

Kippelen

Caillaud

Robert

et al. 2002

Pflügers Arch - Eur J Physiol

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“…The improvement in V '/Q ' with inhaled L-NAME is a novel finding and accords with the results of VENEGAS et al [38], who found that inhaled NO (40 parts per million (ppm)) increased the spatial heterogeneity of V '/Q ' in supine dogs measured by positron emission tomography, although HOPKINS et al [39] found no V '/Q ' deterioration in anaesthetized dogs given 80 ppm NO. Deterioration in V '/Q ' matching with inhaled NO has also been shown in studies of patients with chronic obstructive pulmonary disease [40] and in normal humans [40,41]. Two recent studies found a trend towards better gas exchange with partial elimination or diversion of endogenous NO production.…”

Section: Differences Between Effects Of Nmentioning

confidence: 84%

Pulmonary NO synthase inhibition and inspired CO2: effects on V ′/Q ′ and pulmonary blood flow distribution

Brogan¹,

Hedges²,

McKinney³

et al. 2000

Eur Respir J

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Inhaled carbon dioxide decreases ventilation/perfusion ratio (V '/Q ') heterogeneity in dogs. The aim of this study was to test whether inhaled CO 2 improves the V '/Q ' by inhibition of nitric oxide production and whether inhibition of endogenous NO production in the lung alters gas exchange and V '/Q ' matching.Eleven healthy dogs were anaesthetized and mechanically ventilated. The multiple inert gas elimination technique (MIGET) was used to measure V '/Q ' heterogeneity and regional pulmonary blood flow heterogeneity was assessed in five dogs using fluorescent microspheres. In a separate set of five dogs, exhaled NO levels were measured via chemiluminescence. All dogs were studied before and after 4.8% inspired CO 2 , and then given the NO synthase inhibitor N v -nitro-L-arginine methyl ester (L-NAME, 10 mg . kg -1 ) via nebulization, after which they were studied again with room air and inhaled CO 2 .CO 2 and L-NAME improved arterial and alveolar oxygen tension, but the improvements with L-NAME did not reach statistical significance. Improved V '/Q ' matching, as assessed by the MIGET, occurred under all experimental conditions. Exhaled NO levels were reduced by 40% with CO 2 and 70% with L-NAME. The standard deviation of regional pulmonary blood flow assessed via microspheres decreased only with inhaled CO 2 . Fractal analysis of pulmonary blood flow distributions revealed that regional blood flow was highly correlated with flow to neighbouring pieces of lung in all four conditions with no changes in the fractal dimension.Inspired carbon dioxide improves ventilation perfusion ratio matching and is associated with a more homogeneous distribution of pulmonary blood flow. Although inspired carbon dioxide causes a reduction in exhaled nitric oxide, the differences in pulmonary perfusion distributions found between carbon dioxide and N v -nitro-Larginine methyl ester suggest that the carbon dioxide effect is not mediated by a reduction in nitric oxide production. The improved ventilation perfusion ratio matching with inhibition of nitric oxide synthase suggests the intriguing possibility requiring further study that endogenous production of nitric oxide in the lung does not subserve ventilation perfusion ratio regulation. Eur Respir J 2000; 16: 288±295. Addition of low concentrations (2±5%) of carbon dioxide to inspired gas improves gas exchange and arterial oxygenation in normal lungs [1,2]. Using the multiple inert gas elimination technique (MIGET), it was demonstrated that inspired CO 2 reduces ventilation/perfusion ratio (V '/Q ') heterogeneity even with constant ventilation [3]. Although CO 2 has many effects on the lungs that may promote V '/Q ' matching [4,5], it remains unknown how and at what site(s) CO 2 decreases V '/Q ' heterogeneity.Changes in CO 2 concentration or the accompanying pH may affect airways, parenchyma or vessels directly or indirectly through modulation of effector substances such as prostaglandins [6] or calcium [7]. Of considerable interest, also, is nitric oxide, which is ...

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“…The race time was faster and the expressed perceived exertion was lower with sodium bicarbonate than in response to saline exercise [median of 6 min 21 s (range 6 min 16 s to 6 min 58 s) vs. 6 min 28 s (6 min 23 s to 7 min 10 s) and median of 18 (range [13][14][15][16][17][18][19] vs. 19 (17)(18)(19), respectively; P Ͻ 0.05].…”

Section: Resultsmentioning

confidence: 99%

“…1,14,19,27,48,49) and also, in some athletes, as a reduced saturation of Hb (Sa O 2 ; Refs. 17,23,37,51). Insufficient increase in ventilation (14), a pulmonary diffusion limitation (14), and ventilation-perfusion inequality (21,26) may contribute to reduce Pa O 2 .…”

mentioning

confidence: 99%

Bicarbonate attenuates arterial desaturation during maximal exercise in humans

Nielsen

Bredmose

Strømstad

et al. 2002

Journal of Applied Physiology

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The contribution of pH to exercise-induced arterial O2 desaturation was evaluated by intravenous infusion of sodium bicarbonate (Bic, 1 M; 200-350 ml) or an equal volume of saline (Sal; 1 M) at a constant infusion rate during a "2,000-m" maximal ergometer row in five male oarsmen. Blood-gas variables were corrected to the increase in blood temperature from 36.5 +/- 0.3 to 38.9 +/- 0.1 degrees C (P < 0.05; means +/- SE), which was established in a pilot study. During Sal exercise, pH decreased from 7.42 +/- 0.01 at rest to 7.07 +/- 0.02 but only to 7.34 +/- 0.02 (P < 0.05) during the Bic trial. Arterial PO2 was reduced from 103.1 +/- 0.7 to 88.2 +/- 1.3 Torr during exercise with Sal, and this reduction was not significantly affected by Bic. Arterial O2 saturation was 97.5 +/- 0.2% at rest and decreased to 89.0 +/- 0.7% during Sal exercise but only to 94.1 +/- 1% with Bic (P < 0.05). Arterial PCO2 was not significantly changed from resting values in the last minute of Sal exercise, but in the Bic trial it increased from 40.5 +/- 0.5 to 45.9 +/- 2.0 Torr (P < 0.05). Pulmonary ventilation was lowered during exercise with Bic (155 +/- 14 vs. 142 +/- 13 l/min; P < 0.05), but the exercise-induced increase in the difference between the end-tidal O2 pressure and arterial PO2 was similar in the two trials. Also, pulmonary O2 uptake and changes in muscle oxygenation as determined by near-infrared spectrophotometry during exercise were similar. The enlarged blood-buffering capacity after infusion of Bic attenuated acidosis and in turn arterial desaturation during maximal exercise.

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Effects of nitric oxide inhalation on pulmonary gas exchange during exercise in highly trained athletes

Cited by 18 publications

References 33 publications

Exhaled nitric oxide level during and after heavy exercise in athletes with exercise-induced hypoxaemia

Exhaled nitric oxide level during and after heavy exercise in athletes with exercise-induced hypoxaemia

Pulmonary NO synthase inhibition and inspired CO2: effects on V ′/Q ′ and pulmonary blood flow distribution

Bicarbonate attenuates arterial desaturation during maximal exercise in humans

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